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Contents
Pediatrics - OK .............................................................................................................................................. 6

Respiratory problems .....................................................................................................................8

Digestive problems....................................................................................................................... 12

Immunisation ............................................................................................................................... 23

Optimal time for surgery in children ............................................................................................. 24

Cardiac problems ......................................................................................................................... 25

Urinary problems ......................................................................................................................... 28

Orthopedics ................................................................................................................................. 29

Developmental problems ............................................................................................................. 33

Milestones - TO DO! .................................................................................................................... 37

Pharmacology, drug side effects, drug intoxications - OK ........................................................................ 38

Intoxications ................................................................................................................................ 38

Substances accumulating in the body............................................................................................ 47

Antibiotics ................................................................................................................................... 48

Drugs and drug side effects........................................................................................................... 54

Anticoagulants ............................................................................................................................. 64

Types of drugs by action (useful_medical.doc) ......................................................................... 66bili

Pharmacology .............................................................................................................................. 72

Obstetrics - OK............................................................................................................................................ 76

Pregnancy parameters.................................................................................................................. 76

Infections in pregnancy ................................................................................................................ 78

Conditions in pregnancy ............................................................................................................... 84

Postpartum pathology ................................................................................................................ 108

Congenital anomalies ................................................................................................................. 111

Antenatal care ........................................................................................................................... 113

Labor ......................................................................................................................................... 114

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Gynecology - OK ....................................................................................................................................... 124

Breast pathology ........................................................................................................................ 124

Contraception and OCP .............................................................................................................. 133

Menopause, HRT and osteoporosis ............................................................................................. 141

Amenorrhoea............................................................................................................................. 145

PCOS .......................................................................................................................................... 147

POF ............................................................................................................................................ 149

Bleeding..................................................................................................................................... 149

Dysmenorrhoea ......................................................................................................................... 153

Vaginal discharge and infections & STI ........................................................................................ 153

Other vulvo-vaginal pathology .................................................................................................... 159

Endometriosis and adenomyosis................................................................................................. 160

Ovarian cysts and CA ................................................................................................................. 162

Endometrial CA .......................................................................................................................... 163

Cervical CA ................................................................................................................................. 164

Uterovaginal (genital) prolapse ................................................................................................... 165

Urinary incontinence in women .................................................................................................. 167

Other gynecological stuff ............................................................................................................ 169

Infertility.................................................................................................................................... 170

Medicine ........................................................................................................ Error! Bookmark not defined.

Orthopedics - OK ........................................................................................................................ 172

Trauma and fractures........................................................................................................................ 172

Bone pathology ................................................................................................................................. 187

Neurology - OK ........................................................................................................................... 188

Nerve roles ............................................................................................. Error! Bookmark not defined.

Nerve non-traumatic pathology ....................................................................................................... 190

Nerve traumatic pathology ............................................................................................................... 193

Motor neurone lesions and back pain .............................................................................................. 197

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Tremor .............................................................................................................................................. 198

Seizures ............................................................................................................................................. 202

Syncope ............................................................................................................................................. 205

TIA ..................................................................................................................................................... 207

Stroke ................................................................................................................................................ 209

Brain haemorrhage ........................................................................................................................... 211

Meningitis ......................................................................................................................................... 212

Headaches/ migraine ........................................................................................................................ 214

Raised ICP .......................................................................................................................................... 216

Brain tumors ..................................................................................................................................... 216

Coma and confusion ......................................................................................................................... 217

Other neurological pathology ................................................................ Error! Bookmark not defined.

Dermatology - OK ....................................................................................................................... 223

Acute/ infectious skin eruptions ....................................................................................................... 224

Strepto pathologyk ........................................................................................................................... 232

Lumps and pigmented lesions .......................................................................................................... 234

Common skin conditions................................................................................................................... 243

Hair disorders .................................................................................................................................... 251

Nail problems .................................................................................................................................... 252

Skin ulcers ......................................................................................................................................... 254

Infectious diseases - OK ............................................................................................................... 256

TB ...................................................................................................................................................... 256

Diarrhoea and traveller’s disease ..................................................................................................... 258

Other infectious diseases .................................................................................................................. 263

Hematology - OK......................................................................................................................... 264

Leukemias ......................................................................................................................................... 264

Other hematol. problems ................................................................................................................. 266

Coagulation problems ....................................................................................................................... 267

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Anemia .............................................................................................................................................. 270

Digestive system - OK .................................................................................................................. 277

Jaundice and other biliary problems................................................................................................. 278

Liver pathology.................................................................................................................................. 285

Pancreatic pathology ........................................................................................................................ 289

Abdominal pain ................................................................................................................................. 291

Dysphagia and oesophageal pathology ............................................................................................ 293

Upper digestive haemorrhage .......................................................................................................... 295

Dyspepsia and stomach pathology ........................................................ Error! Bookmark not defined.

Intestinal pathology .......................................................................................................................... 308

Scrotal swellings and hernias - OK ............................................................................................ 30908

Renal, urinary and male pathology - OK.................................................................................... 31615

Male pathology ................................................................................................................................ 329

Electrolytes, ABG, dehydration, burns - OK ................................................................................. 333

Electrolyte disturbances ........................................................................ Error! Bookmark not defined.

ABG ................................................................................................................................................... 337

Dehydration and burns ..................................................................................................................... 338

Respiratory/ lung pathology - OK ................................................................................................ 343

Pneumonia ........................................................................................................................................ 349

Asthma .............................................................................................................................................. 350

COPD ................................................................................................................................................. 353

PE ...................................................................................................................................................... 354

Pneumothorax .................................................................................................................................. 356

Pleural pathology .............................................................................................................................. 357

Lung CA ............................................................................................................................................. 358

Cardiac pathology - OK ............................................................................................................... 356

Heart failure ...................................................................................................................................... 366

Cardiac arrhythmias .......................................................................................................................... 367

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MI ...................................................................................................................................................... 371

ECG .................................................................................................................................................... 377

Vascular pathology - OK ............................................................................................................. 375

Arterial pathology ............................................................................................................................. 383

Venous pathology ............................................................................................................................. 385

Aortic pathology................................................................................................................................ 386

HTN ............................................................................................................................................... 38986

Dyslipidemia ...................................................................................................................................... 388

Rheumatology - OK .................................................................................................................... 391

Autoimmune diseases ....................................................................................................................... 401

Myopathies ....................................................................................................................................... 413

Endocrinology - OK ..................................................................................................................... 414

Hyperprolactinemia .......................................................................................................................... 415

Adrenal glands pathology ...................................................................... Error! Bookmark not defined.

Thyroid pathology ............................................................................................................................. 418

Hyperparathyroidism ........................................................................................................................ 423

DM..................................................................................................................................................... 423

Oral pathology - OK .................................................................................................................... 426

Head and neck masses - OK ........................................................................................................ 427

ENT - OK..................................................................................................................................... 429

Laryngeal pathology .......................................................................................................................... 429

Ear and hearing problems ................................................................................................................. 430

Dizziness ............................................................................................................................................ 436

Ophthalmology - OK ................................................................................................................... 431

Emmergency medicine - OK ...................................................................................................... 4600

CA metastases - OK .................................................................................................................... 467

Genetic diseases - OK ................................................................................................................. 470

Pain - OK .................................................................................................................................... 471

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Radiology - OK............................................................................................................................ 475

Other stuff - OK .......................................................................................................................... 477

Psychiatry - OK .......................................................................................................................................... 483

Main pathology .......................................................................................................................... 483

Defense mechanisms ........................................................................................................................ 483

Personality disorders ........................................................................................................................ 485

Types of disorders ............................................................................................................................. 487

Schizophrenia .................................................................................................................................... 495

Mood disorders ................................................................................................................................. 502

Dementia and mental retardation .................................................................................................... 514

Behavioral emmergencies................................................................................................................. 517

Child psychiatry .......................................................................................................................... 520

Other conditions ........................................................................................................................ 522

Ethics - OK ................................................................................................................................................. 526

Statistics - OK ............................................................................................................................................ 528

Normal values ....................................................................................................................................... 53126

Pediatrics - OK
- By age
o Neonate < 1 mth
o Infant 1 mth – 1 yr
o Toddler 1-3 yrs
o Child
o Puberty
▪ Boys 12 – 16/18
▪ Girls 10 – 15/17
- Neonatal Conjunctivitis:
oImmediately after birth, purulent, sticky
oMarked conjunctival edema = Gonococcal
oIf at 2nd to 3rd wk = Chlamydia
- Umbillical granuloma – Red fleshy tissue at base of umbilicus + discharge
o Topical Silver Nitrate (Caustic pen) ------ for 5 days (MCQ)
o If yellowish (urine) discharge - USG and Surgery (Urachus fistula)
- Umbilical discharge
o types
▪ Mucous
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▪ Pus
▪ Urine
• before delivery – communication = Urachus; if it remains after delivery =
patent urachus
- Dx
▪ Creatinine and urea levels from discharge -> confirm it’s
a urinary discharge
▪ USG – to rule out patent urachus
- Mx – Refer for surgical correction
▪ Feces
▪ Black----Meconium?
o Dx diff
▪ CA
▪ Fistula
▪ Urachal cyst
▪ Umbilical calculus
o Mx
▪ Clean debris
▪ Apply dressing (wound)
▪ Swab for culture and sensitivity
▪ A/B
- Night terrors and sleep walking have many features in common – Murtagh 789
o Sleep walking: – child not awake
▪ sits up in bed, walks around, don’t acknowledge parents even though eyes
might be open
▪ lasts 10-30 min
▪ 1-8 yrs, (child is neurologically & developmentally normal)
▪ Can’t remember episode next morning
▪ usually within 2 hrs after falling asleep
▪ harmless, benign
▪ inherited – family Hx
▪ 2% of children
▪ usually grow out of it by 12 yrs
▪ Rx
• Reassure and educate parents, protect the child (unaware), self limiting
• wake up the child 15 mins before the usual time of attacks for a few dys
• don’t try to calm the child during attack--> it will aggravate the situation
• no indication for sleeping pills, anti-epileptics or sleep EEG.
• no relation with TV viewing or day’s activity
o Night terror:
▪ Sharp screams, violent thrashing movements, sweating, tachycardia
▪ 3N for night terror and sleep walking. No N for nightmate
Night (sleep) terror Sleep walking Nightmare
2-4 yrs 6-9 yrs 3-6 yrs
First 1/3 of sleep (within 2 hrs of First 1/3 of sleep Last 1/3 of sleep
falling asleep)
Non-REM stage Non-REM stage REM stage
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Unarousable Unarousable Easily aroused

Will NOT remember dream Will NOT remember dream Remembers dream
- Breath holding spells:
o usually when trying to get something from their parents (getting his own way): Cry
vigorously -> hold breath -> turn pale -> then blue -> sometimes (rarely) unconscious,
fits or seizures.
o 6 mths – 6 yrs; MC 2-3 yrs
o can last 10-60 sec --> then they will breath again
o Rx
▪ reassurance
▪ educate parents – not harmful, will go away, don’t panic or take any action
during spell (just ignore the baby – be firm!)
- Hypospadiasis: = Urethral opening on ventral aspect of penis
o you can’t do circumcision – they might use that skin later for repair
o look for associated abnormalities:
▪ if no urinary stream – refer immediately
▪ if urinary stream present – reassess by 6 mths + surgery by 12 mths
- Aspirin in children (otherwise always Paracetamol, as aspirin causes Reye’s syndrome)
o Kawasaki
o Rheumatic fever
o Juvenile RA
- Tests for baby at birth: Hypothyroidism, cystic fibrosis, phenylketonuria, homocysteinuria
- Septicemia - child unable to take feed, sleepy most of time, high fever 400C, chest retraction,
tracheal tug, increased respiration.
- Platelets < 40,000 = risk of intracranial bleeding for infant
- Sudden infant death syndrome:
o Unknown cause
o Potential causes/ risk factors:
▪ Smoking of parents (passive smoking)
▪ Parental narcotic/ cocaine abuse
▪ Prone position during sleep
▪ Artificial feeding
▪ Hyperthermia
▪ Extreme prematurity
▪ URTI
- Cow’s milk lacks:
o Iron
o Vitamin C
Respiratory problems
- Stridor:
o Croup (acute laryngotracheobronchitis)
o Epiglotitis
o Inhaled foreign body
o Laryngomalacia
- Foreign body:
o in oesophagus
▪ wait max. 6 hrs – beyond that -> risk of perforation (especially ē Lith batteries)
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▪ could be passed in stool in 3 days

▪ Dx – X Ray
▪ Rx – esophagoscopy to remove object
o in resp. tract
▪ always suspect when symptoms on only 1 side
▪ 1-3 yrs of age
▪ Sx
• Coughing/ choking episodes while eating solid food/ sucking small object
• Sudden onset of first wheezing with no history of allergy
• Persistent coughing and wheezing
• Inspiratory stridor
• All symptoms may disappear if the object passes into lower airways.
- Later wheeze, infection or obstructive emphysema supervene
causing localized rhonchi, crepitations and breathlessness.
• decreaed or absent breath sound over whole or part of a lung
▪ Dx
• inspiratory and expiratory chest X Ray
- Organic foreign bodies such as peanuts will not show,
compensatory hyperinflation, collapse and consolidation will
gradually appear
▪ Rx
• examine nose, etc. under GA
• Complete airway obstruction: Hold head down, deliver 5 blows to back
and 5 chest thrusts. Attempt removal of object or proceed to
cricothyroid puncture.
- epiglotitis vs. croup vs. bronchiolitis – Jay, Alena – p. 47
o Epiglottitis:
▪ Sore thumb/ fingerprint sign on lateral neck X Ray film

▪
▪ Rx:
•O2 by mask
•May intubate or ventilate
•Cricothyrotomy or tracheostomy
•Antibiotics:
- Ceftriaxone
o Croup: (acute laryngo-tracheo-bronchitis)(complications-tracheitis)
▪ Steeple sign on anterior neck X Ray film
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▪
▪ Most ominous sign of deterioration = Retraction of intercostal spaces and
suprasternal fossi and use of accessory muscles. Rx:
• Nebulized Adrenaline
• Corticosteroid Oral/ IM/ IV
• May do intubation
Croup Epiglottitis Bronchiolitis
(Laryngotracheobronchitis)
Cause Viral – Parainfluenza virus (+ Bacterial – H. influenzae type B RsV
adenov., influenza)
Age 6 mths – (3-) 6 years, 6 mths – 6 yrs 2 wks - 9 mths, < 1 yr
sometimes older may also occur in adults
Onset Slow (usually 2 days) – Rapid (hrs) Slow (usually 2 days) –
prodrome of URTI prodrome of URTI
Fever Low grade High (> 40) yes
Dysphagia None Severe None
Drooling None Present None
Stridor Harsh inspiratory stridor Soft expiratory stridor
Cough Barking, brassy, spontaneous Absent Yes
Voice Hoarse Soft, clear to muffled
Wheeze Bilat. Inspiratpry crackles and
or expiratory wheeze
Posture Recumbent/ lying back Sitting forward, quietly & still,
while his eyes follow you
around the room (limited head
movt. to protect obstructive
airway), sits with neck
hyperextended and chin
protruding (“sniffing dog”
position) & lean forward in a
“tripod” position to maximize
air entry
Toxemia Mild Severe
Other Indication of emergency Cherry-Red epiglottis Resp. distress (tachypnea,
intervention: Child is restless It’s a true emergency and can lead intercostal recession, nasal
& irritable to life-threatening airway flaring) widespread fine
obstruction so time should not inspir. crackles (not in
be wasted on ordering an X asthma) hyperinflated chest –
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Ray or examining the throat barrel shaped, subcostal

recession
Rx Corticosteroids Oral/ IM/ IV Remember ABCs: Secure Symptomatic: O2
In mild to moderate cases airway first with endotracheal Corticosteroids are CI!!!
Nebulize Adrenaline in sevre intubation or tracheostomy Indic. for admission:
cases (showing cyanosis and and then give IV antibiotics - Resp. rate > 60
irritability) (ceftriaxone or cefuroxime, - Age < 3 mths
cefotaxime). Can be prevented - Feeding problems
by H. Influenza Vaccination Severe cases – antiviral:
Ribavirin
- Bronchiolitis:
o Vs. Penumonia
▪ Bronchiolitis – with prodrome of 2 days (URTI)
• < 1 year
▪ Pneumonia – abrupt debut with fever, etc.
o Risk factors – parents smoking
o Sx
▪ prodrome of 2 days (URTI) like rhinorrhea
▪ then 3-5 days of severe sympt.
• wheezy breathing, tachypnoea, hyperinflated chest: barrel-shaped,
subcostal recession
▪ widespread fine inspiratory crackles (not in asthma)
▪ frequent expiratory crackles and wheezing
▪ indic. for admission
• resp. rate > 60 (normal < 50/min at 6 months)
• age < 3 mths
• feeding problems and O2 saturation < 94%
• social problems – if parents can’t give adequate care (neglect)
X Ray: Bilateral hyperinflation of lung due to air trapping, apperance of
perihilar infiltrates and multiple areas of atelactatsis
Virus identified by PCR on nasopharyngeal aspirate. Rapid RSV viral test
available. Blood glucose should be assessed in all sick patients.
o Rx
▪ O2
▪ IV fluids
▪ C/S are CI!!
o resolution in 1-2 wks
- Apnoea after birth
o At term
▪ Cause – Resp. suppression by narcotics use during analgesia in mother (e.g.
Pethidine)
▪ Rx – Naloxone
o In preterm – Apnoea of prematurity
▪ Theophylline
▪ Caffeine
- Respiratory Distress in newborn: – 2-3 Qs in exam
o RR > 60
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o 3 causes:
Infantile respiratory distress Transient tachypnoea of Meconium aspiration
syndrome (Hyaline membrane newborn (Wet lungs – can’t syndrome (with meconium
disease) eliminate/squeeze fluids from all over his body)
lungs because delivered by C/S)
Premature, usually < 30 wks wt Term baby, C section Post term baby (Jay – in
<2.5kg (can be in term babies too) prolonged labor)
Not improving with O2 < 30% O2 (< 40% other sources) Sympt. from birth
Longer course, worst prognosis Quick recovery within 72 hrs Usually they improve
X-Ray – ground-glass haze, Coarse streaking/ fluid in lung Hyperinflation, bilateral
fine granularity with hypoareated fissures consolidation because of
lung fields, slightly elevated both inspiration of meconium
hemidiaphragms
Rx:
- Betametasone to mothers up to
34 wks (↑secr. of surfactant)
- Surfactant (Survanta) on ETT for
baby
Digestive problems
- Baby vomits after first and each feeding
o Tracheoesophageal fistula - becomes cyanotic
o Esophageal atresia – does NOT become cyanotic
o Dx
▪ chest X Ray
- Tracheoesophageal fistulae (TEF):
o 1 in 3,000 births
o Associated with polyhydramnios (16%), cardiac abnormalities, vestibular abnormalities,
imperforate anus, and genital-urinary abnormalities
o Various types:
▪ Distal TEF with upper esophageal atresia (85%)
▪ Blind upper & lower oesophageal pouches without a connection to the trachea
(9%)
▪ True H-type fistula (6%)
▪ Proximal esophagus empties to trachea (1%)
o Dx
▪ Passage of a NG tube that meets obstruction 9-13 cm from nares suggests
diagnosis
▪ Chest X Ray with catheter in place demonstrates position of pouch as well as
air in stomach and intestine.
o A standard Ba swallow is not recommended because of possibility of spillage into
pulmonary tree.
- If baby vomits, check serum K:
o Low K – Pyloric Stenosis
o High K
▪ Congenital adrenal hyperplasia (salt losing) presents soon after birth
• Baby vomits, marked decr. Na and Cl, K incr.
▪ Salt losing congenital syndrome?
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▪
- Vomiting in children
o By color
▪ Green (bile stained):
• 1- Duodenal atresia – newborn
- assoc. with Down syndrome
• Small bowel obstruction
• Volvulus – Vomiting and abdominal distension
- Bilious/ green vomiting
- Several small, seedy and yellowish stools (from intestine distal
to point of volvulus)
- Olive shaped mass palpable in epigastrum
- Non-projectile bile-stained vomiting
• Sepsis
• Infection: UTI, Otitis media
▪ Milk stained (Non-bilious), Coffee ground
• 1 - Pyloric Stenosis ----- Projectile
• GERD
• Infection: UTI, Otitis media
o types
▪ 1. 1st day baby vomiting bilious content + baby did not pass meconium
• duodenal or jejunal atresia
- X Ray: Double-bubble sign
• small bowel obstruction or malrotation
• Hirschprung dis.
• imperforated anus
• meconium plug & ileus
• cystic fibrosis
▪ 2. 2-3 wks with projectile vomiting immediately after meal
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• Baby lethargic, hungry, dehydrated, visible peristaltic movement

crossing from left to right during feeding, changes with posture and
respiration
• usually with Olive shaped mass or no mass on exam.
• = Pyloric Stenosis
- Complic: Metabolic alkalosis: (Na+, K+ & Cl- all ↓) HCO3- ↑
▪ Vomiting: Loss of water and HCl
▪ Resulting condition: Hypovolemia with hypokalemic
hypochloremic metabolic alkalosis.
• Na+ <130 (135-145)
• HCO3- >32 (22-28)
• Ph >7.45
• Cl- <100
• K+ normal or low (3.5-5.5)
- 2-6 wks of age
- risk factors:
▪ male
▪ first born baby
▪ Caucasian
▪ family Hx
- Baby appears hungry, dehydrated failure to thrive
- Gastric peristalsis clearly visible in abdominal wall
- Vomiting coffee grounds (not-bile stained)
- Pyloric tumour
- Dx
▪ 1 test – Feeding test
• Feel tumour (wave left -> right abdomen or
immediately after vomiting).
▪ 2nd & best test – USG, as good as surgical exploration
▪ Ba meal is not preferred -> risk of aspiration
- Rx
▪ IV fluid replacement: 0.45% (1/2) NS + 5% Dextrose (DA)
▪ Potassium: Once baby is passing urine
• 20 mmol/l KCl- if mild
• 30 mmol/l KCl- if moderate or severe.
▪ Surgery: Refer to pediatric surg. (Ramstedt pylorotomy)
▪ 3. Morning effortless vomiting + headache
• causes:
- 1.Posterior fossa tumor
▪ Medulloblastoma: 5-7 yrs
• MC tumor in childhood
• round cerebellar tumor (from vermix) – midline
• Sx
o Ataxia, poor balance (frequent falls),
dysmetria, etc.
o Triad Murtagh: dizziness + morning
headache + vomiting
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o raised intracranial pressure (ICP):

nausea, vomiting, headache, change in
behaviour or mental status of child
o signs (Awad):
▪ 1 - disturbed level of
consciousness
▪ 2 - Ipsilateral pupillary dilatat.
▪ 3 - Papilledema
▪ most reliable sign of ICP =
disturbed consciousness level
▪ late signs: Bradycardia, HTN,
Papiledema
▪ Rx: … + hyperventil. (↓CO2 =>
decr. blood sent to the brain)
to prevent brain herniation.
- 2. Infratentorial tumor
• Sx
- headache, vomiting, strabismus, meningismus, blurring of vision,
hydro or macrocephaly, dizziness
▪ 4. Projectile vomiting + headache + rash (with photo)
• Meningococcemia (meningitis)
- Kernig & Brudzinski signs +
- Rx
▪ next step = A/B = Benzyl Penicillin
▪ even better or if allergic = IV Ceftriaxone
▪ 5. Vomiting after each feeding but child is thriving & happy = GERD
• Irritability & crying: Sole manifestation
• Vomitus: Just ingested milk
- Vomitus may be projectile BUT NOT persistent
- The Majority of babies continue to thrive & gain weight
- can be:
▪ Mild – no complications
▪ Severe - w/ complications
• Peptic esophagitis
• Barrett’s oesophagus
• Peptic strictures
• Adenocarcinoma of esophagus
• Failure to thrive: uncommon
• Pulmonary complications: Persistent cough,
wheeze that may result from aspiration
(aspiration pneumonia).
- Mx
▪ Healthy infant whose main symptoms are vomiting and
regurgitation (Mild form):
• Reassurance.
• Upright position after feeding + get rid of air+
decrease spacing between meals, small
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frequent meals+ gaviscam (milk thickener)+

antacid can be added + sleep with head of bed
elevated
▪ If symptoms persist - Severe, with complications
• Barium esophagogram: To exclude anatomical
abnormality such as stricture, gastric outlet
obstruction and malrotation.
• if Acid-reflux-related symptoms suggestive of
esophagitis:
o Endoscopy and biopsies (most
appropriate)
▪ if atypical sympt:
• Aspiration needs to be considered.
• Ba esophagogram.
• CXR
• Ambulatory 24-hour pH monitoring: May detect
presence of GERD but doesn’t prove association
- Rx
▪Medications:
• Mylanta – Stomach protector
• H2 Recep. antagonists– not popular in Aus.,
cause sedation
• Proton pump inhibitors
▪ Surgery: Complications or medical treatment failed.
▪ 6. Vomiting, diarrhoea & fever
• Gastroenteritis:
- cause
▪ Rotavirus: 40-50%, common in Winter
▪ Adenovirus: 7-17%
▪ Bacterial: 5-10%: Salmonella, Campylobacter Jejuni,
Yersinia enterocolitica and E. Coli.
• Salmonella enteritis:
o Back to school/ work after 3 succesive -
ve wkly stool analysis
o MC form = enteric fever
o Usual source = meat, poultry
o Salmonella choleraesus – causes
gastroenteritis
o ampicilin is used to terminate carrier
state
o Blood cultures are usually not positve in
Salmonella gastroenteritis
o Rx – A/B
- Risk – dehydration
▪ Sx - Oral or IV rehydration (if child can’t drink)
▪ 8. Child vomiting + bringing leg to his abdomen (drawing leg up) & looks pale.
The pain is episodic
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• On examination – Sausage shaped mass

• Later sign – Per Rectal - red currant jelly stool = Intussuception
• Mx
- Dx and Rx = air enema--> repeat at leat 3 times if fail --> Surgery
▪ 9. Vomiting + fever + urgency of urination = UTI
▪ 10. Projectile vomiting + lower abdominal pain
• incarcarcerated hernia
• torsion of testis
- Steatorhea:
o Causes:
▪ Celiac disease
▪ Cystic fibrosis
▪ Giardiasis
▪ Malabsorption
▪ Pancreatic enzymes problems
o Dx
▪ Small bowel biopsy
- Failure to thrive
o Definition
▪ < 3rd percentile or drop of > 2 percentile
o causes
▪ Organic:
• Celiac disease
• Cystic fibrosis
▪ Non-organic: more frequent!
• Psychosocial: negligence, child abuse etc.
- Chronic diarrhoea in kids – D/Dx.
o Cystic fibrosis:
▪ AR (1 gene involved = carrier, 2 genes involved = disease)
▪ 12 common mutations
• MC = delta F508 on CFTR gene, on chromosome 7
▪ Defect in an ion channel protein – affects normal transport of Cl- => ↓ Na+ and
water transfer => ↑ Viscosity in secretion (lung, pancreas & gut)
▪ S/Sx
• Triad: FTT + chronic cough + loose bowel actions
• GI and respiratory symptoms
- GIT:
▪ Meconium ileus
▪ Bulky, steatorhic stools
▪ Rectal prolapse: MCQ
- Respiratory:
▪ URTIs, cough
▪ Recurrent pneumonias
▪ Bronchiectasis
▪ Sinusitis, polyps
▪ Clubbing of fingers
• Infertility in males bc of bilateral congenital absence of Vas Deferens
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▪ Dx
• On 1st/2nd day – Newborn screening --> looking for
1. Immunoreactive Trypsin (IRT ) – if > 99 percentile = positive => send
for 2. DNA analysis: Check to see if 1 or 2 allels are affected -->
• If both + = Diseased => refer to Cystic Fibrosis Clinic
• If only 1 + = Carrier--> 3. Sweat Cl- Test: 75 g Sweat (> 60 mEq/L =
positive) => Refer to Cystic Fibrosis Clinic.
- 40-60 – Suggestive of healthy carrier
▪ Rx
• Drainage of airway secretions
• Hypertonic saline solution by nebulizer
• A/B for infection
• Oral pancreatic enzymes
• Lung and liver transplant
▪ Survival in developed countries = 31 yrs (in poor countries – 10 yrs)
o Celiac disease: (Fe deficiency is MC than other metabolits)
▪ triad: fatigue + wt. loss + diarrhoea +hyperactive bowel sounds
• loose stools
• wt. loss (failure to thrive)
• fatigue, due to iron/ folate deficiency (due to malabs.) anemia
- Microcytic – iron deficiency
- Normocytic
- Macrocytic – folate deficiency
- ↑INR due to Vit K malabsorption
- Osteoprosis due to Vit D and calcium malabsorption
▪ Irish nurse
▪ Sx
• usually start after gastroenteritis – acid, watery diarrhoea, smells like
vinegar
• cough
• buttock wasting
• bulky stool
• failure to thrive
▪ Dx
• I test - fecal fat estimation (Steathorea)
- ↑fecal fat
- fat crystals in stool
• IgA
- Anti-gliadin AB – Screening only
- Anti-endomysial – 90% sens./specif. (Maria)
- Anti-transglutaminase – 90% sens./specif. (Maria)
• II test - Small bowel biopsy (best)
▪ Cx
• Increased risk of proximal jejunal lymphoma
▪ Rx
• Remove gluten from diet
19

o Toddler’s diarrhea: Hx of loose stools containing undigested food (peas & other
vegetables)
▪ otherwise child is healthy and gaining weight
▪ resolves spontaneously
- Abdominal pain in children
o 3 mths – 1 year (< 2 yrs)
▪ INTUSSUSCEPTION = Distal ileum telescopes into a distal bowel loop.
• usually in the ileocolic region
• also at other ages
• causes
- Metastatic deposit – MC from melanoma
- Enlarged Pyer’s patches – in children
- Crohn’s
- Meckel’s diverticulum
- lymphoma of small bowel
- benign sumbucous fibrolipoma
- Internal hernia
• Sx
- Intestinal obstruction
- Sudden screaming intermittent attacks of pain with vomiting,
drawing legs up
- Sausage mass in the RIF
- Child looks pale, lethargic, anxious and unwell.
- Bleeding (Red Currant Jelly Stool): Late sign.
• Associations:
- Recent viral gastroenteritis (Adenovirus)
- Infantile Spasm.
- H-S Purpura (Arthralgia, skin rash, nephritis)
• Dx:
- Plain X Ray: Normal or bowel obstruction = I step
- Ultrasound: Target sign
- Barium Enema: Claw sign
- Air or Barium enema – best - Hydrostatic reduction under USG
• Rx
- Air or Barium enema
▪ if it fails, repeat for at least 3 times
▪ risk of recurrence
• monitor for 24 hrs in the hospital
- Surgery: If enema failed, peritonitis or septicaemia
o Usually over 5 yrs
▪ Appendicitis
• Any age, rare under 5 years.
• Sx
- Anorexia, vomiting.
- Localized abdominal pain: Epigastrium, periumbilical region, RIF.
- Tenderness and guarding in RIF
20

- Palpation of left side of the abdomen causes pain in right side of

abdomen
- Typical march of symptoms (J.B Murphy):
▪ Prodromal mild bowel upset
▪ Development of abdominal pain, which progressively
worsens.
▪ Anorexia, nausea, vomiting.
▪ Moderate fever not high
▪ Signs of focal peritonitis over inflamed appendix.
• Rectal examination – not done in children!
• Dx
- Physical examination: Abdominal auscultation, palpation,
percussion.
- First test: FBC and Urinalysis: Leukocytosis to rule out UTI
- Pregnancy test: Female adolescents
▪ if female patient – next test: USG: Female adolescents
(doubt and no peritonitis).
- CT:
▪ Imaging of choice
▪ Neurologically impaired
▪ Immunologically suppressed, or
▪ Obese (doubt and no peritonitis)
- Lactose intolerance: –Murtagh 477
o Normal histology of intestinal mucosa
o Common in Asians
o Normal galactose absorbtion
o Don’t cause steatorhea
o Types:
▪ 1. Genetic – enzyme defficiency/ absence
• Sx
- often asymptomatic or
- 30 minute - 2 hrs after milk consumption
▪ Colicky abdominal pain
▪ Bloating
▪ Diarrhoea
• Dx
- Hydrogen test (Breath test) – if lactose not broken in small
intestine, it will be broken down by bacteria in large intestine
which will also produce gas
- Overload test (Blood glucose test)
▪ give lactose (50g) then check glucose levels
• normal – glucose ↑ > 1mmol/L
• sick – glucose same or ↑< 1mmol/L
- check reducing substances in stool – Clinitest tablets
▪ 2. In children, after acute gastroenteritis:
• watery, frothy, smell like vinegar stools (acidic) => can cause
excoriations of buttocks
21

• but happy baby, thriving

• vomiting subsides but diarrhoea continues
• Dx
- Detection of reducing substances in stool (stool acidity test)
• Rx
- Continue breastfeeding
- If bottle feed – switch to lactose-free formula for 1 month (vilous
glands will recover)
- Galactosemia:
o AR, incidence 1 in 40,000
o Glycogen Storage Disease (Can’t metabolize galactose)
o Sx
▪ Jaundice in first 2-6 wks, vomiting, family Hx of jaundice, family Hx of cataract
▪ toxic levels of galactose in blood,resulting in
• hepatomegaly, jaundice, cirrhosis
• renal failure
• cataracts
• brain damage
• Ovarian failure
▪ lethragy, vomiting, diarrhea
▪ failure to thrive
o Dx
▪ during newborn screening – blood (from heel of infant) or urine test
• Beutler fluorescent spot test
▪ reducing substances (galactose) in urine
o Rx
▪ eliminate lactose & galactose from diet
Important Points:
- Neonatal jaundice in first 24hrs is ABO incompatibility.
- After first 7 days meningitis in neonates is caused by E.Coli. CSF analysis (↓Glucose,
↑WBC and Proteins) suggests bacterial meningitis.
- Neonatal Hypothyroidism: Supra-orbital edema, dry skin, coarse body features, harsh
cry, jaundice, slow feeding, umbilical hernia. Complications: Poor school performance
and permanent intellectual disability. Rx. Thyroid replacement immediately within 2wks
after birth.
- Shock management in children initial bolus of 20ml/ Kg of crystalloids followed by same
20ml/ kg of crystalloids if still shows signs of shock.
- Rubella: Microcephalic and gorwth retarded, hepatosplenomegaly, purpura (from
thrombocytopenia) cataract deafness and cardiac abnormalities.
- Mouth ulcers + hand and feet maculopaular rash + fever + irritability = Enterovirus =
Hand foot mouth disease
- Mouth Ulcers: + fever + irritability = Herpes Simplex Virus.
- Meningococal disease: Fever petechial rash and drowsiness. It’s an emergency.
Rx. 1st choice Ceftriaxone or Benzylpenicillin as 2nd choice.
- UTI in children: Rx 1st line trimethoprim orally, if severe and non responding IV
Gentamycin. Vancomycin has no role in UTI in children.
22

- Meningococcemia: Caused by Nessseria Meningitidis, presents with a child who is

lethargic, drowsy with fever and petechial rash. Its an emergency and is not prevented
by current immunisation programme. Blood cultute is investigation of choice. LP is
contraindicated bc of risk of cerebellar tonsil herniation leading to respiratory arrest.
- Nephrotic syndrome: Acute onset of generalized edema periorbital puffiness. Cause is
minimal change disease. Urine shows heavy proteinuria no glucose or hematura. Rx is
steroids. If there is proteinuria + hemturia + HTN renal biopsy is investigation of choice MCQ
- Acute (Group A Streptococcal) Glomerulonephritis: 1-3 wks history of streptococccal
throat or skin infection followed by less proteinurina, less marked edema, oliguria, child
is HTN and there is marked hematuria.
- Ig A Nephropathy: 1-2 day after throat infection. Less transient Hematuria, HTN and
URTI. No proteinuria or edema. Hematuria disappears after URTI.
- Bronchiolitis: Common in infants under 12 months caused by resp syncytal virus
associated with low grade fever, tachypnea, tracheal tug intercostal recession and nasal
flaring. X Ray Chest: Shows hyperinflation of lungs due to air trapping and perihilar
infiltrates. It’s self limiting and resolves in 1 to 2 wks. Rx: O2 and IV fluids
- Petrol Ingestion: MC complication is aspiration pneumonia.
- Acanthosis Nigricans: Seen in obese girls, often asscociated with PCOD, who have dark
rash around her neck and axilla. Blood sugar levels are raised due to increased insulin
resistance and fasting blood sugar levels lead to diagnosis. Serum insulin level is ↑
- Febrile seizures: 3% of children between 6m to 5yrs show febrile seizures. Among these
risk of developing afebrile seizures or epilepsy is only 3%.
- Absence seizures: seen at school going age = 5yrs, 3Hz spike on EEG.
- Infantile (salaam) Spasm, seen during first yr of life. Cluster of seizure activity + loss of
developed skills. Dx EEG showing classical picture of hypsarrythmia (Chaotic rhytm). Rx:
very resistant treatment most appropriate Rx is Vigabatrin + Steroids.
- Hered. Spherocytosis: Eosin-5-maleimide staining test is done to see osmotic fragility
- Thalassemia: Hb electrophoresis is done
- Fe deficiency anemia: Serum ferritin is ↑
- Duodenal atresia: Associated with Down syndrome, infant presents within 24hrs (high
gut obstruction) with s/s of gut obstruction with bile stained vomiting.
- Volvulus: Presents within 24hrs but no associated with Down syndrome.
- Meconium plug syndrome: 2-3 days later with generalized gaseous distenion.
- Hirschprung disease: 4-5 days after birth progressive distension, vomitinmg and delayed
passage of meconium.
- Necrotising enterocolitis: seen in sick premature infants.
Neonatal conjunctivitis
- Neisseria gonorrhoeae conjunctivitis, within 1–2 days of delivery, requires vigorous
treatment with intravenous cephalosporins or penicillin and local sulfacetamide drops.
- Chlamydia trachomatis usually 1–2 weeks after delivery, with moderate mucopurulent
discharge. It is a systemic disease and may be associated with pneumonia. The diagnosis
is confirmed by PCR tests on the conjunctival secretions. Treatment is with oral
erythromycin for 21 days and local sulfacetamide eye drops.
- Encopresis:
o 4-5 yrs, previously toilet trained.
o previously had constipation and anal fissure, so he avoids going to toilet (e.g. at school)
due to fear => fecal impaction and soiling of underwear
23

o Rx
▪ Day 1 – enema to empty bowel
▪ Day 2 – laxatives PR
▪ Day 3 – oral laxatives
▪ then go back to toilet – put child to toilet after breakfast, before going to school
• address constipation: more fiber, more fluids
- Necrotising enterocolitis:--- in premature newborns
o caused by ischemia of the bowel + inf. (Pseudomonas aeruginosa)
o Risk factors
▪ Septicemia
▪ Low apgar scores
▪ Respiratory distress
o Dx
▪ X Ray
• Pneumatosis intestinalis – air cysts in the intestinal wall
• finding of air in the portal vein = severe illness
o Rx
▪ Supportive
▪ if perforation - remove necrotic intestine
- young child 6 wks – no stool up to 7 days - still OK
- Hirschprung disease = Aganglionosis = congenital megacolon
o Narrowed aganglionic portion + proximal distension
o There is just a delay in passing of meconium (usually on 4th day) and bilious vomiting on
7th day.
o MC in male
o Constipation + distension
o Dx
▪ PR
▪ X ray, Barium enema (distended enema)
▪ full thickness biopsy
o Rx
▪ Resection of affected portion of colon
▪ Preliminary colostomy
Immunisation
- Immunisation schedule – additional notes from Neha + Murtagh – p. 79
o Premature baby < 32 wks – additional HBV vaccine at 1 yr
o > 6 mths – can give Influenza vaccine
▪ free for:
• > 65 age
• indigenous population > 50 yrs (+ free pneumococcal vaccine)
• indigenous population 15-49 yrs who have a high risk of complication
and death.
o Pneumococcal vaccine - Indigenous population at 2, 4, 6 mths, 18-24 mths
▪ in chronic heart failure, chronic renal failure, postsplenectomy
▪ not in chronic HT
o Post-splenectomy
▪ H. influenza B – Hib once (if not immunized)
24

▪ Pneumococcal vacc. 2-3 wks pre-op., repeat after 5yrs

▪ Meningococcal vacc. every 5yrs
▪ e.g.
• after 2 yrs, URTI – A/B
▪ Cx
• Short term:
- ↑ Platelets
• Long term
- severe infections
▪ pneumonia – Rx: Amoxycilin
o Hep. A – indigenous population
▪ 1st dose – 12-24 mths
▪ 2nd dose – 18-24 mths (6 mths later)
▪
o Don’t postpone any immunization for minor illnesses such as mild URTI and mild fever
- CI for vaccination
o absolute CI for vaccination
▪ encephalopathy after DTP
▪ anaphylaxis after vaccine
o relative CI for vaccination
▪ fever --> 38.5oC --> defer
- CI of all vaccines
o > 38.5oC
o Anaphylaxis
o live (attenuated) vaccines – not in immunosupressed and pregnant patients
- CI for Vaccines – Neha (notes)
o Anaphylaxis
o Encephalopathy within 7 days of immunization
o live vaccines CI in immunsupressed
▪ C.I for MMR, Varicella, Oral Polio – if pt. is immunosupressed (e.g. ALL) or on
high Corticosteroids or on chemotherapy
• after systemic Corticosteroids Rx, delay live vaccines for at least 3 mths
• Polio vaccine
- live
- inactivated
o in children doing chemotherapy – booster doses 6 mths after Rx
o ± for all vaccines – fever > 38.50C: wait for fever to go down?
Optimal time for surgery in children
- Murtagh 897
o Squint - 1-2 yrs, absolutely before 7 yrs (otherwise lazy eye will become blind if not
functioning by 7 yrs)
o ear deformity – after 6 yrs
o cleft lip before 3 months
o cleft palate 6-12 months
o Inguinal hernia: 6-2 rule
▪ Dx at birth – 6 wks --> surgery within 2 days
▪ Dx at 6 wks – 6 mths --> surgery within 2 wks
25

▪ Dx at 6 mths – 6 yrs --> surgery within 2 mths

o
Umbilical hernia – do nothing till 4 yrs, then assess:
▪ if strangulated --> surgery
▪ otherwise --> do nothing
o Femoral hernia – immediately
o Torsion of testis – within 4 hrs (absolutely within 6 hrs)
o Undescended testis – best at 6-12 mths
o Hydrocele – leave until 12 mths, then review (90% will resolve by 18 mths)
o Hypospadias – surgery by 12 mths
o Bow legs (Genu varum) – do nothing till 3-4 yrs; refer if intercondylar space > 6 cm
o Knocked nee (Genu valgum) – do nothing till 8 yrs; refer if inter medial malleloar space >
8 cm
o Out toeing – Charlie Chaplin posture – external rotation (internal retraction restricted)
▪ no Rx
o Flat feet (Pes planus) – reassure; if painful –insole special boots
o High archfoot (Pes cavus) --> refer to neurologist
▪ usually normal
▪ can be secondary to neurological conditions (Polio, Spinocerebellar ataxia)
Cardiac problems (MCQ 2143 P 93)
- Cyanosis
o central
▪ heart
▪ lung
o peripheral
- Heart malformations/Anomalies:
o The major presenting features are:
▪ Murmur
▪ Signs of CHF
▪ Central Cyanosis

-
o Cyanotic (Blue babies) - Shunt Right --> Left 5Ts (TOF, TGA, Tricuspid Atresia, Tingle
Ventricle, Truncus areteriosus)
TGA Hypoplastic left heart TOF
DiGeorge syndrome syndrome (HLHS) MC cyanotic heart disease of
(CATCH 22) childhood (DiGeorge
syndrome) presents e nail
clubbing
26

Description Aorta and pulmonary Severe cardiac VSD

arteries arise from failure. Survival RVH
incorrect ventricles depends on patency Pulmonary stenosis
of PDA Overriding of aorta
(MC cause of nail clubbing)
Cyanosis 1st day (first few hrs 4th to 5th day (after > 3 mths, more obvious
detected after birth) (TGA is MC PDA closes) when crying/ on exertion
cyanotic heart disease of Cyanotic spells (Tet spells)
newborns)
Murmur No murmur No murmur (the only Systolic ejection murmur
one!) (Pulmonary Stenosis)
Dx X Ray: Egg on side ECHO X Ray: Boot shaped
appearance of heart ECHO
ECHO
Rx IV PGE1 to keep DA Prostaglandin to IV PGE1→ Surgery
open → Surgey keep DA open Squatting position
o Acyanotic (Pink babies):– Shunt Left --> Right (3D’s)
o ASDs and VSDs rarely present at birth. ASDs, VSDs, and PDAs are acyanotic conditions
unless Eisenmenger’s syndrome has developed (right-to-left shunt, cyanotic).
o
ASD VSD PDA (can become
5-7% MC congnt. heart disease (25%) cyanotic)
Description Not associated with 2 Types: Prematurity
pulmonary HTN 1. Membranous MC infection
Types: 2. Muscular Rubella
1. Septum secundum 50% close spontaneously
2. Septum primum (muscular)
1. Usually Small: Incidental finding.
asymptomatic. MC Medium: Breathlessness failure
2. associated with pul to thrive, recurrent chest infect.
HTN and heart failure MC cause of central cyanosis.
Murmur 2nd intercostal space 5th intercostal space Continous,
(upper left sternal Lower left sternum edge -> machinery
edge)-> ejection systolic loud holoystolic/ pansystolic murmur
murmur (↑blood flow murmur.
thru pulmonary valve) can have thrill +3
Aortic & pulmonary radiating into axilla and back
components of 2nd
heart sound are widely
separated (fixed, widely
split S2)
Dx ECHO ECHO ECHO
Natural Septum primum - Assoc Depends on size:
history with Down syndrome Small to moderate – closes
No need of prophylaxis Large – might not close
for O. secundum, but Can have a tinge of cyanosis if
needed for O. primum with heart failure
(Eisenmenger’s syndrome)
27

Rx Surgery – never closes Surgery Indomethacin –

on its own to close PDA
Surgery if Indo
fails
o q
▪ VSD – SaO2
• AD 60%
• VD 80% incr.
• AS 95%
• VS 95%
▪ ASD
• AD 75% incr.
• VD 75% incr.
• AS 95%
• VS 95%
▪ Hyperoxia test – administer 100% O2 to baby for 10 min
• Respiratory cause – SaO2 will improve
• Cyanotic heart disease – SaO2 will NOT improve
▪ SaO2 – determined with
• blood gas
• pulse oximetry
- Types of murmur:
o Innocent murmur:
▪ mid-systolic, no diastolic component
▪ musical high-pitched sound at the base of heart (just below clavicle)
▪ non radiating ē no associated thrill
▪ changes with posture & respiration
o Organic murmur:
▪ diastolic
▪ loud
▪ palpable thrill (4 + grade out of 6)
▪ radiating to axila or neck ē associated symptoms
- A thrill is felt with ≥ 4 murmurs out of 6.
- Mitral Stenosis – Purple Book p. 171, Q37
o Aboriginals, caused by Rheumatic Fever,
o Diastolic murmur at apex
▪ doesn’t radiate (the only one)
o tapering apex beat
o S1 ↑ loud and usually palpable sound 1
o Loud P2
o Opening snap after S2 = Mitral Valve Stenosis
o AF
- Mitral regurgitation:
o Systolic murmur radiating to axila
- Aortic stenosis:
o loss of consciousness (Syncope) + angina + exertional dyspnea
o fatigue
28

o Systolic ejection murmur

▪ Systolic murmur = aortic stenosis (MC than mitral regurgitation)
▪ Radiates towards neck
• no radiation & exacerbation with Valsalva manouver = HOCM
o Apical impulse is lateral to the mid clavicular line
o Aortic stenosis vs. complete heart block
▪ similar, but hBP in aortic stenosis vs. HBP in complete heart block
- Aortic regurgitation:
o diastolic murmur that radiates down or down and to left
- (Pan) Holosystolic murmurs:
o VSD, TR & MR
Urinary problems
- Enuresis: (MCQ Q bank P32 Vol. 3)
o Child with:
▪ Nocturnal enuresis: night wetting > 5 (6) yrs (by age 5 child should be dry by
night) or
▪ Diurnal enuresis: daytime wetting > 4rs
o types
▪ Primary MC (cause is neurological delay)
▪ Secondary (occurs if baby is dry for 6 months and restarts bed wetting)
• Psychological factors (transitory)
• Asymptomatic UTI (MCQ)
o Risk factors:
o Family Hx (genetic asociation with high incidence in families) having one or two parents
with nocturnal enuresis
o Dx
▪ Urinary exam – UTI.? For secondary
o Rx
▪ Reassurance upto 5 years
▪ Step-wise Mx:
• 1. Bed alarm (conditioning apparatus) in diapers –Ring bell when baby
wets the diaper: wakes him up, child feels guilty, goes to bathroom.
- 3 mths
- 3 mths break
- 3 mths
- 3 mths break
- most effective in children > 8 yrs old
• 2. Desmopressin acetate (DDAVP) intranasal spray – similar to ADH for
school going children
• 3. DDAVP + alarm
• 4. Planned waking
• 5. TCAs----- Imipramine – purple book
▪ Never punish child!
• Praise child when he doesn’t wet the bed
- VUR
o 80% are females
o types
29

▪ 1. Congenital abnormality in UV junction

▪ 2. Boys – posterior urethral valves
▪ neuropathic bladder – spinal anomaly – 25%
▪ urinary tract anomaly
o Grade 1 – 5
▪ 1 proximal ureter distended
▪ 2 whole ureter distended
▪ 3 ureter and calyces distended
▪ 4 significant distension of ureter
▪ 5 even larger distension and tortuosity of ureter
o Cx
▪ Renal scarring
▪ HTN
o Dx
▪ 1: Urine culture
▪ 2: U/S
▪ 3. MCUG (micturating cystourethrogram)
o Mx
▪ Daily prophylaxis with A/B, daily single dose, 1/3rd of required dose
• Trimethoprim
• Nitrofurantoin
Orthopedics
- Urgent referal conditions:
o Leg calve Perthe’s
o Slipped capital femoral epiphysis
o DDH
o tumor
- Hip pain in kids
Transient Perthe’s SCFE Osgood- Septic arthritis/
Synovitis (femoral head Schlatter Osteomyelitis
flattening)
4-8 y female 4-8y Male 10-15y male 10-15 y male Any age
Recent viral inf. Restricted hip Obese child Tibial Local point tenderness –
in Hx Self limiting movement: Prepuberty tuberosity pain Osteomyelitis.
Restricted Abduction & Restricted Self limiting Refuses to walk, don’t
movement: internal movement: let you touch his leg –
Abduction & rotation Internal septic arthritis, Fever,
internal rotation rotation etc.
Dx X Ray: ↑ joint X Ray X Ray X Ray Osteomyelitis:
X Ray – normal space, femoral Femoral head Tibial tubercle Early normal
U/S head lateral epiphysis slips separate from Late: haziness, loss of
displacement, back, ↑neck underlying density, periosteal
wide femoral length bone reaction, sequestrum
neck
Mx Urgent Urgent Rx: limit Mx – 1. Joint aspir. (open
referral (provide referral: Risk activity lavage) + rule out gout
crutches) if no of avascular Self limiting
Rx can lead to necrosis of
30

osteoarthritis femoral head

o Developmental dysplasia of the hip (DDH) – 0-4 yrs
▪ Women: Men 6:1
▪ Asym. 40%, bilat 1/3
▪ Tight adductors, short leg, delay in walking & limping
▪ Rsk factors:
• Breech presentation with extended legs
• Oligohydroamnios
• Congenital anomalies
• 1st born female child
▪ Dx:
• In a normal infant flexed hip should abduct almost to right angle while
in DDH it often stops half way.
• S/S: ↓ abduction in flexion of affected hip, asymmetrical skin crease of
groin and thigh, affected leg is short and rotated externally, a clicking
on hip movement and a palpable jerk or clunk on abducting flexed hip
(Ortolani sign of jerk).
• 2 mths – Ortolani, Barlow
- Ortolani test (abduction + anterior pressure => reduce luxation)
- Barlow manouver (the reverse => cause the luxation)
• USG: under 3-6 mths
• X Ray – helpful after 3 mths (after femoral head epihphysis appears)
▪ Screening
• DO!!
- Before discharge
- At 6 wks
▪ Mx
• Ref to specialist
• 0-6 mths Pelvic Harness = abduction splint
• 3-16 mths Reduction & cast (Pelvic Spica)
• > 18 mths Open reduction & possible osteotomy
▪ Follow up:
• Acetabular dysplasia (underdev. roof of hip) -> premature osteoarthritis
• X Ray for teenager
o Irritable hip (Transient synovitis) – Alena (4-8 yrs Female)
▪ Acutely painful hip in kids
▪ MC cause of limp in pre-school age
▪ Hx of recent viral URTI (1-2 wks ago) (MCQ)
▪ able to walk but with pain (refuses to walk) otherwise afebrile and well
▪ Dx of exclusion after ruling out other conditions
▪ Common synovial inflammation which is self-limiting
▪ sudden onset of limb pain & limp
▪ Moderate ↓in range of hip movement esp. internal rotation
• if severe limitation of hip movement – consider septic arthritis
▪ Dx
• FBE normal
• X Ray normal
31

• Orthopedic surgeon can suggest U/S if fluid present

▪ Mx
• Settles within 7 days
• no complications
• follow up in 4-6 mths to rule out Leg Calve Perthe’s disease
o Leg Calve Perthe’s disease
▪ Avascular necrosis of capital femoral epiphysis (small flattened femoral head)
▪ 2-12 yrs (4-8 majority)
▪ 20% bilateral
▪ Pain + limp + restricted hip movement
o Slipped capital femoral epiphysis – 10-15 yrs Male
▪ Weight > 90% percentile
▪ Pain in hip which is usually referred to knee.
▪ Hip is externally rotated and shorted
▪ Can’t do: internal rotation + abduction
o Juvenile arthritis
▪ very rare in the hip
o Septic Arthrits – any age + fever
▪ consider in any sudden onset of monoarthritis
▪ in doubt-- treat as sepsis
▪ cause – MC Staph. aureus
▪ Sx
• Swollen, red, tender joint
• All movements are painful (child doesn’t move leg at all)
▪ Dx
• Joint aspiration
- will show neutrophils and bacteria
▪ if treated with C/S, bacteria might not be seen
(masking)
▪ Rx
• 1. Arthroscopy & lavage --> blood culture
• 2. A/B – Staph. MC cause
- Flucloxacilin
- in hospital – Ceftriaxone – 3rd gen (Covers gram -)
o Osteochondritis of tibial tubercle = Osgood-Schlatter osteochondritis, traction
apophysitis of tibial tubercle
▪ 10-14 yrs
▪ common in sports with running, kicking, jumping + after injury/fall
▪ Sx
• localized pain in region of tibial tubercle during and after activity
• lump, localized swelling, tenderness at tibial tubercle
• pain is present if any attempts to flex or straighten knee against
resistance
▪ Dx
• X Ray -> widening of apophysis, fragmentation of tibial tubercele
▪ Mx
• abstain from active sports
32

• acute attack – ice packs, simple analgezics

• self limiting, takes 1 yr to resolve
• Quadriceps stretching exercises
- Growing pains – Murtagh 878
o 3-7 yrs
o wakes up due to pain in knee, shin, calf
o may recur during night
o attack lasts 20-30 mins
o family Hx
o benign – no abnormalities are found
o Rx
▪ Reassurance
▪ Analgezics, heat packs
- Juvenile chronic arthritis = juvenile RA = juvenile arthritis = Still’s disease
o Unknown etiology
o < 16 yrs
o Types
▪ Pauciarticular < 4 joints, M.C. - large joints: knee, wrist, ankle
• assoc with uveitis or sacroileitis
▪ Polyarticular > 4 joints
• large & small joints
• RF can be positive, rheumatoid nodules are often present
• cervical spine is involved
▪ Systemic type (with vasculitis) –and spiking fever, Salmon-pink rash on trunks &
extremities, arthritis, myalgia, hepatosplenomegaly, pericarditis
lymhpadenopathy, pleuritis.
o Dx:
▪ ESR↑, FBE (microcytic anemia, lymphopenia, platelet↑)
▪ Pauciartic – ANA +
▪ U/S – pericarditis?
o Diff Dx – rule out septic arthritis -> perform arthrocentesis
o Rx
▪ physiotherapy, occupational therapy
▪ NSAIDs
▪ IV IGs in systemic type ē vasculitis
▪ C/S
▪ methotrexate
▪ joint replacement
▪ synovectomy may be required
- Osteomyelitis
o causes
▪ Hematogenous
• MC – Staph. aureus – 90%
o Sx
▪ fever
▪ point tenderness over bone
• pain in joint = Septic arthritis
33

• pain in bone, outside the joint = Osteomyelitis

o Rx - Flucloxacilin
Developmental problems
Puberty
Begins: girls at age 10, boys at age 12.
Completes: Girls usually by ages 15–17, while boys usually by ages 17 or 18 yrs.

Sequence in girls:
first telarche (enlargement of breast buds)
then growth spurt
then axillary and pubic hair develops
then menarche occurs (2 years after start of puberty)

Sequence in boys:
Scrotal and testicular growth
Pubic hair (after 6 months)
Penile enlargement (within 12-18 months)
axillary hair (after 2 years)
deepening of voice
Tanner stages
Boys Girls
Prepubescent Basal Growth, No penile/ testicular Basal growth, breast buds
Stage 1 enlargement, No pubic hair
Stage 2 Testicular/ scrotal enlargement (9- Growth spurt (8-13 yrs
11 yrs)
Stage 3 Growth spurt/ Pubic hair Axillary and pubic hair
Stage 4 Penile enlargement,axillary hair Coarse pubic hair and menarche
Stage 5 Deepening of voice and facial hair Adult pubic hair distribution

- Development
o Female
▪ I – Telarche 2 yrs till menarche
▪ II – Adrenarche androgen hormones --> axillary & pubic hair, body odor
▪ III – Menarche influenced by her mother’s menarche
▪ IV – Pubarche pubic hair
o Male
▪ I – Testis
- Simple Tanner scale – printout from Neha
o Boys
▪ Scrotal & testis growth --> 6 mths --> pubic hair --> 12-18 mths --> penile
enlargement --> Axillary hair (whole process 2 yrs)
o Girls
▪ 1st = enlargement of breast buds (9 yrs old) -> growth spurt -> axillary & pubic
hair --> menarche (whole process = 2 yrs)
o Average time for puberty = 3 yrs
o Based on secondary sexual characters
▪ Male
34

• size of testis
• pubic and axillary hair
▪ Female
• breast and nipple dev.
• pubic and axillary hair
o Stages:
▪ 1– Preadolescent, no sec. sexual chars.
▪ 2– 9 - 11
▪ 3– 11-13
▪ 4– 13-15
▪ 5– 15+
- Causes of delayed puberty:
o types
▪ Hypogonadotropic hypogonadism
• ↓FSH ↓ LH → ↓ estrogen
• Pituitary problem
▪ Hypergonadotropic hypogonadism
• ↑FSH ↑LH → ↓ estrogen
o Dx
▪
FSH LH
- Normal percentile: 3 – 97% for height & weight
- Speech problems
o Delay
▪ Causes
• Mental retardation – MC
• Deafness
• Cerebral palsy
• Infantile autism
• Social deprivation
o Stammering
▪ Male 3:1
▪ Genetic factors
▪ Recover spontaneously before age 16
o Elective mutism – occurs only in certain situations
- Developmental problems in kids
o Precocious puberty – early secondary sexual characters in girls < 8 yrs, boys < 9.5 yrs
Investigation of preco. Puberty:
1. FSH, LH and Estradiol (usually raised in precocious puberty)
2. Bone age X Ray (Left wrist and elbow)
3. MRI brain (to exclude pituitary tumor) if FSH and LH are ↑
o Premature telarche – isolated breast dev. in girls < 2 yrs
▪ due to hormonal stimulation from estrogen
▪ sometimes with discharge from nipples
o Pubertal gynecomastia – 40-50% boys, transient
- 1st yr of life weight calculation
o ¾ kg monthly first 4 mths = ¾ x 4 = 3 kg
o ½ kg monthly next 4 mths = ½ x 4 = 2 kg
35

o ¼ kg monthly next 4 mths = ¼ x 4 = 1 kg

o Total at 1 yr: 6 kg + wt. at birth
- Obese children are taller than same age children
o MC assoc. of childhood obesity in Aus = above average height
- Gynecomastia
o Causes
▪ Physiological
• first 3 wks – ↑estrogen from mother
• puberty – up to 50% of adolescent boys
- hormonal imbalance: estro/ testosterone ratio ↑
• elderly
- > 50 yrs – due to ↓testosterone
▪ Drugs (DISCOME)
• digoxin
• isoniazide
• spironolactone, steroids
• cimetidine
• omeprazole
• metyhldopa, marijuana
• estrogen
• + calcium antagonists, amiodarone, TCAs
• NOT: Frusemide, Labetalol
▪ Hypogonadal states:
• Klinefelter’s syndrome (XXY)
• Sec. testic. failure (Torsion, orchitis, orchidectomy, traumatic atrophy)
▪ Hepatic failure:
▪ Testicular feminisation sydrome
▪ Estr. secreting tumors
• Adrenal CA
• Leydig cell tumor
o Dx
▪ 1 Testosterone
▪ 2 Estrogen
o Rx
▪ < 18 yrs – reassurance
▪ if persists >18 yrs - find cause: Klinefelter, testicular atrophy, etc.
- Developmental Delay
o ask if child lost some skills recently (even more alarming for neurol. involvement)
o after vaccination – very rare, anecdotal
▪ unusual irritability and prolonged crying, due to low grade fever – after DPT
- Growth Charts – see p. 210 in my notes
o http://www.cdc.gov/growthcharts/clinicalcharts.htm
o http://www.cdc.gov/nccdphp/dnpa/growthcharts/guide.htm interpretation
o there is a wide variation of a normal growth.
o 3% of normal children will be above 97th percentile or below 3rd percentile
▪ 94% of normal children are between the 3rd & 97th percentile (-2 SD to +2 SD)
▪ Other 6% are either below 3rd or above 97th percentile.
36

▪ Even below 3rd & above 97th percentile there are normal kids.
o Short Stature:
▪ 1. Familial (Genetic) short stature
• Bone age BA = CA Chronological age
• Grow on 3rd percentile or below but the rate of growth is parallel to 3rd
• Growth velocity = Normal
• Puberty is at appropriate time
▪ 2. Constitutional delay (delayed puberty) MC
• Boys
• Growth velocity is slower bw 6m and 3yrs
• often family Hx of parent being short as a child with delayed puberty
and eventually he caught up ----- “Late bloomers”
• BA < CA
• Puberty is delayed
• 1st bone age then (testosterone & plasma gonadotrophin levels MCQ)
- e.g. in the recalls
▪ Short with CA = 15 but stature of 12 yrs
• good prognosis? if BA = 9 = constitutional delay
▪ 3. Hypopituitrism
• Usually manifests after 2 yrs
• look for relative obesity w/o any other explanation
▪ 4. Chronic illness or malnutrition
• Celiac, Cystic fibrosis, etc.
▪ 5. Iatrogenic
• e.g. C/S
- fusion of epiphysis
▪ 6. Chromosomal abnormality
• MC – Turner Syndrome
- Girl – Short stature -- 45XO
7. Skeletal Dysplasia—Short limbs
o Alena
▪ most kids 25-75 percentile
▪ <10 = Concern
▪ > 95 = Gigantic
▪ important is trend from birth
• if always high or low percentile = normal!
• drop in wt. > 2% at a certain moment, in a short period of time = FTT
- Short stature
o Genetic
o Intrauterine causes
o Intralabor causes
o Postpartum causes
▪ extensive resuscitation
• Growth hormone retardation
▪ Post delivery hypoglycemia
▪ Hypothyroidism
37

▪ Cystic Fibrosis
▪ Celiac disease
▪ Phenylketonuria
o later
▪ child abuse, nutritional defficiences
▪ CRF
▪ Turner syndrome – female (45XO)
o MC = Constitutional delay
o Combinations:
▪ Bone age = Chronological age => Subnormal adult height
• cause
- Genetic short stature
- low birth weight
▪ Bone age < Chronological age + appropriate to height age => Normal adult
height
• Cause = familial maturation delay
• e.g. jul 2009 – q11
▪ Bone age below height age => severe growth retardation (only height is short,
GH is diagnostic)
• cause = endocrine – hypothyr., growth hormone defficiency
o Dx
▪ FBE – anemia, chronic inflammation (ESR, CRP)
▪ Thyroid function
▪ Growth Hormone level
▪ Blood sugar Level
▪ Karyotyping – Turner
▪ X Ray of left wrist -> bone age
• if it’s younger than age of child => room for it to grow
Milestones - TO DO!(MCQ 2145 P 94)
- Asked so far – Murtagh 866
o Social Smile: 2 mths (0-7 wks)
o Roll over from back to front position (prone to supine): 4 months?
o Roll over from front to back position: 5 mths
▪ Both asked – 4-5 mths
o sits with support: 6m
o sits alone: 8m
o standing with support: 5-10 m (10 m)
o walks with support: 7 ½ - 12 ½ (12 m)
o walks without support: 11 ½ - 15 m (15 m)
o walks up steps w/o help: 2 yrs (14-22 m)
▪ Climbs stairs with alternate foot: 30 m
o hops on one foot: 3-5 yrs
o rides a tricycle: 21m – 3 yrs
o reach for an object: 3 – 5½m
o pass object from hand to hand: 4½-7½m
o pincer grip: 9 –15 m
o wave his hand/ wave goodbye around: 12 m ??
38

o drinks from a cup: 10-17 m (1 ½ yr)

o play peakaboo: 10 m
o draw a triangle/ square: 4 yrs
o draw a 3 part man: 3-5 yrs
o build a tower of 2 to 3 blocks: 2yrs
o build a tower of 8 blocks: 40 mths ??
o says mum, dad w/o meaning (babbling ): 8-10 mths
o says mum, dad w/ meaning: 9-15 mths
▪ speaks 4 words including mama and dada: 9 – 15 m (15 m)?
o says 3 words other than mum and dad: 1.5 yrs (12-20 mths)
o 2 words sentence: 2 yrs
o 3 words sentence: 3 yrs
o give first and last name: 2-4 yrs (4 ys)
o name colors: 3–5 yrs (5 yrs)
o Teeth- 6-12 mths?
Pharmacology, drug side effects, drug intoxications - OK
Intoxications
- Nicotine replacement therapy
o absolute CI
▪ pregnancy
▪ breastfeeding
▪ recent CVA
▪ arrhythmia
▪ children
- CO intox
o in houses using wood-fired heaters
o Carboxyhemoglobin – any percentage is abnormal
▪ ireversible binding with O2
o Sx
▪ cyanosis
▪ blood – is purple red
o Rx
▪ remove CO source
▪ admin. 100% O2
- Urine drug scan
o Regular
▪ Cannabis/ marijuana
▪ Cocaine
▪ Amphetamines
▪ Opiates
o + Benzos - separate
o + TCAs - separate
- Paracetamol intox.
o Regular dose: 4 x 2 tablets/ day
o Toxic dose:
▪ Adult > 10 g (20 tabl) within 48 hrs
▪ Children > 200 mg/kg
39

o plot Nomogram after 4hrs from ingestion

▪ above line in nomogram = Dangerous
▪ below line = Safe -> discharge
o Detoxication:
▪ Phase I => metabolites still hepatotoxic -> phase II (conjugation with Glutathione
– this can get consumed after 4 hrs)
o Rx
▪ IV fluids
▪ Under 1 hr Activated Charcoal
▪ over 1 hr N-acetyl cysteine: dose calculated based on p. plasma levels at 4 hrs
• take blood for p. level
• then NAC within 8 hrs
- Oral
- IV
• based on P serum level, will give another dose of NAC
▪ Methionine – if allergic reaction after first dose of NAC (antiox. – liver
protecting)
▪ Liver failure -> liver transplant
▪ renal failure is more rare (10% acute tubular necrosis), sec. to liver failure
• Peritoneal dialysis – after 8hrs
- Iron intoxication (in child who took iron pills)
o Sx
▪ Intial symptoms (within 20 min)
• lack of symptoms within 6 hrs makes toxicity unlikely
• nausea, vomiting, abd pain, HTN, hematemesis, fever
• GI symptoms are due to corrosive nature of iron
▪ Latent period (6-24 hrs) –initial symptoms resolve before systemic symptoms
▪ Systemic symptoms – appear at 6-24 hrs, last 12-24 hrs
• tachycardia, vasoconstriction, HTN, shock
- fluid shifts from intravascular to extravascular compartment and
cellular hypoxia
• Metabolic acidosis can occur
▪ Multiple organ failure at 12-48 hrs
• Cerbral ataxia 12-24 hrs
• Hepatic failure 12 hrs
• Seizures 12-24 hrs
o Cx
▪ Pyloric stenosis (scarring)?
o Mx
▪ ABC
• Supportive Rx – maintaing BP and electrolyte balance
• IV fluid resuscitation 20ml/ kg
• K + and glucose admin. as necessary
▪ Asympt. Pts.
• if tablet ingestion→ X Ray Abdomen→ Negative: no need for further
investigation, only observe
- if no sympt. and clear X Ray = everything is OK
40

• if unknown amount or > 60 mg/kg ingested, need serum Fe levels every 4

hrs until falling
▪ Symptomatic patients
• Dx
- Abdominal X Ray if tablet ingestion
- ABGs
- Glucose (hyperglycemia)
- Serum iron
▪ Peak usually at 4 hrs
• after 4 hrs might underestimate toxicity
▪ slow release or entericoated – levels repeated at 6-8
hrs
- clotting – in hepatic injury
• Decontamination
- whole bowel irrigation – until rectal efluent is clear
▪ if abd. X Ray reveals tablets or capsules
▪ in sympt. patients
- Activated charcoal – of no benefit
• Antidote = Desferroxamine
- Indication:
▪ Serum iron > 90 µmol/L
▪ level 60-90 & tablets visible on X Ray or sympt. patient
▪ any patient with significant sympt. (HTN, tachycardia,
tachypnoea, etc.) or worsening sympt.
▪ if altered conscious state, shock, severe acidosis
(pH<7.1) commence desferroxamine without delay,
without waiting for Fe+ levels
- Usually requires 12-16 hrs
▪ Continue until:
• Pt. is asympt.
• Fe level < 54 µmol/L
• Aninon gap acidosis has resolved
- Desferroxamine has been assoc. with pulmonary toxicity if used
> 24 hrs
- Antidotes:
o CO antidote – Hyperbaric (100%) O2
o Opiods – Naloxone (post delivery use morphine in neonates), Methadone maintenance
o Alcohol dependence----Naltrexone
o Paracetamol – N-actetylcysteine
o Iron - Desferoxamine
o Methanol and ethyleneglycol - Ethanol –> inhibits alcohol dehydrogenase
o Organophosphorous poisoning (pesticides, insecticides) - Atropine
o Lead, mercury – Chelating agents
o TCA – IV Sod. bicarbonate to protect from cardiac arrhythmias + Intubate and
hyperventilate
- Aspirin intoxication:
o Sx
41

▪ tinnitus, nausea, vomiting, dehydration, hyperventil. (Resp. AlKalosis), sweating

o Rx
▪ first 1 h – activated charcoal
▪ best way to eliminate: ionized form in alkaline urine
• make urine alkaline
▪ induce diuresis
▪ hemodialisis
- Petrol sniffing
o aboriginals
o cough, bilat. wheeze and tachycardia, due to aspiration pneumonitis. Dx: CXR
o drowsy, ataxic, convulsions
o long term: kidney, gut, liver, myocardium toxicity
o Mx
▪ admit
▪ CXR
- Alcohol
o levels
▪ < 0.05 accepted when driving or for any offense (> 0.05 = drunk)
▪ Breath level > 0.4 (blood level > 86.8 mmol/L) – very dangerous – lethal!
o what to ask an alcoholic: CAGE
▪ did your think about Cutting your alcohol consumption?
▪ did anybody get Annoyed about your drinking?
▪ did you feel Guilty about drinking alcohol?
▪ did you need an Eye opener in the morning?
o Sx of intoxication
▪ nausea, vomiting, abdominal pain
▪ ataxia, lethargy, coma, convulsions
▪ hypoglycemia, hypothermia
▪ hypokalemia, metabolic acidosis
▪ respiratory depression
▪ Unexplained drowsiness, hypothermia or hypoglycemia in an adolescent
might be alcohol poisoning (frequently assoc. with other drugs) MCQ
o Mx
▪ 1. Check breath alcohol concentration
▪ 2. Check for fractures, other lesions
▪ 3. Wait till GCS comes back to 15
▪ 4. Send him home
o Rx
▪ Charcoal doesn’t help
▪ Glucose – since alcohol causes hypoglycemia
▪ Asympt or mild symp.
• observe every 2hrs
• carbonated drinks
▪ Sympt.
• Blood ethanol measurement
• IV fluid
• Temperatue regulation
42

• Admit
o 1 Standard drink = 10g
▪ 250 ml glass of Beer 4.8%
▪ 100 ml glass of Wine 13.5%
▪ 30 ml glass of Spirit 40%
▪ http://www.health.gov.au/internet/alcohol/publishing.nsf/Content/standard
o High risk/ harmful drinking
▪ > 6 standard drinks for men
▪ > 4 standard drinks for women
o Alcohol limit for driving in Australia: < 0.05 g/ 100ml (2.5 g alcohol/ 5L blood volume)
▪ for a 70 kg man, this means not to drink more than:
• 2 std drinks in 1h
• 3 std drinks in 2h
• 4 std drinks in 3h (1 std drink eliminated in 1 h)
o Lethal dose: 0.45-0.5 g/100 ml (%)
o Intoxication
▪ Potentially fatal
▪ BAC is around 0.45% to 0.5%
▪ Use a breath analyzer to estimate BAC & observe pt, until BAC falls below 0.2%.
▪ BAC normally declines at a rate of 0.015% to 0.02%/ hr, although rate of decline
may be ↑in heavy drinkers.
▪ Sx
• hearing voices (like in Schizophrenia)
▪ TREATMENT:
• Supportive and symptomatic
• Careful monitoring of:
- BAC
- Level of consciousness
- Responsiveness
- O2 saturation
o Alcohol withdrawal:
▪ Characterised by:
• Anxiety
• Tremor
• Sweating
• Nausea & vomiting
• Agitation
• Headache and perceptual disturbances
• Seizures: Uncommon
• Alcoholic hallucinosis
- rare complication of alcohol withdrawal in alcoholics. This
develops about 12 to 24 hrs after drinking stops and involves
auditory hallucinations (accusatory or threatening voices).
▪ these begin with simple sounds (whispering, muted
laughter, clink of glasses, simple words)
43

▪ then progress to formed sentences and frequently

offensatory and derogatory voices which accuse the
person of shameful actions.
▪ command hallucinations can occur and can lead to
violence or suicide.
- This condition is distinct from delirium tremens since it develops
and resolves rapidly, involves a limited set of hallucinations and
has no other physical symptoms.
- The risk of developing alcoholic hallucinosis is increased by long-
term heavy alcohol abuse and use of other, illicit drugs.
- Some severely dependent patients will progress to delirium
tremens.
▪ Symptoms usually appear within 6-24 hrs of last consumption.
▪ Symptoms persist for 72 hrs. May last for several weeks.
▪ TREATMENT:
• Most of them require no medication.
• Supportive care.
• Monitoring.
• Information on withdrawal syndrome.
• MEDICAL TREATMENT – in severe cases
- Benzodiazepine loading dose technique
- The patient is given repeated doses of diazepam until symptoms
have diminished to an acceptable level.
- As alcohol-dependent patients are usually deficient in thiamine,
use:
▪ Thiamine 100 mg IM as a single dose, followed by 300
mg orally, daily in 3 divided doses.
▪ Delirium tremens
• can lead to death
• visual and tactile hallucinations with affected sensorium
• if lasts longer, more dangerous
• Most severe manifestation of alcohol withdrawal
• It usually commences 3 to 4 days after cessation of drinking
• High mortality rate (if untreated) principally from heart failure
• CLINICAL FEATURES:
- Gross tremors
- Fluctuating levels of agitation
- Visual hallucinations (e.g. spiders, pink elephants)
- Disorientation
- Impaired attention
- Fever, tachycardia and dehydration
• COMPLICATIONS - frequent
- Infections and trauma
- Anemia, dehydration
- Metabolic disturbances
- It may be associated with: Wernicke's encephalopathy (thiamine
defficiency) and hepatic encephalopathy
44

• TREATMENT:
- Hospitalization
- Correct dehydration and infection if any
- Benzodiazepine loading dose technique.
▪ Diazepam 10 to 20 mg orally, 2 hrly until symptoms
subside.
- Thiamine 100 mg IM as a single dose, followed by 300 mg orally,
daily in 3 divided doses.
- Haloperidol 1.5 to 10 mg orally If psychotic features (e.g.
hallucinations and delusions). Add haloperidol– only if
benzodiazepines didn’t work.
- Wernicke’s Encephalopathy:
o in alcoholics due to thiamine defficiency
o Sx – CONA
▪ Confusion
▪ Opthtalmoplegia
▪ Nystagmus
▪ Ataxia
• Nystagmus & Ataxia (DD)
- with alcohol – Wernicke’s encephalopathy
- cerebellar stroke
▪ no tongue fasciculations
▪ Korsakoff amnestic confabulatory syndrome
• Anterograde amnesia
• Retrograde amnesia
• Confabulation – to make up missing details from affected memory
• meager content in conversation
• lack of insight
• apathy
o Rx
▪ Thiamin IV or IM
▪ followed by glucose/ dextrose
• if we administer glucose first, before thiamin, it might cause
dehydrogenation of piruvate, which will consume thiamin
- Drug intox.
o CNS depressors, stupor, coma
▪ miosis, bradycardia, hT
▪ Drugs:
• OPIODS:
- 1. Morphine
▪ SE
• Miosis (pin-point pupils)
• drowsiness & respiratory depression – most
dangerous
o in high single dose adm.
o usually in terminal patients
45

o now no longer adm. this way, but in

gradually increasing doses
• orthostatic hT
• nausea – in short-term use (not in long term)
• euphoria, sedation and addiction
• constipation (MC and troublesome)
• causes ODI sphincter constriction – CI adm. in
biliary colic (but actually still used)
- 2. Heroin
▪ no fever
▪ CNS and resp. depression
▪ in pregnancy
• IUGR
• premature labor
• drug withdrawal for neonate
- Rx in intox.
▪ Naloxone, short acting, IV
• (Naltrexone, long acting > 24 hrs, P.O. – in
alcohol dependance)
▪ Methadone - Synthetic Opioid, with different structure
than opiods but acting on same receptors and
producing same effects.
• used as anti-addictive in heroine and morphine
addictions.
▪ Clonidine
• SE: postural hT, insomnia
- Opiod withdrawal
▪ uncontrollable yawning, runny eyes and nose,
goosebumps, muscle spasms (twitches), diarrhoea,
colicky abdominal pain, irritability, restlessnes,
sleeplessness, mydriasis & emotional depression
• Benzodiazepine
- Rx – flumazenil
▪ Dx - Urine drug screen
o CNS Stimulant
▪ Sx – Hallucination, mydriasis, tachycardia, HT
▪ Drugs:
• Cocaine:
- fever
- dilated pupils, sweating, nausea, vomiting, pulse/ temperature
/BP instability, agitation, aggressiveness, blurred vision.
- tactile hallucinations, seizures
- can aggravate or produce a paranoid schizophreniform psychosis
- “stimulant psychosis”
▪ paranoia and persecutory delusions
▪ ideas of reference
▪ auditory and visual hallucinations
46

- Effects in prenancy
▪ IUGR
▪ placental abruption
▪ premature labor
▪ intraventricular hemorrhage
▪ developmental delay
▪ stillbirth
▪ teratogenic effect not proven
- Post-withdrawal – can cause depression
- RX Cold blanket and cool normal saline MCQ party intoxication
• Amphetamine
- Sx
▪ rush with grandiosity, feelings of well-being and
overconfidence, heightened sense of sexual feeling
▪ can aggravate or produce a paranoid schizophreniform
psychosis - “stimulant psychosis” (by increasing
dopamine in the synaptic clefts of brain)
• paranoia and persecutory delusions
• ideas of reference
• auditory and visual hallucinations
▪ persecutory auditory hallucinations
▪ visual illusions and hallucinations
▪ tactile hallucinations of bugs or vermin crawling under
the skin (formication) – can lead to scratching
▪ anxiety, hostility, aggressiveness
- Rx
▪ admission
▪ cessation of amphetamines
▪ antipsychotics – haloperidol, phenothiazines
- In pregnancy
▪ amphetamines - MC associated with congenital
anomalies and
• cleft palate
• HT and pre-eclampsia
• IUGR
• preterm labor
- withdrawal – with depression and high suicidal risk
- Ecstasy – type of amphetamine
▪ euphoria, anxiety, agitation
▪ dehydration
• sec. hyponatremia due to excessive water
consumption
▪ muscle jerks
• Marijuana (Cannabis)
- only drug that has its own receptor
- potentiates the effect of sleeping pills – risk of overdose
- mix of stimulant/ depressant / hallucinogen effects
47

- causes sedation, somnolence, sleep problems

- hydroponically grown cannabis has higher concentration of THC
(Tetrahydrocannabinol)
- withdrawal – in chronic users only (not in occasional use)
▪ influenza-like: hot flashes, sweating, hiccups, irritability,
insomnia and restlessness
• Hallucinogens {lysergic acid (LSD) and phenycyclidine}
- could cause a “bad trip” = visual hallucinations, perceptual
distortions and intense emotions (frightening, unpleasant)
▪ flashbacks to this “bad trip” may recur in the future
- does not produce a withdrawal syndrome
• Alcohol
▪ Dx – Urine drug screen
▪ Rx
• IV fluids
• Diazepam
- Detergent powder/alkaline ingestion (children)
o pH > 11.5
o causes significant GI ulcerations (oesophagus!)
o Sx
▪ nausea, vomiting, drooling, refusing to eat or drink
▪ stridor, respiratory distress
o Rx
▪ if sympt. (pain, vomiting etc.) – refer to surgery immediately (for endoscopy)
▪ if asympt.
• give water or milk (to dilute and wash out the content) - max. 250 ml
(10ml/kg)
- if after 4 hrs still asympt. + able to eat and drink -> discharge
- don’t do lavage and don’t use charcoal (Charcoal is CI)!
Substances accumulating in the body
- Lead poisoning (Pb) MCQ 2115 p 84
o Sx
▪ microcytic hypochromic anemia, basophilic stippling of RBCs
▪ crampy, colicy abd. pain, nausea, vomiting
▪ diarrhoea
▪ encephalopothy, ataxia, seizures
▪ muscle weakness
▪ foot drop – common peroneal n.
▪ wrist drop (radial nerve palsy)
▪ gum lines (blue lines)
o in old houses and lead pipes (was used everywhere before) and paint
o All Australians should have a blood lead level below 10 mcg/dL (though there is no known
safe level of lead).
o Levels above 10 mcg/ dL are associated with decreased IQ levels.
- Mercury: CNS toxicity with intention tremors excitiability, memorty loss and delirium.
o Its found in contaminated fish , dentists removing amalgam fillings, and hat (millinery)
industry.
48

o peripheral neuropathy (presenting as paresthesia or itching, burning or pain)

o skin discoloration (pink cheeks, fingertips and toes), swelling, and desquamation
(shedding of skin).
o Because mercury blocks degradation pathway of catecholamines, epinephrine excess
causes profuse sweating, tachycardia (persistently faster-than-normal heart beat),
increased salivation, and hypertension (high blood pressure). Mercury is thought to
inactivate S-adenosyl-methionine, which is necessary for catecholamine catabolism by
catechol-o-methyl transferase.
- Arsenic
o Chronic poisoning: tasteless and odorless, skin rashes, gastrointestinal symptoms
▪ Chronic exposure to inorganic arsenic may lead to hypertension, involuntary
muscular dysfunction (including incontinence), diabetes, neuropathy,
depression, obesity and any other condition related to the altered role of
intercellular voltage-dependent potassium channels, including cutaneous
hyperpigmentation.
- Hemochromatosis
o lack of cell surface of HFE due to C282Y or H63D mutations
o Cx
▪ Cirrhosis, liver CA
▪ Arthritis
▪ Pituitary gland
• fertility problems
• testic. atrophy
▪ Tanned skin
▪ DM – bronzed DM
▪ Cardiomyopathy, AF
o Dx
▪ Screening - Serum ferritin > 250 µg/L
▪ Key diagn. - Transferrin saturation > 70%
o Rx – no cure, just prevent the Cx
▪ Venesections
• 500 ml weekly till Fe is N, then 500 ml 3-4 times/yr
• MCQ: improve his DM, skin pigm., cardiomyopathy, ↓ size of liver
- Can’t improve his risk for cirrhosis and liver CA
- Wilson’s dis. - AR
o Copper deposits in tissues
▪ Liver – Chronic hepatitis -> Cirrhosis
• flapping tremor
▪ Brain – parkinsonism, ataxia, dystonia
o Kayser-Fleisher brown ring around iris
o Dx Serum cerruloplasmin
Antibiotics:
- A/B used in various conditions:
o Scabies
▪ Permethrin cream 5% or
▪ Benzyl benzoate 25% emulsion
o Toxoplasmosis
49

▪ Pyrimethamine + Sulfadiazine + Folate (to counteract their antifolate activity)

o Cellulitis:
▪ Strepto. & Staphylococcus
• Severe: Flucloxacillin IV
• Less severe: Flucloxacillin P.O.
▪ in DM
• Penicillin + Metronidazole + Gentamycin (empirical) (Alena)
o Mastitis Flucloxacilin ( for Candida – Fluconazole or Nystatin)
o Orbital cellulitis Flucloxacillin + Ceftriaxone
o Conjunctivitis - Chloramphenicol eye drops
▪ Gonococcal (hyperacute onset)
• Topical Sulfacetamide
• IV Cephalosporins or Penicillin
▪ Chlamydia
• Neonates Erythromycin
• Children > 6 kg Azithromycin
o UTI
▪ Rx - TG (Alena)
• 1 – Trimethoprim – not in pregnancy
• 2 – Amoxyclav. – in pregnancy
• 3 – Cephalosp. - cefalexin
• 4 – Nitrofurantoin – not in pregnancy?
▪ In pregnancy - Amoxyclav or Cefalexin
o Prostatitis: Amoxycillin + Gentamicin
o Epididymo-orchitis
▪ STI (gonococci + chlamydia): Ceftriaxone + Doxycycline
▪ Instrumentation (E. coli): Amoxyclave or trimethoprim
o Bacterial vaginosis
▪ 1 - Metronidazole 400 mg P.O. 12 hourly for 7 days
▪ 2 - Clindamycin 20% P.O. or Vaginal cream – in:
• resistant inf.
• pregnancy
▪ in pregnancy
• 1. Clindamycin 300 mg Orally 12 hrly for 7 days
• Metronidazole 400 mg P.O. 12 hrly for 7 days
- not very safe – categ B2
o Trichomonas
▪ Metronidazole P.O.
▪ pregnancy – Clotrimazole vaginal tablets
o Candidiasis
▪ Topical Clotrimazole (Miconazole, etc.) – first line, 1-7 days
• V aginal tablet + cream
▪ Recurrent
• Nystatin cream + pessaries
▪ Recalcitrant, not pregnant
• Fluconazole or Itraconazole P.O.
50

▪ Pregnancy - Clotrimazole pessaries! (local, not systemic)

▪ in Candidata glabrata - Boric acid (not in pregnancy)
o Chlamydia
▪ 1. Azythromycin (preferred) or doxycycline
▪ 2. Erythromycin – in pregnancy
o Trachoma
▪ non-pregnant woman, child – Azythromycin
▪ pregnant woman, child < 6 kg – Erythromycin or Roxythromycin
o Gonorrhoea
▪ if penicillin-resistant gonococci (PPNG)
• Ceftriaxone + Azithromycin or Doxycycline
▪ if PPNG prevalence is low
• amoxycillin + probenecid + azythromycin (if Chlamydia hasn’t been ruled
out)
▪ in pregnancy
• Erythromycin or Roxythromycin
o Syphilis
▪ procaine benzylpenicillin or benzathine penicillin
• if sensitive to penicillin
- doxycycline
o STD prophylaxis after unprotected sex
▪ penicillin (gonococal) or azithromycin or doxycycline (chlamydia)–
prophylactically.
o PID
▪ Mild to moderate/ outpatient: Azithromycin 1g orally + Ceftriaxone 250 mg IM
+ doxycycline 100 mg BD. Orally + Metronidazole 400 mg b.d. For 14 days.
▪ Severe/ hospital: Cefotaxime (or ceftriaxone) + Doxycycline + Metronidazole
▪ in pregnancy: Cefotaxime (or ceftriaxone) + Roxithromycin + Metronidazole
o Post-partum endometritis or pyrexia {fever, tender uterus, foul smelling lochia
(brownish discharge)}:
▪ Ampicillin (or amoxycillin) + Metronidazole + Gentamycin
o Otitis media
▪ 1st line Amoxicillin
▪ still not resolving after 48 hrs
• 2nd Cefaclor or
• Amoxycillin + Clavulanic acid – if resistance is suspected
o Bronchitis – Amoxycillin or Doxycycline
o Pneumonia
▪ Staphylococcus Flucloxacilin
▪ Lower lobe consolidation – Streptococcus pneumonia
• Rx – Penicillin or Amoxyclave
▪ Atypical pneumonia
- Azithromycin – the best
▪ covers Mycoplasma, Legionella, Chlamydia
- Erythromycin, Roxithromycin
▪ don’t cover Legionella
- Doxycycline, Tetracycline
51

▪ Pneumocystic - Cotrimoxazol
▪ Klebsiella - Cefuroxime
o Lung abscess
▪ Cephalosporin (Ceftriaxone) + Clindamycin
▪ Cephalosporin + Flucloxacillin
o Tonsilitis – Penicilin
o Rheumatic fever Penicilin
o Scarlet fever Penicillin
o Impetigo Topical antiseptic – Bactroban (Mupirocin)
▪ if extensive, systemic A/B
• Flucloxacilin
• Cephalexin
o Meningitis - Ceftriaxone (3rd gen) + Benzylpenicillin
▪ Ceftriaxone 2 g IV
• + Benzylpenicillin 2.4 g IV (ampicillin for Listeria) in immune-
compromised or Listeria
▪ if Penicillin/Cephalosporin hypersensitivity:
• Vancomycin + Ciprofloxacin
▪ prophylaxis in contacts: Ciprofloxacin or Rifampicin
o Typhoid fever – Ciprofloxacin
o other diarrhoeas – see Diarrhoea chap.
o Whooping Cough – Clarithromycin/ Erythromycin
o Epiglotitis – Cephalosporin (3rd gen): Ceftriaxone, Cefotaxime
o Infective endocarditis - start ASAP empiric Rx with Benzyl Penicillin + Flucloxacilin +
Gentamycin IV
o Osteomyelitis – (staph.) Flucloxacilin
o Septic arthritis (staph.) Flucloxacilin
▪ in hospital – Ceftriaxone – 3rd gen (covers gram -ve)
o Cholecystitis - Gentamicin, Ampicillin.
o Cholangitis: Ceftriaxone, Penicillin, Aminoglycosides
o Peptic ulcer
▪ 1st line: PPI + Clarythromycin + Amoxycilin
▪ 2nd line: PPI + Metronidazole + Amoxycilin
▪ 3rd line if sensitive to Penicilin: PPI + Clarythromycin + Metronidazole
o Peritonitis (after viscus rupture): Gentamicin 5 mg/kg IV + Ampicillin 1 g IV +
Metronidazole 500 mg IV
o TB
▪ Active TB
• 4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2 mths
• then 2 drugs (rifampicin and isoniazid) for 4 mths
- total 6 mths
▪ Latent TB (Mantoux positive, no symptoms, no X Ray findings)
• when active TB is excluded: Isoniazid mono-therapy for 6-9 mths
▪ Pregnant
• Isoniazid, Rifampicin, Ethambutol – 9 mths treatments
▪ Isoniazid resistant TB
52

• Streptomycin or Amikacin instead of isoniazide

- A/B:
o Gram +ve – Penicilin, if allergic -> Erythromycin; Cephalosp. 1st gen; Ampicilin
o Gram -ve – Gentamycin (nephro, neuro, ototox.); Cephalosp. II & III gen (higher the
generation, better gram -ve coverage)
o Chlamydia, Mycoplasma – Tetracyclin, Doxycycline
o Staph. aur – Amoxycilin (if resistant staf.) + Clavulanic acid., Flucloxacilin, Dicloxacilin
(penicilins)
o UTI- Trimethoprim, Cefalexin (3rd gen)
- Cross sensitivity 4-6 % between Penicillin & Cephalosporin
- No topical A/B in Aus.
o Exception – Ocular inf. (Chloramphenicol)
- A/B
o Classification
▪ Bactericidal
- Beta lactams
▪ Penicilins
▪ cephalosporins
- Aminoglycosides
▪ Bacteriostatic
• Macrolides
• Tetracyclines
o I. Beta lactams – interfere with the synthesis of bacterial wall
▪ 1. Penicillins:
• Types:
- Narrow spectrum (have “penicilin” in the name)
▪ Benzyl penicilin
▪ Procain penicilin
▪ Benzathine penicilin
▪ Phenoximethyl penicilin - Oral
- Broad spectrum – modified in order to have a broad spectrum
▪ Ampicilin
▪ Amoxycilin
- Antistaph. – resistant to beta lactamase
▪ Methiciline
▪ Cloxaciline
▪ Flucloxaciline
• SE: Cholestatic Jaundice
▪ Dicloxaciline – preferred over flucloxaciline, but not
very stable
- Antipseudomonal
▪ Piperacilin
▪ Ticarcilin
• Resistance to penicilin – mechanisms:
- Production of Beta lactamase enzymes (destroy beta lactam ring
of a beta lactams)
53

▪ use of beta lactamase inhibitors: Clavulanic acid

(Amoxicilin + Clavulanic acid = Amoxiclav), sulbactam,
tazobactam
- Reduction in cell wall permeability
▪ e.g. Gram negative bacteria
- Occurrance of modified penicilin binding sites
▪ MRSA – Methicillin Resistant Staph. Aureus
• use Vancomycin
▪ 2. Cephalosporin (higher the generation better gram -ve coverage)
• 1st Gen.
- active on gram +ve and modest on gram -ve
- e.g.
▪ Cefalexin – Oral
▪ Cefazolin – IV
Worst combinations causing Acute renal failure (ATN)
- Cefazolin (1st gen)+ Gentamycin
- 1st gen + Furosemide or Vancomycin
▪
• 2nd Gen.
- Strongest on gram +ve and moderate on gram -ve
- Cefaclor, Cefuroxim
• 3rd Gen.
- strongest on gram -ve and less than second gen. on gram +ve
- ex. Cefotaxime, Ceftriaxone
• 4 Gen.
th

- strong on gram -ve, moderate on gram +ve, also cover other bact.
- ex. Cefclidine, Cefepime
▪ 3. Imipenam – Very broad spectrum (Gram +ve, Gram -ve, Aerob/Anaerob,
Pseudomonas, most enterobact. etc. – almost all bact.)
▪ 4. Meropenam – also very broad spectrum
o II. Aminoglicosides
▪ Gentamycin, Streptomycin, Amikacin, Kanamycin, Neomycin
▪ spectrum: good for gram -ve, also on gram +v
▪ SE
• Ototoxic - Vit. E should be added to prevent ototoxicity of gentamycin
• Nephrotoxic – monitor renal function
▪ prefered dosage: once daily
o III. Macrolides
▪ Erythromycin, Clarithromycin, Azithromycin
▪ spectrum
• more on gram +, less on gram –
• active on Mycoplasma, Chlamydia, Bordetella
• Azithromycin – very active on legionella
o IV. Tetracyclins
▪ Tetracyclin, Doxycyclin
▪ spectrum:
• Gram +, Gram -, Chlamydia, Mycoplasma
54

• A/B of choice for atypical bact.: Mycoplasma, Chlamydia, malaria

prophylaxis, plague, brucellosis, cholera, Lyme dis. + in mixed inf.
o V. Glycopeptides:
▪ Vancomycin
• to treat multiresistant staph.
- Pseudomembranous colitis (No.2 choice; No. 1 choice =
metronidazole)
o VI. Metronidazole
▪ Drug of choice for Pseudomembranous colitis
o VII. Nitrofurantion
▪ UTI
o VIII. Quinolones: A/B affecting the tropoisomerase 2 enzyme
▪ Ciprofloxacin, Norfloxacin
▪ SE:
• CI in children < 14 yrs: risk of joint difformity (not in growing yrs)
• Ciprofloxacin + Theophylin interaction => theophylin toxicity
o IX. Anti-TB – all are hepatotoxic (RIPE)
▪ 1st line:
• Rifampicine
- SE: Red urine
• Isoniazid
- SE: Hepatotoxic
• Etambutol
- SE: Optic neuritis
• Pyrazinamide
- SE: Peripheral neuropathy (add Vit. B12 to prevent it)
- Not used in pregnancy
▪ 2nd line
• Streptomycin
• Ciprofloxacin
Drugs and drug side effects
- Adverse drug reactions
o dose related?
▪ type A – dose related
• MC
• predictable
• for drugs having low Therapt. index = toxic dose/ therapeutic dose
- e.g. Digoxin, Lithium, Antiarrythimcs, Theophyiline, etc.
• caution in renal failure
▪ type B – non-dose related, idiosyncratic
• rare
• unpredictable
• high mortality
• e.g. anaphylaxis – MC
o type of hypersensitivity reaction
▪ type I – Anaphylaxis MC
55

• e.g.
- Penicilin
- Cephalosporin (cross-reaction with penicilin)
- Sulphur drugs
- IV contrast mediums (CT, etc.)
▪ type II – Cytotoxic
• sub-types
- hemol. anemia – sulphonamides (sulfur drugs), peniciline – rare,
quinidine (anti-arrhythmic), methyldopa
- Agranulocytosis – clozapine, carbimazole, ACE inh.
- Thrombocytopenia – heparin (HIT), quinidine
▪ type III – Immune-complex mediated
• e.g.
- penicilin
- sulphur drugs
- thiazides
▪ type IV – T-cell mediated
• e.g.
- penicilin
- cephalosporin
- local anesthetics
- phenitoin
- Drugs to be avoided in pregnancy – Murtagh 1063
o A/B
▪ Tetracyclines (e.g. doxycycline) – incorporated into fetal bones and teeth
▪ Aminoglycosides
▪ Trimethoprim
o Anti-HTN
▪ ACE inhibitors
▪ Diuretics – as in pre-eclampsia and pregnancy induced HT the intravasc. volume
is already low.
▪ Beta blockers – have potential problems
▪ (best evaluated to use in pregnancy = Methyldopa)
▪ Verapamil
o C/S systemic
o Anticonvulsants
▪ Phenytoin – hydantoin syndrome (facial, nail and other abnormalities)
o Estrogen
▪ Diethystilbestrol
• causes reproductive tract abnormalities in both genders
• ↑risk of clear cell carcinoma of vagina in female children
• ↑ abortion rate
o Danazol – Androgenisation: Clitoral hypertrophy & labial fusion in female fetuses
- Drugs to be used in Breastfeeding
o Antiphyschotic
▪ Olanzapine
▪ Risperidone
56

▪ No typical antipsychotics
▪ Clozapine – as much as possible avoid but can be given
o Antidepressants
▪ SSRI except fluoxetine
▪ prefer short acting SSRIs (Paroxetine, Sertraline)
o Bipolar drugs
▪ Na valpropate---- Drug of choice
▪ Lithium – CI (blue book), but Shipra said: as much as possible avoid, but can be
given (check level in the infant as well)
o Benzodiazepines
▪ short acting cause sedation and poor sucking in baby
▪ long acting, like diazepam, cause floppy infant syndrome
o Opioids – safe
- Danazol
o Androgenic SE, especially in long term Rx
▪ Weight gain
▪ Fluid retention
▪ Voice change
▪ in pregnancy: androgenisation: clitoral hypertrophy & labial fusion in female
fetuses
- Inotrop drugs
o Positive inotrops
▪ Ca
▪ Ca sensitizer – levosimendan (in CHF)
▪ Cardiac glycosides – Digoxin
▪ Catcholamines – adrenaline, noradrenaline, dopamine, dobutamine
▪ PG
▪ Phosphodiesterase inh. – theophylline
o Negative inotrops
▪ Beta blockers
▪ Ca channel blockers – only diltiazem, verapamil
• amlodpidine (long acting metabolite of nifedipine) – replacing nifedipine
• decr. the afterload resitance (vasodil.)
• SE:
- edema – nifedipine
- reactive tachycardia
- Chronotrop. neg. Drugs (decreasing HR)
o digoxin
o verapamil, diltiazem
o adenosine
o beta blockers
- Antiarrhythmic Drugs - http://en.wikipedia.org/wiki/Antiarrhythmic_agent
Known
Class Examples Mechanism Clinical uses [5]
as
57

• Ventricular arrhythmias
fast- • Quinidine (Na+) channel block • prevention of paroxysmal recurrent
channel • Procainamide (intermediate atrial fibrillation (triggered by vagal
Ia
blockers • Disopyramide association/dissociation) overactivity), *procainamide in
Wolff-Parkinson-White syndrome

• treatment and prevention during

and immediately after myocardial
• Lidocaine infarction, though this practice is
• Phenytoin (Na+) channel block (fast now discouraged given the
Ib
• Mexiletine association/dissociation) increased risk of asystole
o ventricular tachycardia
o atrial fibrillation

• prevents paroxysmal atrial

fibrillation
• Flecainide
(Na+) channel block (slow • treats recurrent tachyarrhythmias
Ic • Propafenone
association/dissociation) of abnormal conduction system.
• Moricizine
• contraindicated immediately post-
myocardial infarction.
• Propranolol
• Esmolol
beta blocking • ↓ myocardial infarction mortality
Beta- • Timolol
II Propranolol also shows • prevent recurrence of
blockers • Metoprolol
some class I action tachyarrhythmias
• Atenolol
• Bisoprolol
• In Wolff-Parkinson-White
• Amiodarone
K+ channel blocker syndrome
• Sotalol
• (sotalol:) ventricular tachycardias
III • Ibutilide
Sotalol is also a beta and atrial fibrillation
• Dofetilide
blocker[6] • (Ibutilide:) atrial flutter and atrial
• E-4031
fibrillation
• prevent recurrence of paroxysmal
slow- • Verapamil supraventricular tachycardia
IV channel • Diltiazem Ca2+ channel blocker • reduce ventricular rate in patients
blockers with atrial fibrillation

Used in supraventricular arrhythmias,

• Adenosine Work by other or
especially in Heart Failure with Atrial
V • Digoxin unknown mechanisms
Fibrillation, contraindicated in ventricular
(Direct nodal inhibition).
arrhythmias.

- Ca channel blockers: Nifedipine, Amlodipine, Diltiazem, Verapamil

o Amlodpidine (long acting metabolite of nifedipine) – replacing Nifedipine
o ↓ the afterload resitance (vasodilatation)
o SE:
▪ edema – nifedipine
▪ reactive tachyc.
58

▪ verapamil intox.
• AV block I-III
• LBBB, RBBB
- Beta Blockers
o Types
▪ Non-selective: Propranolol (acts on both heart and lung)
▪ Selective: Metoprolol, Atenolol, Sotalol (acts only on heart)
o Indications
▪ HTN
▪ heart failure – decr. Mortality (cardioselective only)
▪ after MI – decr. mortality
▪ rate control
▪ rhythm control – sotalol
o CI
▪ Pregnancy
▪ heart block
▪ Prinzmetal angina (due to coronary spasm)
▪ asthma, COPD (propranolol – neselective)
▪ DM
▪ peripheral vascular disease
o SE
▪ bronchospasm – non-selective
▪ hyperkalemia
▪ hyponatraemia
▪ ↑risk of DM
- ACE inhibitors
o Indications
▪ HTN
▪ Heart failure – ↓mortality
▪ MI – ↓ mortality
• especially with:
- renal condition
- HTA
- DM
▪ Renal condition (renoprotectors)
▪ DM nephropathy in beginning stage (microalbuminuria)
▪ Progressive renal failure
o SE
▪ Dry cough
▪ Angioedema (C1 estrase)
▪ Agranulocytosis (cytotoxic)
▪ Hyperkalemia
▪ Acute renal failure – in (unilateral or bilateral) renal artery stenosis
▪ Orthostatic hypotension
o CI
▪ Pregnancy
59

▪
Renal failure (in advanced stages when creatinine > 3.5 & worsening with their
use)
▪ Renal artery stenosis
▪ Diastolic heart failure (hypertrophic heart) – M 1337
• hypertrophic cardiomyopathy
• aortic stenosis
• HT
• Rx
- Beta blocker
- Calcium antagonists
- Spironolactone (causes hyperkalemia)
o indic.:
▪ Diuretic
• Heart failure
• HTN
▪ Antiandrogen (Aldosterone antagonist) causes gaynocomastia
- Thiazides
o SE
▪ hypokalemia
▪ hyperuricaemia
▪ impaired glucose tolerance –↑risk of DM (like the Beta Blockers)
▪ hypercholestrolemia
o indic.
▪ diuretic
• HTN
• heart failure
▪ protect from oxalate stones (renal stones)
- Nitrates
o Types
o Short acting
▪ GTN – spray, patch
• duration of action – 30 min
▪ Long acting
• isosorbid mononitrate
• isosorbid dinitrate
o SE
▪ Postural hypotension and Headaches – bc of vasodilation
▪ reflex tachycardia (prevent with β blockers)
- Hyperkalemia
o causes
▪ Drugs
• K⁺ sparing diuretics (spironolactone & amiloride)
• ACE inhibitors & AIIRA
• Digoxin
• Beta Blockers
• NSAIDs: Indomethacin, etc.
• IV Benzyl Penicillin (contains K)!
60

▪ ↑ K intake: banana, low fat milk, beans, sweat potato.

▪ ↑ production – when cellular membranes are ruptured! e.g. rhabdomyolysis,
burns, ischaemia, hemolysis.
▪ ↓ renal excretion:
• Acute and chronic renal failure
• Addison’s disease
• hypoaldosteronism
▪ Transcellular compartmental shift: acidosis, hyperglycaemia, low insulin
- Prolonged QT = risk of Torsades de Pointes (polymorphic VT) -> VF -> death
o causes:
▪ hypokalemia
▪ TCAs
▪ antipsychotics
• haloperidol, droperidol
• chlorpromazine
- Digoxin intoxication – Oxford 100
o Digoxin works on Na+-K+ pump
o narrow therap. range
o Effects:
▪ Inotrope positive
▪ Chronotrope negative (↓HR)
▪ Dromotrope negative (slows down conduction in AV node and increases its
refractory period)
o Usage:
▪ Atrial fibrillation, atrial flutter (along with Beta- and Calcium-blockers)
▪ Congestive heart failure (but diuretics and ACE inhibitors are the first choices)
o CI
▪ HOCM
▪ WPW
o Precautions – when digoxin intox. is more often/ severe
▪ elderly
▪ ischemia
▪ hypothyroidism
▪ renal failure
▪ hypokalemia
▪ decr. Mg
▪ decr. Ca
o intox

▪ increased gastrointestinal motility (loss of appetite, nausea, vomiting, diarrhea)

▪ blurred vision, yellow-green halos & color perception problems (Xanthopsia)
▪ Nausea, vomiting, anorexia
▪ Confusion
▪ Severe toxicity will cause hyperkalemia
▪ ECG
• Arrythmia – ANY
- acute – usually bradycardia
- irregular pulse
61

- tachycardia
• various arrythmias
- shortened QRS complex, atrial or ventricular extrasystoles,
paroxysmal atrial tachycardia with AV block, heart block
- PR interval prolongation
- Pulses bigeminy, V. tach. or fibrillation
• nodal bradycardia, bradyarrythmia
• ST depression with T negative wave (“sagging” )
• hypokalemia – small T wave, proeminent U wave
- hyperkalemia – tall tented T wave, widened QRS complex, absent
P waves
• hypocalcemia: long QT, small T wave
- hypercalcemia: short QT
• ventricular ectopics
• never prolonged QTc (corrected QT -> predispose to torsade de pointes)
▪ Rx
• Stop digoxin
• Check K+
• Treat arrythmias
• Consider giving digibind IV – AB to digoxin
- NSAIDs:
o not in renal failure/ insufficiency
▪ ↓ GFR
▪ ↑ proximal tubular reabsorption
• can ↓ Lithium clearance -> Lithium toxicity (MCQ)
- Oral antidiabetics
o Glibenclamide
▪ SE
• hypoglycemia
• cholestatic jaundice
o Metformin
▪ GI upset
• diarrhoea, ↑flatulence
▪ no hypoglycemia
- Amphotericin B IV
o only in potentially lethal fungal infection, as a last resort
o SE
▪ Phlebitis at the site of infusion
▪ anemia
▪ hypokalemia
▪ renal problems (irreversible)
• renal failure
• renal tubular necrosis
- Azathioprine
o hepatotoxic
o acute pancreatitis
62

- Phenytoin
SE
o P 450 inducer
o Gum hypertrophy
o Teratogenic --hydantoin syndrome (facial, nail and other abnormalities)
o Osteomalacia & osteopenia (not osteoporosis)
o interferes with folate metabolism – Megaloblastic anemia
o neuropathies (vertigo, headache and nystagmus)
o Yellow-brown pigmentation of skin
o hirsutism
o lymphadenopathy
o risk of cardiac arrythmias when injected rapidly
- Valproate
o Hepatotoxic (monitored in plasma)
o Teratogenic
- Benzodiazepines
o SE
▪ drowsiness, dizziness
▪ upset stomach
▪ blurred vision
▪ dreaming
▪ depression
- Amitryptilline (TCA)
o SE
▪ ED
▪ ↑ QT interval
- Erythromycin:
o Abdominal Pain
o Anorexia
o Loose bowel motions
- CorticoSteroids
o SE – Oxford 371
▪ Short term
• mood changes: euphoria, depressive
• mild hypokalemia
• mild hyperglycemia – counter-insulin effect
▪ Long term (Cushing – like syndrome)
• insomnia, increased appetite
• fluid retention – mineralocorticoid effect
• HTN
▪ adrenal suppression
▪ avascular necrosis of the bone
▪ myopathy
▪ cataract
▪ gynecomastia?
▪ osteoporosis
▪ growth suppression
63

▪ pancreatitis
▪ oesophageal and peptic ulceration
▪ infections – ↑frequency and severity
• candidiasis
• chickenpox
- Teratogenic drugs
o class
▪ A – safe
▪ B – not fully studied, Metronidazole
▪ C
• Lithium – defintely teratogenic in the 1st trimester and should always
be suspended, preferrably before an intended pregnancy!
• Methadone
- should be taken during the 1st trimester
- discontinue gradually in the 2nd trimester
- taken again during breastfeeding to prevent or minimise
withdrawal or abstinence in the neonate
• Phenytoin and all entiepileptics
• Warfarin
• ACE inh.
• Danazol (androgenisation) Clitoral hypertrophy & labial fusion
• Retinoids
• A/B:
- tetracyclines (growth retardation, etc.)
- metronidazole (its now proven to be safe)
- chloramphenicol
- aminoglycozides
- Drugs causing pulmonary infiltration
o Amiodarone -> fibrosis, alveolitis
▪ other SE:
• hypothyroidism (inf. the conversion of T4 -> T3)
• photosensitivity
• skin pigmentation
• peripheral neuropathy
• ARDS
o Bleomycin
o Busulphan
o Gold compounds (rheumatoid arthritis)
o Nitrofurantoin
o Methotrexate
o Methylsergide
- Nephrotoxic drugs
o A/B
▪ Aminoglycosides: gentamycin, etc.
▪ Cephalosporins – some
• worst combinations causing ARF (acute tubular necrosis):
- Gentamycin + Cefazolin (1st gen)
64

- 1st gen + furosemide or vancomycin

▪ Vancomycin
▪ Tetracyclines
o NSAIDs, COX-2 inhibitors
o ACE inh (in early stages protective & toxic in advanced stages) & AIIRA antagonists
o Lithium
o Radio contrast
- Ototoxic drugs
o Aminoglycosides (+ nephrotoxi)c
o Furosemide
- Methotrexate
o SE - Pancytopenia
- Aspirin
o CI:
▪ Peptic ulceration
▪ Asthma
▪ Children (Rye syndrome)
Anticoagulants
- Heparin
o Types
▪ Unfractioned
▪ LMW (fractioned)
o adm. IV or SC
o monitored by APTT
o inactivates thrombin
o Cx
▪ Heparin induced thrombocytopenia (HIT)--- Cytotoxic
• Petechiae of skin, bleeding, hematuria
• thrombosis – most characteristic
• usually when using unfractioned heparin, rarely with fractioned heparin
• ↓ platelets but thrombotic disorder
• 4-15 days after administration of heparin -> Sx of thrombosis
• Rx
- Withdrawal of heparin
- Antidote: Protamine Sulphate
- Replacement with warfarin
- Warfarin
o Antivit. K, depresses factor II (prothrombin), VII, IX, X
o effect starts after 2-3 days
o full effect after 5-7 days
o Antidote:
▪ Vit. K
▪ FFP
▪ Prothrombin complex concentrate
o Monitored with INR (normal INR = 0.8-1.1)
▪ Target INR:
• 2-3 for most indications
65

• 2.5-3.5 for mechanical prosthetic heart valve

▪ INR measured
• before starting –> baseline (modified in certain dis., e.g. liver dis.)
• 3rd day -> effect started
• 5-7th day -> max. effect
• daily for 1 week – adjust the dose
• weekly for next 4 wks
• then monthly
o indic:
▪ Prosthetic cardiac valve
▪ DVT, PE
▪ A Fib. selected cases
▪ Post-coronary bypass & lower limb surgeries
▪ Thrombosis in antiphospholipid antibody syndrome
o CI
▪ active bleeding
▪ intracranial bleeding
▪ uncontrolled HTN
▪ impaired liver function
▪ Pregnancy: in 1st trimester it causes fetal chondrodysplasia punctata and in
2nd and 3rd trimester it causes fetal optic atrophy and mental reatrdataion.
o Cx
▪ Skin necrosis
▪ Purple toes syndrome
▪ Rx – stop warfarin
o Intoxication
▪ INR 3-5
• Lower dose or omit next dose of warfarin
• Resume therapy at a lower dose when INR is in therapeutic range
▪ INR 5-9:
• Cease Warfarin
• Give Vit. K
• Measure INR after 24 hrs
▪ INR > 9
• Low risk of bleeding
- Cease warfarin
- give vit. K
- Measure INR in 6-12 hrs
• High risk of bleeding
- Cease warfarin
- Give FFP
- Give vit K
- Measure INR in 6-12 hrs
▪ if bleeding, no matter what the INR is - FFP
o Pre-op:
▪ Elective surgery
• Stop it 1 wk before surgery + start heparin (LMW heparin)
66

• Stop heparin 12-24 hrs before surgery

• after surgery, start heparin and warfarin
• Stop heparin when desired INR has been achieved
▪ Emmergency surgery
• Give FFP + prothrombine concentrate + Vit. K
o Admin. for
▪ 3 months if cause of DVT is known
▪ 6 months if cause of DVT is unknown
- Anti-platelets
o Aspirin
▪ Thromboxane A2 inhibitor
▪ 100 mg tabet – 1x/ day
o Clopidogrel
▪ ADP inhibitor
▪ 75 mg
o Dipyridamole
▪ Phosphodiesterase inh.
▪ indic. – prosthetic valves in young patient
▪ also a vasodilator (with more SE)
o GP IIb/IIIa glycoproteins
▪ Eptifibatide, Alciximal
▪ for interventional cardiology
Types of drugs by action (useful_medical.doc)
Antibiotics
- Penicillin – 14% of Streptococcus pneumoniae is resistent to penicillin in Australia
o Benzylpenicillin IV – the first choice in uncomplicated lobar pneumonia
- Group B streptococcus
o Benzylpenicillin
▪ if allergic – clindamycin or erythromycin
- Amoxycillin + clavulanic acid = Augmentin – very broad spectrum
o in urinary infections (E. coli)
- Cefalexin
o in urinary infections (E coli)
- Cotrimoxazole + metronidazole
- Doxycycline – in Atypical pneumonia: Chlamydia pneumoniae, Mycoplasma pneumoniae
- Flucoxacillin + gentamycin – broad spectrum
- Gonorrhoea
o currently: Doxycycline + Metronidazole – but N. gonorrhoea increasingly resitent to
tetracyclines, so replace with:
▪ probenecid (increases the serum concentration of antibiotics by inhibiting their
renal excretion) + ceftriaxone + doxycycline
▪ clindamycin
▪ gentamicin
▪ azithromycin
- Syphillis
o Procain benzylpenicillin
▪ Doxycycline for people sensitive to penicillin
67

- Toxoplasmosis
o Pyrimethamine + Sulfadiazine (+ folic acid, to counteract their antifolate activity)
- Clostridium difficile
o 1. Metronidazole
o 2. Vancomycin– if 1 fails

o Antiemetic, nausea:
a. side effect of morphine – haloperidol, prochlorperazine (Stemetil)
b. poor gastric emptying – metclopramide, cisapride, domperidone
c. cytotoxic chomotherapy or radiotherapy – ondansetron (Zofran) = serotonin receptor
antagonist

Antivertigo – Betahistine - dilate blood vessels within middle ear which can relieve pressure from
excess fluid and act on smooth muscle. In Meniere’s syndrome.
Antipsychotics:
- Tranquilizing psychiatric medication primarily used to manage psychosis (including delusions or
hallucinations, as well as disordered thought) particularly in schizophrenia and Bipolar Disorder.
- All antipsychotic drugs tend to block D2 receptors in dopamine pathways of brain. This means
that dopamine released in these pathways has less effect. Excess release of dopamine in
mesolimbic pathway has been linked to psychotic experiences. It is blockade of dopamine
receptors in this pathway that is thought to control psychotic experiences.
- 1st generation (Typical) antipsychotics – 1950 - the first typical antipsychotics to enter clinical
use were the Phenothiazine (Chlorpromazine)
o Butyrophenones
▪ Haloperidol (Haldol, Serenace)
▪ Droperidol (Droleptan)
o Phenothiazines
▪ Chlorpromazine (Thorazine, Largactil)
▪ Fluphenazine (Prolixin) - Available in decanoate (long-acting) form
▪ Perphenazine (Trilafon)
▪ Prochlorperazine (Compazine)
▪ Thioridazine (Mellaril, Melleril)
▪ Trifluoperazine (Stelazine)
▪ Mesoridazine
▪ Periciazine
▪ Promazine
▪ Triflupromazine (Vesprin)
▪ Levomepromazine (Nozinan)
▪ Promethazine (Phenergan)
▪ Pimozide (Orap)
o Thioxanthenes
▪ Chlorprothixene (Cloxan, Taractan, Truxal)
▪ Clopenthixol (Sordinol)
▪ Flupenthixol (Depixol, Fluanxol)
▪ Thiothixene (Navane)
▪ Zuclopenthixol (Cisordinol, Clopixol, Acuphase)
68

- 2nd generation (Atypical) antipsychotics - less extrapyramidal motor control disabilities in

patients, which include unsteady Parkinson's disease-type movements, body rigidity and
involuntary tremors. These abnormal body movements can become permanent even after
medication is stopped. During the course of treatment atypical antipsychotics are associated
with the following benefits; higher rate of responders, efficiency in patients with refractory
disease, lower risk of suicides, better functional capacity and an improved quality of life.
o Clozapine (Clozaril) -Requires wkly to biwkly CBC due to risk of agranulocytosis. – New
gold standard in Schizophrenia
o Olanzapine (Zyprexa) - Used to treat psychotic disorders including Schizophrenia, acute
manic episodes and maintenance of Bipolar Disorder. Dosing 2.5 to 20 mg/day.
o Risperidone (Risperdal) - Dosing 0.25 to 6 mg/day and is titrated upward. Divided dosing
is recommended until initial titration is completed at which time the drug can be
administered once daily. Used off-label to treat Tourette syndrome & anxiety disorder.
o Quetiapine (Seroquel) - Used primarily to treat Bipolar Disorder, Schizophrenia and "off-
label" to treat chronic insomnia & restless legs syndrome. It is a powerful sedative.
Dosing starts at 25 mg and continues up to 800 mg maximum per day, depending on the
severity of the symptom(s) being treated.
o Ziprasidone (Geodon) - Approved in 2006[citation needed] to treat bipolar disorder.
Dosing 20 mg twice daily initially up to 80 mg twice daily. Side-effects include a
prolonged QT interval in the heart, which can be dangerous for patients with heart
disease or those taking other drugs that prolong the QT interval.
o Amisulpride (Solian) - Selective dopamine antagonist. Higher doses (greater than 400
mg) act upon post-synaptic dopamine receptors resulting in a reduction in the positive
symptoms of schizophrenia, such as psychosis. Lower doses, however, act upon
dopamine autoreceptors, resulting in increased dopamine transmission, improving the
negative symptoms of schizophrenia. Lower doses of amisulpride have also been shown
to have antidepressant and anxiolytic effects in non-schizophrenic patients, leading to
its use in dysthymia and social phobias. Amisulpride has not been approved for use by
the Food and Drug Administration in the United States.
o Asenapine (Saphris) is a 5-HT2A- and D2-receptor antagonist under development for the
treatment of schizophrenia and acute mania associated with bipolar disorder.
o Paliperidone (Invega) - Derivative of risperidone that was approved in 2006.
o Iloperidone (Fanapt) - Approved by the FDA on May 6, 2009.
o Zotepine (Nipolept, Losizopilon, Lodopin, Setous)- An atypical antipsychotic indicated for
acute and chronic schizophrenia. It was approved in Japan circa 1982 and Germany in
1990, respectively.
o Sertindole (Serdolect, and Serlect in Mexico). Sertindole was developed by the Danish
pharmaceutical company H. Lundbeck. Like the other atypical antipsychotics, it is
believed to have antagonist activity at dopamine and serotonin receptors in the brain.
Antidepressants:
- Selective serotonin reuptake inhibitors (SSRIs) - current standard of drug treatment
o A possible cause of depression is an inadequate amount of Serotonin, a chemical used
in brain to transmit signals between neurons. SSRIs are said to work by preventing
reuptake of serotonin (also known as 5-hydroxytryptamine or 5-HT) by presynaptic
neuron thus maintaining higher levels of 5-HT in the synapse.
o This class of drugs includes:
▪ Citalopram (Celexa, Cipramil)
69

▪ Escitalopram (Lexapro, Cipralex, Seroplex, Lexamil)

▪ Fluoxetine (Prozac, Sarafem, Symbyax)
▪ Fluvoxamine (Luvox)
▪ Paroxetine (Paxil, Aropax)
▪ Sertraline (Zoloft)
o These have fewer adverse effects than tricyclics or MAOIs. Although effects like
drowsiness, dry mouth, nervousness, anxiety, insomnia, decreased appetite, long-term
weight gain and decreased ability to function sexually may occur. Some side effects may
decrease as a person adjusts to drug but other side effects may be persistent. Though
safer than first generation antidepressants, SSRIs may not work on as many patients as
previous classes of antidepressants, suggesting the role of norepinephrine in depression
is still important.
- Serotonin-norepinephrine reuptake inhibitors (SNRIs)
o newer form of antidepressant that work on both norepinephrine and 5-HT. They
typically have similar side effects to SSRIs though there may be a withdrawal syndrome
on discontinuation that may necessitate dosage tapering.
o These include:
▪ Desvenlafaxine (Pristiq)
▪ Duloxetine (Cymbalta)
▪ Milnacipram (Ixel)
▪ Venlafaxine (Effexor)
- Tricyclic antidepressants (TCAs)
o Oldest class of antidepressant drugs. Tricyclics block reuptake of certain
neurotransmitters such as norepinephrine (noradrenaline) and serotonin. They are used
less commonly now due to the development of more selective and safer drugs. Side
effects include ↑ heart rate, drowsiness, dry mouth, constipation, urinary retention,
blurred vision, dizziness, confusion and sexual dysfunction. However, TCAs are still
used because of their effectiveness especially in severe cases of major depression.
o These include:
▪ Tertiary amine tricyclic antidepressants:
• Amitriptyline (Elavil, Endep) – also used in neuropathies, e.g. in
diabetes, shingles, ankylosis spondylitis, etc. for pain relief
• Clomipramine (Anafranil)
• Doxepin (Adapin, Sinequan)
• Imipramine (Tofranil)
• Trimipramine (Surmontil)
▪ Secondary amine tricyclic antidepressants
• Desipramine (Norpramin)
• Nortriptyline (Pamelor, Aventyl, Noritren)
• Protriptyline (Vivactil)
- tetracyclic antidepressants (TeCAs)
o named after their chemical structure which contains four rings of atoms and are closely
related to the tricyclic antidepressants (TCAs) which contain three rings of atoms.
o Pharmaceutical Drugs
▪ Amoxapine (Asendin)
▪ Maprotiline (Deprilept, Ludiomil, Psymion)
▪ Mazindol (Mazanor, Sanorex)
70

▪ Mianserin (Bolvidon, Norval, Tolvon)

▪ Mirtazapine (Remeron, Avanza, Zispin)
▪ Setiptiline (Tecipul)
- Monoamine oxidase inhibitors (MAOIs)
o may be used if other antidepressant medications are ineffective. MAOIs work by
blocking enzyme monoamine oxidase which breaks down neurotransmitters dopamine,
serotonin and norepinephrine (noradrenaline).
o Because there are potentially fatal interactions between this class of medication and
certain foods (particularly those containing tyramine) as well as certain drugs, classic
MAOIs are rarely prescribed anymore. However, this does not apply to Emsam, the
transdermal patch form of selegiline, which due to its bypassing of the stomach has a
lesser propensity to induce such events.
o MAOIs can be as effective as tricyclic antidepressants, although they are generally used
less frequently due to the fact that they have a higher incidence of dangerous side
effects and interactions. A new generation of MAOIs has been introduced; moclobemide
(Manerix), known as a reversible inhibitor of monoamine oxidase A (RIMA), acts in a
more short-lived and selective manner and does not require a special diet.
o The MAOI group of medicines include:
▪ Isocarboxazid (Marplan)
▪ Moclobemide (Aurorix, Manerix)
▪ Phenelzine (Nardil)
▪ Selegiline (Eldepryl, Emsam)
▪ Tranylcypromine (Parnate)
- Noradrenergic and specific serotonergic antidepressants (NaSSAs)
o newer class of antidepressants which purportedly work to increase norepinephrine
(noradrenaline) and serotonin neurotransmission by blocking presynaptic alpha-2
adrenergic receptors while at the same time blocking certain serotonin receptors.
o Examples include:
▪ Mianserin (Tolvon)
▪ Mirtazapine (Remeron, Avanza, Zispin)
- Norepinephrine (noradrenaline) reuptake inhibitors (NRIs)
o act via norepinephrine (also known as noradrenaline). NRIs are thought to have a
positive effect on the concentration and motivation in particular.
o These include:
▪ Atomoxetine (Strattera)
▪ Mazindol (Mazanor, Sanorex)
▪ Reboxetine (Edronax)
▪ Viloxazine (Vivalan)
- Norepinephrine-dopamine reuptake inhibitors (NDRIs)
o inhibit the neuronal reuptake of dopamine and norepinephrine (noradrenaline).
o These include:
▪ Bupropion (Wellbutrin, Zyban)
- Selective serotonin reuptake enhancers (SSREs)
o Tianeptine (Stablon, Coaxil, Tatinol)
- Norepinephrine-dopamine disinhibitors (NDDIs)
o act by antagonizing the serotonin 5-HT2C receptor which normally acts to inhibit
norepinephrine and dopamine release, thereby promoting outflow of these
neurotransmitters.
71

o Examples:
▪ Agomelatine (Valdoxan, Melitor, Thymanax)

Lithium:
- A mood stabilizing drug, primarily in treatment of Bipolar Disorder, where it has a role in
treatment of depression and particularly mania, both acutely and in the long term. As a mood
stabilizer, it is probably more effective in preventing mania than depression and may ↓ risk of
suicide in certain bipolar patients. In depression alone (unipolar disorder) Lithium can be used to
augment other antidepressants. Lithium carbonate (Li2CO3), sold under several trade names is
MC prescribed while the citrate salt lithium citrate (Li3C6H5O7) the sulfate salt lithium sulfate
(Li2SO4), lithium aspartate and the orotate salt lithium orotate are alternatives.
- Upon ingestion, it becomes widely distributed in CNS and interacts with a number of
neurotransmitters and receptors, ↓ norepinephrine release and increasing serotonin synthesis.
Parkinson: Levo-dopa (precursor of cathecolamines: dopamine, epinephrine, norepinephrine),
Quetiapine (at night, = antipsychotic,= Seroquel, also used in Schizophrenia, Bipolar syndrome, restless
legs syndrome and chronic insomnia )

Cholinesterase inhibitors: Donepezil, galantamine, rivastigmine – in Alzheimer’s disease, Dementia

(modest delay of dementia progression)

Alzheimer’s disease: Cholinesterase inhibitors (donepezil), aspartate (NMDA) antagonist (Memantine)

Antiepileptics:
- Carbamazepine (+ also used in Trigeminal neuralgia)
- Valproate
- Ethosuximide
- Gabapentin (+ diabetic neuropathy, post-herpetic neuralgia)

Hiccoughs – Chlorpromazine (antipsychotic), Haloperidol (antipsychotic)

Anticoagulants:
- Warfarin = Antivit. K (coumadins) Oral
o in patients with atrial fibrillation, if > 65 and with no other contraindications
o full effect reaches after 5-7 days
o maintain an INR = 2 to 3
o Antidotes:
▪ Vit. K – effect is not immediate
▪ FFP --brings all required coagulation factors. Effect is immediate
- Heparin: (Ati- thrombin)
o long term treatment: start with heparin (SC or IV) until oral warfarin starts to take effect
(5-7 days)
o can be:
▪ Unfractioned – short half-life so adm. frequently or as an infusion, HIT
▪ Fractioned (LMWH) – daily usage
• Enoxaparin
• Dalteparin
o Antidote: Protamine Sulphate -Reverses anticoagulant effects of heparin by binding to it
Antiplatelet drugs:
72

- Aspirin
o it has half the effectiveness of warfarin in preventing strokes!!!
- Dypiridamole
- Ticlopidine, Clopidogrel

Thrombolytics:
- These drugs are most effective if administered immediately. The advantage of administration is
highest within first 60 minutes, but may extend up to 6 hrs after start of symptoms.
- examples:
o tissue plasminogen activator - t-PA - alteplase (Activase)
o reteplase (Retavase)
o tenecteplase (TNKase)
o anistreplase (Eminase)
o Streptokinase (Kabikinase, Streptase)
o urokinase (Abbokinase)
- Side-effects:
o Hemorrhagic stroke is a rare but serious complication of thrombolytic therapy.
o If a patient has had thrombolysis before, an allergy against the thrombolytic drug may
have developed (especially after streptokinase).

Edema – dexamethasone, prednisolone (corticosteroids)

Muscle spasm – diazepam, clonazepam, baclofen, dantrolene

Terminal distress/ restlessness – clonazepam, midazolam

Antispasmodic – hyoscine

Death rattles – hyoscine (dries the secretions), atropine

Hypercalemia – biophosphonates (APD)

Anorexia – metoclopramide, corticosteroids

Pharmacology
o Pharmacodynamics = mec. of action of a drug
▪ includes the concentration-effect rship.
o Pharmacokinetics = time course of the body handling the drug
▪ includes the concentration-time rship
o EC50 – effective concentration that causes 50% of the effect
▪ the smaller the more potent the drug
o types of kinetics
▪ First-order kinetics
• drug elimitation is proportional with the conc. of the drug
• half-life is constant
• most drugs
• chart:
- regular (with conc. and time) – exponential curve
73

- with logarithm of conc. and time – straight line

▪ Zero-order kinetics
• Removal of a constant amount of the drug
• Chart:
- regular (with conc. and time) – straight line
• e.g.
- aspirin
- alcohol
- phenytoin
o Drugs with effect on liver enzymes
▪ Liver enzyme inducers - ANTIEPILEPTICS
• Antiepileptics
- Phenytoin
- Carbamazepine
• Barbiturates: Phenobarbitol (used in jaundice)
• Rifampicin
▪ Liver enzyme inhibitors – A/B
• Erythromycin
• Isoniazid
• Metronidazol
• Ketoconazol
• Cimetidine
• Ethanol
• SSRI (e.g. Fluoxetine, F luvoxamine) inh. the clearance of benzos,
Clozapine, Warfarin => toxicity
- Venlafaxine, Citalopram, Sertraline are less causing this
interaction
- 1st pass metabolism of a drug– what’s left after being absorbed & partially degraded by liver
o By passed by
▪ Inhalation
▪ IV
▪ Sublingual
▪ IM
▪ PR admin.
- Drugs by effect:
o Cholinergic drugs
▪ Physostigmine
• is a parasympathomimetic, a reversible cholinesterase inhibitor
• used to treat myasthenia gravis, glaucoma, Alzheimer's disease and
delayed gastric emptying. Recently, it has begun to be used in the
treatment of orthostatic hypotension.
• Because it is a tertiary amine (and does not bond Hydrogen, making it
more hydrophobic) it can cross blood-brain barrier & physostigmine
salicylate is used to treat CNS effects of atropine, scopolamine and
other anticholinergic drug overdoses.
▪ Neostigmine
▪ Succinylcholine – muscle relaxant (intubation, ECT)
74

o Anticholinergic drugs – in extrapir. effects of antypsychotics

▪ benzatropine
▪ benzhexol
▪ atropine
▪ scopolamine (hyoscine) – smooth muscle relaxant
▪ TCAs -- Amitryptiline, chlomipramine, imipramine
▪ antypsychotics: chlorpromazine, thioridazine
o ↑dopamine
▪ dopaminergic – in Parkinson
• Levodopa, Carbidopa
▪ dopamine agonists – in Parkinson
• Bromocriptine – also in hyperprolactinemia
• OPergolide
• Cabergoline
o ↓dopamine
▪ antipsychotics
• haloperidol, droperidol, amisulpride, risperidone
• chlopromazine
- Anticholinergic delirium – caused by the anticholinergic drugs
o agitation, confusion, motor restlessness,dysarthria, myoclonus, hallucinations, convulsions
o dry mouth, constipation, flatulance, urinar ret., tachycardia, HT, dilated and sluggishly
reactive pupils
o Rx
▪ Physostigmine IV
• if cholinergic SE – admin. atropine
- Vitamins
o Fat soluble – A, D, E, K
o Water sol. – B complex, C
▪ Vit C
• defic. – Scurvy:
- irritability – MC presenting complaint
- gum bleeding
▪ Vit. D
• defic.
- rickets (children)
- adults (osteomalacia)
▪ incr. ALP
▪ incr. costochondral junction
▪ Vit. B1 (thiamine)
• defic. Beri-Beri
- Baby is restless, sleepless, breathless, eats less (anorexia),
Cardiomegaly, neuropathy, memory loss.
- Chronic def. results in Wernick’s Encephalopathy.
▪ Vit. B3 (Niacin, Nicotinic acid)
• Deficiency = Pellagra
- 3Ds:
▪ diarrhoea
75

▪ dermatitis
▪ dementia
- Regular monitoring of plasma level of drugs – for:
o Lithium
o Digitalis
o Theophylline
Therapeutic value Toxic value
Digitalis 0.5-1.5 2
Lithium 0.6-1.2 2
Theophylline 10-12 20
o Clozapine
▪ monitor FBE (neutropenia) and glucose tolerance (DM)
o nortryptiline
o (Amit) +
▪ Aminoglycosides: gentamicin
▪ Antiepileptics: phenytoin, valproate, carbamazepine
▪ antiarrhythmics
▪ antidepressants
- Drug interactions
o Erythromycin and Theophylline
o ACE inhibitors and Diuretics
o Amiodarone and Beta Blockers
o NOT - Digoxin and Warfarin
- Drug administration changes in pre-op for elective surgery
o Oral hypoglycemic
▪ No change for minor procedure
▪ Switch over to insulin at least 48 hrs before surgery
o OCP
▪ Combined OCPs: Stop pill 4 weeks before surgery (risk of DVT due to ↑
estrogen in OCP)
▪ Mini-pill: can be continued
o Oral anticoagulants
▪ Warfarin
• Elective surgery
- Stop it 1 week before surgery + start heparin (LMW heparin)
- Stop heparin 12-24 hrs before surgery
- After surgery, start heparin and warfarin
- Stop heparin when desired INR has been achieved
• Emmergency surgery
- Give FFP + prothrombine concentrate + Vit. K
o Aspirin, Clopidogrel - Stop 1 week before surgery
o Antianginal, Anti-HT – continued
o Antidepresants
▪ MAOI – Stop 3 weeks before surgery
▪ Lithium – Stop 48-72 hrs before surgery
o C/S
76

▪ if taken for > 1 week in last year (external C/S have suppressed the endogenous
production of C/S): give hydrocortison supplement before or during surgery to
keep up with the stress of the surgery
- Drugs that can be delivered by endotracheal tube
o O2
o Naloxone
o Lignocaine
o Atropine
o Adrenaline
o Asthma
▪ Beta 2 agonists: Salbutamol (Ventoline)
▪ Cholinergic blockers: Iprotropium bromide (Atrovent)
- Statin (HMG-CoA inh.)
o SE
▪ Hepatotoxic
▪ Myositis
• Statins + fibrates = bad combination -> risk of myopathy (simvastatin
myopathy)
- even worse with erythromycin – liver enzyme inhibitor
- causes rhabdomyolysis:
▪ check serum CK and urine myoglobin
▪ hemoglobinuria (not hematuria) – no RBCs on
microscopy
o CI in pregnancy
o Dx
▪ LFT, CK – follow up for 6 mths
- Follow up LFT test
o Anti-TB drugs
o Anti-epileptics
o Li
o Statins
Obstetrics - OK
Pregnancy parameters
- Implantation:
o 5 days for fertilized egg
o 10 days from ovulation
- Don’t monitor baby up to 24 weeks
o until then – only monitor mother
- Term baby > 37 weeks
- Characteristic of pregnancy
o immunological suppresion
o leucocytosis
- Gestational age - most appropriate examination:
o U/S in first trimester, 8th to 9th week, before 18 wks (not reliable after 18th week)
▪ the earlier the more accurate
▪ measures the crown-rump legnth (CRL)
o if no U/S then pelvic/ bi-manual examination in first trimester
77

▪ measure the uterine size----fundal height

- Engagement of the fetal head
o 36-40 wks – in primigravida
o during labor – in multigravida
- Fetal Heart Sound
o heard with Doppler amplifier at 9-12 weeks
o heard with the stethoscope at 20 weeks
- Fetal movements felt by
o 18 wks – multigravida
o 20 wks – primigravida
- Characteristic for pregnancy
o LH very elevated – because beta sub-units of LH and HCG are almost identical so the
HCG is measured in the LH assays
▪ > 200 mIU/mL -> indicative of pregnancy

Gravida/ para/ abortus (GPA) or sometimes just gravida/ para (GP), is a shorthand notation for a
woman's obstetric history.

- Gravida indicates the total number of times a woman has been pregnant, regardless of whether
these pregnancies were carried to term. A current pregnancy, if any, is included in this count.
- Para indicates the number of viable (>20 wks) births. Pregnancies consisting of multiples, such as
twins or triplets, count as ONE birth for the purpose of this notation.
- Abortus is the number of pregnancies that were lost for any reason, including induced abortions
or miscarriages. The abortus term is sometimes dropped when no pregnancies have been lost.

Pregnancy stuff:
duration: 37-42 wks (40 weeks since last normal menstrual period, LNMP or 38 wks from conception)
Prenatal care:
monthly visits during the first two trimesters (from week 1–28)
biweekly from 28 to week 36 of pregnancy
weekly after week 36 (delivery at week 38–40)
total: 14 (can be reduced to 7-10)

Weight gain: 12.5 kg (9-15) of which 9 kg in the last 20 weeks

6 weeks after birth the woman should weigh 3 kg more than before pregnancy
6 months after birth the woman should weigh 1 kg more than before pregnancy

Supplimentation:
Folate 0.5 mg last 3 months and first 3 months of the pregnancy
Iron – in vegans/ vegetarians
Calcium and vit. D (10 µgrams/ day) – maybe
Vit. A excess is harmful to the baby!

Screening:
- Chorionic villus sampling: 9-11 weeks, result in 48 hrs
- Amniocentesis: 15 weeks, result in 3 weeks
- Ultrasound
- Immunisations:
78

- Influenza
- Typhoid or cholera – if travelling abroad
- Polio – if not vaccinated yet

Symphisis – Fundal height: approx. match height in cm = No. of weeks (e.g. at 20 weeks – 20 cm)

Evolution:
by 10 weeks (70 days) the placental development is complete
uterus becomes palpable from 12-13 weeks
fetal movements felt after 18 weeks
morphology ultrasound scan at 18-20 weeks
uterine fundus reaches the umbilicus – 20 weeks
Infections in pregnancy
- Pregnancy doesn’t lower the woman’s resistance to inf.?
o exception: poliomyelitis
- baby – immunocompetent at 14 wks, but the efficacy is low till the second ½ of the pregn.
- Mx
o offer mother termination of pregnancy if active infection with:
▪ Erythema infectiosum (Slppped cheek, 5th disease)
▪ Rubella
- Types
o a. Bacterial
▪ 1. Group B Streptococcus:
• (15) 18-27% of mothers are carriers
• during labour > 50% of babies born through an infected vagina are
colonized
- 1% of them will develop early onset GBS neonatal sepsis ->
difficult to treat with high neonatal death
▪ 25-30% of premature babies
▪ 2-8% of term babies
▪ 15-40% neurological sequelae in survivors
• risk incr. in
- PROM – mother can develop chorioamniotitis
- Vaginal delivery – especially in premature babies
• Mx – 2 approaches:
- 1. test for it at 36 weeks
▪ Swab low vagina + rectum
- 2. treat if positive risk factors
▪ premature labor < 37 weeks
▪ when anticipated ROM > 18 hrs before delivery
▪ intrapartum fever > 38o C
▪ previous early onset GBS dis.
▪ GBS bacteriuria during pregnancy
• Rx.
- for mother
▪ come to hospital if early labor
79

▪ Benzyl Penicillin every 6 hrs during labor or after ROM

- crosses the placenta and goes to the baby
• if allergic to penicillin: Clindamycin or
Erythromycin
- for baby
▪ optional if baby is normal
▪ mandatory if baby is infected or in prolonged PROM
▪ 2. Gonorrhoea
• can cause:
- septic abortion
- chorioamnionitis during pregnancy
- neonatal blindness from conjunctivitis. Neonates coming through
the birth canal are given erythromycin ointment in eyes to
prevent blindness from infection. The underlying gonorrhea
should be treated; if this is done then usually a good prognosis
will follow.
• investigate whether mother is infected – culture on Thayer-Martin
medium
• Rx:
- Erythromycin or Roxythromycin
- For non-pregnant woman - currently: Doxycycline +
Metronidazole – but N. gonorrhoeae increasingly resitent to
tetracyclines, so replace with:
▪ Probenecid (increases the uric acid in urine + increases
the serum concentration of antibiotics by inhibiting
their renal excretion) + ceftriaxone + doxycycline
▪ Clindamycin
▪ Gentamicin
▪ Azithromycin
▪ 3. Syphilis
• extremely rare now
• able to penetrate the placenta after 15th week -> congenital syphilis in
20-50%, perinatal death in 20-30%
• can cause early and late congenital syphilis: stillborns, prematurity,
Hutchinson's triad (deafness, Hutchinson's teeth (centrally notched,
widely-spaced peg-shaped upper central incisors) and interstitial keratitis
(IK), an inflammation of the cornea which can lead to corneal scarring
and potential blindness), mulberry molars (6th year molars with multiple
poorly developed cusps), frontal bossing, poorly developed maxillae,
enlarged liver and spleen, etc.
• screening at first antenatal test + repeated at 30 wks
- VDRL
- rapid plasma reagin (RPR) test
• confirmed with more specific tests:
▪ TP haemagglutination test (TPHA)
▪ fluorescent treponamal AB test (FTA-ABS)
▪ TP immobilisation test (TPI)
80

• Rx
- Procaine benzylpenicillin or benzathine penicillin
- Non-pregnant: if sensitive to penicillin
▪ Doxycycline
- in case mother was infected and not fully treated -> baby also
treated with procaine benzylpenicillin for 10 days
▪ since baby’s sympt. are non-specific + serology is
inacurate
o b. Viral – smaller than bact. => higher chance of passing through the placenta
▪ most of them infect baby only if very severe infection in mother
• exceptions:
- Rubella
- CMV
- Herpes
▪ 1. Rubella (German Measles)
• very rare now, due to the immunization program
- 85% had the inf. and 90% of them are immune
• if active inf. in first 14 wks => fetus will almost certainly be inf. (90%),
with 40% of them being damaged by virus (5% risk in last trim.)
• causes “Congenital Rubella Syndrome”:
- Prematurity
- "blueberry muffin" rash
- Cataract, blindness
- Deafness
- Heart malformation - PDA
- IUGR
- Thrombocytopenic purpura, hepatosplenomegaly
- Vasculitis, renal artery stenosis
• Prevention
- Immunize all women between 11-13 yrs
- Screening
▪ when she wants to get pregnant
• if not immune – get vaccine and don’t get
pregnant in next 3 months
▪ at first pregnancy test – if vaccinated, extremely small
risk of infection
• Mx in case of inf. (rubelliform rash – 50% of rashes are not due to
rubella) or contact with infected person
- Pregnancy test neg.
▪ IgM neg., IgG neg. -> immunize and don’t get pregnant
in next 3 mths
▪ IgM pos., IgG neg. -> supportive Rx + don’t get
pregnant till sympt. disappear and IgG becomes pos.
▪ IgM neg., IgG pos. = immune, safe to get pregnant
- Pregnancy test pos.
▪ IgM neg., IgG neg. -> do not immunize + avoid contact
with inf. person + repeat test in 3 weeks
81

• if IgM become pos. -> discuss therapeutic

abortion if first trimester
• amniocentesis can be used to confirm the
infection of the baby
▪ IgM pos., IgG neg. -> discuss therapeutic abortion if
first trimester
▪ IgM neg., IgG pos. = immune, continue pregnancy
▪ 2. CMV
• MC non-bacterial pregnancy inf. in Aus.
• CMV is the MC cause of congenital infection in humans and intrauterine
primary infections are 2nd only to Down's syndrome as a known cause
of mental retardation.
• 1% of women may become inf. during pregnancy
- most of them asymptomatic
- Dx: Urine culture for virus (MCQ), PCR for amniotic fluid
- Cx
▪ ↑perinatal mortality
▪ 3-7% with congenital abnormalities
• Microcephaly, hepatosplenomegaly, petechial
rash on skin, hearing loss, visual impairment or
diminished mental and motor capabilities,
pigmented retina and no cataract (MCQ)
• no screening since there is no vaccine available
▪ 3. Genital herpes
• primary inf. is usually asympt. MCQ
• transm.
- during pregnancy – rare: 1:11.000
- during labour (+ GBS)
▪ 40-50% if active primary inf.
▪ 5% if active recurrent inf.
• Dx – endocervical swabs every 2 wks from 34wk – can be abandoned
(not a good predictor)
• Mx
- if no current active inf. (primary or recurrent lesions have
healed) => vaginal delivery
- if active herpetic lesions during ROM or labor => C-section
- acyclovir prophylactic from week 38?
- + Rx the baby with acyclovir if
▪ clinically ill
▪ positive cultures
• Cx - severe neonatal inf.
- 30% risk of neonatal death
- in 40% of survivors - neurological damage
▪ 4. Chickenpox (Varicella)
• 80% of women are immune
• causes the: malformations, microcephaly, optic atrophy, psychomotor
retardation etc.
82

• primary infection during pregnancy

- in 1st trim. => 0.4% of babies are inf.
- in 2nd trim. => 2% of babies are inf.
▪ Congenital Varicela Syndrome
• limb hypoplasia
• microcephaly
• optic atrophy
• cortical atrophy
• cataracts
• psychomotor retardation
• convulsions
• IUGR
• disem. inf. in baby – if inf. is 7 days before or
after the delivery
• Dx
- IgM neg., IgG neg: but sympt. -> give mother VZV Ig 12.5 U/kg
IM within 4 days of exposure + if severe inf. Acyclovir
- IgM pos., IgG neg: -> give mother VZV Ig 12.5 U/kg IM withing 4
days of exposure + if severe inf. Aciclovir
- IgM neg., IgG pos. = Shingles – Rx mother with Acyclovir
- + infected infant
▪ VZV Ig. + Acyclovir
▪ 5. HIV
• 30% chance to pass the inf. to the baby
• inf. has no adverse reaction on the pregnancy and vice versa
• Mx
- with Rx of mother => risk drops to 2%
▪ Retroviral drugs antenatally and intrapartum
▪ C-section – reduces risk by 50%
• vaginal delivery – if viral load < 1000 copies/ml
▪ Bottle feeding
▪ coexisting STIs, chorioamniotitis or ROM for > 4 hrs =>
4x risk of transm.
▪ avoid invasive manouvers: CVS, amniocentesis,
cephalic version, etc.
▪ after delivery – baby is washed and given
Azathioprine for 6 wks
• Dx
- screening – ELISA:
▪ positive - repeat in 12 weeks
▪ unprotected intercourse + negative – repeat in 12
weeks
- confirmation – Western blot (ELISA can be positive in EBV inf.)
▪ 6. Hepatitis B
• predom. in migrant mothers
• transm. to the baby probably during birth (only 1-5% during pregnancy)
83

• ↑ risk if both HBsAg and HBcAg are pos. in mother’s blood

• Rx
- Babies are given
▪ Hep. B Ig (only if mom is infected) +
▪ (otherwise only) Hep. B Vaccine at birth, 2 and 6 mths
• Dose: 0.5 ml in the anterolat. thigh
o Adult: 1 ml in deltoid (Engerix B)
- Without Rx- high risk of liver CA when babies become adults
▪ 7. Hepatitis C
• Prevalence = 1.3%
• Risk of vertical transm. = 5%
- if assoc. with HIV + high viral load => 25%
• Rx
- no methods to avoid transm.
▪ avoid fetal scalp blood sampling and fetal scalp
electrode application (MCQ)
- Rx in mother (ribavirin + interferone) is teratogenic
- if HCV RNA is pos. in baby after 12-18 mths -> refer baby for Rx
▪ 8. Parvovirus B19 - Erythema infectiosum/slap cheeck disease/ arthritis
• pregnant lady exposed to this in 1st trimester => Hydrops
(erythroblastosis) fetalis – fever, cardiac failure -> discuss termination
• if inf. in 2nd trim – U/S of the baby
• Dx – check AB
o c. other
▪ Toxoplasmosis
• Rare – 0.2-1%
- highest risk in first trimester
• 90% asympt.
• Cx – in 25% of fetuses
- most asymptomatic – with developmental delays
- Small baby (IUGR)
- eyes and CNS may be severely damaged
- miscarriage
• TORCH infections that lead to congenital abnormalities:
- TOxoplasmosis
- Rubella
- Cytomegalovirus.
- Herpes simplex
• Screening
- antenatal + retest in each trimester
• Precautions
- avoid touching cat feces
- when handling raw meat
▪ avoid touching eyes or mouth
▪ wash hands
- only eat well-cooked meat
- wash fruits and vegetables thoroughly before eating them
84

- wear gloves when gardening

• Rx
- Pyrimethamine + sulfadiazine + folate (to counteract their
antifolate activity)
o d. UTI
▪ ↑ due to urinary stasis
▪ asymptomtic bacteriuria in pregnant women
• 6% of women (pregnant or not)
- 30% of them will develop symptomatic UTI = Pyelonephritis
• screening in early pregnancy
- Mid Stream Urine -> culture
• 85% - E. coli
• Rx for 7 days with amoxiclave (1st timst) or cefalexin or nitofurantoin
(2nd timst)
- repeat culture after 7 days
▪ if not cured, continue A/B
▪ Pyelonephritis
• usually after 20 wks
• Sx
- mild
▪ tiredness,↑ urinary frequency, dysuria
- more severe
▪ chills and rigors, fever
▪ pain over one/ both renal areas
▪ dehydration
▪ nausea
• Dx
- MSU -> culture
• Cx
- in baby
▪ low birth weight
- in mother
▪ Premature labour
▪ PROM
▪ Postpartum endometritis
▪ Perinatal death
• Rx
- correct dehydration
- AB - amoxiclav or cefalexin
▪ repeat culture every 2 wks
o e. Vaginitis
Conditions in pregnancy
- I. Early pregnancy
o a. Bleeding
▪ 1. Ectopic pregnancy
• MC location = ampula
• RISK FACTORS:
85

- Previous ectopic pregnancy

- Pelvic inflammatory disease
- Previous tubal surgery or scarring
- IVF treatment
- IUCD
- 50% with no predisposing risk factors
o Sx
- Triad: Amenorrhoea + lower abd. pain + abnormal vaginal
bleeding
- mass usually can’t be palpated
- if ruptured: rebound tenderness and a small amount of guarding
o Dx
▪ U/S
• empty uterus (absent gestational sac)
• tubal mass, tubal ring
• fluid in the pouch of Douglass
o Mx
▪ Beta HCG
▪ if < 1500 UI, repeat after 48 hrs
• if > 1500 UI, transvaginal U/S
o if gestational sac in uterus = abortion
o otherwise = ectopic pregnancy
• Rx
▪ Methotrexate
• indic.
- Beta HCG < 3500 U/L
- no FCA
- tubal mass < 3.5 cm
- tubes must be unruptured
- stable pt.
▪ normal LFT
▪ normal U & E
▪ normal FBC
- pt must use contraception (OCP) and not get
pregnant for at least 3 mths
- if methotrexate is CI –> laparoscopic surgery (salpingectomy or
salpingostomy)
o Cx
▪ Rupture
• MC location of rupture = Isthmus of fallopian tubes
• CLINICAL HISTORY:
- 5th – 9th weeks of pregnancy.
- History of breast tenderness, nausea or recent
unprotected intercourse.
- Predominant feature: Lower abdominal pain
(90%).
- Vaginal bleeding (mild), collapse.
86

- Tenderness and guarding to one side.

- Discomfort and swelling in that lateral fornix
on vaginal examination.
- Smaller uterus than expected for amenorrhoea
- shock: hT, tachycardia
• DIAGNOSIS:
- First step: Pregnancy test:
▪ Urinary dipstick in emergency deptt.
and β-hCG in blood
- Next: TVS:
▪ Empty uterus, a tubal ring, adnexal
mass and fluid in the pouch of Douglas
• MANAGEMENT:
- Hemodynamically unstable:
▪ High-flow O2
▪ IV resuscitation.
▪ Urgent referral to gynaecological team
- Haemodynamically stable:
▪ Admission.
• Give all Rh-ve mothers anti-D Imglblns.
▪ Refer for laparoscopy
▪ 2. GESTATIONAL TROPHOBLASTIC DISEASE/ NEOPLASIA
o a. Benign hydatiform mole (Molar pregnancy)
▪ Most pts (80-90%) follow a benign course with their disease
remitting spontaneously
▪ Incidence: 1 every 1500-2000 pregnancies.
▪ Higher incidence in women in Asia (Taiwan): 1 every 125-200
pregnancies.
▪ Younger than 20 years, older than 40 years.
▪ Sx
• Irregular, heavy vaginal bleeding during 1st or 2nd
trimester
• Usually painless.
• The patient may expel molar ‘vesicles’ from vagina –
clots that look like grapes
• Uterus large to date
• Excessive nausea, hyperemesis gravidarum (due to ↑β
HCG from large placenta)
- also present in multiple pregnancies
▪ Dx
• Absence of fetal heart sounds
• Ultrasound: ‘Snowstorm’ pattern is diagnostic
• β-hCG titres can be high for early pregnancy
▪ TREATMENT:
• Evacuation under GA
• Manual evacuation
• dilat. and evacuation
87

• D&C
▪ followed by U/S + prophylactic inj. of methotrexate
• FOLLOW –UP: Wkly serum or urine β-hCG.
• They should fall to undetectable levels within
12-16 wks after evacuation
• if not back to normal -> oncology assessment
for possible metastases
o MC location = lung
o brain
o bones
▪ Precaution: no pregnancy for 1 yr (use OCP)
o b. Invasive mole (chorioadenoma destruens).
o c. Choriocarcinoma.
▪ 3. Spontaneous miscarriage
o Intrauterine death – MC cause = Unknown
o Expulsion of products of conception before 24th wks of pregnancy
o Occurs in 10-20% of all early pregnancies
o MC in 1st trimester
o Miscarriage
▪ 1st trimester – Chromosomal (MC - 60%, mostly trisomies) and
fetal abnormalities
▪ MC > 35 yrs
▪ 2 trimester
nd

▪ genetic disease
▪ infection
▪ uterine malformation
▪ Fetal fibronectin test: if + even when cervix is still
closed risk of premature delivery is markedly ↑.
▪ cervical incompetence
• 20% of women with recurrent misscariage
after 12 wks have this (usually at 16 wks)
• gradual dilatation of internal cervical OS ->
intrauterine pressure will break amniotic bag at
cervical OS.
• Sx
o Recurrent miscarriage: painless leaking
of amniotic fluid (PROM)
o painless cervical dilatation + ↑ cervical
mucous discharge
o miscarriage after painless labour
o contractions – only rarely
o usually no or small bleeding – differ
from other type of miscarriages
• Dx
o U/S or vaginal examination – before
• Rx - Cervical Cerclage – sutures like a ring on
outside of cervix at internal OS
88

o at 12-14 wks (before they usually

miscarriage) Indications:
o 2 or more consecutive previous 2nd
trimester pregnancy losses.
o 3 or more preterm births before 34wks
o not after ROM.
o results
▪ 10% will still abort
▪ 10% will deliver prematurely
▪ 80% normal delivery
o sutures removed 7 days before delivery
or when she presents with labor or
ROM
o STAGES of abortion:
Threatened Inevitable Incomplete Complete Missed
(Dx. after (Dx. after U/S) (silent)
clinical exam)
POC Present, alive Present, alive Some parts No Present but
Uterine size are still dead
compatible present inside
with duration uterus
of pregnancy
Cervix Closed Open ≥ 5 mm Open Closed Closed
Fetal heart Good Good No No No
sounds
Will Normal Incomplete or Complete a. Abortion
continue pregnancy in complete a.
with 90-95% cases
Rx Observation & Minimal Minimal U/S – confirm If
bed rest bleeding: wait bleeding: wait that uterus is hemodynamic
& watch & watch empty stable and no
Heavy Heavy signs of inf.,
bleeding: bleeding: D&C patient agrees
D&C to wait + lives
close to
hospital.
- otherwise ->
D&C
▪ 1. Threatened miscarriage.
• Most common up to 14 weeks of gestation.
• Chance of successful outcome of pregnancy in
threatened abortion: 90-95%, provided ultrasound
examination is normal.
• Mild cramps and transient vaginal bleeding
• Uterine size compatible with duration of pregnancy
• External cervical os is closed on speculum examination
▪ 2. Inevitable miscarriage.
89

• Can’t be arrested/stopped
• Bleeding is heavier, abdominal cramps more persistent
(typical here)
• External OS is open (5 mm ≥).
• POC may be found in vagina or protruding from cervical
canal.
▪ 3. Incomplete miscarriage.
• Parts of fetus/placental material retained in uterus
• The bleeding remains heavy.
• Cramps persist even following passage of clots and
POC
▪ 4. Complete miscarriage.
• All fetal and placental material has been expelled from
uterus
• Bleeding and cramps stop.
• Signs of pregnancy disappear.
• Cervical OS is closed.
▪ 5. Silent or missed micarriage.
• All the POC are retained
• Cramps and bleeding are replaced by an asymptomatic
brownish vaginal discharge
• USG fails to detect fetal heart motion.
o Dx
▪ First: Pregnancy test.
• If β-hCG is positive, check β-hCG level to assess
usefulness of ultrasound of USG.
- Β-hCG greater than 1000 U/L: USG.
▪ To confirm the gestation.
▪ To check the sac size.
▪ Liquor volume.
▪ Presence or absence of fetal heart
activity
o MANAGEMENT:
▪ Stable or Unstable?
▪ IV resuscitation
▪ Transfusion if needed
▪ Refer to Gynaecological team for surgical or non-surgical
management
▪ Give Rh negative mothers anti-D immunoglobulin
▪ 4. Septic abortion
• Result of criminal abortion.
• Pelvic infection with salpingitis, peritonitis, pelvic and pulmonary
thrombophlebitis.
• Can lead to septicaemia, DIC, shock and death.
• CLINICAL FEATURES:
- Fever > 37.8
90

- Abdominal pain
- Foul-smelling vaginal discharge and bleeding.
• MANAGEMENT:
- First step: Swabs for microscopic assessment and culture.
- Immediate antibiotic therapy: Gentamicin 5mg/kg IV, ampicillin
2g IV and metronidazole 500 mg IV
- Refer for curettage or emergency hysterectomy
- II. Late pregnancy
o a. Bleeding = ANTEPARTUM HEMORRHAGE = Vaginal bleeding after 24 wks of gestation
▪ 1. Placenta praevia
• The placenta is implanted, either partially or wholly, in the lower uterine
segment and lies below the fetal presenting part.
• incidence – 1%
• MC obstetric cause of coagulopathy
• classif.
- total, complete, central – completely covers the cervical os
- partial
- marginal – edge min. 2 cm away from cervical os

-
• RISK FACTORS:
- Three times as common in multiparous women as in primiparae.
- Cesarian section.
- Submucous fibroids.
- History of placenta praevia.
- Advanced maternal age
• Sx
- PAINLESS vaginal bleeding
▪ may be precipitated by
• trauma
• coitus
• pelvic/ vaginal exam
▪ can stop then resume
- Uterine Hypotonia: Uterus is non tender
- Fetal head is still mobile above the pelvic brim
- Blood loss is MATERNAL.
- Bleeding in 2nd half of pregnancy is placenta praevia until proven
otherwise.
• DIAGNOSIS:
- First: Fetal heart sounds
- Ultrasound: Dx is confirmed only after 30 weeks of pregnancy (at
32-34 weeks)
91

▪ wait till 30 weeks as usually the lower part of placenta

atrophies and upper part hypertrophies => placenta
migrates up in 80-90% of cases
- NEVER perform a vaginal or speculum examination, as this may
precipitate torrential vaginal haemorrhage!!!
• MANAGEMENT:
- First step: Admission
▪ resuscitate mother
▪ give anti-D if mother is Rh neg.
▪ confirm Dx by U/S
▪ aim: prevent prematurity – prolong the pregnancy
• wait for fetal lung maturity: confirmed with
Amniocentesis – L/S ratio (Lecithin-
Sphingomyelin ratio)
o >2 lungs are probably mature
o < 1.5 risk of hyaline membr. Dis (RDS).
- Minor: Continue pregnancy until term.
▪ vaginal delivery can be attempted
• if abnormal bleeding starts, change to C-
section
- Major: C Section at 37-38 weeks
▪ before term/ labour starts
▪ earlier if severe bleeding
• Cx
- Sheehan’s syndrome
- acute tubular necrosis
- no engagement of the fetal head – blocked by the placenta
praevia
▪ oblique or transverse presentation
▪ 2. Placental abruption
• Premature separation of a normally situated placenta.
• incidence – 1%
• Risk factors:
- Maternal HTN, Pre-eclampsia.
- Cigarette smoking, cocaine abuse
- History of placental abruption.
- Trauma, MVA
- Multiple pregnancy, polyhydramnios
• CLINICAL FEATURES:
- Abdominal pain with or without vaginal bleeding
▪ usually external bleeding
▪ sometimes concealed placental abruption - internal
bleeding => retroplacental hematoma =>↑ fundal
height
• Dx diff. with
o red degeneration of fibroid
92

o complication of an ovarian cyst

(torsion, rupture)
▪ shock out of proportion with vaginal bleeding
- Hard/ tense and tender uterus
▪ Dx. diff with polyhydroamnios
- Maternal and fetal blood loss
▪ Fetal distress
▪ Shock
• DIAGNOSIS:
- Clinical: painful vaginal bleeding + normal implantation
- USG: It is not an accurate tool.
• MANAGEMENT:
- Mild: <500 ml
▪ Mother and fetus are well
▪ Pt may go home if bleeding ceases or induction of
labour if pregnancy has advanced to 37 wks.
- Moderate: 500-1000 ml
▪ Signs of shock, fetus is hypoxic
▪ Rapid blood transfusion, possible cesarean
- Severe: 1500 ml
▪ Treatment of shock (as pre-eclampsia is associated, BP
may be in normal range)
▪ most coaglopathies occur here
▪ Fetus is almost always dead: Amniotomy (spontaneous
labour)
▪ If still alive: Urgent delivery
• COMPLICATIONS:
- Maternal:
▪ DIC – release of tissue thromboplastin from ruptured
placenta
▪ hypovolemic shock
▪ acute renal failure - ATN
▪ post-partum hemorrhage
- Fetal: IUGR, pre-term delivery, anemia
▪ 3. Vasa previa (loss of fetal blood)
• Rare
• when fetal blood vesels traverse placental membranes => rupture of
fetal blood vessels during rupture of membranes
• Risk factors
- Multiparity
- Placental accessory (succenturiate) lobes
• Sx
- Triad: rupture of membranes + painless vaginal bleeding + fetal
tachycardia then bradycardia (due to exsanguination)
- loss of fetal blood
- bleeding usually doesn’t stop
- fetus usually dies
93

• Dx
- clinical
- Apt test – distinguish between fetal blood and maternal blood
• Mx
- emmergency C-section, otherwise fetus will die
▪ 4. Placenta Accreta
• rare: 1:500 - 1:2500
- incidence is ↑due to↑incidence of C-sections
- risk proportionately increases after multiple C-sections
• risk factors
- previous C-section + anterior low lying placenta
• when placenta implants over a previous C-section scar -> trophoblast
penetrates through scarred decidua and myometrium becoming
morbidly adherent.
• Sx
- Excessive vaginal bleeding leading to frequent DIC
• Mx – Cesaren hysterectomy to preserve mother’s life
▪ 5. Rupture of uterus
• RESULT OF:
- Obstructed labour – during uterine contractions
- Trauma
- Dehiscence of a cesarean scar
- Inappropriate use of oxytocins
• Sx
- Vaginal bleeding
- Abdominal pain which becomes constant
- Shock in some cases
- Some can be asymptomatic
• TREATMENT:
- Hysterectomy
- In few cases uterine tear can be sutured
▪ 6. Polyp
• Sx
- Bleeding can occur after coitus
- More limited bleeding
▪ best way to monitor adequacy of blood volume replacement = urine output
• since body can compensate through vasoconstriction for a while (Pulse,
BP normal) but urinary output will be ↓ in hypovolemia.
o b. HTN in pregnancy – Classification:
▪ 1. Chronic HT
• Essential HT – prior to conception or in 1st ½ of the pregnancy, without
an underlying cause
• Secondary HT – caused by renal, renovasc. or endocrine disorders or
aortic coarctation
▪ 2. Gestational HT
• arises after 20 wks
• without any features of pre-eclampsia
94

• resolves within 3 months after delivery

• good prognosis
• Rx
- monitoring to exclude development of pre-eclampsia
- if BP >140:90 give antihypertensive drugs
▪ maintain BP at 110-140/80-90
▪ 3. Pre-eclampsia
• after 20 wks
• multisystem disease
- HTN – usually first symptom followed by proteinuria
• resolves within 3 months after delivery
• RISK FACTORS:
- MC in Primigravida
▪ 1/3 of them will recur
- in multigravida, if
▪ maternal dis.: Family history of hypertension/ pre-
eclampsia, DM, chronic renal dis., SLE
▪ placental problems: hydatiform mole, placental
abruption
▪ fetal problems: Multiple pregnancy, Hydrops fetalis.
• SEVERE P. = BP > 160/110 mmHg plus proteinuria.
• Imminent eclampsia – severe p. +
- Severe headache
- Blurring of vision
- Epigastric pain
- Hyperreflexia
- Oliguria
• Dx
- HTN that arises after 20 wks of gestation
▪ Hypertension: > 140/90 mmHg or
▪ Rise in BP of more than 25 mmHg systolic or 15 mm Hg
diastolic
- plus one of the following:
▪ Proteinuria: > 300mg/ 24 hrs or urine protein/
creatinine ratio > 30 mg/mmol
▪ Renal insufficiency
• serum creatinine > 0.09 mmol/L or
• oliguria
▪ Liver dis.
• raised AST/ALT and/or
• severe epigastric/RUQ pain
▪ Neurol. problems
• convulsions (eclampsia)
• hyperreflexia with clonus
• severe headaches with hyperreflexia
• persistent visual disturbances (scotomata)
▪ Hematological problems
95

• Thrombocytopenia
• hemolysis
• DIC
▪ fetal growth restriction
• COMPLICATIONS:
- Mother
▪ HELLP syndrome = severe form of pre-eclampsia
• triad:
o Hemolytic anemia
o Elevated Liver enzyme
o Low Platelets
• Rx – deliver the baby
▪ DIC
▪ Oliguria, ARF
▪ Eclampsia (tonico-clonic seizures and coma)
- Baby
▪ Intrauterine death.
▪ IUGR
▪ Premature delivery.
• MANAGEMENT:
- Admission: BP > 150/100 (twice), maternal symptoms,
compromised fetal well being.
- Treat HTN:
▪ moderate – Oral
• Methyldopa 250 mg two-three times daily.
• Labetalol or atenolol
• Nifedipine
▪ Severe – IV
• Hydralazine 5 mg IV bolus every 20 min
- < 32 wks: try to continue pregnancy until 35 wks
▪ steroids for pulmonary maturity
▪ daily fetal movement count (kick count chart)
▪ 3 CTGs/ week
▪ Doppler umbilical blood flow
▪ Platelet count – to detect HELLP syndrome
• if platelets > 100.000 – keep monitoring
• if platelets < 100.000
o Give C/S – 2 doses, 24 hrs apart -> to
prevent hyaline membrane disease
o Correct thrombocytopenia, then
o induction
- 32-35 wks: Same management, but if delivery is indicated, can
do C-section or induction of labor
- > 35 wks
▪ pregnancy should be terminated rapidly with induction
of labor or C-section, depending on cervix and feto-
maternal situation.
96

- Eclampsia
▪ delivery
▪ prevent convulsions with MgSO4
• can be used in first 48-72 hrs after delivery
• Initial dose of 4g IV over 5-10 min then infusion
1g/ h for at least 24 hrs.
• if woman has eclampsia, hyperreflexia, fits or
headache
• monitor tendon reflexes, resp. rate (>16/min)
and urine output (>25 ml/h)
• SE/toxicity
o diminished or abolished reflexes (knee
jerk = patellar reflex) – first sign
o decr. resp. rate -> resp. paralysis
o decreased urinary output
• Rx
o stop MgSO4
o give antidote – Cal. Gluconate
▪ if convulsions occur, treat with Diazepam 0.1-0.2
mg/kg IV or Phenytoin
▪ 4. Pre-eclampsia superimposed on chronic HT
• after 20 wks
• systemic features of pre-eclampsia develop on top of existing chronic HT
o c. PROM
▪ in most cases (80-90%) the baby is born within 7 days
▪ for best prognosis of baby, most important is administartion of C/S
▪ Mx
• lithmus paper test (Nitrizine test) – is there amniotic fluid in discharge?
• monitor for signs of Chorioamniotitis
- cause: anaerobes, GSE
- Sx
▪ fever
▪ tachycardia
▪ abd. pain, tenderness
▪ offensive vaginal discharge
- Dx
▪ FBE: incr. WBC, CRP – every 2-3 days
- Rx
▪ A/B
▪ expedite the delivery
• Sterile speculum exam. – under strict sterile conditions
• NO PV!! – risk of inf.
• U/S – amount of amniotic fluid around the baby (oligohydramnios?)
• Doppler for umbilical blood flow: is the baby receiving enough blood?
• CTG – every 2-3 days
• WBC and C reactive protein every 2-3 days.
• high and low vaginal swab, rectal swab
97

- then erythromycin – 250 mg every 5 hrs

▪ usually ceased if swabs come back negative
• fetal fibronectin – labor?
• Valsalva manouver -> examine pouring of amniotic fluid in the fornices
• 2 C/S inj. 24 hrs apart (for 48 hrs)
• check indic. and CR for Tocolytics
- if contracn. have started before C/S therapy is concluded
▪ -> admin. Ca channel blocker (nifedipine) or
Salbutamol.
- otherwise rarely used, since the contr. might signify subclinical
uterine inf. -> in this case delivery should be expedited
• transport ASAP to tertiary hospital
• if OK and no immediate labor, send home
- monitor fever
- no sexual intercourse
- no strenuous exercise
- urgent readmission in hospital if
▪ fever
▪ vaginal discharge
▪ ↓fetal movement
• > 35 wks
- if cervix is favorable -> induction with oxytocin (Syntocinon)
- if cervix is unfavorable -> delay induction by 48-72 hrs, to give
time to cervix to ripen (=> induction will be easier)
• 26-35 wks = PPROM (preterm premature ROM)
- try to delay the delivery but incr. risk of inf.
- Group B streptococcus: About 15-20% of women are colonised with it in vagina. Most of them
are asymptomatic although some do have GBS UTIs. Antenatal treatment wil’nt eradicate
oraganism. Penicillin given parenterally to mother when she is in labour (6hrly) will protect the
baby from svere infection. Screening for this organism is done in routine at 36 wks. Without
such treatment 1% of babies delivered will develop severe infection (Meningitis, septocemia).
- Immunisation
o severity of blood group sensitisation can be assessed by:
▪ 1. maternal serum anti-D titres
• not very accurate
• useful
- if very low or very high
- in the first pregnancy
▪ 2. previous obstetric performance – gets worse with succeeding pregnancies
▪ 3. 2nd best: liquor bilirubin levels at 26-34 wks
▪ 4. The best: measurement of fetal Hb sampled from fetus at 20-36 wks
• in order that
- fetal blood transfusion can be given if Hb is low
- fetal blood group to be determined
- direct Coombs test to be performed
▪ detects RBC AB on the RBCs (direct) or in serum
(indirect) by using rabbit anti-serum against RBC
98

▪ 5. U/S – looking for ascites and/or hydrops (late signs)

o Any jaundice in first 24 hrs is pathological – ABO, Rh
o Rh incompatibility is MC and severe cause of HDN. Incompatibility may occur when an Rh-
mother and an Rh+ father have an Rh+ baby. Cells from baby can cross placenta and enter
mother's bloodstream, causing mother to make anti-D antibodies. Unlike ABO antibodies,
structure of anti-D antibodies, cross placenta and enter baby's bloodstream. There they
destroy baby's RBCs, causing severe fatal anemia.
o ABO incompatibility
▪ when mother is group O and baby is group A or B
▪ more frequent but milder jaundice on 1st day
• rarely with severe hemolytic anemia in baby
▪ Dx
• Coomb’s test
▪ Rx – to prevent kernicterus
• Phototherapy
o Rh incompatibility
▪ Due to anti-D antigen. Mother Rh- father and baby Rh+
▪ present on erythrocytes of Rh+ fetuses as early as 7 wks => mothers become
immunised if they receive a feto-maternal transfusion as early as 7 wks (e.g.
termination of pregnancy as early as 7 wks, fetomaternal transfusion during the
pregnancy)
▪ Sx
• hemolytic anemia
• jaundice in first 24 hrs
• hepatosplenomegaly
• heart failure
▪ Cx
• MC cause of Hydrops fetalis
• Stillbirth
▪ screening of mothers
• at first presentation
• at 28 wks
• at 34-36 wks
▪ Dx
• Coomb’s test
- Direct – from baby
▪ Detects anti-RBC antibodies or complement proteins
that are bound to surface of RBCs
- Indirect – from mother
▪ Detects anti-RBC antibodies that are present unbound
in patient's serum
• Kleihauer test - blood test used to measure the amount of fetal HB
transferred from a fetus to a mother's bloodstream.
- performed on Rh- mothers to determine the required dose of
Rho(D) immunoglobulin (RhIg) to destroy fetal RBCs and thus
inhibit formation of Rh antibodies in mother and prevent Rh
disease in future Rh+ children.
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▪ Indications for anti-D:

• all Rh- unsensitised women who have an abortion
- -> inj. 250 IU within 72 hrs of abortion
• all Rh- unsensitised women who require/ have:
- CVS, amniocentesis
- Ectopic pregnancy
- Threatened abortion
- Antepartum hemorrhage
- Abdominal trauma
- Need an external cephalic version
- -> inj. 250 IU before 20 wks or 625 IU after 20 wks
• all Rh- unsensitised women whose pregnancy has progressed to 28 wks
or 34 wks
- -> 625 IU prophylactically
• all Rh- unsensitised women who gave birth to an Rh+ baby
- -> 625 IU within 72 hrs if Coombs test is neg.
- perform Kleihauer test on mother’s blood
▪ if 80 => 5 ml of fetal blood was transfused to mother ->
inj. an additional 625 IU
▪ if second pregnancy in Rh- mother with Rh+ baby --> perform amniocentesis
• if bilirubin is present -> intrauterine blood exchange
▪ Rx – to prevent kernicterus.
• Before birth:
- Intrauterine blood transfusion/ Exchange
- Early induction of labor – after fetal lungs are mature
- Plasma exchange in mother – to reduce level of ABs by 75%
• After birth:
- Phototherapy
- Blood transfusion
- Exchange transfusion
- Jaundice in pregnancy
o Viral hepatitis – 40% (bilirubin is significantly raised)
▪ Hepatitis A – MC hepatits during pregnancy
• similar course as in non-pregnant women
• worst prognosis if chronic hepatitis is present
• ↑risk of premature labour
o severe pre-eclampsia, eclampsia and hyperemesis gravidarum – can cause hepatic
damage with jaundice
o 3rd trimester
▪ 1. MC cause - acute fatty liver of pregnancy
• rare
• high mortality – 50%
• causes
- disordered metabolism of fatty acids by mitochondria in the
mother, caused by deficiency in the LCHAD (long-chain 3-
hydroxyacyl-coenzyme A dehydrogenase) enzyme
- admin. of hepatotoxic agents in debilitated mother
100

• Week 35-36
• Sx
- nausea, anorexia, vomiting
- jaundice and fever
• Cx
- renal failure
- fulminant hepatitis with hepatic encephalopathy
- pancreatitis
- DIC
• Dx
- liver and renal failure (urea and uric acid ↑)
- AST and ALT ↑(but not as high as in viral hepatitis: 200 not 400)
- Bilirubin ↑
- ALP usually normal
- liver biopsy – confirms Dx
• Rx
- urgent admission to ICU
- urgent termination of pregnancy (life-saving for mother and
baby)
- prevent/ treat DIC
- may require liver transplant
▪ 2. Intrahepatic cholestasis of pregnancy (hepatosis)
• MC in 3rd trimester, but can start anytime
- usually in second ½ of pregnancy
• due to estrogen sensitivity
• Cx
- fetal distress
- fetal death
- preterm delivery
- meconium ingestion
- meconium aspiration syndrome
• Sx
- intense itching, usually without a rash
▪ Generally, itching is localized to abdomen, legs, palms,
and soles, but can be generalized.
▪ Itching that increases in evening
▪ Itching that doesn’t respond favorably to anti-
histamines or other remedies
- Often, elevated LFTs and serum bile acid counts
- Less common:
▪ Darker urine
▪ Lighter stools
▪ ↑ clotting time (due to associated vitamin K deficiency)
▪ Fatigue
▪ Increased nausea
▪ Decrease in appetite
▪ Jaundice - only in relatively small subset of cases
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▪ Upper right quadrant pain

• Dx
- ALP incr.
- AST/ALT and bilirubin only mildly incr.
▪ if bilirubin significantly incr. = MC viral hepatitis
• Rx
- monitor fetus – deliver if in distress
• Prognosis
- usually clears up rapidly after delivery
- often recurs in future pregnancy or if using OCP (which are CI)
- Diabetes Mellitus
o 1. Existing (pre-gestational) DM
▪ Effects on fetus:
• large for date (macrosomia)
• ↑fetal abnormalities
- neural tube defects
- cardiac – VSD, ASD, TGA
- kidney
- small left colon
• hypoxia
• intrauterine death
• miscarriage
• malpresentation
• IUGR
• preterm delivery
• postnatal
- early hypoglycemia – jitters, tremors
▪ should be checked @ 4 hrs after delivery or after 2nd
feeding, whatever comes first
- ARDS
- jaundice
▪ Effects on mother: – incr. risk of:
• pre-eclampsia
• DKA
• polyhydramnios
• intercurrent inf.
• first trim. miscarriage
• obstructed labor (incr. shoulder dystocia)
• placental abruption
• C-section
▪ aim for diabetic control:
• 4-7 mmol/L
• HbA1c < 7%
▪ type II - stop oral hypoglicaemic pills during pregnancy and breastfeeding -> use
insulin instead
▪ type I – insulin requirements will incr. (especially in the last trim.) but will go
back to normal after delivery
102

o 2. Gestational DM
▪ screening test is glucose challenge test (non-fasting) at 26-28 wks (not OGTT)
• N = 8 mmol/l
• > 8 abnormal -> then do OGTT (fasting)
• Criteria for diagnosis of gestational DM: Fasting > 5.5mmol/l and >
8mmol/l 2hrs after 75gms oral glucose.
- also do OGTT if high risk:
▪ previous Hx of gestational DM
▪ DM
▪ family Hx of DM or gestational DM
▪ Hx of macrosomia
▪ PCOS
▪ glycosuria
• common in pregnancy – 25-50%
• only 2-3% of them have DM
• if present on 2 occasions, should do OGTT
▪ Rx – like in pre-gestational DM
▪ follow up with OGTT at 6 weeks and then every 5 yrs
• likely to recur in subsequent pregnancies
• 30% developing DM later in life
- Vomiting
o causes
▪ normal pregnancy
▪ multiple pregnancy
▪ hydatiform mole
▪ UTI
▪ intestinal obstruction
o Dx
▪ U&E and creatinine – to assess the dehydration
▪ U/S – multiple pregnancy? hydatiform mole?
▪ urine culture – UTI?
▪ single erect abd. X-ray – intest. obstr.?
- Acute pancreatitis in pregn. is assoc. with:
o cholelithiasis – MC
o alcohol intake
o cocaine use
o hyperparathyroidism
o abdominal trauma
- pain in lumber area while walking, 3rd trimester - refer to physiotherapy
- fetal movements felt by
o 18 wks –multigravida
o 20 wks - primigravida
- can’t feel fetal movement
o 1st step – intermittent auscultation
▪ don’t hear anything -> 2nd step = U/S
▪ hear something that worries you (bradycardia, etc.) -> II step = CTG
• CTG normal
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- Mx
▪ < 32 wks – U/S
▪ > 32 wks – repeat CTG
o (another approach) if normal auscultation (hypoxia)
▪ CTG
• if ok discharge + do kick count chart (normal: 10 movements/day)
▪ if abnormal auscultation
• CTG + U/S
- Multiple pregnancies
o assoc. with
▪ ↑perinatal morbidity and mortality (5-10x)
▪ ↑post-partum hemorrhage (uterine atony)
▪ ↑IUGR of one or both twins
▪ ↑umbilical cord prolapse (esp. for 2nd twin)
o not associated with feto-maternal hemorrhage
- Oligohydroamnios
o Mx
▪ U/S
▪ RFT
▪ regular CTG
▪ lupus AB
- Polyhydroamnios
o risks
▪ PROM
▪ preterm labor
▪ cord prolapse
▪ APH
▪ malpresentation
- Pubic symphysis diastasis (pelvic osteoarthropathy)
o separation of pubic bones (due to relaxation of ligaments during pregnancy)
o II-III trim or early postparthum
o Sx
▪ pubic pain aggravated by walking/ moving
▪ pubic joint is very tender
o Dx
▪ confirmed by U/S
▪ post-partum – X Ray
o Rx
▪ bed rest on firm mattress
- Abdomen big for date (fundus > age)
o wrong date
o polyhydramnios
▪ fetal malformations
▪ multiple pregnancy (twins)
▪ DM
▪ infection: CMV, toxoplasmosis
▪ chorioangioma of placenta
104

o DM – macrosomia
o fibroids
o twins
o Rh incompat. – MC cause of hydrops fetalis
o ABO incompatibility
- Abdomen small for date (fundus < age)
o Wrong date
o Small baby – in fetal malformation
o Oligohydramnios– in fetal malformation
o IUGR
- CTG:
o usually performed after 26 weeks (before not very accurate)
o not usually done
▪ not superior to intermittent auscultation
▪ has not ↓ incidence of cerebral palsy or other neonatal developm. anomalies
▪ rarely a predictor of previous fetal oxygenation – unless profoundly abnormal
▪ poor predictor of current fetal oxygenation - unless profoundly abnormal
o Indications
▪ high risk pregnancy: HT and DM mom, etc.
▪ overdue pregnancy > 40 wks (2 times/ week)
▪ on Oxytocin
▪ color of water is brown or green
▪ bad baby heart beats
o Side Effects
▪ ↑ risk of obstetric intervention (instrumental delivery or C-section)
o 2 lines:
▪ above - baby’s heart
▪ below - uterus contractions
o we check fetal heart rate, fetal movements and uterine contractions to identify the
presence of fetal hypoxia
▪ 1. Baseline FHR = mean level of FHR when this is stable (excluding accelerations
and decelerations)
• Normal: 110-160 (150?)
• < 110 Bradycardia
- ↑ vagal heart tone
- fetal heart block
- cord compression
- fetal hypoxia
• >150 Tachycardia
- fetal inf.
- fetal hypoxia
- maternal fever
• > 200 – fetal arrhythmia
▪ 2. Baseline variability – minor fluctuations of baseline
• normal: 5-15 (10-15?)
• reduced or incr = fetal distress
• lost:
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- pre-term fetus who is sleeping

- drug effect – diazepam, morphine
• incr.
- maternal fever, drugs, hypoxia
▪ 3. Accelerations
• transient incr. in FHR > 15 bpm lasting at least 15 sec
• simultaneous with the uterine contractions
• usually normal – at least 2 in 15 min
- if absent baby might be sleeping
▪ wake up baby then repeat CTG
▪ 4. Decelerations
• transient decr. in FHR lasting for at least 15 sec of > 15 bpm
• a. Early – start with uterine contr. (coinciding with uterine contr.)
- normal, due to incr. vagal tone in response to uterine
contractions (HEAD compression)
• c. Variable No relation with uterine contraction, V shaped with a
shoulder before and at end.
- sign of UMBILICAL CORD compression/ prolapse
▪ Rx – change position of mother
- if severe = severe fetal compromise
• b. Late (PLACENTA) starts after uterine contraction
- sign of fetal hypoxia (utero-placental insufficiency) -> rule out
placental abruption!
▪ Rx – if cervix dilatd delivery otherwise C-Section
- if persistent = severe fetal compromise
o Types of results
▪ Normal antenatal CTG
• baseline FHR = 110-160
• variability of FHR 5-25
• decelarations are absent or early
• accelerations 2 within 15 mins
- normally present
- if absent baby might be sleeping
▪ wake up baby then repeat CTG
▪ Stress CTG (in labour)
• Normal
- Baseline FHR 110-160
- Variability 5-15 (Beat to beat variability is considered normal,
indicative of active CNS)
- Decel. absent or early
- (accelerations are not considered during labour – their
significance is unknown)
• Non-reassuring pattern – one of the following features is present:
- borderline FHR 100-109 (slight bradycardia) or 161-170 (slight
tachycardia)
- variability is reduced to 3-5
- variable decelerations
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- Mx
▪ non-reassuring pattern in I stage of labor
• reposition woman (left, right position)
• give O2 via face mask
• if she was on oxytocin, slow it or stop it
• -> then check CTG again
o if it didn’t improve -> perform fetal
scalp blood sampling (with
amniotomy)
▪ if Ph <7.2 -> C-section
• Abnormal CTG – 2 of the following features in the non-reassuring type
are present or
- baseline FHR < 100 or > 170
- variability is absent (<3) = monotonous trace
- late decelerations (especially prolonged > 3 min)
▪ => immediate delivery
• vaginal – if cervix is fully dilated
• C-section – if cervix is not fully dilated
• Most ominous – indicating severe fetal compromise
- 1. persistent late decelerations - worst
- 2. severe variable decelerations
- Appendicitis in pregnancy:
o Dx
▪ difficult, due to:
• the displacement of appendix by enlarged uterus – higher the later the
condition occurs during pregnancy
• tenderness more difficult to localize, since appendix is behind large
uterus
• confusion with other diseases
- UTI
- hyperemesis gravidarum
- right ovarian cyst complication
- red degeneration of fibroid
- small concealed placental abruption
o Rx – Appendicectomy
- DVT in pregnancy
o Anticoagulant throughout pregnancy
▪ use Heparin instead of Warfarin (therapeupric doses for 3 months then prophylactic
doses for remainder of pregnancy until 6 wks postpartum)
• Heparin = Large molecule size => can’t cross placenta (no anticoagulant
effect on baby). Therapeutic dose = 2 times prophylactic dose.
• reversal of anticoagulant effects can be achieved faster than warfarin
▪ Warfarin
• SE
- Can’t be used in 1st trimester (Teratogenic)
▪ can be given during 13-36 wks but its effect is slower
to reverse
107

-miscarriage risk
-stillbirth
-neurological problems in baby
-crosses placenta and has anticoagulant effects on baby as well ->
hemorrhg. in mother and baby
o 6 wks post-partum heparin
- Impaction of a retroverted uterus (e.g. 16 wks - MCQ)
o Sx
▪ lower abd. pain, urinary retention
- Thrombocytopenia
o causes
▪ incidental thrombocytopenia of pregnancy– MC
• not significant unless < 50x109/L
▪ pre-eclampsia – when severe = HELLP syndrome
▪ immune thrombocytopenia
▪ SLE
- Maternal mortality
o 1:10.000 in Aus.
o causes
▪ Primary pulmonary HT – 50% die during pregnancy or puerperium
▪ Severe pre-eclampsia and eclampsia
▪ PE
▪ Postpartum hemorrhage
▪ Amniotic fluid embolism
▪ Anesthetic accidents
- IUGR
o viscera least affected is the brain
o can be
▪ Asymmetric
• MC- AC is affected
• due to placental dysfunction
• Biparietal head diameter (BPD) is last one to be affected
▪ Symmetric
• more rare
• causes
- intrauterine infections
- other intrauterine abnormalities
• All parameters are reduced, BPD is reduced alongwith others
- Premature delivery
o causes
▪ increased uterine size
• macrosomia
• polyhydroamnios
• multiple pregnancy
▪ shortened cervix < 1.5 cm
▪ open cervix especially if:
• internal OS is open
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• bacterial vaginosis is present

• Hx of premature delivery
o Dx
▪ fetal fibronectin test on cervical secretions is +ve, even if cervix is closed –
most conclusive!
Postpartum pathology
- Postpartum hemorrhage
o causes:
▪ 1. Uterine atony: MC cause of bleeding
• causes:
- Previous atony
- Big uterus/ baby: Polyhydramnios, macrosomia, twins, large
fibroids
- After prolonged/ obstructed labour
- old age mother
- Halothane anesthesia
- Oxytocin can cause it
• Sx
- massive bleeding
• Rx.
- for atony
▪ Oxytocin IV
▪ Massage the uterus
▪ if failed -> (step ladder approach)
• ergometrine
• bilat uterus compression for 3 min
• PGs
• uterine artery ligation
• hysterectomy
- for bleeding
▪ IV fluids + O2, pulse/ BP monitoring every 15 min
▪ urinary catheter – monitor urinary output
▪ 2. Retained placenta – (baby born normal + bleeding)
• 2nd MC cause of bleeding
• Rx – step-ladder approach
- Oxytocin drips
- curretage under GA
- uterine artery ligation
- hysterectomy
▪ 3. Laceration – baby born normal + bleeding + placenta delivered normal + BP
80/60
• in precipitated (fast) labour (e.g. 4 hrs), elderly grand-multigravida
• contracted uterus
▪ 4. DIC
• contracted uterus in 3 and 4 (excludes 1 and 2)
▪ 5. Uterine inversion
109

• due to overtraction on cord or Dubin expression of placenta without

waiting for firm uterine contraction
• placental delivery then vaginal bleeding + profound shock, out of
proportion with the bleeding (due to autonomic stimution caused by
drawing the ovaries and their nerve supply)
• pain is not very severe (more shock)
• can lead to death through shock + hemorrhage
• Rx
- immediate replacement of the uterus
▪ manual
▪ if uterus is firmly contracted – use hydrostatic method
- if unsuccessful - surgery
▪ 6. Uterine rupture
• Hx of C-section + prolonged labour + late 2nd stage: suddenly bleeding
(no delivery of baby)
- the bleeding might not be important (concealed bleeding)
- shock out of proportion with the bleeding (like in inversion)
• can also occur after a normal stage 3 (abnormal stage 3 – pulling on the
cord -> inversion)
• MC in grand multipara, when delivering a large baby
▪ 7. Amniotic fluid embolism
• very very rare
• amniotic fluid, fetal cells, hair, or other debris enters the mother's blood
stream via the placental bed of the uterus and triggers an allergic
reaction. This reaction then results in cardiorespiratory (heart and lung)
collapse and coagulopathy
• On the list of causes of maternal mortality, it’s 5th
• Sx
- massive bleeding
- convulsions, coma, death
o Dx
▪ evaluation of blood loss with
• observation of clotting and estimation of blood clotting time by the
bedside -> giving most info in shortest time
- does not clot or clotting time > 8 min – pathol.
• FBE – Hb: useful only when low
• coag. profile (Platelets, fibrinogen, APTT, Prothrombin time – takes 30-
60 min to assess
• D-dimers or fibrin degradation product (FDP)
- Puerperium – up to 6 wks after delivery
o vascular and lymphatic engorgement of the breasts
o colostrum secretion: 2-3 days -> then milk secretion
o transient leucocytosis
o lochia: postpartum vaginal discharge, containing blood, mucus & placental tissue
▪ Lochia discharge typically continues for 4 to 6 wks after delivery
▪ It progresses through 3 stages:
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• Lochia rubra (or cruenta) is the 1st discharge, red in color because of
large amount of blood it contains.
- It typically lasts no longer than 3 to 5 days after birth.
• Lochia serosa is the term for lochia which has thinned and turned
brownish or pink in color. It contains serous exudate, erythrocytes,
leukocytes and cervical mucus.
- This stage continues until around the 10th day after delivery.
• Lochia alba (or purulenta) is the name for lochia once it has turned
whitish or yellowish-white. It contains fewer red blood cells and is
mainly made up of leukocytes, epithelial cells, cholesterol, fat & mucus.
- It typically lasts from 2nd through 3rd to 6th week after delivery
- Puerperial fever/ sepsis (1 to 10th day after delivery)
o > 38OC
o > 24 hrs
o causes
▪ 3 Bs
• Birth canal – endometritis (MC, 75%, with high grade fever)
- post-partum endometritis or pyrexia (fever, tender uterus, foul
smelling lochia):
▪ Ampicilin (or amoxycylin) and metronidazole
• if not improving add Gentamycin
• Breast - mastits
• Bladder – UTI
• + DVT
▪ MC
• UTI – E.coli
• breast inf – Staph. aureus
• wound inf. – if C-section
▪ less common
• Genital – endometritis – strepto.
• DVT?
o Dx
▪ U/S: bulky uterus
▪ inspection of lower tract for infected tears or lacerations
▪ MSU for microscopy, culture, sensitivity
▪ vaginal swab
▪ signs of mastitis
o Rx
▪ 1 - init. empirical: penicilin + metronidazole + gentamycin
▪ after result, adjust for sensitivity
- After birth - http://en.wikipedia.org/wiki/Fetal_circulation
o Umbilical vein closes and becomes ligamentum teres
o Closure of ductus venosus
o Lateral umbilical artery becomes lateral umbilical ligament
o Ductus arteriosus is closing due to increased local PG
o increased venous return from the lungs causes pressure to increase in the left atrium,
which closes the foramen ovale flap valve
111

o Opening up of lungs causes a massively increased pulmonary artery blood flow

Congenital anomalies
o eyes far from each other (wide palpebral fissure + wide philtrum + wide face): Down,
chromosomal anomaly
o eyes close to each other (short/ narrow palpebral fissure + short/ narrow philtrum +
narrow face/ microcephaly): Alcoholism
- Down syndrome
o types
▪ 95% - Trisomy 21, due to failure of disjunction (separation) during meiosis
▪ 5 % - can be:
• translocation involving chromosome 21
- often inherited, risk of recurrence = 10%
• Mosaicism
o risk factors
▪ increased maternal age
o incidence
▪ 20 yrs – 1:2000
▪ 30 yrs – 1:700
▪ 35 yrs – 1:400
▪ 37 yrs - 1:250
▪ 40 yrs – 1:100
▪ 43 – 1:50
• we say increased risk if > 1:300
▪ risk of recurrence = 1%
o Sx
▪ varying degrees of intellectual impairment and developmnetal delay
▪ premature aging & Alzheimer-like changes develop in mid life (4th - 5thdecades)
▪ Head
• moon-shaped face with small mouth and teeth
• transverse furrowed tongue, high arched palate
• sloping/ oblique palpebral fissures and epicanthic folds
• flattened occiput and face
• short squat nose
• sparse, coarse hair
▪ Hands
• short and broad with hyperextensible fingers
• abnormalities of thumb and little finger
• single transverse palmar crease
▪ hypotonia, hyperreflexia
▪ gentle and good natured temperament, lively and affectionate, cheerful and
sociable with affinity for music, dance, rhythm
▪ associated disease
• very frequent: atlanto-axial subluxation -> sports are CI
- Dx – Cervical spine X Ray
• congenital heart malformation (septal defects)
• duodenal atresia
o Screening (BHCG and Inhibin A are ↑ all others are ↓)
112

▪ 1st trimester – combined test – tripple test:

• 11-12 wks - U/S –1. Nuchal translucency (if thick > 2 mm: Down; not
compulsory: normally at 18 wks, at 13 wks woman will have to pay for it)
• 10-12 wks –blood tests:
- 2. β HCG increased
- 3. Plasma protein decr. – PAPPA (pregnancy associated plasma
protein)
▪ 2nd trimester
• 15-18 wks –tripple or quadruplet test
- 1. βHCG increased
- 2. Alfa fetoprotein decreased (Down syndrome)
- 3. Unconjugated estriol decreased
- 4. Inhibin A increased (Down syndrome)- optionally
▪ high risk mother: old age, previous Down, etc. -> invasive methods
• Amniocentesis – 15-18 wks
- most accurate
- abortion rate: 1 in 200
• Chorionic villus sampling – 9-11 wks
- less accurate
- abortion rate: 1 in 100
- Neural tube defects: AMC clinical assessment p. 105-106
o types:
▪ Spina bifida
• Dx - U/S can be seen at 16-18 wks
• ↑α fetoprot. in mother at 12-15 weeks (screening only – not
diagnostic)
- amniocentesis - incr. alfa fetoprotein
▪ Anencephaly
• happening during 5-8 wks
• Dx - U/S can be seen at 11-12 wks
• women are offered the option to
- terminate
- continue the pregnancy
▪ MC Cx = polyhydramnios
o incidence = 1:1000
o recurrence if not taking folate = 2-5%
▪ screening in subsequent pregnancies: α fetoprot. in maternal serum at 16 wks
o Prevention
▪ Folic acid - up to 12 wks
• 0.5 mg/day
• 5 mg/day – if:
- previous neural tube defect
- on antiepileptic drugs
- DM?
▪ Vit. B (B6, B12)
▪ Vit. D
- Cleft palate, Cleft lip
113

o MC cranio-facial malformation
o causes
▪ Benzodiazepine
▪ Antiepileptics - carbamazepine
▪ Amphetamines
▪ Rubella
▪ Genetic factors
• Kalman syndrome
▪ Smoking
▪ Alcohol
- Alcohol abuse:
o from 80 g alcohol/ day => Fetal alcoholic syndrome
▪ Microcephaly
▪ Mental retardation
▪ Poor muscle tone
▪ short palpebral fissure
▪ long and smooth philtrum
▪ underweight till puberty
▪ short stature
▪ septal defect
▪ facial hypoplasia
▪ joint deformities
▪ low IQ
▪ attention deficit
▪ forebrain malformation
- Cocaine abuse:
o IUGR
o Placenta abruption
o Premature labour
o Intraventricular hemorrhage
o Developmental delay
o Stillbirth
o Teratogenic effect not proven
- fetal malformations can be assoc. with umbilical cord vessel anomalies
o Normal – 2 arteries & 1 vein (3 vessels cord)
o MC anomaly assoc. with fetal malformation = only 2 vessels in cord
▪ 1 artery + 1 vein – baby can survive
▪ otherwise – stillbirth in 1st trimester
Antenatal care
o 1st antenatal checkup
▪ Confirm pregnancy
▪ FBE
▪ Blood group, Rh, Coomb’s test
▪ Blood sugar level
• Random
• Fasting
▪ MSU, urine analysis, electrolytes
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▪ LFT
▪ Infections
• Rubella
• Hep. B
• HIV
• Syphillis - VDRL
• CMV
- consider Varicella, Hep. C
o Hb electrophoresis – Thalassemia
o for Gestational DM
▪ Screening test is Glucose challenge test (non-fasting) at 26-28 wks (not OGTT)
• Normal = 8
• > 8 is abnormal -> then do OGTT (fasting)
- also do OGTT if high risk: Previous Hx of gestational DM, DM,
family Hx of DM or Gestational DM, Hx of macrosomia, PCOS,
Glycosuria.
▪ Insulin requirements
• ↑ in last trimester
• ↓ immediately after delivery
▪ Fetal hypoglycemia
• should be checked @ 4 hrs after delivery or after second feeding,
whatever comes first
o International travel/ flight
▪ after 28 wks – Better to avoid
▪ after 36 wks – Prohibited
o Pregnancy + cardiac disease
▪ never give ergometrine
▪ don’t put in lithotomy position
▪ watch for fluid balance
o VSD in pregnancy
▪ if only VSD – can go for vaginal delivery
▪ if VSD + transverse lie – C-section
o ≥ 42 wks (41 wks + 6 days) = Postdated pregnancy
▪ Induction and C/S then
• U/S – check amniotic fluid index – N > 5
• CTG – if CTG abnormal, do pH test (fetal scalp)
▪ Meconium stained indicates fetal distress
• We have to do CTG before Dx of fetal distress
• pH < 7.2 = fetal hypoxia
- have to check cord prolapse too
o after ROM – check for cord prolapse
o C/S in
▪ Breech presentation
▪ Fetal distress
▪ Labour progress is slow
Labour:
Contractions:
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< 30 weeks: small localized contractions every 1 min + higher amplitude contraction every 30-30 min
after 30 weeks: more intense (Braxton Hicks contractions)
after 36 weeks: increasing progressively until labour starts
labour starts: 1 contraction every 10 min, lasts 20 sec
late labour: 2-4 contractions every 10 min (1 every 2-4 min), last 40-90 sec
contractions still occur for 48 hrs after delivery with decreased frequency

Cervix dilatation:
anytime after 34 weeks, but usually later (especially in primigravida)
dilatation of min. 1 cm/h during labor

Onset of labour: dilatation of cervix more than 2 cm + painful contractions at least every 10 min with
increasing frequency

Duration of labor: 6 (multipara) – 9 (nullipara) hrs (90% within 12 – multiparae to 16 – nulliparae – hrs)

Stage I – till complete cervical dilatation (10 cm); only passive uterine contractions
- has a:
o passive phase
o active phase – from cervix dilated 3-4 cm to fully dilated; cervix dilates faster,
contractions become more painful
Stage II – till birth: passive uterine contractions + active abdominal contractions
- if it lasts more than 2 hrs -> vacuum extraction or forceps
Stage III: placenta expulsion: 15-30 min after birth of baby. Wait 2-3 min after birth before clamping the
umbilical cord

Loss of blood: 400 ml

Premature birth – less than 37 weeks of gestation
Normal: 2500-4000 g
Low birth weight: < 2500 g
Big baby: > 4000-4500 g

- Labour
o epidural – up to 7 cm dilatation
o monitoring of fetal well being
▪ uncomplicated labor – intermittent auscultation (stethoscope with Doppler)
▪ complication - CTG
o There are 3 signs of onset of labor:
▪ A bloody show
• passage of a small amount of blood or blood-tinged mucus through
vagina near the end of pregnancy
• It can occur just before labor or in early labor as the cervix changes
shape, freeing mucus and blood that occupied the cervical glands or
cervical OS
▪ Rupture of membranes (waters breaking)
▪ Onset of contractions
o 1st stage
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▪starts when
• cervix is at least 2 cm dilated
• contr. become painful and regular, at progressively shorter intervals (3-
5 min), and lasting > 1 min
▪ Duration
• average 8.25 hrs in nulliparae, 5.5 hrs in multipare
▪ Phases
• a. latent: onset -> 4 cm dilat.
• b. active: 4 cm -> 10 cm dilat.
- 1 cm/ hr dilatation
▪ Pulse, temp., BP every 2 hrs
▪ monitor contr.
▪ monitor FHR every 15 min
▪ PV exam every 4 hrs
• if ROM – check for cord prolapse
▪ every woman should receive Syntometrine (ergometrine + oxytocin), to
• promote contr.
• minimize bleeding (16 x less)
nd
o 2 stage – begins when cervix is fully dilated
▪ duration
• < 45 min – multiparous (average 15 min)
• < 2 hrs – nulliparous (average 1 hr)
• > 2 hrs – can be:
- 1. Obstructed labor - very low chance woman will deliver
naturally
▪ if on epidural (no urge to push) we can wait up to 3 hrs
▪ causes:
• Pelvic swellings: Ovarian tumors, fibroids,
ectopic pelvic kidney, very distended urinary
bladder
o (not cystocele or rectocele – are soft,
can easily be pushed out of the way)
• Cephalopelvic disproportion
• Large baby: DM, hydrops fetalis, etc.
• Postterm pregnancy
▪ MCQ: MC finding = 4 cm of head is palpable in abd.,
although bony head is at ischial spines on pelvic
assessment.
▪ Rx
• if good contr. -> assisted delivery
o Forceps
▪ more traumatic for mother not
for baby
▪ ↑in vaginal tears
▪ ↑need for episiotomy
o Vacuum extraction
▪ more traumatic for baby
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▪ The baby may be left with a

temporary lump on its head,
known as a chignon.
▪ A possible cephalohematoma
formation or subgalial hemorg.
• if not effective contract. -> give oxytocin drips
o if effective contr. -> assisted delivery
o if still not effective -> C-section
• if Cephalopelvic disproportion: C-section
▪ e.g. Shoulder Dystocia:
• after delivery of head, anterior shoulder of
infant can’t pass below pubic symphysis or
requires significant manipulation to pass
below pubic symphysis. It’s diagnosed when
shoulders fail to deliver shortly after fetal head
• In shoulder dystocia, it is chin that presses
against the walls of perineum.
• causes
o large baby (DM) - MC
o post term pregnancy – MC
o mid-forceps delivery
• Rx – Various manouvers – MC – McRobert’s
manouver.
• Cx
o Shoulder dystocia is an obstetrical
emergency and fetal demise can occur
if infant is not delivered due to
compression of umbilical cord within
birth canal.
o Major concern of shoulder dystocia is
damage to upper brachial plexus.
Klumpke paralysis - form of paralysis involving muscles of forearm & hand, resulting from a
lower brachial plexus injury in which C8-T1 nerves are injured. Affects principally intrinsic
muscles of hand and flexors of wrist and fingers ± dilators of iris and elevators of eyelid (both
of which may be seen in case of associated Horner's Syndrome). Classic presentation of
Klumpke's palsy is “Claw Hand” where forearm is supinated, wrist & fingers are
hyperextended. If Horner syndrome is present there is miosis (constriction of pupils) in
affected eye

▪
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Erb's Palsy - Paralysis of arm caused by injury to upper group of arm's main nerves,
specifically if upper trunk C5-C6 is severed - loss of sensation in arm, paralysis and atrophy of
deltoid, biceps & brachialis muscles. Position of limb under such condition is characteristic:
arm hangs by side and is rotated medially; forearm is extended and pronated. Arm can’t be
raised from side. All power of flexion of elbow is lost as is also supination of forearm.
Resulting biceps damage is main cause of this classic physical position commonly called
"waiter's tip." Risk factors – breech presentation, shoulder dystocia

▪
- 2. Inefficient or incoordinated labor
Feature on PV examination Obstructed labor Inefficient/ incoordinate labor
Moulding of fetal head ++ Usually none
Caput formation on fetal head ++ ±
Cervical oedema Anterior lip oedema Usually none
Fetal tachycardia ++ and progressive +
Station of fetal head – relation Just at or above ischial Can be above or below ischial
of lowest part to ischial spines spines spines
Amount of head palpable above > 2 finger breadths Usually < 1 finger breadth
pelvic brim when lower point of (most important feature)
head is at ischial spines
▪ monitor FHR every 5 min
• if FHR falls < 100 + for > 2 min => PV (cord prolapse?)
▪ monitor contr. – normal: 60-90 seconds every 2-4 min
• if not good give oxytocin
o 3rd stage:
▪ duration
• 15 min in both nullipara and multipara (90%)
• If placenta still not delivered after 15 min
- encourage contraction by rubbing uterine fundus
- no effect => manual removal
▪ MC SE = Uterine inversion
o total duration of labor:
▪ 9.5 hrs in nullipara
▪ 6 hrs in multipara
o Cardinal movements of labor:
▪ engagement
▪ descent
▪ flexion
• first 3 occur simultaneously
▪ internal rotation
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▪ extension
▪ external rotation
▪ expulsion
o sign of progress of labor
▪ incr. strength, duration and frequency of uterine contraction
▪ descent of fetal head into pelvis
▪ rotation of fetal head (occipito-transverse to occipito-anterior) on abd.
palpation
▪ best sign of progress – progressive increase in cervical dilatation (1cm/hr)
• with effacement (shortening) of the cervix
▪ rotation of fetal head (occipito-transverse to occipito-anterior) on pelvic exam.
▪ descent of head within and through the pelvis
▪ above spines -> spines level -> below spines -> coccyx -> vulva
- Induction of labor
o indic.
▪ Prolonged pregnancy > 42 weeks
▪ Hypertensive disorders in pregnancy
• Pregn. induced HTN
• Pre-eclampsia
• Eclampsia
▪ PROM
▪ Intrauterine fetal death (IUD)
▪ IUGR
▪ Antepartum hemor.
▪ Isoimunisation
• ABO incompat.
• Rh incompat.---Hydrops fetalis
o CI
▪
absolute
• Cephalopelvic disproportion
• Placenta praevia
• Vasa praevia
• Fetal distress
• previous classical C-section (not low segmental)
• invasive cervical CA
• cord presentation
• some abnormal presentations
- Breech pres.
▪ complete – ok (bent knee)
▪ frank – ok (knee extended)
▪ incomplete – NOT OK (with feet down)
o when to start: when cervix is ready/ favorable -> assesed with Bishop score
▪ 1. Cervix dilatation
▪ 2. Cervix length
▪ 3. Cervix consistency
▪ 4. Cervix position
▪ 5. Head station (in raport to ischial spines)
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0 1 2 3
Dilatation (cm) <1 2 3 >4
Length (cm) >4 3 2 <1
Consistency Firm Mild Soft
Position Post. Ant. Central
Head station -3 -2 -1 >0
▪ score 0-4 – cervix not ready for induction (very high risk to fail induction)
▪ score at least 5 to start induction (with amniotomy)
o Procedure:
▪ start with intravaginal PG gel
• PG E2 – Dynoprostone – for alive baby
• PG F2 alpha – Dynoprost
- indic.
▪ dead fetus
▪ missed abortion
▪ termination of pregnancy
▪ evac. of hydatidiform mole
▪ wait until cervix will be ready (if no fetal distress) with Bishop score ≥ 5
▪ then do amniotomy
• SE
- cord prolapse
- inf.
▪ after amniotomy, deliver within 5-8 hrs
▪ after amniotomy, use oxytocin infusion (drips) to promote contr.
▪ then proceed with normal delivery
Preterm premature rupture of membranes: rupture of membranes before 37 wks
Premature rupture of membranes: rupture of membranes after 37 wks without onset of labor.
Position of baby: important after 28 wks
Lie:
- longitudinal (99%)
- cephalic – 95%
- breech – 4%
- oblique
- transversal
Presentation:
- Cephalic – 95%
- Vertex – head flexed, occiput leads
- Face - head extended, face leads
- Brow – head slightly extended (between vertex and face)
- Breech (buttocks down) – 3.5%
- Shoulder – 0.5%

- Malpresentations
o Breech presentation
▪ 15% at 30 weeks, but only 3% at birth
▪ ↑ risk for fetus
- due to
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▪ intracranial hemor.
▪ asphyxia
▪ fractues of humerus, femur or clavicle
- preterm and late post term babies – mortality 12%
- term babies – mortality 1%
▪ Types
- with extended legs (frank) – 65-70%
- with flexed legs (complete)- NVD can be attempted
- footling (incomplete) – one foot comes first (rare)
▪ Rx
▪ if still breech pres. at 37 wks, attempt cephalic version - easier if the baby has
flexed legs
• Ext. cephalic version @ 36 wks or end of 37 week + tocolytic
▪ CI
• Cephalopelvic disproportion
• Placenta praevia
• Multiple pregnancies
• Antepartum bleeding
• Hx of uterine scar, HTN, bad obstetric Hx
• PE
• Hx of unstable lie
• Small for date baby
▪ absolute indic.
• shoulder presentation
• face presentation
• Risk of cord prolapse: first do PV to exclude cord prolapse
- Rx
▪ if the cord is still puslating, push the presenting part
and cord as far in as possible (MCQ).
▪ place mother in knee – chest position
▪ urgent delivery
• C-section – preferred
• Vaginal delivery with forceps or vacuum
extraction avoiding cord pressure
- C-section – preferred, with decr. perinatal mortality (from 1.15% to 0.6%)
- normal delivery can also be used
• baby with normal size
• complete breech or extended legs
• eyebrow presentation
• head flexed
• CPD excluded
• labor onset spontaneously
• e.g. if unexpected breech presentation with full cervical dilatation with
insufic. time to organize a C-section
o Transverse or oblique presentation
▪ may convert to a longitudinal one later on
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▪ Dx – 1st - U/S to rule out placenta previa (this is what might be causing the baby
to have this presentation, prevents him from having a cephalic presentation)
▪ Mx
- at 36 weeks – Cephalic version
- > 36 weeks: wait for normal labor
▪ if beyond 37 wks (term) best Mx is C-Section
- Malpositions
o types
▪ Occipito-posterior – MC
• 11 cm (vs. 9.5 for normal position)
• assoc. with poor quality uterine contraction
- if this is excluded – Cephalopelvic disproportion
• incoordinate uterine action -> ↑ intrauterine pressure -> incr. fetal
distress (MCQ).
- CTG is recommended for monitoring
- even more common when oxytocin and epidural were used
▪ in this case CTG is mandatory
• slow labor
- Rx
▪ labor can be stimulated with
• amniotomy
• oxytocin
▪ epidural is often necessary
▪ C-section may be necessary in case of obstructed
labour or fetal distress
▪ occipito-transverse
▪ (occipito-ant. = N)
▪ face
▪ brow
o Rx
▪ if no other problems – vaginal delivery in most of them (especially in occipito-
post. and occipito-transverse)
• exception: Face – vaginal delivery may be impossible => C-section
▪ C-section – in prolonged labor with maternal exhaustion, obstructed labor, CPD,
fetal distress, selected primigravida, face and brow (only in nulliparous not
multiparous) presentation .
Post partum depression occurs in 30% of women in first 6-12months postpartum
Post partum Blues occur during first 2 weeks after delivery.
- Anesthesia
o Epidural:
▪ Anaesthetist conducting an epidural places catheter in the mid-lumbar, or lower
back region of spine.
▪ In adults, spinal cord terminates around the level of disc between L1 and L2 (in
neonates it extends to L3 but can reach as low as L4), below which lies a bundle
of nerves known as cauda equina ("horse's tail"). Hence, lumbar epidurals carry
a very low risk of injuring the spinal cord.
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▪ A common solution for epidural infusion in childbirth or for post-operative

analgesia is 0.2% ropivacaine or 0.125% bupivacaine with 2 µg/mL of fentanyl
added. This solution is infused at a rate between 4 and 14 mL/hr, following a
loading dose to initiate the nerve block.
▪ CI (purple book)
• previous surgery to vertebrae in that area
• skin infection near the point of intended insertion
• significant maternal haemorrhage (it may make the extent of
haemorrhage more difficult to assess)
• Bleeding disorder (coagulopathy) or anticoagulant medication (e.g.
Warfarin) - risk of spinal cord-compressing hematoma
- e.g. thrombocytopenia < 40.000/mm3
• cardiac condition (e.g. primary pulmonary HT) where heart can’t cope
with the vasodil. caused by the epidural
• severe fetal distress – better to give GA and expedite the delivery
▪ SE
• slows down labor significantly
• bloody tap
• Vasodilation leading to hypovolemic shock.
• Neurological injury lasting less than 1 yr (rare, about 1 in 6,700)
• Epidural abscess formation (very rare, about 1 in 145,000).
• Epidural hematoma formation (very rare, about 1 in 168,000).
• Neurological injury lasting longer than 1 yr (extremely rare, about 1 in
240,000)
• Paraplegia (1 in 250,000).
• Arachnoiditis (extremely rare, fewer than 1000 cases in past 50 yrs)
• Death (extremely rare, less than 1 in 100,000).
o Pudendal anaesthetic block
▪ produced by blocking pudendal nerves (which arise from S2,3,4) near the ischial
spine of pelvis.
▪ A local anesthetic such as lidocaine or chloroprocaine (Lidocaine is usually
preferred for a pudendal block because it has a longer duration than
chloroprocaine which usually lasts less than 1hr) is injected into pudendal canal
where pudendal nerve is located.
▪ This allows quick pain relief to the perinium, vulva and vagina. A pudendal block
is usually given in 2nd stage of labor just before delivery of baby. It relieves pain
around the vagina and rectum as the baby comes down the birth canal. It is also
helpful just before an episiotomy.
- Oxytocin
o SE
▪ Uterine hypertonus and tetany -> Fetal distress (MC)
▪ water intoxication
▪ uterine rupture – in multiparous
• rare
▪ hT
o CI – if cervix is closed
- APGAR score
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o at 1 and 5 min
0 1 2
Appearance/ color Absolutely blue Centrally pink, Pink
peripherally blue
Pulse/ heart rate Absent < 100 > 100
Grimace/ response to No response Some facial grimace Cries
stimulation (place
suction catheter in
nose of child)
Activity/ muscle tone Floppy, flaccid & Some flexion Good active
hypotonic limbs movement
Respiration effort Absent Gasping, irregular & slow Normal good crying
▪ Good > 7
▪ How ready is this child =
• heart rate
• resp. effort
• irritability
• tone
• colour
▪ low score at 1 and 5 min => child needs resuscitation
▪ causes
• significant hypoxia
• perinatal asphyxia
Apgar score

The test is generally done at 1 and 5 min after birth and may be repeated later if score is and
remains low.
- Scores 3 and below are generally regarded as critically low.
- 4 to 6 fairly low
- 7 to 10 generally normal.
A low score @ 1min indicates neonate requires medical attention[3] but is not necessarily an
indication that there will be long-term problems, particularly if there is an improvement @
5min. If Apgar score remains below 3 at later times such as 10, 15, or 30 minutes, there is a risk
that child will suffer longer-term neurological damage.
Gynecology - OK
Breast pathology
- Mastalgia:
o 30-50 yrs (MC 35-45 yrs)
o Causes:
▪ MC – Cyclical mastalgia
▪ Pregnancy
▪ Caffeine
▪ Breast CA
• risk is < 10%
• e.g. mastitis carcinomatosa – red and hot breast, during lactation
▪ Fibroadenoma
▪ Mastitis
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▪ Drugs
• OCP
• HRT – Diffuse bilateral pain
- Rx – ↓ estrogen dose
• Theophylline
o Types
▪ diffuse, bilateral and cyclical = Cyclical mastalgia
• 30-50 (35) yrs
• hormonal basis
• causes
- MC = benign mammary dysplasia (fibroadenosis, chronic
mastitis, cystic hyperplasia, fibrocystic breast dis.)
▪ 30-50 yrs
▪ Dx
• mammogram – if diffuse lumpiness > 40 yrs
o shows calcifications
• U/S
• biopsy
▪ Mx
• large cysts - aspiration
• Sx
- pain in breasts (mid-cycle till end of period) & feeling of lumpy
breasts
▪ pain extend down inner aspect of upper arm
- possible - straw-like or green grey discharge from the nipple
- breasts diffusely nodular or lumpy
• Rx – Murtagh 969
- Mild
▪ reassurance
• rule out fear of CA in patient
▪ analgesic (paracetamol)
▪ lifestyle advice
• low fat, eliminate caffeine
• wear good quality, comfortable bra
• lose weight
- Moderate
▪ Mefenamic acid (NSAID - inh. of PG synthesis)
▪ add Vit B1, Vit B6
▪ (Primrose oil – contains an essential fatty acid - Awad)
- No response
▪ Danazol (progestogen = modified testosterone –
inhibits ovarian synthesis of estrogen)
▪ norethisterone – progestogen
▪ Diffuse, bilat. non-cyclical mastalgia
• poorly understood
• causes (may be)
- duct ectasis
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- periductal mastitis
• Rx
- much more difficult to treat
- exclude caffeine & lose weight
- Vit B1, Vit B6
- norethisterone – progestogen
▪ Unilateral difuse non-cyclical
• Mastitis – cellulits of interlobular connective tissue
- in lactating women with
▪ cracked nipple
▪ poor milk drainage
- causes
▪ bact
• MC cause – Staph. aureus (coagulase-positive)
o Rx
▪ Flucloxacilin
▪ Erythromycin
• E. coli
▪ Candida – after A/B
• severe breast pain (hot knife, hot shooting
pains)
- Sx
▪ a sore lump at first
• then red tender area
▪ fever
- Cx – Breast abscess
▪ if persisting > 48 hrs + area of tense induration
develops
▪ Rx
• surgical drainage (under GA) or aspiration with
a large bore needle (under LA)
• A/B
- Rx
▪ Breast feeding should continue from both sides (milk
production not affected)
• empty the breast well
▪ flucloxacilin
• or cephalexin
▪ for candida – fluconazole
• or nystatin
▪ localised
• Costochondritis (Tietze’s syndrome)
- constochondral junction becomes strained in persistent cough
- palpable swelling about 4 cm from sternal edge (enlargement of
costochondral cartilage)
- initiated or aggravated by deep breathing and coughing
- Self-limiting – may take a few mths
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- Rx – infiltration with local anesthetic and C/S

o Dx
▪ Mammography > 40 yrs
▪ U/S – for localised pain
• not useful in postmenopausal breast – fatty and looks like CA
▪ excision biopsy – in lumps
- Nipple discharge: Breast CA can produce any type of discharge!
o Bloody discharge
▪ one breast – benign
• both breasts – probably malignant
▪ intraductal papilloma -----(benign) MC
▪ intraductal CA
▪ mamary dysplasia
o Green-grey (toothpaste like)
▪ duct ectasia (green toothpaste)
o mamary dysplasia
o Yellow
▪ Mamary dysplasia
▪ intraductal CA (Clear, serous)
▪ breast abscess (pus)
o Milky white
▪ Lactation & lactation cyst
▪ Hyperprolactinemia
▪ Drug induced e.g. Chlorpromazine, risperidone, amisulpride
o Straw like color
▪ Fibroadenosis (mammary dysplasia, fibrocystic disaes)
- Cracked nipples
o cause
▪ wrong breast feeding
▪ aggressive suckling by baby
o Mx
▪ teach appropriate breastfeeding technique
▪ continue breast feeding
• even in mastitis and with breast abscess from both breasts
• CI – HIV
- Breast lumps
o Mammary dysplasia (fibrocystic disease, fibroadenosis) – 32%
o Fibroadenoma – 23%
▪ 15-35 yrs
▪ types:
• Juvenile – soft, rapidly-growing tumor
• adult
▪ Rx
• firm, smooth and mobile (“ breast mouse”)
▪ Dx
• U/S
• FNAC
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o Carcinoma – 22%
o Cysts – 10%
▪ 40-50 yrs, painful solid lumps.
▪ associated with mammary dysplasia
▪ regress after menopause
▪ Dx
• for breast cyst – 1st test is always U/S!
• mammography
• FNAC
▪ MCQ: 45 yrs, painful solid lump in the breast – breast cyst (tense)
• rapid growth – pain
o Breast abscess - 2%
o Duct ectasia
▪ Looks like CA
▪ A whole breast quadrant is indurated and tender
▪ Green toothpaste-like nipple discharge
▪ Dx – widespread linear and globular calcifications on mammography
▪ Rx - Surgery
o Duct papilloma
▪ Benign-----not premalignant
▪ Bloody discharge
▪ Rx – excision of duct and affected breast segment
o Lactation cyst (Galactocele)
▪ Rx - Aspiration
o Paget’s syndrome of nipple
o Fat necrosis (traumatic)
▪ after large bruise or trauma (e.g. protracted breast feeding)
▪ with skin and nipple retraction
• looks like CA
▪ it usually disappears
▪ Dx – excision biopsy
- Breast CA
o MC CA in women
o Lifetime risk: 1 in 11 women in Aus.
▪ 1 in 11 women will develop CA by age 75 – max around 60 yrs
o 1 in 25 women die of breast CA
o incidence rises with age and incr. in higher socioeconomic class
o Types:
▪ MC - non-invasive: intraductal CA
▪ invasive
• invasive duct CA – 90%
• lobular CA
o risk factors
▪ Sex -100 x MC in women
▪ Caucasian race
• low in Asian countries
▪ Age:
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• > 40 yrs (uncommon under 30 yrs)

- mean age of Dx = 60 yrs
▪ Greatest risk – positive family Hx
• 1st degree relatives (mother, sister, daughter) with breast CA, especially
< 50 yrs: highest risk (risk incr. 3X)
• strong predisposition from mutations in genes BRCA1 & BRCA2
▪ Personal Hx
• Hx of Breast CA
- including CA of other breast
• Hx of benign proliferative disease or lumps - especially mammary
dysplasia (with cellular atypia)
▪ Hormonal facts:
• early menarche
• late menopause (>53)
• nulliparous at 40 yrs – one of most offending risk factors
- having 1st child over 30 yrs
• no breast feeding
• HRT > 5 yrs
▪ Obesity after menopause
▪ Alcohol
▪ Ionising radiation
o Not risk factors:
▪ OCP
▪ Smoking
▪ Sedentarism
o Screening
▪ monthly self-examination
• false positive rate is high < 40 yrs
• recommended > 35 yrs
▪ Mammography
• at least every 2 yrs for all women 50-70 yrs
• + 40-49 yrs – on demand
• Specificity = 90%
▪ in high risk genetic inheritance pattern: Murtagh 982
• monthly self-examination
• > 40 yrs - annual GP examination
• mammography every 2 yrs > 50 yrs
• aspiration of cysts
• mammography, U/S and FNAC to Dx any localised mass
• U/S for young dense breasts (< 40 yrs)
o Sx
▪ Lump: painless, hard, irregular, attached or fixed to underlying tissues or skin
(dimpling)
• < 10% with pain
▪ Nipple changes: retracted (not inverted), distortion, discharge (blood stained)
▪ Skin: dimpling, peau d’orange
▪ Paget’s syndrome of breast – Dx diff. with eczema
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Paget’s syndrome Eczema

Unilat. Bilat.
Older patients Reproductive years/ lactation
Possible nipple discharge No discharge
Not pruritic Pruritic
No pustules Pustules
Deformity of the nipple Normal nipple
Possible palpable lump No lump
▪ Spread:
• Local:
- skin
- muscles
• Regional:
- I - axillary lymph nodes
- internal mammary
- supraclavicular nodes (right side)
▪ (left – gastric; small % of gastric – to right as well)
• Distant:
- 1 - other breast
- 2 - bones
- brain
- liver
- lung – cannon ball metastases (many round opacities)
o Dx
▪ Tripple test:
• Clinical examination
• Imaging: mammography +/- U/S
• FNAC +/- core biopsy
▪ Approach:
• < 35 yrs – bilateral U/S
- U/S
▪ in dense breasts (< 35 yrs) especially with cysts
▪ for Dx diff between solid lump and cyst
▪ palpable masses at periphery of breasts (not screened
with mammography)
• > 35 yrs - bilateral mammography + U/S
- mammography
▪ established benefit over 50 yrs!
• possible benefit in 40s
▪ Pattern: irregular infiltrating mass with focal spotty
microcalcifications
• if
- Cystic -> aspirate
- Solid -> fine needle biopsy -> only cytology (can’t Dx CA) –
surgeons do this
▪ for
• cyst aspiration
131

• solid lumps
▪ FNAC: 90-95% accuracy – better than mammography
▪ indications for biopsy or excision of lump:
• cyst fluid is blood stained
• lump dn’t dissapear completely with aspiration
• swelling recurs within 1 mth
- unsure/suspicion of CA: core biopsy -> histology (can Dx CA) –
radiologists do this under U/S guidance
▪ FNAC can’t distinguish between CA in situ & invasive!
• core biopsy can do that
▪ tumor markers
• estr. receptors – in 2/3 of breast CA
- good prognostic factor
• progesterone receptors
o Staging
▪ Manchester
• I - Confined to breast
• II - Confined to breast + palpable mobile axillary lymph nodes
• III - Skin changes (fixation, cutaneous ulcers, peau d’orange) + fixed
axillary nodes, supraclavicular nodal involvement
• IV - Distant metastasis
o Rx
▪ workflow (dr. Gaya)
• a. for younger women - wide local excision (quadrantectomy), with a 1
cm margin
- “sentinel node” procedure to detect if first node draining from
the breast (sentinel node) is involved
▪ single most powerful predictor of subsequent
metastases and death = lymph node involvment
▪ radiopharmaceutical injected at nuclear medicine
centre a day before surgery + on the day of surgery we
inject some blue dye close to the nipple:
• we remove sentinel node during surgery, send it
to pathology & check it
o if not affected, we don’t remove lymph
nodes
o if affected, we remove all nodes
(axillary disection)
▪ if more nodes are involved, we
do chemotherapy
- plus Radiotherapy – otherwise 40% chance of recurrence
▪ indications
• tumor > 5 cm
• axillary node involvement > 3 nodes
• positive of close tumor margins
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• b. for an older woman or a large tumor - modified radical mastectomy

(compared to the regular radical mastectomy we don’t remove the
pectoralis major muscle) + axillary lymphadenectomy
- no radiotherapy required
• if post-menopausal woman with invaded nodes, we do antiestrogen
therapy (tamoxifen)
- will be effective especially if estrogen-receptive but we will
administer it any way
• Advanced stage
- radiotherapy & chemotherapy
▪ Pregnancy: terminate preg + radio & chemotherapy.
• Breast reconstruction
- rectus abd. or latissimus dorsi flap
- immediate reconstruction
▪ Breast surgeon + cosmetic surgeon (8 hr surgery)
- later reconstruction
▪ Step 1 - breast surgeon puts in a tissue expander, to
expand the skin
▪ Step 2 – cosmetic surgeon – completes the surgery later
in time
• for nipple – skin from labia majora
• Microcalcif. might be DCIS = ductal carcinoma in situ
- breast screening – looking for microcalcification
▪ microcalcif. are irregular (“crushed rock”) or punctuate
- Stereotactic biopsy – tridimensional biopsy with 2 probes to
locate small CAs (core biopsy)
- hook-wire pre-op localization done by the radiologist
▪ area removed -> radiologist will do a mammogram on
tissue to make sure all the microcalcif. were removed
• no chemotherapy, no radiotherapy is required
• cancer comes back in the same location
- chest wall radiotherapy + tamoxifen (if menopausal)
▪ types of Rx (Maria)
• surgery:
- breast conserving
- Modified radical mastectomy – indic.:
▪ > 5 cm
▪ multifocal CA
▪ Peau d’orange of overlying skin is wide (extends into
another quadrant)
▪ Previous radiation
▪ Patient’s wish
• adjuvant
- Radiation: after surgery (always), axillary nodes (>3)
- Chemotherapy: pre-menopausal
- hormonal Rx: post-menopausal (tamoxifen)
- + aromatase inhibitors: anastrozole, etc.
133

- + monoclonal AB: trastuzumab (Herceptin)

- + progesterones: medroxyprogesterone acetate
o Poor prognostic factors:
▪ tumors > 2 cm
▪ tumors 1-2 cm + estr./progest. receptor negative or high histological grade
▪ lymph node involvement
- Suppresion of lactation – if woman dn’t want to breastfeed or wants to stop breastfeeding
o 1. Tight fitting bra +/- fluid restriction
o 2. Ice application to relieve pain + simple analgezics
▪ with 1-2 lactation usually subsides in a few days
o 3. Bromocriptine
▪ reserved for severe engorgement + if 1 and 2 have failed
▪ risk of severe HT, seizures and strokes in post-partum women
- Galactorrhoea
o in multigravid woman with normal prolactin levels
▪ is common
▪ Rx
• reassurance
• Bromocriptine – if very profuse and troublesome
Contraception and OCP
- Ovulation
o detect the time when it will occur
▪ LH surge at midcycle – ovulation will occur in next 24 h (12-36) – most exact
▪ plasma estradiol peak at midcycle – oculation will occur in 36-48 hrs
• less accurate
▪ alteration in cervical mucus, which becomes more abundant/maximal (and
clear and slippery) immediately before ovulation
• less accurate
• After ovulation the discharge will become cloudy and sticky or disappear
entirely
o confirm that ovulation has occurred by
• Progesterone level surge at day 21 (luteal phase) will confirm that
ovulation has occurred – the best (MCQ)
• Biphasic change in temperature chart
- temperature steadily ↑ for min. 3 days (by < 1 degree) after
ovulation
• Endometrial biopsy
o ovulation occurs always 14 days before her period (luteal phase is always 14 days)
- Ovulatory menstrual cycles
o usually regular with dysmenorrhoea – best predictor of ovulation
o have premenstrual abdominal and breast distension, sometimes acne
o ↑ midcycle mucus production
o sometimes with midcycle bleeding (when estr↓)
- Contraceptive methods
o Pearl Index = No. of pregnancies/ 100 women/yrs (100 women using it for 1 yr) using a
certain conctraceptive
o Types (in order of preference)
134

▪ COCP
▪ Barrier methods
• condoms
- < 5 pregnancies/ 100 women/ yr
• diaphragms
▪ IUD (can be inserted any time within first 12 days of start of menstrual bleeding)
• with
- copper – affect sperm motility and transport
- progest. (Mirena – with levonorgestrel)
• 96-99% pregnancy protection
• Post-partum
- 6 wks after vaginal delivery
- 12 wks after C-section
• CI
- absolute
▪ pregnancy
▪ active PID
▪ undiagnosed abnormal genital tract bleeding
▪ previous ectopic pregnancy
▪ severe uterine cavity distortion
- in nulliparous women?
▪ Cx
• risk of infection
• bleeding
• Side Effects:
- risk of ectopic pregnancy 10x > than with COC
- if pregnancy occurs, 40-50% risk of abortion or intraut. sepsis in
2nd trimester
- incr. risk of PID in 1st 30 days after insertion -> prophylactic
doxycycline (especially if having multiple sexual partners)
- extrusion, perforation and translocation of uterus
- may incr. bleeding for 2-3 mths, then disappears
▪ if it persists, remove IUD
▪ – Mirena reduces or stops bleeding
- lower abd. cramp-like pains
▪ Spermicidal agents
• adjuvants
• when used alone < 10 pregnancies per 100 women/ yrs
▪ Rhythm
• coitus interruptus
• calendar method
- facts
▪ ovulation occurs always 14 days before her period
(luteal phase is always 14 days)
▪ sperm survival is up to 6 days
▪ ovulated egg can be fertilized during 24-36 hrs following
ovulation
135

- method
▪ keep track of length of cycles: e.g. between 26-29 days
=> ovulation between day 12-15
▪ safe periods -
• up to 12-6 (how much sperm survives) =1st 6dys
• after day 15 + 2 (how much time ovum can be
fertilized) = day 17
• unsafe from day 6 to 17
• Basal body temp.
- 2-3 days after ovulation, body temp.↑0.3o C for the rest of cycle
(over temp. of previous 6 days) -> safe from 2 dys after rise of
temp. (4-5 dys after ovulation) until next period.
- + calendar method for safe period at the beginning of her cycle
• Billing method
- fertile mucus – clear, watery, stringy, incr. in amount, feels
lubricative
▪ on ovulation – highest secretion
• ovum survives for 2 days + 1-2 days extra for
safety => safe = 4 days after maximal mucus
secretion (spinbarkiet phenomenon)
(ovulation) MCQ
▪ then abrupt change to non fertile mucus
- not fertile mucus – more whitish, thick, sticky
- failure rate: 1-2 (average 3) / 100 women/ yrs
• Lactational amenorrhoea - Awad
- during breastfeeding
- < 1% risk of pregnancy (90% safety – Awad)
- conditions
▪ exclusive breastfeeding
▪ < 6 months
▪ mother didn’t get her period yet
▪ + Progest. Only Pill (POP) (main action is thickening of cervical mucus)
• mini-pill
- not as efficacious as OCP bc it doesn’t inhibit ovulation (but
almost same) and are taken regularly for 28 days of cycle (no
inactive pills).
- pregnancy rate 3/ 100 women/ yr
- contains
▪ lovenorgestrel 30 µgms/ day
▪ norethisterone
- Side Effects (only few)
▪ cycle irregularity (oligomenorrhea, irregular bleeding
or amenorrhea) and weight gain
• reduces cycle to < 25 days
- Indications
▪ > 45 yrs
▪ smokers > 35 yrs
136

▪ contraindiactions of estrogen, like CA Breast

▪ DM, HTN, DVT
▪ Migraine, Epilepsy
▪ chloasma
▪ lactating women
▪ well-controlled HTN
- Contraindication:
▪ pregnancy
▪ undiagnosed vaginal bleeding
▪ Hx of ectopic pregnancy
▪ enzyme-inducing drugs (carbamazepine, barbiturates, phenytoin)
▪ obesity
▪ active liver disease
▪ + Injectable contraceptives:
• Depo-provera – with progest. Only x inj. IM
- effective for up to 14 wks (3 mths)
- pregnancy rate: 1/ 1000 women/ yr
- Side Effects:
▪ weight gain
▪ amenorrhoea – 70%
▪ prolonged or irregular bleeding
▪ infertility for 6-9 mths after 3rd shot
- CI - Obesity
• Etonogestrel implant (Implanon) - with progest. = etonogestrol
- 3 yrs system
- SE
▪ irregular bleeding
▪ weight gain
- CI - Obesity
▪ + Vaginal ring – Nuva Ring
• with estrogen + progesterone
▪ + Sterilisation
• Male
- Vasectomy:
▪ confirm absence of spermatozoa in ejaculate 2-3 mths
after surgery
▪ it takes 12-15 ejaculates to clear existing sperm
▪ reversal – successful in 80% of pts
▪ 1:500-1000 risk of recanalisation
• Female
Ttubal ligation:
▪ clips or rings are applied to each Fallopian tube
• e.g. Filshie clip
▪ reversal – successful in 50-70%
▪ pregnancy risk: 3-4/ 1000 women sterilized
▪ mortality < 1:10.000
• MC cause of death - anesthesia
137

- Essure procedure
▪ introduction of microinsert in tubes-> occulsion of tubes
▪ + Yasmin contraceptive pills (Awad)
• can also help for wt. loss
• decr. fluid retention
• decr. acne formation, decr. greasy skin
- Post-partum contraception
o C.I. - OCPs or NUVA ring – combined estr. or prog. (estr. would suppress lactation)
o can give any progesteron
- Combined Oral Contraceptive Pills: (act on hypothalamus MCQ)
o inhibits hypothalamic and pitutary function => Anovulation
o risk of pregnancy: 1-3 ideally (2-6 in practice)/ 100 women/yr
o OCP – safe to be used for 10 yrs, up to the age of 50 yrs
o contain
▪ estr – MC ethinyl estradiol (20-30ug)
▪ prog.– MC levonorgestrel
o types
▪ microgynon 30 – first line
▪ microgynon 50 – indic:
• in epileptics and other enzyme inductors
• if with microgynon 30 she has breakthrough bleeding that doesn’t
resolve in time
• for control of menorrhagia
• failure of microgynon 30
o Woman > 35 yrs
▪ smoker -> mini-pill (POP)
▪ non-smoker -> mono-phasic OCPs
o Advantages
▪ effective Rx for most menstrual cycle disorders
• primary dysmenorrhoea & menorrhagia
▪ ↓ Fe-deficiency anemia
▪ ↓ benign breast dis.
▪ ↓ Ovarian cysts
▪ 50% ↓ in PID
▪ ↓incidence of ovarian, endometrial and colorectal CA.
• does NOT protect from cervical CA (slightly ↑ probably due to ↑ sexual
activity)
▪ + decr. sebacous disorders
▪ + decr. thyroid disorders
▪ + decr. endometriosis, fibroids?
o SE
▪ Thromboembolic dis.
• Venous:
- DVT
▪ PE
- rarely mesenteric, hepatic and kidney thrombosis
• Arterial:
138

- MI
- stroke
▪ thrombotic
▪ hemorrhagic
- rarely retinal and mesenteric thrombosis
▪ CAs
• possible incr. In
- Cervical CA {Breast CA minimal (has no effect latest research
shows)}
• protective in
- endometrial, ovarian and colorectal CA
▪ OCP are not recommended with any antihypertensives. Condoms can be used.
▪ Migraine – Rx: discontinue COC and give POP
▪ depression – Rx: decr. or change the progest.
▪ Acne – Rx: ↑ estr. dose (estr. will clean acne)
▪ Breast feeding, DM and smoking >35 yrs: POP
▪ Chloasma – Rx: POP
▪ Amenorrhoea – Rx: incr. estr. and decr. progest.
▪ PCOS: An OCP containing ethinyl estrsadiol + cyproterone acetate
▪ Excessive fluid retention: ethinyl estrsadiol + drospirenone
▪ Dysmenorrhoea or menorrhagia – Rx: increase progest.
▪ Breakthrough bleeding
• 20% at beginning
• 3% after 3-6 mths
- Rx - keep using OCPs at same day, every day at same time
▪ if persists after 3 mths, ↑ dose or change to different
type
• early to mid cycle bleeding – ↑ estr. –
Microgynon 50
• late cycle – incr. prog. or change type
▪ Breast problems
• fullness/ tenderness: decr. estr.
• mastalgia: decr. progest.
▪ Libido loss: incr. estr.
▪ Weight gain
• constant – decr. or change progest.
• cyclic – decr. estr.
▪ nausea, vomiting – decr./change/stop estrogen
▪ post-pill amenorrhoea
▪ delayed onset of ovulation after stopping OCPs (Usually periods resumes 2–3 days
after stopping tablets).
• 50% - after 2 weeks
• 90% - after 6 weeks
• 1% - hasn’t occurred after 12 mths
▪ HTN? (blue book 3.201)
• stop OCP, use a different contraception method & reassess in 3 months
- HT will usually settle
139

o Special interactions:
▪ warfarin and oral hypoglycemics doses have to be adjusted
• if using warfarin – STOP OCPs (warfarin is more important)?
▪ High doses of Vit. C, griseofulvin, rifampicin, anticonvulsants (except Sod.
valproate) interact with COCs. Phenobarbitone, phenytoin, primidone,
carbamazepine, oxacarbezepine, topiramate all are enzyme inducing anti-
epileptics. If we have to use these drugs along with hormonal contraceptive
methods either ↑ dose of estrogen in pill or use mirena or barrier method.
▪ Following anti-epileptic drugs are non inducers and don’t effect efficacy of
hormonal contraceptives. Valproic acid, gabapentin, levetricetam , pregabalin,
vogabatrin.
▪ if using A/B or if vomiting/ diarrhea: they might inh. the effect of OCPs -> use
another contraceptive method beside OCPs (condoms)
o Contraindications:
▪ Absolute – Murtagh 961
• 1
- Pregnancy
- First 2 wks post-partum/ post abortion – there’s still bleeding
happening and OCPs would increase risk of clots, thrombosis
• 2
- Thrombembolic Hx
▪ DVT
▪ PE
▪ Thrombophilia
- Coronary artery disease
- Cerebrovascular history
- Migraine
• 3 Estrogen dependant tumors
- Breast
- Cervix
- Ovarian
- Uterus
• 4
- Active liver diseases
- Polycythemia vera
▪ Relative
• heavy smoking/ smoker > 35 yrs old (prescribe POP)
• diagnosed abnormal vaginal bleeding
• HTN
• DM
• hyperlipidemia
• long term immobilisation
• complicated valvular heart disease
• breast feeding – mini-pill (progest)
• 4 wks before surgery and 2 wks after
• gall blader or liver dis.
• Chloasma (prescribe POP)
140

• severe depression (Dec. progest)

o Missed pill:
▪ < 12 hrs
• take it now then take the pills normally
▪ between 12 and 24 hrs
• take 2 pills for that day
- 1st as soon as you remember
- 2nd at regular scheduled time
• + use additional contraception method for 7 days (condom) (rule of 7)
• if pill missed in wk 3 – skip the pill-free wk
- blue book p. 532: woman who skipped her 2nd last active pill ->
start her 7-day hormone-free period when she forgot her pill
(last night) -> then start next course of hormone pills.
• if pill missed in 1st week – wait 7 days of continuous pills to be
protected + additional contraception method in meantime.
▪ > 24 hrs
• if 2 pills of 20 µgms estr. or 3 pills of 30 µgms estr. were missed -> use
additional contraception method for 7 days (condom) (rule of 7)
- Unprotected sex with unknown person
o 1. emergency contraception
o 2. test for STD
▪ Chlamydia, gonococal – first void urine or swabs
▪ HIV, Syphilis, Hepatitis – from serum
o 3. Penicillin (gonococal) and azithromycin or doxycycline (chlamydia)– prophylactically
o 4. review patient in 2-3 weeks
▪ if no period – pregnancy test
- Emergency contraception:
o No absolute CI
o 1. normal method (within 72 hrs)
▪ Postinor-2 – with 750 micrograms levonorgestrel
• less/ no nausea/vomiting (only 1%)
• 1 tablet + another tablet after 12 hrs
• failure rate 2-3%
• inh. ovulation in 60%
• progesterone only
- thickens cervical mucous
▪ prevents penetration of sperm
▪ inh. sperm motility
• within 72 hrs
- best within first 8 hrs
- most important Q to ask: time of unprotected intercourse
• menstruation within 3 weeks – else might be pregnant
▪ Yuzpe – most women will experience nausea & vomiting (due to estr. in pills)
• microgynon 50 – has 50 mg estrs.
- needs at least 100 mg estr.--> give her 2 pills
- then after 12 hrs another 2 tabl
• failure rate: 2.6%
141

▪ Danazol 200 mg – 2 tabl. + another 2 tabl. after 12 hrs

o 2. IUD – within 5 days but only in couples (no risk of STD; if STD – incr. risk of PID)
o Levonorgestrel releasing IUD is 1st line contraceptive choice for women using enzyme
inducing antiepileptics.
Menopause, HRT & Osteoporosis
- Menopause
o age it occurs at is
▪ genetically determined
▪ not influenced by
• age at menarche
• age when pregnant
• lifestyle (dev. countries)
▪ earlier if
• smoking
• XXX females
• ovarian surgery or radiotherapy
• some cytostatic agents
• some autoimmune dis.
o Phases:
▪ Premenopausal – 5 yrs before LMP
▪ Perimenopausal – early menopausal sympt. + irregular bleeding
▪ LMP
▪ Menopausal – after 12 mths of amenorrohea
▪ Postmenopausal – 5 years after menopause
o Sympt.
▪ hot flushes
• MC in women with
- premature menopause
- thin women
- ↓ estr. production (high GnRH)
▪ night sweats
▪ Vaginal sympt.:
• atrophic vaginitis
• dyspareunia
o 2 main risks of decr. estr:
▪ Osteoporosis
▪ Ischemic heart disease
o Dx
▪ Estrogen (Estradiol E2) and progesterone are ↓. FSH, LH and LDL all are ↑
- HRT
o Duration: 2 yrs, then review.
o indic
▪ Distressing symptoms
▪ significant osteoporosis
▪ especially if
• HTN
• dyslipidemia
142

• cardiac disease
o Protective for:
▪ Bowel CA but not for ovarian CA
▪ Cardiac dis.
▪ Alzhimer dis.
• if given from time of menopause
- decline in cognitive fc. (= early manifestation of Alzhimer)
- BUT
▪ doesn’t decr. the rate of progression of Alzheimer
▪ doesn’t make advanced Alzhimer less severe
• if started at 60-65 yrs, incidence of Alzheimer is ↑
o SE
▪ Premenstrual syndrome
▪ Nausea and breast disorders
▪ Bleeding problems
• ↑ risk of Breast CA
• after 5 yrs of combined estrogen + progesteron
• after 7.2 yrs of estrogen only
▪ ↑risk of stroke!
o CI
▪ estr.-dep. CAs (Estrogen containing HRT is CI in Breast CA)
• Breast CA
- Rx just Biphosphonates to prevent osteoporosis
• Endometrial CA
▪ recurrent thrombembolism
▪ Hx of coronary artery disease
▪ uncontrolled HT
▪ undiagnosed vaginal bleeding
▪ active liver disease
▪ active SLE
▪ otosclerosis
▪ acute intermittent porphyria
▪ smoking?
o Rx
▪ with uterus present, no CI
• first 2 yrs after LMP
- Best choice: Cyclical HRT: Continous daily estr. + cyclical
progest.(MPA) (12 dys/ mth)
▪ need to add progesteron (min. 12 dys/ cycle) to protect
uterus.
▪ usually causes predictable periods, generally
comencing 2 days after progesteron course was
completed.
▪ can cause breakthrough bleeding -> is she can’t tolerate
it -> continuous estr. + progest.
• 2 yrs after LMP – Continuous HRT: continuous estr. + progest (MPA).
143

- if given in first 2 yrs after LMP -> high likelihood of unpredictable

breakthrough bleeding
▪ hot flashes, vaginal dryness, Hx of DVT –> transdermal patches of estrogen
▪ hot flashes, hysterectomy, Hx of DVT –> transdermal patches of estrogen
▪ severe sympt. (hot flashes) but CI for HRT (e.g. Breast CA)
• Rx
- SSRI – Venlafaxine, paroxeteine, gabapentin
- Clonidine
▪ CI to estr. -> POP
▪ Vaginal dryness only – vaginal estrogen cream
▪ Post-Hysterectomy:
• we can do unopposed estrogen
- for upto 7 yrs (no risk of Breast CA)
- 3-4 women in 100 will dev. endometrial CA
• start with ultra low and go up
• types:
- estriol valerate (Progynova)
▪ ultralow -> 1 mg alt. days
▪ low -> 1 mg every day
▪ high -> 2 mg every day
- conjugated equine oestrogen (Premarin)
▪ ultra low -> 0.3 mg alt days
▪ low -> 0.3 mg every day
▪ medium -> 0.625 mg every day
▪ high -> 1.25 mg every day
- Osteoporosis
o risk factors:
▪ female
▪ thin (low BMI < 19)
▪ anorexia nervosa
▪ family Hx
▪ early menopause before 45 yrs
▪ race – Asian, Caucasian
▪ prolonged amenorrhoea
▪ modifiable factors:
• cigarette smoking
• high coffee intake > 4 cups/day
• high alcohol intake > 2 std. drinks/day
• low calcium intake
• sedentary life
• chronic C/S usage
▪ Endocrinal:
• Cushing
• acromegaly
• hyperparathyr. & hyperthyr.
• hypogonadism
• DM
144

▪ Chronic renal failure

▪ Coeliac dis.
▪ + multiple myeloma
▪ anticonvulsants
▪ pronlonged immobilization
o Protective factors:
▪ thiazides
▪ overweight
o Dx
▪ 1st test – X Ray –is of limited value, not detectable until 40-50% of bone is lost
• typical – compression fracture
- woman – back pain when working in garden: compression
fracture due to osteoporosis
▪ 25 hydroxy Vit. D (most useful test – Murtagh)
▪ Bone densitometry (Dexa Scan) – most specific/ best current modality
• Femoral neck – most useful index
• T-Score:
- -1 Normal
- -1.5 to -2.5 Osteopenia
- < -2.5 Osteoporosis
- < -2.5 with fracture severe osteoporosis
▪ Serum Ca, Serum phosphate, ALP – usually Normal
▪ Exclude multiple myeloma
o Rx
▪ Biophosphonates – best (↓ bone absorption) first line treatment of
osteoporosis in breast CA
• Alendronate (Fosamax), Risedronate and zoledronic acid are first line
therapy in treatment of postmenopausal osteoporosis and prevent
vertebral, non vertebral and hip fractures.
• MCQ: Old woman with GERD history and oesophageal scarring present
and taking PPI, T score given -2.5 in vertebra and -2.5 in femur, in labs
details was given, Ca Vit D was normal and asking treatment.
• Alendronate (causes esophagitis and jaw necrosis)
• HRT
• Strontium ranelate: Answer
• MCQ: Elderly woman with steroid use taking risedronate has frequent
thoracic vertebra fractures. Which is next?
Change to Alendronate
Increase it/ Continue
Change to IV Zoledronic acid********* (reduce vertebral fracture risk by
75 % while oral alendronate and risedronate reduce it by 40 %) Davidson
1123
▪ HRT
▪ SERM -Selective estrogen receptor modulator
• Raloxifene -> only in post-menopausal women. It prevents post
menopausal bone loss, ↓ vertebral fractures but doesn’t prevent non
vertebral fractures. ↑hot flushes & DVT. ↓Breast CA
145

•other SERMs
- Tamoxifen
- Clomiphene
▪ Calcitriol = Vit. D metabolite
• if using this, don’t use Ca
▪ Good dietary intake of Ca
• 800 mg/ day premenopause
• 1000 - 1500 mg/day postmenopause
- 1.5 glass of milk = 1.5 g Ca = enough/ day in osteoporosis (Calin)
• Ca supplementation is poorly absorbed after menopause => inefficient in
preventing bone loss, even when combined with vit. D, unless estrogen
suplementation is given. Ca citrate is better absorbed than carbonate.
o Prevention:
▪ Menopause – patches of HRT, for 2-3 yrs
▪ increased dietary intake of Ca
▪ incr. exercise
▪ decr. smoking, alcohol, coffee
▪ monitor with regular bone density scans
Amenorrhoea
- Primary amenorrhoea
o types
▪ Sexually infantile
• Short stature and non functioning ovaries (streak gonads)
- Turner syndrome – 45X0
▪ gonadal dysfunc. – infertility, lack of breast develop.
▪ Non functioning ovaries, uterus and vagina normal
▪ web neck (cystic hygroma)
▪ wide carrying angle, widely spaced nipples
▪ low ear insertion & low hairline
▪ vision and hearing problems
▪ lymphedema, chromatin negative buccal smear
▪ coarctation of aorta, bicuspid aortic valve
▪ horseshoe kidney
- hypothyroidism
• Normal stature
- Kalman Syndrome – hypothalamo-hypogonadism
▪ deficit of GnRH => lack of FSH and LH
▪ anosmia, hyposmia
▪ optic problems: color blindness or optic atrophy
▪ cleft palate
- true gonadal agenesis
▪ Masculinized
• Congenital adrenal hyperplasia
- 95% due to 21-hydroxylase defic. - AR
▪ normal male genitalia , ambiguous female genitalia /
enlarged clitoris
▪ baby vomits, decr. Na, K incr. – salt-wasting
146

- (rare – in 17 hydroxylase deficiency – AR

▪ ambiguous male genitalia, normal female genitalia)
• True hermaphrodism
- XX/XY mosaique
• androgen-secreting ovarian tumor
▪ Normally feminised
• Mullerian agenesia
- absent uterus (Ut. develops from mullerian duct) +
- vaginal hypoplasia (Vag. does not develops from mull. duct) or
- tranverse vaginal septum or
- imperforate hymen
▪ cyclical recurrent lower abd. pain
▪ suprapubic mass
▪ may have urinary retention
• androgen insensitivity syndrome
o Dx
▪ 1. Check breast development
▪ 2. then U/S -> check for normal uterus
Breast +, uterus + Pregnancy, vaginal agenesis, imperforate hymen, vaginal septum), anorexia
nervosa, excessive exercise OR secondary amen.
Breast +, uterus - Muellerian agenesis, Androgen insensitivity
Breast -, uterus + Gonadal dysgenesis (Turner syndr.), hypothalamico-pituitary failure
Breast -, uterus - Rare
o Double vagina and cervix
▪ Dx – Hysterosalpingography
o No uterus
▪ Dx – Hysterosalpingography
- Secondary amenorrhoea > 6 mths
o causes:
▪ pregnancy, menopause
▪ metabolic
• uncontrolled DM
• renal failure
• hepatic failure
• hypothyr., hyperthyr.
• Post OCP
• hyperprolactinemia
▪ Hypothalamic
• eating disorders: anorexia nervosa, bulimia
• emotional stress
• strenuous exercise
▪ Pituitary causes
• microadenoma
• tumors
• infarction = Sheehan’s syndrome
- Post partum hemorrg. then amenorrhoea = Sheehan’s syndrm.
147

- Necrosis of anterior pituitary gland due to excessive blood loss --

> hypovolemic shock during and after delivery.
- Sx
▪ Agalactorrhea (no lactation)
▪ hypothyr. sympt., adrenal insuffic. sympt. (Addison),
gonadotropin defic. (oligo- or amenorrhoea, hot
flashes, decr. libido)
▪ Ovarian causes
• PCOS
• POF
▪ Uterine causes
• Asherman’s syndrome
- amenorrhoea after termination of pregnancy – after D&C for
abortion, incomplete miscarriage, etc.
- intraut. adhesions due to scars
- Dx – hysteroscopy
o Rx
▪ Ovulation-induction therapy
• with
- Clomiphene
- Gonadotrophins
• Primary infertility with secondary amenorrhoea: most value to predict a
poor response to ovulation induction therapy = low serum estrogen?
• Poor response to it: most accurate predictor is if FSH is ↑(=menopause)
- if FSH is normal – it’s usually effective

PCOS
PCOS POF Ovarian resistant syndr. Menopause
FSH slightly ↑ or normal Very incr. Incr. Incr.
LH Very incr. Very incr. Incr. Increase
(LH:FSH = 2:1/3:1)
Estr. N Decr. Incr. Decr.
Testosterone Incr.-->
(free, DHEA) Hirsutism
U/S > 10 cysts <10 cysts 3-4 cysts
o Sx
▪ irreg. cycles (anovulatory), oligo- or amenorrhoea, infertility
▪ obesity
▪ hirsutism, acne
▪ ± DM
o MC cause of anovulatory infertility
o causes
▪ insulin resistance
▪ incr. androgens (LH and FSH)
o risk of endometrial hyperplasia -> endomet. CA (unopposed estrogen)
o Dx.
▪ Very high LH (LH > FSH, LH:FSH = 2:1/3:1) – normally FSH > LH
148

▪ estr. N
▪ ↑ Androstendione (testosterone)
▪ ± insulin incr., blood sugar level incr.
▪ sex hormone binding globulin decr.
▪ transvaginal U/S
• if thickness > 5 mm
- hysteroscopy + biopsy
• if thickness < 5 mm – CA very unlikely
▪ Rostterdam Dx criteria – at least 2 of the following:
• 1. Oligo- or amenorrhoea
• 2. Signs of hyperandrogenism:
- Clinical: Acne, hirsutism, deepening of voice, clitoromegaly
- Labs.: ↑ Testosterone & DHEA
• 3. U/S ≥ 10 (12) cysts in any of ovaries or both (at the periphery)
o Rx
▪ lifestyle modification
▪ Metformin – Best Rx
▪ OCP
• ↓ Cyst formation, acne & testosterone
▪ for hirsutism
• wax
• laser
▪ wants to get pregnant: metformin and clomiphene have equal efficacy, but:
• BMI > 25 – Metformin
• BMI normal – Clomiphene
• Blue book p. 527 says:
- 1. Metformin &
- 2. Clomiphene but both are equally effective
- 3. Laparoscopic ovarian drilling, IVF, gonadotrophin therapy –
when 1. and 2. have failed
▪ PCOS with normal prolactin:
• Rx – Clomiphene citrate
- SERM
- stimulates pituitary gland to produce more (mainly FSH) & LH =>
ovulation and superovulation
- effects
▪ Excessive estrogen
• fluid retention, breast enlargement
• hot flushes (vasomotor sympt.)
o cold and warm feeling on face, neck
and upper thorax
• dev. of more than 1 follicle and release of
more than 1 ovum => multiple pregnancy (5-
10% risk)
• inadequate ovulation (corpus luteum dysfc.)
• enlarged ovaries with multiple cysts, pain and
↑risk of torsion
149

• Ovarian hyperstim. syndr. – enlarged ovaries,

ascites, hypovolemia, hemo-concentration
• NO ↑ in birth defects
POF (very high FSH, LH and Low estradiol (estrogen and progesterone )
o causes
▪ autoimmune?
▪ ran out of ovums?
o types
▪ < 12 mths of amenorrhoea
• POF
• resistant ovarian failure (if no POF option)
▪ > 12 mths of amenorrhoea
• premature menopause
USG: 3-4 follicles in both ovaries
o Dx diff
▪ Pituitary tumors
• Prolactinoma – MC
- ↑ prolactin
• Gonadotrophin-producing tumors – extremely rare
▪ Craniopharyngioma - brain tumor derived from pituitary gland embryonic
tissue
• with deposit of Ca on X Ray in suprasellar region
• low FSH and LH
▪ double (ballooning) floor of sella turcica – can be an anatomical variant (if
prolactin is normal)
o Sx
▪ hot flashes, dry vagina, mood swings (like in menopause), ↓libido
o Rx: (if high levels of FSH most of ovulation induction therapies fail)
▪ HRT
▪ infertility – ovum donation from a young woman -IVF
Bleeding:
- Menorrhagia
o causes
▪ General
• thyroid dis.
• liver dis.
• renal dis.
• coag./ platelet dis.
▪ Local
• Fibroids – with regular periods
- enlarged uterus
• Adenomyosis – with regular periods
- enlarged uterus
• Endometrial polyps – with regular periods
• Endometrial CA – MC post menopausal
• PID
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• Physiological - DUB
- ovulatory (regular cycle)
- anovulatory cycles (irregular cycle)
▪ MCQ: MC cause of menorrhagia (irregular cycles)
suddenly occuring in a 45 yrs old woman, previously
OK (disorder of ovulation)
▪ Iatrogenic
• hormonal – HRT
• non-hormonal – IUD
• anticoagulants
- Uterine fibroids: (Regular cycle + enlarged uterus)
o encapsulated uterine smooth muscle fiber tumors (leiomyoma – pl. is leiomyomata)
o types
▪ intramural - MC
▪ submucosal (in muscle beneath the endometrium) – MC to cause menorrahgia
▪ subserosal (underneath the peritoneal surface of uterus)
▪ intrauterine – pedunculated causes continuous bleeding
o Estrpgen dependat decrease by menopause
o in fertile women, especially in obese women
o Sx
▪ totally asympt or
▪ menorrhagia
▪ dysmenorrhea, pelvic discomfort (if big)
▪ dysuria, constipation, back pain
▪ if pedunculated – torsion
▪ infertility
▪ calcification
▪ in pregnancy
• red degeneration of fibroid
- mostly in 2nd trimester of pregnancy
- low grade fever, severe abd. pain, local tenderness, guarding
- but no shock (no blood loss)
- Dx diff. with
▪ torsion of ovarian cyst
▪ placental abruption
▪ appendicitis (if right sided)
• effects of pregnancy on fibroid:
- incr. in size
- softens
• effects of fibroid on baby:
- incr. risk of miscarriage
- premature labor
- malposition
- post-partum hemorrhage – lack of contraction
- may prevent vaginal labour (if big and located near internal OS)
o Dx
▪ U/S
151

▪ in case of bleeding, 1st step = Uterine curettage (Dx and Rx)!

o Rx
▪ in pregnancy
• myomectomy – not recommended in pregnancy or during C-section; do
nothing
• red degeneration in pregnancy – just analgesics
▪ not pregnant
• < 14 wks in size (measured like a baby) + no symptoms
- leave it and observe
• > 14 wks or infertile woman, young, wants babies
- Rx: Blood transfusion (if needed), then myomectomy
▪ admin. GnRH (for max 6 mths) before surgery, to ↓size
• old lady, doesn’t want babies, severe signs & symptoms
- Rx: Hysterectomy
- DUB
o 10-20% women at some stage
o types
▪ Ovulatory – 35-45 yrs --- regular
▪ Anovulatory – 12-16 & 45-55 yrs---Irregular
o Sx
▪ Menstruation > 8 days
▪ Heavy bleeding > 4 days
▪ Frequent bleeding – periods occur more often than every 21 days
o Dx of exclusion
▪ FBE, coagulation profile, FSH, LH, etc.
▪ D & C, hysteroscopy, biopsy
• -> if all normal = DUB
o Mx – Step-ladder approach:
▪ Conservative/ medical
• 1. Mefenamic acid (PG inh.) - NSAID
- or Naproxen, Ibuprofen, Indomethacin
- can ↓ bleeding in up to 50% of pts (blue book p. 533)
• 2. Tranexamic acid (antifibrinolytic agent)
• 3. OCP
- Provided it’s not CI (e.g. in HTN)
• 4. GnRH agonist – induce a medical menopause
- SE – significant menopausal sympt. (when admin. before
menopause)
- e.g.
▪ Nasal spray - Synarel
▪ Monthly implant – Zoladex
• 5. Oral progest.
- e.g.
▪ Norethisterone
• Blue book p. 532: recommended in a 45 yrs
woman with DUB, HTN and regular cycles
(Ovulating)
152

▪ medroxy progesterone acetate (MPA)?

• 6. Depo-provera
• 7. Implanon- a matchstick like device implanted SC for 3 yrs containing
progesterone
• 8. Mirena IUD
- Blue book p. 532: recommended in a 45 yrs woman with DUB,
HTN and regular cycles (ovulating)
• 9. Danazol
- Virilization SE on long term Rx
• 10. D & C
▪ Surgery: for women who have finished their family + DUB Dx is established
• 11. if fibroid – myomectomy
• 12. Uterine artery embolization
• 13. uterine a. ligation
• 14. Endometrial ablation
- methods
▪ laser
▪ diathermic
- difficult to perform and with poor long-term cure rate if uterus is
significantly enlarged (blue book)
• 15. Hysterectomy – most invasive but also most effective
- especially if severe bleeding and severe anemia
- Postmenopausal bleeding
o causes
▪ in first 2-3 yrs after LMP – MC = episodes of ovarian follicular activity
• + ↓in hot flushes, ↑vaginal lubrication, breast and abd. size
▪ > 3 yrs after menopause:
• 1. MC – Vaginal atrophy
• 2. Cervical or endometrial polyps
• 3. Endometrial or cervical CA – 10% together – we shouldn’t miss
• cystic endometrial hyperplasia – in obese women
• Ectropion – MC in postcoital bleeding
o Dx
▪ 1st step: TVS
• endometrial thickness < 5 mm -> OK
• endometrial thickness > 5 mm -> suspect of CA
- -> do hysteroscopy – most appropriate
- causes of Post-coital bleeding
o Ectropion - MC cause in young women
▪ central columnar epithelium protrudes out through external OS of cervix
▪ due to excess estrogen, in
• young women ovulating
• pregnant women
• OCP
▪ CIN is often located inside it
▪ Sx
• mucous discharge (not purulent) which can be abundant
153

• lesion that looks like an erosion – used to be called cervical erosion

- red ring around cervical OS
• can cause bleeding, e.g. post-coital
▪ Rx
•
if asymptomatic - reassurance
•
if troublesome - cautery
- healing in 4 wks
o CA – always to rule out in elderly
o chlamydial cervicitis
o cervical polyp
o trauma
Dysmenorrhoea
o types
▪ Primary
• common
• often commencing 2 yrs after menarche, when ovulatory cycles begin
- not present during anovulatory cycles
• less common after pregnancy or cervical dilatation
• Sx
- pain starts before period and continues 1-2 days into period
• Rx – success in 95%
- anti-prostglandins, inh. of prostaglandin synthetase
▪ NSAIDs (First line agents), Mefanamic acid
- OCPs
▪ MCQ: young virgin with severe dysmenorrhea - OCP
• placebo is also effective in 20-50%
▪ Secondary
• Sx
- pain persists through the menses
• causes
- submucousal fibroids
- endometriosis and adenomyosis
- PID
• Rx – treat primary disease
Vaginal discharge, Infections & STI:
- Vaginal pH - N = 4-4.7 (acidic)
- Dx
o pH
o Smears -> before initiating Rx
▪ Amine or whiff test – add a drop of KOH to vaginal secr. -> for bacterial
vaginosis
▪ Wet film
o Culture
o STI workup
▪ first-pass urine and Thin Prep samples -> for Chlamydia and gonorrhoea PCR
▪ swabs from cervix for Chlamydia and gonorrhoea: cervix then endocervix
▪ viral culture (herpes simplex)
154

▪ GBS – swabs from endocervix, urethra, rectum

▪ Pap smear
- Causes
Color Consistency Odor p Wet film Assoc. sympt.
H
Physiological Milky- No No (no
discharge white/clear itchiness)
mucoid
Atrophic Yellowish, Non- Tenderness,
vaginitis Non offensive dyspareunia,
offensive post-coital
bleeding
Candida White Thick (cream No 4 Lactobacili, no Itch,
cheese) polymorphs, + soreness,
spores, hyphae redness
Trichomona Yellow- Bubbly/frothy, Malodorous, 5- Numerous Soreness, itch
s (SEXUALLY green profuse fishy, foul 6 polymorphs,
TRANSMITTE (mucopurulent) smelling Trichomonas
D) (with flagella &
moving)
Bacterial Grey Watery, Malodorous, 5- Numerous No pain no
vaginosis( profuse, bubbly fishy 6 polymorphs, itch
NOT SEXUALLY) Clue cells
o 1. Physiological discharge
o 2. Atrophic vaginitis – after menopause
▪ vaginal dryness, reduced elasticity and turgor of the vulvar skin
▪ loss of vaginal acidity -> more prone to infection
• yellowish non-offensive discharge
• tenderness, dyspareunia
• post-coital bleeding
▪ Rx
• Vaginal estrogen replacement
• Oral HRT
o 3. Bacterial Vaginosis – 40-50% (MC cause of vaginal irritation and discharge)
▪ not transmitted sexually
▪ caused by a mixed flora:
• Gardnerella vaginalis
• Mobiluncus species
• Mycoplasma hominis
▪ Sx
• fishy foul smelling discharge
• no pain, no itch
▪ Dx
• Clue cells – aggregates of squamous vaginal epithelial cells with bacter.
attached to them (cytoplasm appears granular & borders are obscured)
▪ Rx
• 1 - Metronidazole 400 mg PO 12 hourly for 7 days
155

• 2 - Clindamycin 20% PO or vaginal cream – in:

- resistant inf.
- pregnancy
• in pregnancy
- 1. Clindamycin 300 mg orally 12 hrly for 7 days
- Metronidazole 400 mg p.o. 12 hrly for 7 days
▪ not very safe – categ B2
• no need to trace and treat the partners
o 4. Trichomonas – 10-20% (TTTT)
▪ Flagellated protozoan
▪ Transmitted sexually
▪ Sx
• soreness, itch
• yellow-green profuse thin discharge, with small bubbles in 20-30%
• diffuse erythema of cervix and vagina
• punctate appearance on cervix – characteristic
• Dyspareunia and dysuria
• Infertility in both male and female and preterm delivery
▪ Dx – Culture (95% sesnitive), (Wet prep 30-80% sensitive).
▪ Rx
• Metronidazole PO x 2g as a single dose
• Pregnancy – Clotrimazole vaginal tablets
• Trace and treat partner!
o 5. Candidiasis – 20-30% (2nd MC)
▪ Sx
• Thrush, white discharge (curdy, cheesy, yogurt), itchy
• Risk factors
- endogenous
▪ DM
▪ pregnancy
▪ debilitating dis. – immunocompromised, AIDS
- exogenous
▪ A/B
▪ OCP, HRT, IUD
▪ long term use of corticosteroids and other
immunosupressants
▪ carbohydrate-rich diet
▪ orogenital/ anogenital intercourse
▪ tight-fitting jeans, nylon underwear, humidity/ wet
bathing suit
▪ Dx
• high vaginal swab
• culture
▪ Rx
• First lin Clotrimazole (miconazole, etc.) – 1-7 days
- Vaginal tablets/ cream
• Recurrent
156

- Nystatin cream + pessaries

• Recalcitrant, not pregnant
- Fluconazole or itraconazole PO
• in pregnancy – Clotrimazole pessaries! (local, not systemic)
• in Candidata glabrata - Boric acid (not in pregnancy)
- resistant to imidazoles
• other advice
- good hygiene, no creams, warm water and vinegar, avoid sex
(painful)
- dryness
- no need to trace and treat partners
- change from OCPs to condoms
o 6. GBS
▪ Screening done at 35 to 37 weeks thru recal or vaginal swab
▪ in pregnant woman, Benzylpenicillin in labour 6hrly
▪ If GBS bacteriuria Rx immediately with penicillin
▪ non-pregnant woman – amoxycillin if significant pyogenic inf.
o 7. Retained vaginal tampon
▪ extremely offensive vaginal discharge
o 8. Tampon toxic shock syndrome
▪ due to exotoxin produced by staph. aureus
- STI
o Vaginitis:
▪ Bacterial vaginosis
▪ Candida
▪ Trichomonas vaginalis
o Urethritis:
▪ Sx
• asympt. or
• dysuria, penile discharge (clear, white, yellow) – men
• dysuria, vaginal discharge
▪ Cx
• Epididymo-orchitis, prostatitis, urethral stricture in men
• PID, infertility in women (MC in NSU)
▪ causes:
• Chlamydia
• Gonorrhoea
• Non-specific urethritis (NSU)
- C. trachomatis
- Ureaplasma
- Mycoplasma hominis
▪ Chlamydia:
• most frequent STD in Australia (3x more frequent than gonorrhoea)
- always first tested for
• incubation 1-2 wks (5 days – 12 wks)
• Sx
- usually asympt. (until severe urethritis or salpingitis occurs) or
157

- milky-white or clear discharge

• Cx
- common cause of infertility due to tubal obstruction
• Dx.
- 1st pass urine (1st 10 ml after not urinating for 4 hrs) -> PCR (95%
specificity)
- wire swab (2-3 cm into urethra + endocervical canal in women)
▪ PCR and LCR (ligase chain reaction) – in men
• Rx.
- 1. Azythromycine (preferred) or doxycycline
- 2. Erythromycin – in pregnancy
- trace and treat (the same way) all partners (even if asympt.)
▪ no sexual intercourse until healing
• Screening for higher risk
- all sexually active females < 25 yrs
- all sexually active teenagers, especially females, Aboriginals and
Torres Islanders
- unsafe sex (no condom)
▪ anal sex
▪ 6-12 mnths post-inf.
▪ Gonorrhoea:
• incubation 2-3 days (up to 3 wks)
• Sx – 2-7 days after vaginal/ anal/ oral sex
- creamy-pus like discharge
- oropharynx – dysphagia, sore throat
- anus – mucopurulent anal discharge, anal discomfort
• Dx
- Gaam stain and culture of urethral pus standard swab (into
urinary meatus) Investigation of choice.
- first pass urine -> PCR
▪ less reliable than an endocervical specimen
- + throat swab
- + rectal swab – gay people
• Rx
▪ Ceftriaxone IM or azithromycin (Single dose)
- in pregnancy
▪ erythromycin or roxythromycin
- if it doesn’t respond to Rx – probably suprainf. with Chlamydia
- trace and treat partners
o Cervicitis
▪ mucopurulent c. often a foreruner of PID
▪ agents:
• C. trachomatis
• gonococcus
▪ Rx – as for urethritis
• Ciprofloxacin + Doxycycline
o PID
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▪ Includes Endometritis, salpingitis, tubo-ovarian abscess, pelvic peritonitis.

▪ Recurrent infections: Risk of infertility and ectopic pregnancy
▪ Causes: not always a STI
• Sexually transmitted:
- Chlamydia MC
- Gonococcus
• Following instrumentation of cervix or recent insertion of an IUCD.
- Mycoplasma
- vaginal pathogens
- E. coli - sometimes
• following a suction curettage for unwanted pregnancy, especially if
having multiple sexual partners
- Chlamydia (15%) + vaginal pathogens
▪ CLINICAL FEATURES:
• Acute
- for Dx:
▪ must be – all these 3:
• moderate to severe bilateral lower abdominal
pain (+/- rebound)
• On vaginal examination adnexal tenderness &
• cervical motion tenderness.
▪ one of the following must be present
• Fever ≥ 38
o if fever is present = systemic inf. = PID,
rather than just a local inf. (vaginitis,
etc.)
• WBC ≥ 10.500/mm2
• purulent fluid obtained via culdocentesis
• inflam. mass present at bimanual pelvic exam.
or U/S
• ESR ≥ 15 mm/h or CRP > 1 mg/dL
• evidence for the presence of Chlamydia or
gonococcus in the endocervix
• > 5 WBC per oil immersion field on Gram stain
of endocervical discharge
- other sympt.
▪ malaise, dyspareunia, menstrual irregularities and
vaginal discharge, dysuria or frequent urination
• Chronic PID
- Sx – ache in lower back, mild lower abd. pain
▪ DIAGNOSIS:
• Send endocervical swab for gonococcal and chlamydial culture.
• FBE and blood culture.
• Pregnancy test.
▪ Cx
• Infertility
▪ MANAGEMENT:
159

• Remove IUD or retained products of contraception if present.

• Admit:
- Systemically unwell.
- Pregnant.
- Intolerant to oral medication.
- Tubo-ovarian abscess.
• Antibiotic therapy:
- Mild to moderate/ outpatient: Azithromycin 1g orally +
Ceftriaxone 250 mg IM + Doxycycline 100 mg b.d. orally +
Metronidazole 400 mg b.d. For 14 days.
- Severe/ hospital: Cefotaxime (or ceftriaxone) + Doxycycline +
Metronidazole
- Pregnancy: Cefotaxime (or ceftriaxone) + Roxithromycin +
Metronidazole
• Follow-up.
• Partner needs to be tested and treated.
o Ulcers
▪ Genital herpes
▪ Syphillis
o Lumps
▪ Warts
o Itch
▪ Scabies
o Pubic lice extragenital STI
Other vulvo-vaginal pathology
- Vaginal and vulvar formations
o Anterolat. wall
▪ Wolffian duct cyst – within vagina, suburethral low in vagina, then more lateral
the higher in vagina.
• Gartner duct cyst
- Gartner duct is part of Wolffian duct
o Post. wall
▪ Bartholin glands
• 2 glands located at the posterior end of the labia majora. They secrete
mucus to lubricate vagina and are homologous to bulbourethral glands in
males
• Pathology
- Cyst – MC JM 1169
- Rx – A simple, non-infected cyst can be left alone and may resolve
spontaneously. If it becomes infected an abscess may result,
causing a painful, tender, red vulval lump. It may resolve with
antibiotic or discharge spontaneously. Otherwise drain and
perform a micro and culture. The usual organism is E. coli. If the
cyst persists and becomes large, a surgical marsupialisation
procedure, which allows permanent drainage, can be performed
- Vaginal invasive malignancies
o Vulvar pruritis and redness – rule out vulvar CA
160

o types:
▪ extension of squamous CA spread from cervix - MC
▪ metastatic adenoCA from endometrium
▪ primary invasive squamous cell CA of vagina
▪ clear cell CA following diethylstilbestrol Rx
▪ CA of the urethra, Bartholin gland, Gartner duct
- Cyclical (recurrent) vulvitis
o MC cause – Candida
o exacerbates premenstrually
o Sx – chronic vulvar itch, burning, swelling, dyspareunia, aggravated with systemic A/C
▪ with or without discharge
o Dx
▪ low vaginal swab
o Rx
▪ topical antifungal: Imidazole, Nystatin
▪ oral antifungal: Ketokonazol, fluconazol, itroconazole
▪ severe itching – C/S
▪ Pregnancy – Nystatin pessaries
- Sebaceous cysts – in labia majora
Endometriosis & adenomyosis
- Endometriosis
o 10% incidence.
o Ectopically loca ted endometrial tissue responds to sex hormones.
▪ locations:
• MC - ovary (60%), uterosacral ligament (60%)
• 28% - cul de sac of Douglas
• 15% - broad ligament
• 15% - bladder
• 12% - rectum
• 7% - sigmoid colon
• 5% - round ligament
• 2% - appendix
o Puberty to menopause: Peak 25-35 yrs.
o MC in nulliparous women and resolves with pregnancy
o CLINICAL FEATURES:
▪ most patients are asymptomatic
• Dx made when a laparoscopy is done to investigate infertility
▪ pain
• Secondary dysmenorrhoea.
- painful period
- pain usually starts before period and continues through the
period, then ↓
• Acute pain with rupture of endometrioma.
• Dyspareunia
• Non-specific pelvic pain or dyscomfort, low back pain
• pain at urination and or defecation
▪ abnormal bleeding
161

• Menorrhagia
• Premenstrual spotting
• irregular spotting
▪ Infertility
▪ diarrhoea/ constipation, bloating
▪ (almost) never undergoes malignant change
o DIAGNOSIS:
• The most suggestive sign is tenderness, mass or nodularity in the pouch
of Douglas or uterosacral ligaments. MCQ
• cervical excitation (motion tenderness)
▪ 1st exam. – U/S
• rule out: ovarian cysts, fibroids, etc.
▪ Gold stand. of Dx: direct visual inspection at laparoscopy or laparotomy
o Rx
▪ Analgesics.
▪ MEDICAL:
• 1. OCP: once daily for 6 mnths
• 2. Progestogens
• 3. GnRH analogues (treatment of choice)
• 4. Danazol
▪ SURGICAL:
• indic
- if medical Rx fails
- causing infertility
- if significant impact on patient’s life
• Laser or microsurgery
- removal of tissue
- endometrial ablation or electrodiathermy excision
- hysterectomy
- Adenomyosis:
o invasion of the myometrum by the basal endometrium of the uterine cav., with ectopic
glandular tissue (adenomyotic glands) found in the muscle
o 35-50 yrs
o not MC in nulliparous (diff. from endometriosis)
o Sx
▪ dysmenorrhoea
▪ menorrhagia
▪ dyspareunia
▪ slightly enlarged (bulky) and tender uterus
o Dx
▪ D&C not helpful
▪ core biopsy of myometrum
▪ removed uterine specimen (after hysterectomy)
o Rx
▪ if severe sympt. -> hysterectomy (adenomyotic glands repond poorly to
hormonal suppression)
162

Ovarian cysts and CA

- ruptured ovarian cyst
o prior to ovulation, after coitus
o 15-25 years
o types of cysts
▪ follicular – MC: unilocular, with thin wall
▪ dermoid cyst
▪ chocolate cyst of the ovary = endometriosis in the ovary
▪ ovarian CA: multilocular, with solid elements
▪ PCOS
o Sx
▪ sudden onset of pain in iliac fossa, ± nausea, vomiting
▪ tenderness and guarding in iliac fossa
▪ no fever
▪ PR – tenderness in rectovaginal pouch
o Dx
▪ U/S
▪ color Doppler
o Rx
▪ reassurance
▪ analgesia.
▪ Referral to Gynaecological team
▪ conservative
• in simple cyst
- < 4-5 cm (most likely a follicular cyst) -> rescan in 6 wks
▪ if size unchaged:
• CA-125 - incr. in follicular cyst & endometriosis
• OCP
• laparoscopic assessment and or aspiration
- > 6 cm – laparoscopic aspiration
• internal hemorrhage, hemodynamically stable
• no pain
▪ laparoscopic surgery (cyst excision), if:
• complex cyst
• > 4-5 cm
- risk of torsion
• severe external bleeding
• painful
- Torsion of ovarian cyst
o Sx
▪ severe diffuse cramping lower abd pain which may radiate to flanks, back or
thigh
▪ severe vomiting, pelvic tenderness, patient is very ill
▪ palpable mass in abdomen
▪ tenderness and guarding if leakage
o Dx
▪ U/S
163

▪ color Doppler
o Rx
▪ laparotomy and surgical correction
- Ovarian CA – M 998
o often Dx late (not many Sx), usually an incidental finding
o > 45 yrs, peak 60-65 yrs
o risk factors
▪ nulliparity
▪ age
▪ family Hx
▪ hereditary breast - ovarian CA syndrome – BRCA1, BRCA2
o protective factors
▪ pregnancies
▪ OCP (they suppress/ shut down ovaries)
o Sx
▪ non-specific: lower abd. pain or discomfort, bloating, constipation, pelvic
heaviness, urine frequency, dysuria, vaginal bleeding, menstr. dysfc.
(dyspareunia, dysmenorrhoea)
▪ ascites
▪ adnexal mass on physical or bi-manual exam.
• any ovarian enlargement detected after menopause must be
considered malignant until proven otherwise!
• large adnexal mass developed in a postmenopausal woman – e.g. 60
yrs (+vaginal bleeding) – MC cause = Ovarian CA (Ovarian cysts or
benign tumors are unusual at this age)
o Dx
▪ 1. Pelvic Doppler U/S
▪ No FNAC – risk of spreading the CA!
▪ 2. tumor markers:
• CA-125 – most specific
- (still not very specific) also ↑ in follicular cyst & endometriosis
• AFP
• Beta HCG
• CEA
o Dx and Sx
▪ 3. urgent referal to gynecologist: excision (Oophorectomy)
- CA metastases in ovaries (blue book p. 531) – only 5% of the CA in the ovaries
o in Aus. MC from colon CA -----Colonoscopy is advised for screening
o in underdev. countries – MC from breast CA
o in Japan (with a very high incidence of stomach CA) – MC from stomach CA (Krukenburg
tumor in both ovaries)
Endometrial CA
o Risk factors
▪ Anovulatory cycles
▪ Old age
▪ Obesity
▪ nulliparity
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▪ late menopause
▪ DM
▪ PCOS
▪ NOT - smoking
o Dx
▪ U/S
• if thickness > 5 mm
- hysteroscopy + biopsy
• if thickness < 5 mm – CA very unlikely
Cervical CA
o risk factors
▪ all women who were sexually active
▪ higher risk
• Early age at 1st intercourse
• Multiple partners or partner who had multiple partners
• Smoking
• OCP
• Radiotherapy
• Diethylstilbestrol (DES)
• HPV – especially with high risk strains (16, 18)
- 4 of 5 women get HPV after they start sexual life, most clear
infection in 1-2 yrs
- condoms give limited protection from transmitting disease
o Prevention
▪ Vaccine = Gardasil – for types 6, 11, 16, 18
• 6, 11 – anogenital warts
• 16, 18 - cervical cancer
• also prevents some vulval and vaginal cancers
• admin. 0, 1-2 mths, 4-6 mths IM
• Girls – any age (9-26 yrs)
- in school free, then they have to buy it
• Boys – 9-15 yrs, safe but not proven to be effective
• useful until 26 yrs
• not in pregnant women
- always do a pregnancy test first
• S.E. - mild fever, allergy
• useful in existing warts
• after admin., continue with PAP smears as usually
o Screening
▪ PAP smears (cellular level) – every 2 yrs until 70 yrs
• if (LSIL CIN I) -> repeat PAP in 12 mths
- -> if normal -> repeat in 12 mths
▪ -> if normal -> normal screening every 2 yrs
- if LSIL CIN I-> colposcopy + biopsy (tisular level – how deep and
extensive is the lesion)
▪ -> if LSIL -> ablation
165

• cryo
• laser
• sugical
• if HSIL (CIN II or CIN III) -> Colposcopy + biopsy
- if HSIL -> ablation
▪ cryo
▪ laser
▪ sugical
- if invasive -> Cone biopsy
▪ SE
• bleeding
• cervix incompetence
• cervix stenosis
• premature labor in future
• PROM
▪ in Pregnancy – cone biopsy and vaginal delivery are CI
• IF LSIL – follow same 12 months protocol
• If HSIL-- first Colposcopy then
< 20 wks – termination of pregnancy + Rx the CA
> 20 wks – discuss with mother:
o terminate pregnancy
o continue but risk of advanced CA
▪ best to wait till 36 wks, then C-
Section (vaginal delivery is CI)
o Stages
▪ I – limited to cervix
▪ II
• IIa – upper 2/3 of vagina
• IIb – upper 2/3 of vagina + parameters
▪ III – lower vagina
▪ IV
• IVa - bladder and rectum
• IVb – distant metastases
o Rx
▪ I – Cervical conization
▪ II – Radiation + chemotherapy
▪ III, IV – radiation + chemotherapy
Uterovaginal (genital) prolapse
o 50% of parous women
o Risk factors/ causes
▪ multiparity – after long 2nd stage labor
▪ obesity
▪ old women at menopause/ post-menopausal – decr. estr. -> decr. collagen
strenght -> weak vaginal muscles
▪ delivering large baby
▪ smoking
o types:
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▪ 1st degree – cervix in vagina

▪ 2nd degree – cervix protruded out on straining
▪ 3rd degree – cervix protruded out without straining
o Sx
▪ heaviness, dragging pain, sense of something coming out
▪ incontinence, urinary or fecal retention
▪ recurrent cystitis
▪ back ache
o Cx
▪ Stress urinary incontinence
• unwanted urinary leakage, loss of small amounts of urine when coughing
or sneezing, incomplete emptying of bladder
o Dx
▪ exam in left lat. position – Speculum – ask woman to cough -> prolapse visible
o Px (prevention)
▪ reassurance and education
▪ pelvic floor exercises
▪ loose weight
o Rx
▪ Asympt – same as Px
▪ Ring pessaries
• individually fitted
• if unfit for surgery or waiting for surgery or she wants kids
▪ Surgery
• transvaginal hysterectomy
- Enterocele:

o
▪ vaginal hernia, which occurs when small intestine (small bowel) descends into
lower pelvic cavity and pushes at the top of vagina, creating a bulge.
▪ Enteroceles MC occur in women who have hysterectomy done
▪ Rx – Surgery
- Rectocele:

o
▪ If muscles of posterior wall of vagina are damaged, rectum will begin pressing
into vagina. This is called a rectocele.
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▪ MC symptoms of rectocele are:

• a bulge in vagina
• constipation and difficulty completing bowel movements
• a feeling of rectal pressure
• painful sexual intercourse
o Cystocele:
▪ If muscles in ant. wall of vagina are weak, bladder will begin to bulge into
vagina. This is called a cystocele.
▪ The MC symptoms are:
• difficulty emptying your bladder
• leaking of urine, esp. when you cough, sneeze or laugh
• pain during sexual intercourse
o Urethrocele – urethra bulges into vagina
Urinary incontinence in women
o 9%
o MC contributing factor = weakness of pelvic floor muscles
o Causes: DIAPERS
▪ Delirium
▪ Infection – UTI
▪ Atrophic urethritis
▪ Pharmocol. (drugs), psychological (acute distress)
• Drugs:
- Stress incont.
▪ anti-HTN and vasodil.
• ACE inh.
• prazosin
• labetalol
- Overflow incont.
▪ bladder relaxants
• anticholinergic
• TCA
- Urge incontinence
▪ Bladder stimulants
• cholinergic agents
• caffeine
▪ Sedatives
• antidepressants
• antipsychotics
• hypnotics
• tranquillizers
▪ others
• alcohol
• diuretics
• lithium
▪ Endocrine (hypercalcaemia), environmental (unfamiliar sounds)
▪ Restricted mobility
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▪ Stool impaction, sphincter damage or weakness

o Dx
▪ exclude UTI
▪ Urodynamic studies
o types
▪ 1. Simple, genuine stress incont. (GSI)
• invol. loss of small amounts of urine during sudden ↑ in intra abd.
pressure
- coughing
- sneezing
- straining
- lifting and during pregnancy
• Mechanism = Sphincter incompetence
• demonstrable: patient coughs while standing with a full bladder
• Rx
- Pelvic floor exercises – 3 months, under supervision
▪ 75% improved, 25% cured
- bladder training
- wt. loss:
- Surgery: If urodynamic studies show genuine stress incontinence
(GSI) due to urethral sphincter weakness, (suprapubic urethral
suspension)
▪ 2. Urge incontinence/ Detrusor instability
• urgent desire to void, followed by involuntary loss of large amounts of
urine
- no residual urine?
- often happens at night when she is asleep
- she has a desire to empty bladder again after an incontinence
episode
• Mechanism = Unstable/ overactive bladder (detrusor instability) and/or
sphincter weakness
• Rx
- bladder training
▪ void more urine less often
▪ delay urination by 10-15 min when she wishes to void
- Anticholinergics (MCQ)
- neurol. signs? -> refer to neurologist
▪ overflow incont.
▪ quiet dribble incont. – sphincter incompetence + unstable bladder or overflow
▪ continuous leakage – fistula
▪ reflex incontinence – neuropathic bladder
▪ + voiding dysfc./ bladder instability
▪ If bladder atony → anticholinergic drugs
• Rx
- Anticholinergic drugs
▪ propantheline
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Other gynecological stuff

- Septic shock in O & G – MC with E. coli
- MC complic. after major gynecological surgery = UTI
- Sexual activity disturbances
o Sexual desire:
▪ can be inhibited by
• menopause
• fear of pregnancy
• hysterectomy
• “empty nest” syndrome
o excitement phase during sexual activity
▪ inh. by marital discord
- causes of Dyspareunia
o Vaginismus-----fear of pain
o Atrophic vaginitis
▪ Menopause, perimenopause, POF, premature menopause
▪ Postpartum, in lactating amenorrhic women (↑prolactin causes ↓GnRH and
thus ↓ estr.)
o Endometriosis pain is resolved during pregnancy and adenomyosis
o Vulvitis, vaginitis (MC in candida, herpes) monilial and trichomonal infections
o Vaginal introital narrowing – e.g. lichen sclerosis et atrophicus
o PID
o Retroverted uterus after surgery
- Retroverted uterus
o Rx - no longer surgery since 100% of treated patients will present dyspareunia
- Chancroid – haemophylus Ducreyi
o Painful ulcers + lymphadenopathy
- Condylomata acuminatum – cauliflower like mass
- Lyphogranuloma venereum – chlamydia trachomatis
o STD
o painful genital ulcers
o painful lymphadenopathy (merging nodes)
- Pre-menstrual syndrome
o 2-14 days before period
o can get worse in the 30s or 40s
o varies from one month to another
o Sx
▪ during luteal phase
▪ physical sympt.
• Weight gain (0.5-1 kg), breast soreness, bloating
▪ Psychological sympotoms
• depression, anxiety (tearful), irritability, ↓ libido, headache
o Dx – normal estrogen and progesterone
o Rx
▪ reassurance, explain problem
▪ ask to write a diary of what happens every month for 3 mths
▪ improve lifestyle – exercise, meditation
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▪ Premenstrual syndrome + dysmenorrhea - Mefanamic acid

▪ Premenstrual syndrome + fluid retention - Spironolactone
▪ Premenstrual syndrome + Mastalgia – Evening primrose oil (1st line) Danazol
2nd line
▪ Premenstrual syndrome + Mastalgia + depression and mood changes =
Premesntrual dysmorphic disorder – SSRI
▪ Bromocriptine and Vit. E have very weak role in PMS.
- Pre-menopausal syndrome
o Sx
▪ irregular periods, ↓flow of blood (less blood and less days)
▪ migraine (decr. progesterone)
▪ rosacea (hormonal imbalance)
Infertility
- Male infertility (Murtagh 1108-1110):
o causes
▪ I. ↓ sperm prodution
• congenital cryptorchidism
- varicocele – does not affect risk (Murtagh)!
• inf.: mumps
• antispermogenic agents: chemotherapy, irradiations, drug, heat
▪ II. Hypothalamic-pituitary dysfunction
▪ III. Disorders of coitus:
• Erectile Dysfunction
• Retrograde ejaculation
- in DM
- after prostate surgery
• Psychosexual ejaculation failure
▪ IV. Idiopathic
o Dx
▪ Normal sperm analysis
• Volume > 2 ml
• Sperm concentration
- > 20 million/mL
▪ < 20 mil. = Oligospermia -> IVF
▪ < 5 mil. = Severe Oligospermia -> ICSI
• Morphology (shape)
- > 20% normal
- < 60% abnormal
• Motility – most important (> concentration)
- > 40% motility after 4 h
- > 25-30 % moving very fast
• Velocity > 30 microns/s
• antibodies against sperm
- < 50 % in cervical mucous
▪ Normal hypothalamic function
• GnRH
▪ Hormal pituitary function
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• FSH, LH
▪ testosterone
o Rx
▪ Inj. with FSH – if sperm analysis isn’t very bad (can improve it)
▪ Regular IVF - if sperm analysis isn’t very bad (5-20 mill/ml)
• if very bad – 2%/ cycle treated success rate
▪ IVF with ICSI – if severe Oilgospermia
• 20% per cycle treated success rate
o MCQ
▪ no fructose = no sperm coming from testicles
▪ 0-3 ml – coming from prostate
- Female infertility
o Dx
▪ Ovulating?
▪ Patency of tubes?
▪ Cervical factor?
• Post-coital test – 2 hrs after check:
- spermatozoids
- cervix – mucus consistency
- IVF
o indic.
▪ Male
• Oligospermia (5-20 mill/ml)
• Presence of sperm AB
▪ Female
• endometriosis
• damaged or absent fallopian tubes
• unexplained infertility
- ICSI (Intracytoplasmic sperm injection)
o indication
▪ severe oligospermia or azoospermia (<5mill/ml)
▪ failure of IVF
- Fertility treatment – Monash IVF
o infertility rate – 15%
o cause of infertility
▪ 1/3 woman
▪ 1/3 man
▪ 1/3 man and woman
o Safety Net – out of 7500 you get 5000 back
o in Vivo:
▪ Ovulation induction – Clomiphene (only if FSH not raised)
▪ Intrauterine insemination (IUI) – 2000 AUD
• 10% success rate
• risk of multiple pregnancies
o in Vitro:
▪ IVF – try this first
• no good sperm
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• donor program
- donor types
▪ Known
▪ Unknown =altruistic – when child becomes 18 has the
right to find who is biological mother/ father
- for
▪ Sperm
▪ Ovum
• Method: Put sperm and ovum together for (short insemination protocol)
2 or 16 hrs (long)
▪ Intra Cytoplasmic Sperm Injection – if IVF failed or we need to do testicular
aspiration, go for this one
• low sperm count
• inject sperm
o Overall success rate is 90% in 3 attempts.
Orthopedics - OK
Trauma and fractures
General stuff
- MC causes of post-traumatic arterial thrombosis
o 1. fracture of femur
o knee dislocation
o hip fracture
- MC cause of artery injury – posterior knee dislocation (Popliteal A.)
- nerves that regenerate most after traumatic laceration:
o Digital N.
o Sural N.
- after visit to chiropractor = dissection of vertebral artery: neck pain, facial hemisensory loss,
ataxia
- Compartment syndrome – haematoma within a fascia, compressing on close structues
(nerves, arteries, etc.)
o Sx – e.g. leg swollen, post. tibial pulse not felt, pain on moving toes
o Rx - fasciotomy
- MVA
o thoracolumbar pain – transport in supine position on a flat surface
o with blood in urethra -> retrograde urethrogram
o main cause of death after MVA - disruption of great vessels, hypoperfusion and shock
- Compound/ open fracture – first step = debridement
- internal organ rupture in trauma
o MC source of air under diaphragm = ruptured intestine
o blow in the abdomen – Organ least often to rupture = Stomach
o MC organ injured in abd. trauma – Spleen 45%
▪ 2 – Liver: 40%
- Splenic rupture
o Mx
▪ Stable pat.
• U/S and CT scan
▪ isolated splenic rapture
173

• conservative Rx
- if it fails -> splenectomy
▪ hT -> splenectomy
▪ other organs are affected -> splenectomy
- Greenstick fracture
o Hx of trauma
o usually occur most often during infancy and childhood when one's bones are soft
o Because a child's bones are much more pliable than adult bone, an incomplete, or
'greenstick,' fracture may occur. A "greenstick fracture" means that one side of bone is
broken and one side is bent; therefore it is classified as an incomplete break.
o The name for a greenstick fracture comes from the analogy of breaking a young, fresh tree
branch. The broken branch snaps on one side (the outer side of the bend), while the inner
side is bent and still in continuity.
o Rx: Most often greenstick fracture must be bent back into the proper position (called a
"reduction") and then casted for about 6 weeks. Greenstick fractures can take a long time
to heal because they tend to occur in the middle and slower growing parts of bone.
- Stress fractures
o normal bone but repeated stresses/ injury on it
▪ diff. from
• pathol. fractures
• acute traumatic fractures
o Athletes, soldiers
o locations
▪ MC – neck and shaft of 2nd metatarsal bone----March troopers
▪ Spinal vertebra in cricket players
▪ Neck of 1st rib in COPD (coughing)
▪ neck of fibula and proximal tibia in runners
• perpendicular fracture starts from the cortical in -> advances till it
becomes transversal
• Rx – rest!
o Sx – pain worse on weight bearing, point tenderness
o Dx
▪ 1. X Rray – Usually normal
▪ 2. Nuclear bone scan – ↑uptake at the point of fracture
o Mx
▪ rest
▪ healing takes 6-8 wks
▪ walking boots
- Insufficiency fractures
o anorexia
o women from Middle East all covered (insuf. Vit. D)
- Flail chest
o 3 or more ribs broken
o Sx
▪ Paradoxical resp. -> gas exchanage impaired -> resp. distress
o Rx
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▪ Immediate intub. and positive pressure ventilation, even if assoc.

pneumothorax (risk of aggravating)
Dislocation/ fracture Main problem or MC injured structure
Shoulder dislocation (ant. disloc. 95%) Axillary N. injury
Fracture of shaft of humerus Radial N palsy
Fracture of surgical neck of humerus Non-union
True pseudo-arthrosis
Supracondylar fracture Impingement of Brachial artery
Elbow dislocation Injury of median and ulnar N
Fracture of head of radius Elbow stiffness
Post-traumatic osteoarthritis
Colle’s fracture Rupture of extensor policis longus tendon
Stiffness of wrist and fingers
Regional pain syndrome
Scaphoid fracture Avasc. necrosis of proximal fragment
Subcapital fracture of femoral head Avascular necrosis of femoral head
Hip dislocation (post. MC) Usually no injuries
Femoral N. and vasc. injury
Injury of knee Popliteal artery injury
Ankle fracture Mortise view – to see if stable or unstable:
If gap between tibia and fibula is uneven = Unstable
=> Rx – refer
Head and neck
- Cervical collar
o 1st test –Check for midline cervical point tenderness
▪ if no tenderness -> remove cervical collar, all OK
▪ 2nd test – X Ray + CT scan
- Temporal Bone Fractures
o Symptoms
▪ Hearing loss, nausea, vomiting and vertigo
▪ signs
• Battle’s sign (post-auricular ecchymosis)
• “Raccoon” sign (periorbital ecchymosis) – involvement of the middle or
anterior cranial fossa

-
▪ External Auditive Conduct laceration with bony debris in the canal
▪ Haemotympanum
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▪ CSF otorrhea or rhinorrhea

o Tests
▪
Tuning fork tests
▪
CT scan
▪
Special tests: audiometry, facial nerve testing (nerve excitability test,
electroneuronography)
- Temporal Bone/ Basal Skull Fractures

o
o Longitudinal Fractures
▪ 70-90% of temporal bone fractures
▪ Extending to EAC, ME, ET, & foramen lacerum
▪ Presentation: bleeding from EAC, CHL, CSF otorrhea, facial paralysis
o Transverse Fractures
▪ 20-30% of temporal bone fractures, usually more severe occipital bone injury
▪ Presentation: hemotympanum, CSF rhinorrhea, SNHL, facial paralysis in 50% of
cases
o Treatment
▪ Stabilize for other neurologic & life-threatening injuries
▪ Observation
▪ Antibiotic coverage
▪ Surgery for persistent Tympanic Membrane perforation – paper patch
myringoplasty or standard tympanoplasty
▪ CHL – hemotympanum resolves in 3-4 weeks with no sequaelae
▪ Facial paralysis – facial nerve decompression & exploration
▪ CSF leak – head elevation, stool softeners, acetazolamide (to decrease CSF
production), placement of a lumbar drain, repair of CSF leak
• fracture of the base of skull – CSF leak
- don’t touch the nose (use orogastric tube)
- AB prophylaxis to prevent meningitis
- Orbital floor (blow-out) fractures
o Fracture of the orbital floor caused by blunt, non-penetrating force
o Direct blunt trauma to the globe causes ↑ intraorbital pressure, causing thin bones of the
orbit to “blow out”
o Inferior orbital wall is most commonly involved
o Ocular globe is protected by the orbital fat
o Forced duction testing is done to evaluate possible muscle/ nerve entrapment
o Inferior oblique muscle is tested, other muscles tested if necessary
o Plain films (tear drop sign on Water’s view)
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o
o CT scan
Clinical features
Enophthalmos MC sign
• Swelling of cheek
• Circumocular haematoma
• Subconjunctival haemorrhage
• Palpable step in infraorbital margin
• Flat malar eminence when viewed from above
• Paraesthesia/diplopia due to infraorbital nerve injury
o • Loss of function (i.e. difficulty opening mouth
o Indications for surgical repair of orbital floor (blow-out) fracture
▪ Rapid onset of intraorbital bleeding & decreased visual acuity
▪ Entrapment (diplopia)
▪ Enophthalmos
o infraorbital nerve entrapment -> diplopia with restricted upward gaze
- Zygomatic fracture
o enophtalmos

Arm
- Lateral epicondylitis = Tennis elbow = Source of extensor tendons (M 714)
On examination the elbow looks normal, and flexion and extension are painless
o pain on pressing on lateral epicondyle
o pronated forearm inc pain (MCQ) + extended wrist (MCQ)-> pain
o resisting extension of wrist -> pain
o Rx
▪ Dumbell exercise with palm facing down
▪ RICE (rest, ice, compression, elevation)
▪ C/S local inj. (1-2)
- Medial epicondylitis = Golf elbow = Source of flexor tendons
o pain on pressing on medial epicondyl
o resisting flexion of wrist -> pain
o Rx
▪ Dumbell exercise with palm facing up
▪ RICE (rest, ice, compression, elevation)
▪ Brace below elbow
▪ C/S local inj. (1-2)
- De Quervain tenosynovitis = Washerwoman’s sprain– M 689
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o tenosynovitis of first dorsal extensor compartment tendons:

▪ Extensor policis brevis
▪ Abductor policis longus
o 40-50 yrs
o Sx
▪ tenderness in thumb, extends along the radial side of thumb down to the radial
side of forearm
▪ pain on pinching or writing
▪ Triad: tenderness to palpation of proximal radial styloid process + firm tender
localized swelling over radial styloid + positive Finklestein’s sign
(pathognomonic)
o Dx
▪ Finklestein test =Put thumb between other 4 fingers, move hand medial <->
lateral => causes pain
o Rx
▪ Rest in splint that involves thumb
▪ NSAIDs are CI!
▪ local inj. of C/S under U/S guidance
▪ last resort: Surgical release of tendons
- Dupuytren contracture (palmar aponeuritis)
o risk factors
▪ smoking
▪ alcoholism
▪ heavy manual labor
▪ trauma
▪ DM
▪ Phenytoin
o fibroting thickening of palmar fascia with skin puckering & tethering
o ring and little finger diformity (but any finger can be affected)
▪ flexion at MCP and PIP joints, DIP joints are spared
o often bilat. and symmetrical
o similar
▪ Peyronies dis.= Fibrotic disease of penis (discomfort & difformity on erection)
▪ Plantar fasciitis = Subcut. nodule on the feet = rare
o Causes
▪ Genetic – AD
▪ Alcoholism
▪ Antiepileptics
o Rx
▪ Fasciectomy surgery – remove affected fascia
▪ Tendency to recurrence
- Carpal tunnel syndrome
o pins and needles, then pain in the median N teritory (fingers 1-3.5)
▪ awakening from their sleep due to this - pathognomonic
• MCQ: man walks up during the night due to painful wrist
o Rx
▪ Rest
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▪ Splinting
▪ C/S infiltration
▪ Surgery
- Injuries to the wrist and hand
o Colle’s fracture
▪ Fracture of distal radius usually within 2.5 cm of wrist.
▪ MC of wrist fractures.
▪ Elderly women with osteoporosis
▪ Fall on outstretched hand
▪ Dorsal angulation and dorsal displacement of the distal radial fragment or
radial displacement.
▪ CLINICAL FEATURES:
• Swelling, ecchymosis & tenderness.
• ‘Dinner fork’ deformity.
• ASSESS neurovascular status: Acute carpal tunnel syndrome.
• Common association
- Ulna
- Scaphoid
- Radial or ulnar styloid fracture
▪ X-Ray: distal fragment is:
• Dorsally displaced with dorsal comminution
• Dorsally tilted fragment with apex or fracture volar
• Supinated
• Radially deviated
• Shortened
▪ Cx
• 1. Stiffness of wrist and fingers (MCQ)
- + Most frequent LATE complication of a Colle’s facture in an
elderly woman
• 2. Osteoarthritic changes
• 3. Malunion
• 4. Non-union – Rx: internal fixation
• 5. Delayed union
▪ MANAGEMENT:
• Colles’ backslab: Permit full elbow flexion & thumb movements
extends from below elbow to metacarpal heads (thumb not included)
- include thumb if associated scaphoid fracture
• Types:
- Undisplaced or minimally displaced (stable):
▪ Colle’s backslab
▪ No manipulation (reduction)
▪ 7-10 days
- Displaced, angulated fractures with radial deviation:
▪ Reduction (Bier’s block = regional nerve block for all the
wrist and hand fractures using a blood pressure cough
on the arm + injection with anestetic in hand).
▪ Circumferential plaster cast for 6-8 wks
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• hand fully pronated

• full ulnar deviation
• with the wrist slightly flexed.
▪ Check within 24 hrs: Discoloration, Swelling,
neurovascular status.
• too tight plaster
o I – discoloration
o II – tingling, numbness & point
tenderness
• Rx – cut the plaster open
▪ Physiotherapy.
o Smith’s fracture
▪ Distal radial fracture with volar displacement.
▪ Fall on the dorsum of hand, a hyperflexion or a hypersupination injury.
▪ Usually unstable.
▪ Localized swelling.
▪ ‘Garden spade’ deformity.
▪ The patient is unable to extend the wrist.
▪ Pain on supination and pronation.
▪ Assess for damage to Median N.
▪ MANAGEMENT:
• Reduction (Bier’s block).
• Place a long-arm plaster.
• Elbow in 90° flexion, forearm in full supination and wrist dorsiflexed.
• Extend plaster above the elbow.
o Barton’s fracture-dislocation
▪ Intra-articular fracture of distal radius with associated subluxation of carpus.
▪ It moves in a volar or dorsal direction.
▪ MANAGEMENT:
• Refer immediately to Orthopaedic team as this injury is unstable and
open reduction with internal fixation is required.
o Scaphoid fracture
▪ MC fractured carpal bone.
▪ Fall on the outstretched hand.
▪ Blood supply is from distal to proximal poles of scaphoid: Risk of avascular
necrosis of proximal half of bone
▪ CLINICAL FEATURES:
• Pain on dorsiflexion or ulnar deviation.
• Pain and weakness of pinch grip.
• Pain and tenderness in palpation of anatomical snuff box or along
thumb metacarpal.
▪ DIAGNOSIS:
• I - X-RAY: AP/ lateral/ scaphoid views required.
- X Ray alone may not reveal scaphoid fracture
• Bone scan.
• II best - CT scan.
▪ MANAGEMENT:
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• Normal X-ray: removable splint 2 wks, follow up

• if
- Confirmed fracture without displacement or angulation: plaster
from mid-shaft of forearm upto metacarpal heads & around
base of thumb to below the interphalangeal joint.

-
▪The wrist should be (like holding an apple – Awad):
• Fully pronated
• Radially deviated
• Partially dorsiflexed
• Thumb held in mid-abduction
- displacement > 2 mm and or angulation – open reduction &
fixation
▪ COMPLICATIONS:
• Non union.
• Avascular necrosis of proximal half of bone.
- circulation (sama as for femoral head)
▪ central to periphearl – usually closes
▪ periphearal to center – from the capsule (main one)
• Osteoarthritis.
o MALLET FINGER:
▪ Injury to extensor digitorum tendon at DIP joint
▪ It results from hyperflexion of extensor digitorum tendon.
▪ Sx
• Full passive but incomplete active extension at DIP joint
▪ TREATMENT:
• Mallet splint for 6-8 wks.
• Elevate hand
• Analgesics
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- Injuries to elbow
o Pulled elbow - Subluxation of radial head
▪ Children 2-6 years.
▪ Axial traction applied to an extended arm.
▪ The radial head is subluxed out of annular ligament.
▪ CLINICAL FEATURES:
• Anxious child
• Local pain
• Loss of use of arm, particularly supination
• Elbow semi-flexed and pronated on examination.
• There is no neurovascular compromise
• Motor activity is normal
▪ X RAY:
• Only to exclude a fracture if extensive swelling.
• Reduction is not successful after two or 3 attempts.
▪ MANAGEMENT:
• Reduction
- Apply pressure to the region of the radial head with one hand.
- Apply axial compression at the wrist.
- Supinate the forearm.
- Gently flex the elbow with other hand.
▪ supination + force flexion of elbow while holding the
thumb over radial head, to feel it move into position, in
the anular ligament-> moves into position
• No immobilization is required.
- Injuries to shoulder & upper arm
o Acromioclavicular dislocation
▪ Fall on to the apex of shoulder with arm held in adduction
▪ types
• Subluxation: Causes local tenderness to palpation with minimal
deformity.
• Full dislocation: Prominent outer end of clavicle (step deformity)
▪ CLINICAL FEATURES:
• Local tenderness and swelling.
• Palpable step between distal clavicle and acromion.
• Pain with adduction.
• Assess the clavicle and scapula for associated fractures.
▪ DIAGNOSIS:
• X Ray: Apparent on stress view. Patient holding a weight in each hand,
compare the shoulders.
▪ TREATMENT:
• Minor: Ice, oral analgesics sling immobilization, daily range of motion
exercises.
• Complete: Same initial treatment, refer to Orthopedic team for possible
operative intervention.
o Glenohumeral joint dislocation
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▪ ANTERIOR DISLOCATION - MC
• Caused by forced abduction and external rotation of shoulder
• Young adults from sports, traffic crashes or elderly from a fall.
• It tends to become recurrent.
• CLINICAL FEATURES:
- ‘Squared off’ shoulder: arm held in slight abduction & external
rotation.
- Loss of deltoid contour (MCQ)
- Humeral head can be palpated anteriorly
- Loss of internal rotation
- Pt can’t rise arm above head (but can move his head to that
position)
▪ most specific – can’t scratch in interscapular region
with his hand
- All shoulder movements are painful.
• ASSOCIATED WITH (These result in recurrent dislocations)
- Hill-Sachs lesion: Flattening or a wedge-shaped defect in
posterolateral aspect of humeral head.
- Bankart lesion – after the first dislocation: Avulsion of capsule
when shoulder dislocates. Occurs in 85% of all anterior shoulder
dislocations.
• COMPLICATIONS:
- Look for complications before any attempt of manipulation
- Axillary N damage:
▪ Check sensation over lateral deltoid (police patch)
▪ check motor function with isometric contractions of
deltoid muscle – Murtagh 1394
- Posterior cord of brachial plexus.
- Axillary artery damage.
- Fracture of the upper humerus.
• DIAGNOSIS:
- X Ray: Always to rule out associated humeral head fracture
▪ Mercedes Benz sign on lateral oblique view – normal
• humeral head displaced anterior or posterior
• ant dislocation – humeral head under coracoid
process of scapula
• post dislocation – humeral head over coracoid
process of scapula
- Humeral head is displaced anteromedially with loss of contact
with glenoid fossa
• TREATMENT:
- Pain relief: Morphine 2.5-5 mg IV
- Conscious sedation with fentanyl (analgesic) and midazolam
(sedative, muscle relaxant)
▪ or fentanyl and propofol (used currently)
- Perform the reduction:
▪ Kocher’s manoeuvre
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▪ Hippocratic method
▪ Jay: straight arm, pull forward (in axul bratului) +
upward (flexion) + abduction + supination
- Sling
- Test again for neurovascular damage
- X Ray to confirm reduction
o Fractures of upper humerus
▪ location:
• Greater tuberosity
• Lesser tuberosity
• Surgical neck of humerus
• Supracondylar
▪ Usually in elderly patients
▪ CLINICAL FEATURES:
• Localized pain.
• Loss of movements.
• Swelling and tenderness.
▪ COMPLICATIONS:
• Dislocation of humeral head.
• Complete distraction of the humeral head from the shaft.
• Axillary N damage -> anaesthesia over lateral deltoid & loss of deltoid
movement.
• Axillary (circumflex) vessel damage.
• in supracondylar fracture (just above epicondyles)
- Sx – huge hematoma
- Cx = Brachial A. injury => Volkmann's ischemic contracture
▪ Permanent flexion contracture of hand at wrist,
resulting in a claw-like deformity of hand and fingers.
It is more common in children. Passive extension of
fingers is restricted and painful. On examination fingers
are white or blue, cold and Radial pulse is absent.
▪ It’s caused by obstruction of brachial artery near elbow
• results from acute ischaemia/ necrosis of
muscle fibres of flexor group of muscles of
forearm, specially flexor digitorum profundus
and flexor pollicis longus which become fibrotic
and short.
▪ Causes:
• Any fracture at elbow or upper arm may lead
to Volkmann's ischemic contracture but
commonly caused by supracondylar fracture of
humerus.
• improper use of a tourniquet
• improper use of a plaster cast – too tight
• compartment syndrome.
▪ Rx
• surgery to fix the damaged tissues
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• cut open the tight plasters + fasciotomy

▪ MANAGEMENT:
• 1. Check pulse
• 2. Closed reduction of fracture
• 3. Check pulse again
• 4. Backslab half-cast at 100 degrees
• Immediately refer (high risk of neural/ vasculary injury):
- Gross angulation or total distraction of humeral head.
- Fractures associated with a dislocation: High incidence of
neurovascular injury.
- Associated neurovascular damage.
• in elderly with fractures of head of humerus
- usually w/o dislocation => rest arm in sling + shoulder movt. as
early as possible.
• Pain relief.
• Velpeau sling for one wk.
• Elderly: Social services.
- Torn shoulder Rotator cuff mechanism: As an acute injury results in inability to abduct arm >
40° in presence of an actively contracting deltoid muscle.
o No deformity on shoulder

Leg
- Dislocation of hip
o Occurs in violent trauma such as:
▪ Traffic crash.
• knee strikes dashboard w/ thigh abducted
▪ Blow from back while in squatting position
▪ Fall from height.
▪ Direct fall on hip.
o location
▪ The MC is posterior dislocation (85%)
• The posterior capsular ligaments are weaker than anterior
▪ Central and anterior dislocation are rare
o CLINICAL FEATURES:
▪ The hip is held slightly flexed
▪ Adducted
▪ Internally rotated
• externally rotated – for anterior dislocation (rotation is more specific in
determining whether anterior or posterior dislocation)
o DIAGNOSIS:
▪ X Ray of pelvis, hip and shaft of femur in all cases.
o Cx:
▪ Avascular necrosis of fem. head: ↑dramatically after 6 hrs of hip dislocation
▪ Assess L5 & S1 of ankle: Sensation over medial side of ankle (L5) and lateral
border of foot (S1).
▪ Sciatic nerve neuropraxia: 15%
o MANAGEMENT:
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▪ Pain relief: Morphine 2.5-5mg and antiemetic.

▪ Refer for immediate reduction under GA
▪ Check associated knee lessions.
- femur fractures
o Fractures of neck of femur
▪ types
• Subcapital
- internal fixation
- hemiarthroplasty – preferred, especially in elderly
• Transcervical (e.g. stress fracture in young person) – dynamic hip screw
(internal fixation)
- high
- med
- low
• Intertrochanteric – arthroplasty? (Murtagh – pin and plate)
• Subtrochanteric – arthroplasty?
• Femoral shaft – intramedullary nail
• Supracondylar – internal fixation
• Condyle
- Undisplaced – plaster or internal fixation
- Displaced – internal fixation
▪ Rx
• displaced fracture - best – arthroplasty
- total – better, more expensive, more disclocations
▪ preferred
- hemiarthroplasty
• if surgery is CI, intramedullary nailing (if no osteoporosis) – dynamic hip
screw
• if displaced – multiple screw fixation
▪ Cx
• Non-union – most important to discuss (MCQ)
- => best Rx is hemiarthroplasty (not internal fixation)
• Avascular necrosis of fem. head
- Circ.
▪ central to periph. – usually closes
▪ periph. to center – from capsule (main one)
- more often if subcapital
- Knee exam. (hinge joint, flex-ext)
o Effusion
▪ check for skin dimplings lateral from patella and above it – if they disappeared =
effusion
▪ patellar tap test
▪ patellar bulge test
o Medial & lateral collateral ligaments
▪ Genu valgum (knocked legs)
• stress test
- >10 degrees pathol.
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• children
- do nothing till 8 yrs
- refer if inter medial malleloar space > 8 cm
▪ Genu varum (bowed legs)
• where is my horse?
• stress test
• children
- up to 3 yrs normal
- Mx
▪ reassurance
▪ 3 yrs – observe
▪ refer if intercondylar dist. > 6 cm
▪ Genu recurvatum
o Cruciate ligament
▪ Ant (ACL) – MC than post.
• Soccer player accident – MC = Injury to anterior cruciate ligament
• Knee giving way
• tests
- Ant drawer test – with knee at 90 degrees (> 10 degree pathol.)
- Lachmann’s test – with knee at 15-20 degrees (> 5 mm pathol.)
- Pivot shift test
▪ Post (PCL)
• tests
- post drawer test
- post. sac test?
o Meniscus – in twisting movts.
▪ Medial
• more frequent (75%) than lateral
• most common knee injury
• Sx
- giving away sensation
- locking of joint – MC cause of locking
▪ Knee locking in flexion
▪ lateral
▪ tests
• Apply grind/ distraction test
• McMurray test
- Knee pain – frequent in hip problems, with knee joint being normal
- Fractures of patella
o Usually by direct trauma:
▪ Traffic crash
▪ Fall
▪ Indirect force from violent quadriceps contraction
o CLINICAL FEATURES:
▪ Acute knee pain.
▪ Swelling and bruising.
▪ Loss of function, especially inability to extend knee.
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o DIAGNOSIS:
▪ 1st: X Ray of both knees.
• Confusion may arise from congenital bipartite or tripartite patella but
these are BILATERAL.
▪ Consider CT scan when a suspected fracture is not seen on X-ray.
o MANAGEMENT:
▪ Refer immediately: Distracted or comminuted fractures.
▪ Stable: Aspiration of haemarthrosis.
▪ Place the leg in a padded plaster cylinder from the thigh to the ankle.
▪ Refer to fracture clinic.
- Flat feet (pes plano valgus)
o painless, asympt.
o refer if painful, stiff
o majority: Physiological
o by 6th birthday: 80% resolve
Bone pathology
- Osteosarcoma
o primary – in adolescents: knee (in the metaphysis)
o sec. – metastases to lungs
o Sx
▪ Pain + swelling
▪ Stress fractures
o Dx
▪ X Ray typical:
• Sunburst appearance
• Codman’s triangle – due to periosteal elevation
• + new bone formation
o Rx
▪ surgery
▪ chemotherapy
- Paget’s disease of bone
o Normal bone replaced by new soft (medullary) bone:
▪ Osteoclastic activity then osteoblastic activity
o 10% at 90 yrs
o Sx
▪ Male 2:1
▪ 95% asymptomatic
• Dx. during X Ray or incr. ALP level
▪ Bone pain, joint pain, stiffness and waddling gait,
• MC bones affected: pelvis, femur, skull
• his hat don’t fit him anymore!
▪ deafness
▪ hyperdynamic circ. -> heart failure (hight output cardiac fail)
o Dx
▪ Marked incr. of ALP (asympt. incr. of ALP)
▪ Normal Ca and Phosphate
▪ X Ray – dense, expanded bone (bigger, thicker bone)
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• X Ray features
- larger bone/ bony extension
- thickened cortex
- coarse/ thicker trabeculation
• Metastases of prostate CA and transitional cell CA of bladder =
Osteosclerotic -> have to be excluded (Do PSA)
o Cx
▪ Fractures
▪ Cardiac failure – in bones more AV shunts, bypassing capillaries (more input
blood coming back to heart => High output cardiac failure)
▪ Osteogenic sarcoma – rarely
▪ Deafness----Cranial nerve involvement
▪ Deformities
o Rx
▪ 1. Bisphosphonates
• SE – Oesophagitis (don’t go to sleep right after taking it)
Neurology - OK
- Cranial nerves
o Only 1st and 2nd pair emerge from cerebrum; remaining 10 pairs emerge from brainstem.
-
Sensory,
Name Motor Origin Nuclei Function
or Both
Cranial nerve zero olfactory trigone, New research indicates CN 0 may
(CN0 is not medial olfactory play a role in detection of
0 Sensory
traditionally gyrus, and lamina pheromones. Linked to olfactory
recognized.)[1] terminalis system in human embryos[4]

Purely Anterior olfactory Transmits sense of smell; Located

I Olfactory nerve in Olfactory foramina in Cribriform
Sensory nucleus
plate of ethmoid.
Purely Ganglion cells of Transmits visual information to
II Optic nerve
Sensory retina[5] brain; Located in optic canal.
Innervates levator palpebrae
superioris, superior rectus, medial
rectus, inferior rectus, & inferior
Oculomotor nucleus, oblique, which collectively perform
Mainly
III Oculomotor nerve Midbrain Edinger-Westphal most eye movements; Also
Motor
nucleus innervates sphincter papillae m.
located in superior orbital fissure
PARALYSIS: Ptosis, down-&-out,
dilated non reactive pupil.
189

Innervates superior oblique muscle,

which depresses, rotates laterally
Trochlear nerve Mainly (around optic axis) & intorts
IV Midbrain Trochlear nucleus eyeball; Located in superior orbital
SO4 Motor
fissure.
PARALYSIS: Vertical diplopia on
looking downward (stays behind)
Principal sensory
Receives sensation from face &
trigeminal
innervates muscles of mastication;
Mixed nucleus,Spinal
Located in superior orbital fissure
(Sensory trigeminal
V Trigeminal nerve Pons (Ophthalmic nerve V1) foramen
& nuc.Mesencephalic
rotundum (Maxillary nerve V2) &
Motor) trigeminal nuc.
foramen ovale (Mandibular nerve
Trigeminal motor
V3)
nuc.
Innervates lateral rectus, which
abducts eye; Located in superior
Abducens nerve Mainly Posterior margin orbital fissure
VI Abducens nucleus
LR6 Motor of Pons PARALYSIS: eye stays behind
(towads middle) when looking
outward (lateral diplopia)
Provides motor innervation to
muscles of facial expression,
posterior belly of digastric muscle
& stapedius muscle. Receives
Pons Facial nucleus, special sense of taste from anterior
Both
(cerebellopontine Solitary nucleus, 2/3rd of tongue & provides
VII Facial nerve Sensory
angle) above Superior salivary secretomotor innervation to
& Motor
olive nucleus salivary glands (except parotid) &
lacrimal gland; Located & runs
through internal acoustic canal to
facial canal & exits at stylomastoid
foramen.
Senses sound, rotation and gravity
Vestibulocochlear (essential for balance &
nerve (or auditory- Lateral to CN VII movement). More specifically:
Mostly Vestibular nuclei,
VIII vestibular nerve or (cerebellopontine vestibular branch carries impulses
sensory Cochlear nuclei
statoacoustic angle) for equilibrium and cochlear branch
nerve) carries impulses for hearing.
Located in internal acoustic canal
Receives taste from posterior 1/3rd
of tongue, provides secretomotor
Both Nucleus ambiguus, innervation to parotid glnd & motor
Glossopharyngeal Sensory Inferior salivary innervation to stylopharyngeus.
IX Medulla
nerve and nucleus, Solitary Some sensation is also relayed to
Motor nucleus brain from palatine tonsils.
Sensation is relayed to opposite
thalamus and some hypothalamic
190

nuclei. Located in jugular foramen.

Supplies branchiomotor innervation
to most laryngeal & all pharyngeal
muscles (except stylopharyngeus).
Provides parasympathetic fibers to
nearly all thoracic & abdominal
Both Nucleus ambiguus,
viscera down to splenic flexure; &
Sensory Posterolateral Dorsal motor vagal
X Vagus nerve receives special sense of taste from
and sulcus of Medulla nucleus, Solitary
epiglottis. Major function: controls
Motor nucleus
muscles for voice and resonance &
soft palate. Symptoms of damage:
dysphagia (swallowing problems),
velopharyngeal insufficiency.
Located in jugular foramen.
Controls Sternocleidomastoid and
Accessory nerve
Trapezius muscles, overlaps with
(or cranial Nucleus ambiguus,
Mainly Cranial and functions of vagus. Symptoms of
XI accessory nerve or Spinal accessory
Motor Spinal Roots damage: inability to shrug, weak
spinal accessory nucleus
head movement; Located in jugular
nerve)
foramen
Provides motor innervation to
muscles of tongue (except
palatoglossus, innervated by Vagus
Mainly
XII Hypoglossal nerve Medulla Hypoglossal nucleus N) and other glossal muscles.
Motor
Important for swallowing (bolus
formation) and speech articulation.
Located in hypoglossal canal.

Nerve (non-traumatic) pathology

- Facial nerve paralysis
o IDIOPATHIC
▪ Bell’s Palsy
▪ Recurrent Facial Palsy
o CONGENITAL
▪ Mobius Syndrome
▪ Congenital Lower Lip Paralysis
▪ Melkersson-Rosenthal Syndrome
▪ Dystrophic Myotonia
o TRAUMATIC
▪ Temporal bone fractures
▪ Birth trauma
▪ Facial contusions/lacerations
▪ Penetrating wounds to the face or temporal bone
▪ Iatrogenic injury
▪ Barotrauma
o INFECTION
▪ Herpes zoster oticus (Ramsay Hunt syndrome)
▪ Otitis media with effusion
191

▪ Acute mastoiditis
▪ Malignant otitis externa
▪ Acute suppurative otitis media
▪ Tuberculosis
▪ Lyme disease
▪ AI+DS
▪ Infectious mononucleosis
▪ Influenza
▪ Encephalitis
▪ Sarcoidosis
o NEOPLASIA
▪ Cholesteatoma
▪ Carcinoma (primary or metastatic)
▪ Acoustic neuroma
▪ Meningioma
▪ Facial Neuroma
▪ Ossifying hemangioma
▪ Glomus jugulare or tympanicum
▪ Schwannoma of lower cranial nerves
▪ Benign and malignant parotid tumors
▪ Leukemia
▪ Hemangioblastoma
▪ Histiocytosis
▪ Rhabdomyosarcoma
o METABOLIC/ SYSTEMIC
▪ Diabetes mellitus
▪ Hyperthyroidism/hypothyroidism
▪ Pregnancy
▪ Autoimmune disorders
o NEUROLOGIC
▪ Guillain-Barre’ syndrome
▪ Multiple sclerosis
▪ Millard-Gubler syndrome
- Bell’s palsy – idiopathic
o MC cause of acute facial paralysis (70% of cases)
o LMN
o Can occur in any age group, prevalent in 3rd decade of life
o Recurrent paralysis in 10-12% of cases, more often on contralateral side
o Positive family history in 14% of cases
o Association - Type I Herpes virus (HSV-1)
▪ Viral infection induces an inflammatory response resulting in neural edema and
vascular compromise of facial nerve
o Sx
▪ paralysis of all facial muscles, including frontalis (MCQ)
▪ can’t close eye (NOT PTOSIS – Horner)
▪ mouth pulled to opposite direction and up when opening it
▪ unilat. loss of taste (ant 2/3rd of tongue)
o isolated, with no other sympt. (e.g. dysphagia – brainstem infarct)
192

o Treatment is controversial
o Treatment options:
▪ Steroid therapy (Prednisolone) – always, 7 days
▪ artificial tears (can’t blink or close eyes)
▪ surgical decompression – if steriods dn’t help
▪ antivirals – sometimes

-
- Herpes zoster oticus – Ramsay Hunt syndrome
o Vesicular eruptions on ear or ear canal (crusts) + ipsilateral facial paralysis
o Other symptoms:
▪
o Nerve degeneration is more progressive and severe than Bell’s palsy!
o Prognosis for recovery is worse!
o Treatment:
▪ antivirals – within first 72 hrs.
▪ steroids
▪ pain management – very painful
- Trigeminal neuralgia
o males > 40 yrs
o paroxystic burning pain in the maxillary and mandibulary region (nerve V distribution)
▪ no Ophtalmic N involv.
o lasts seconds – 1-2 min
o recurs many times during day and night
o triggered by
▪ touching of skin of affected area
▪ washing
▪ shaving
▪ eating
▪ talking
o Unilateral
▪ 2nd mandibular division of Vth nerve
▪ 3rd maxillar division of Vth nerve
o cause
▪ local pressure on nerve root entry zone by tortuous pulsatile dilated small
vessels – 75%
▪ MS
▪ neurosyphillis
▪ tumor in posterior fossa
o Rx
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▪ Carbamazepine
▪ (amytriptiline)
▪ Phenytoin
▪ Gabapentin
▪ Surgery
- Postherpetic neuralgia
o Unilateral or bilateral
o Ophtalmic area involved
o Rx
▪ Amytriptiline – Murtagh, we used to be told to select this
▪ Carbamazepine – less SE
▪ Gabapentin
Nerve traumatic pathology
- Hand
o Brachial plexus C5-T1 - http://en.wikipedia.org/wiki/Brachial_plexus
▪ Axillary nerve
• Deltoid muscle
• Small area of overlying skin – “police patch”
▪ Musculocutaneous nerve
• Biceps brachii
▪ Radial nerve C5-C8 (goes more towards back of arm-forarm-hand)
• all extensors: triceps = elbow extension, wrist extension
- Injury
▪ above elbow: dropped elbow and wrist (can’t extend)
▪ elbow level: dropped wrist (can’t extend)
- Rotation of thumb (thumb up – antenna, 90 degrees to Palm, in
same plane as palm) – Alena
• Post. interosseous n. (branch of radial n.) – extension of finger lost but
hand extension intact
▪ Median nerve C6-T1
• Motor – grasp (hand) and flexors + thenar muscles (under thumb)
• tests
- above elbow (cubital fossa)
▪ Clasping test (Ochsner’s test) – can’t flex index finger
on affected side when asked to clasp hands firmly
together.
- below elbow (wrist)
▪ Pen touch test – can’t do flexion of thumb, 90o
perpendicular on palm’s plane
• injury -> median claw affecting fingers 2-3
• opposition (adduction OK) of thumb to index finger (OK – O –
Opposition) alena
▪ Ulnar nerve C8-T1
• Ulnar paradox: higher the lesion, less sever the injury
- high – flexor digitorum profundus paralized => less severe “Claw
hand” affecting fingers 4-5
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- low – flexor digitorum not paralized => more severe “Claw hand”
affecting fingers 4-5
• can’t adduct (opposition) thumb (can’t hold a piece of paper between
thumb & index finger = Froment’s sign)
• all small muscles of hand except thenar: interosseus + hypothenar
(under fingers 2-5) (sparing thenar muscles) + abduction and adduction
of fingers (spread fingers) – alena
▪ C8
• Loss of sensation of ring finger, may be extending to little finger
• Weakness of extensors of wrist.
▪ T1 (both Ulnar & Median N)
• all small muscles of hand, including thenar and hypothenar eminences
including all fingers (1-5)
- diff. from medial or ulnar injury
• difficulty of precision grip and opposition of thumb to fingers,
weakness spreading and bringing together fingers
• in time – claw hand
o Sensory
▪ Palm
• 3 ½ median (fingers 1-3.5)
• 1 ½ ulnar (fingers 3.5-5)
▪ Dorsum
• 3 ½ radial (fingers 1-3.5)
• 1 ½ ulnar (fingers 3.5-5)
o Erb's Palsy - Paralysis of arm caused by injury to upper group of arm's main n,
specifically upper trunk C5-C6 is severed- loss of sensation in arm, paralysis and atrophy
of Deltoid, Biceps and Brachialis muscles. The position of limb, under such conditions is
characteristic: arm hangs by side and is rotated medially; forearm is extended and
pronated. The arm can’t be raised from side; all power of flexion of elbow is lost, as is
also supination of forearm. The resulting “Biceps” damage is main cause of this classic
physical position commonly called "Waiter's tip."
▪ Risk factors – breech presentation, Shoulder dystocia due to macrosomia
materanal or gestational DM.
o Klumpke palsy- Paralysis involving muscles of forearm and hand, resulting from a lower
brachial plexus injury (C8-T1 severed)- affects principally intrinsic muscles of hand and
flexors of wrist and fingers".± dilators of iris and elevators of eyelid (both of which may
be seen in case of associated Horner's Syndrome). The classic presentation of Klumpke's
palsy is “Claw Hand” where forearm is supinated, wrist and fingers are hyperextended.
If Horner syndrome is present there is miosis (constriction of pupils) in affected eye
(Complete claw).
195

o
o
Syringomyelia
- Leg – Murtagh 714, Blue book 190-191
o Sciatic N, coming from sacral (or lumbosacral) plexus – branches above popliteal fossa
into: Common peroneal and tibial N
▪ PED: P = Common Peroneal n (at front of leg) damaged => E = Eversion, D =
Dorsiflexion
• L5-S1
• Complic. of lithotomy position -> compression of common peroneal n
• branches:
- deep peroneal N – dorsiflexors: tibialis ant., extensor hallucis
longus, extensor digitorum longus, fibularis brevis
- superf. peroneal N – eversion muscles: fibularis longus, fibularis
brevis
- L4-L5-S1-S2
• Muscles supplied by P:
- Extensor hallucis longus
- Extensor digitorum longus
- Tibialis anterior
- Peroneus brevis
- Short head of biceps femoris
▪ TIP: T= Tibial n (at back of leg) damaged => I= Inversion, P= Plantar flexion
• L4-L5
▪ SEDIP => Sciatic n damaged (peroneal n and tibial n are branches)
Power loss Reflex Sensory loss
C5 Abduction of arm Biceps
C6 Elbow flexion, extension of wrist Biceps
C7 Elbow extension Triceps
C8 Hand grip
T1 Finger spread (abduction / adduction of fingers)
L3 Extension of knee Knee jerk Ant. Aspect of thigh
L4 Inversion of foot Knee jerk Medial aspect of ankle
L5 Dorsiflexion of great toe Dorsum of foot
S1 Plantar flexion & eversion Ankle Plantar Lateral aspect of ankle
- Nerve roots asked in MCQs – Oxford p. 457
o Biceps jerk: C5-C6 (Erb’s palsy)
o Triceps jerk: C7
o Hip flexion L1-L2
196

o Knee extension L2-L3

o Knee jerk: L3-L4
o Ankle jerk: S1
o Dorsiflexion: L4 (DIEP – going down)
o Inversion: L4
o Eversion: L5-S1
o Plantar flexion: S1-S2
- Foot drop – L5 (common peroneal n), sciatic nerve
- Bladder – low sacral nerves
- Quadriceps – L2-L4
- L5 and S1 radiculopathies are MC
- L4
o dorsiflexion (extension)
o inversion
o knee jerk
o skin on medial side of the leg below the knee
- L5 (Hx of back pain, sciatica) & common peroneal n. (Hx of knee injury, iatrogenic compression
of n.)
o dorsiflexion, including dorsiflexion of great toe
▪ foot drop
o inversion
o eversion
o no reflex
o skin on lateral aspect of leg below knee
- S1
o Plantar flexion
o Eversion
o Ankle jerk
o Plantar jerk
- Sciatic n.
o Plantar flexion
o Dorsiflexion
▪ foot drop
o Widespread sensory loss on leg
- Nerves affected by prolonged stretching/ compression during surgery
o Common peroneal n – lithotomy position
o Ulnar n. – at elbow (with abducted and supinated arm) MCQ
o Radial n. – in spiral groove

Upper limb: Biceps reflex C5/C6 · Brachioradialis reflex C6 · Extensor digitorum reflex
Tendon reflexes C6/C7 · Triceps reflex C7/C8
Lower limb: Patellar reflex L2-L4 · Ankle jerk reflex S1/S2 · Plantar reflex L5-S2

- Corneal reflex
o V – afferent
o VII – efferent
- Gag reflex
o Glossopharyngeal IX - afferent –
197

o Vagus X – efferent
- Oculocephalic reflex (doll’s reflex) – Brainstem integrity
Motor neurone lesions and back pain
o types:
UMN LMN
Weakness Yes Yes
Power Decr. Decr.
Muscle Wasting Absent/mild Marked
Tone Incr. (spasticity) Absent or decr. (flaccid)
Fasciculations No May be present
Reflexes Brisk Absent or diminished
▪ UMN – above anterior horn cell: cerebral cortex, internal capsule, brain stem,
spinal cord (stroke, tumors, MS, etc.)
▪ LMN – lesion from anterior horn cell = spinal reflex arc (peripheral neuropathy,
Bell’s palsy, GBS, motor neuron dis., poliomyelitis, etc.)
o Motor neuron dis. (MND)
▪ progressive neuromusc. disorder due to death of motor neurons in brain, brain
stem and spinal cord.
▪ no sensory loss (MCQ)
▪ no sphincter involvment
▪ cause
• 5-10% inherited AD
• rest – sporadic
▪ types
• amyotrophic lateral sclerosis (ALS)
- LMN muscle atrophy + UMN hyper-reflexia (progressive
spasticity)
• progressive muscle atrophy
• progressive bulbar and pseudobulbar palsy
▪ Sx
• Triad: LMN + fasciculations (in hands – wasting of all muscles) and UMN
signs (hyper reflexia in legs)
• weakness or muscle wasting
• difficulty with swallowing, speech
• fasciculations & cramps
▪ Dx
• clinical
• neurophysiological tests
▪ no Rx
▪ incurable – death in 3-5 yrs from respiratory failure/ aspiration pneumonia
- Back pain:
Without neurological sympt. With neurological sympt.
1. Muscular spasm 1. Disc prolapse – compress on nerve roots
After heavy weight lifting Limited neurol sympt. = sensory abnormality (no motor) –
Diffuse tenderness numbness, shooting pain in leg
2. Vertebral crush/ collapse 2. Cauda equina syndrome (L1-5, S1-5)
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Old lady with osteoporosis Urinary retention (> 500 ml after urination) Saddle shape
Point tenderness paresthesia (numbness in groin area) +↓ anal tone (ask
patient to squeeze + do you feel my finger in your anus?)
LMN only
3. Spinal canal stenosis 3. Spinal cord compression
Pain relieved by trunk flexion Urinary & fecal retention/ incontinence
LMN + UMN
- Examples:
Spinal cord compression/ lesion:
▪MCQ: Pain in mid-thoracic region & spastic paraparesis progressing over last 2
mths.
▪ Sx
• Above lesion - normal
• At the level of lesion - ipsilateral LMN signs
• below lesion – ipsilateral UMN signs + ipsilateral loss of position
- this is after a few wks; initially we have flaccid motor paralysis +
loss of all sensory modalities
• contralat. sensory loss, temperature and pain
• + spinal root pain, precedes weakness
▪ Rx
• Acute – high dose steroids to lower edema!
o Cauda equina syndr. – Murtagh p.37
▪ pain at back of thigh and legs, shooting to leg
▪ saddle anesthesia (numbness of inner buttocks, perineum and upper medial
thigh), back of legs, soles of feet,
▪ bowel and bladder involvement (urinary retention)
▪ weakness of legs and feet
▪ atrophy of calves
▪ Rx – Surgical decompression
o Spinal canal stenosis – neurogenic claudication: Murtagh p. 710
▪ pain in buttocks related to walking, relived by trunk flexion or rest
▪ pain relieved when going up hill and amplified when extending spinal column
(going down hill)
• Dx diff from vascular claudication = pain relieved at rest or going down
hill
▪ Bowel/ bladder involvement
Tremor
o Types
▪ Resting – Parkinsonism
▪ Action or postural
• Benign Essential tremor (MCQ)
- AD in 50% of cases
- can be present in Parkinson
- Sx
▪ Triad: tremor with little disability + normal gait +
family Hx
▪ tremor
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• begins with slight tremor in one of the hands ->

spreads to other over time
• may involve head (titubation) chin and tongue
• interferes with writing, handling of cups, etc.
• tremor most marked when arms held out =
postural tremor
• exacerbated by anxiety
• relieved by alcohol
- Dx diff from Parkinson
▪ faster tremor (8-13 Hz, vs. 4-6 in Parkinson)
▪ normal gait (vs. loss of arm swing & short steps in
Parkinson)
- Rx
▪ Reassurance
▪ Drugs
• 1 – propranolol
• benzos – in stress
• alcohol – 1 std. drink
• Anxiety/emotional (with increased heart rate)
• Hyperthyroidism (with increased heart rate)
• Alcohol
• Drugs/ drug withdrawal (heroine, cocain, alcohol)
▪ Intention tremor – exacerbated by action and ↑ as target is approached
• in cerebellar lesions
▪ Flapping tremor (asterixis)
• COPD with CO2 narcosis (↑ CO2, ↓ O2)
• Hepatic encephalopathy, Wilson’s disease
• Uremia
- Parkinsonism
o MC and disabling chronic neurol. disorder
o Male = female
o Degeneration of dopaminergic neurons in substantia nigra => ↓dopamine in basal ganglia
-> causes movts. to become smaller and slower
o Parkinsonism can be drug induced: Phenothiazines (chlorpromazine), Butyrophenones
(haloperidol, droperidol), reserpine
▪ All these drugs are CI in Parkinson.
o Sx
▪ slow and insidious onset, around 58-62 yrs
• only 50% have rest tremor at onset
• first signs = loss of dexterity in rapid alternating movts. + abscence of
arm swing
▪ triad: rest tremor + rigidity + bradykinesia (poverty of movt.)
▪ tiredness, lethargy, restlessness
▪ tremor
• hemi-parkinsonism – at start
• 4-6 Hz (low freq)
• Pill-rolling – severe cases
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▪ cogwheel ridigity
▪ slow and shuffling gait with flexed trunk and short steps
• no arm swing
▪ bradykinesia
• slowness to start movements
• micrographia
• ↓ blinking
• slow monotonous speech
▪ progressive forward flexion of trunk
▪ poor balance – suspect Parkinson in a fractured hip
▪ constipation (common)
▪ congnitive impairment – due to:
• progressive Parkinson-associated dementia in 30-40% usually after 10
yrs
• Alzhimer
• medication
▪ normal reflexes
o Dx
▪ clinical!
▪ Dx. diff.
• Parkinsonism – doesn’t respond to levodopa
▪ Lewy bodies in the neurons – pathognomonic
o Rx
▪ 1. drugs:
• types:
- Dopaminergic
▪ Levodopa – best drug, baseline and gold standard of Rx
• initiate Rx ASAP
• start low: 100 mg/day
• ↑if needed:Max. tolerated dose = 450-600
mg/day
▪ + Carbidopa or Benserazide – with onset of disability
(motor disturbances)
▪ improves rigidity, dyskinesia, gait disorder but not
tremors
- Dopamine agonists
▪ Bromocriptine
• SE - severe psychiatric disturbances -> not in
elderly with confusion or dementia
▪ Pergolide – assoc. in Rx for levodopa “on-off”
phenomenon
• SE - severe psychiatric disturbances -> not in
elderly with confusion or dementia
▪ Cabergoline
- Anticholinergic – for tremor (in young people)
▪ benztropine
▪ benzhexol
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- COMT inhibitors
▪ entacapone – levodopa potentiation
- others
▪ amantadine
▪ selegiline
• approach:
- Mild (minimal disability)
▪ levodopa + carbidopa or
▪ selegiline (can be use as first line monotherapy)
▪ amantadine
- Moderate (disabled but independent)
▪ levodopa
▪ + dopamin agonist: pergolide or bromocriptine or
cabergoline
- Severe (disabled, dependent on others)
▪ levodopa + pergolide or cabergoline
▪ + entacapone
• Long term problems – after 3-5 yrs of Rx with levodopa
- Dyskinesia: Choreiform, involuntary flickering movt. of mouth
(lips, tongue), face, eyelids, cheeks, limbs, trunk – 80-100% of
patients.
▪ Rx: ↓ Levodopa and carbidopa + add pergolide or
cabergoline
- end of dose failure (effect lasts for only 2-3 hrs)
▪ Rx:
• Add entacapone
• dosages closer together
- “on-off” phenomenon (sudden inability to move – recovery in 30-
90 min)
▪ Rx:
• Apomorphine (+ domperidone to prevent
vomiting) for off phase
• add pergolide
- early morning dystonia (clawing of toes)
▪ Rx – slow release levodopa
- nocturnal akinesia
▪ Rx – slow release levodopa
- sundown effect: pts often go psychotic as sun goes down
▪ 2. Surgery:
• Alleviates only tremor and rigidity
• Does not prevent progression to bradykinesia, dysarthria and dementia
• types:
- Pallidotomy
- Stereotactic thalamotomy
• indic:
- tremor or rigidity not responding to drugs
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- for younger patients with unilat. Tremor

Seizures

-
▪ types:
• Partial (non-convulsive, no loss of consciousness)
- Simple
▪ e.g. Jacksonian march: starts from a part of body and
moves to other area of body
- Complex
▪ with impaired (altered or cloudy but not lost)
consciousness
• e.g. temporal lobe epilepsy – with olfactory
hallucinations.
• Generalized (convulsive, with loss of consciousness)
- Grand-mal (tonic – clonic)
▪ Sx
• usually last 1-2 min
• loss of consciousness
tonico-clonic contractions: This is a generalized
seizure with varying phases of muscular rigidity
(tonic) followed by jerking of muscles of body
for several minutes (clonic).
• tongue-biting
• incontinence
• post-ictal confusion
▪ Dx diff with functional or pseudo-seizures = means of
coping with stress (exams, etc.)
• Atypical: no loss of consciousness, no tongue-
biting, no incontinence, etc.
▪ Nocturnal epilepsy – Involuntary vocalisation
followed by grand-mal.
• blood on pillow & enuresis noticed in morning
- Petit-mal (absence) Consciousness is impaired only briefly (few
seconds). Pt often remains upright and gives a normal appearance
or seems to be staring into space. Absence seizures occur more
often in children.
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▪ absence seizures: Observe child during running and

swimming – might have a seizure and die!
▪ can have a motor component
- Myoclonic seizures –> Sodium valproate
- febrile seizures
▪ with surprised or scared look (not a blank look), lip-smacking, mouth movement
= Temporal lobe epilepsy
▪ Valproate:
• SE
- Hepatotoxic (LFT done every 2 mths upto 6 mths)
- very teratogenic
o EEG features
Absence seizures Infantile spasm
3 Hz spike and wave pattern Hypsarrhythmia -> Chaotic pattern
o Pregnancy
▪ stop Valproate use Carbamazepine + folic acid 5 mg/ day to prevent neural tube
defects
o Eye-witness account is crucial to establish true diagnosis
o DD: syncope, fall or episode of vertigo (pseudo-seizures)
o Helpful indicators: Bitten tongue, urinary incontinence, preceding aura or drowsiness,
known epilepsy. Seizures of unclear etiology are called epilepsy. If there is a clear cause, it
is not epilepsy.
o MC causes in known epileptics:
▪ Not taking their medications (check levels!) or rarely medication toxicity.
▪ Alcohol abuse, either excess or withdrawal
▪ Intercurrent infection (meningitis)
▪ Head injury
▪ Hypoglycemia
o Secondary causes (if not an epileptic): Exclude first.
▪ Hypoglycemia.
▪ Head injury
▪ Hypoxia
▪ Infection especially meningitis, encephalitis, cerebral abscess, HIV or a febrile
seizure in a child.
▪ Acute poisoning: Alcohol, tricyclic antidepressants, anticholinergics,
theophylline, cocaine, amphetamine and isoniazid.
▪ Drug withdrawal.
▪ Intracranial pathology: SOL, cerebral ischemia, subarachnoid or intracerebral
hemorrhage.
• usually post. circulation (anterior – Amaurosis fugax, paralysis, etc.)
▪ Hyponatraemia (K+ for cardiac problemes), hypocalcaemia, uremia and
eclampsia.
o DIAGNOSIS:
▪ after 2 fits = Dx of epilepsy
• EEG
• CT – less used in children - irradiation
▪ Urgent anticonvulsant levels if patient is on treatment.
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▪ Blood glucose test strip: If low

• 1 mg IM glucagon (if difficult venous access), or
• 50% dextrose 50 mL IV
o Rx
▪ Proceed as indicated clinically.
▪ High dose of O2
▪ first choice = Lorazepam 0.07mg/ kg, diazepam 0.2mg/ kg or midazolam 0.1mg/
kg if patient is having a seizure or if recurs.
▪ Advise the patient not to drive, operate machinery, bath a baby alone etc.
- GENERALIZED CONVULSIVE STATUS EPILEPTICUS
o 2 or more grand mal seizures without full recovery of consciousness in between.
o Recurrent grand mal seizures for more than 5-10 minutes.
o Over 50% patients have no prior history of seizures (look for acute causes).
o phases
▪ tonic
▪ clonic
o Rx
▪ O2 (> 94% saturation).
▪ 50% dextrose 50 mL IV if sugar low.
▪ Thiamine 100 mg IV if chronic alcoholism – Wernike - or malnutrition (WE).
▪ Lorazepam 0.07mg/kg, diazepam 0.2mg/ kg or midazolam 0.1mg/kg. Repeat
until seizures cease.
• if seizures don’t stop -> Phenytoin 15-17 mg/ kg IV by slow bolus or as
an infusion in 250 mL of NS over 30 min.
o If failure to regain consciousness – rule out:
▪ hypoxia
▪ Hypo-hyperglycemia
▪ Hypotension
▪ Cerebral edema
▪ Lactic acidosis
- Febrile seizures = only high fever + fits
o benign condition with no brain damage and no death
o after fever in viral inf.
o always assoc. with febrile illness > 38o C
o family Hx
o type
▪ simple – doesn’t repeat within 24 hrs
▪ complex – repeats within 24 hrs
o generalized seizure, self-limiting
o incidence 2-5% in general population
o Peak at 3-6 mths – 5-6 yrs
o no evidence of acute intracranial disease, metabolic disturbance or CNS inf.
o high rate of recurrance
▪ Younger the age, higher the chance of recurrence
o before and after febrile illness child will be absolutely normal
o 1-10 mins
o 3% risk of epilepsy (normal 0.5%) – not very high risk (MCQ)
o risk factors for seizures/ epilepsy in future
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▪ > 10 min
▪ multiple convulsions during 1 episode (complex)
▪ family Hx of epilepsy
o prognosis – excellent
o Mx
▪ reassurance
▪ control temperature - Paracetamol
▪ > 10 min -> rectal diazepam (0.2-0.4-0.5 mg/kg)
• if seizures during examination: Observe -> if not improving in 5-10 min -
> rectal diazepam
• Oral or nasal midazolam 0.3-0.5 mg/ kg
▪ recurrance > 30-40%
• 30% in first 24 hrs
- Infantile spasm = Sallam attacks = West syndrome = hypsarrythmia (high amplitude irregular
EEG waves) (M 588)
o funny turns (flexion/ bending forward of trunk and extended limbs)
o first year of life
o assoc. with HSP and intussusception
o Dx: Increased CRH – (corticotrope releasing hormone)
o Rx
▪ ACTH (lowers CRH) – best
- Tourette syndrome (boys)
o Multiple motor tics & 1 or more vocal tics that are recurrent many times a day for > 1 yr
o starts with motor tics
o echolalia
o coprolalia (10% only)
o 3-8 (4-15) yrs
o any stress may exacerbate it
o Rx
▪ 1. Clonidine
▪ 2. Resperidone
▪ 3. Haloperidol
▪ electrode on brain?
- Habitual tics
o Sx
▪ recurrent tics > 1yr
▪ NO echolalia, coprolalia
Syncope
o Transient loss of consciousness.
▪ Associated with blurred vision, dizziness, sweating and loss of postural tone,
followed by spontaneous full recovery results from ↓ cerebral perfusion.
o Causes vary from benign to imminently life threatening.
▪ Dx diff.
• Vaso-vagal: with prodrome – vomiting
- syncope after going to bathroom or post-op (pain), change of
position
▪ posture change by standing
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▪ pro-drome before syncope

• warning feeling (dizziness), nausea, hot or skin
sensation, blurred vision
▪ sliding to ground, rapid return to consciousness
▪ Sx
• palor, sweating
• hBP, bradycardia
▪ triggering factors: emotional upset, pain
hBP Bradycardia Vaso-vagal attack
hBP Tachycardia Shock
If ↓ central venous pressure = hypovolemia, septic shock
If ↑ central venous pressure and JVP = cardiogenic shock
HTN Bradycardia (but > 50) Incr. intracranian pressure (ICP)
HTN Bradycardia (but < 50) Complete heart block
• Cardiac - sudden onset, short duration
- Arrhythmia, either tachycardia or a bradycardia.
▪ Complete heart block
• Pulse 25-50/m
• Large volume pulse
• ↑ JVP, cannon wave (large wave produced by
atrial contraction)
• Systolic murmur
- Myocardial infarction.
- Stenotic valve lesion (aortic stenosis).
▪ Aortic stenosis = Dyspnea + chest pain + syncope +
syst. murmur
• slow rising pulse
• non-displaced apex beat
• aortic thrill
• ejection systolic murmur radiating to carotids,
better heard at upper left sternal edge and
aortic area
• brain hypoperfusion because of fixed decr.
cardiac output => syncope.
- Hypertrophic cardiomyopathy.
- Drug toxicity or side effect.
• Vascular
• Carotid sinus hypersensitivity: Hypersensitive baroreceptors cause
excessive reflex bradycardia ± vasodilatation on minimal stimulation
(Head turning or shaving).
• Pulmonary embolism
• Hemorrhage or fluid loss:
- Hematemesis and malena.
- Concealed hemorrhage (such as an abdominal aortic aneurysm or
ectopic pregnancy)
- Vomiting and diarrhoea with dehydration.
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• Neurological:
- Subarachnoid haemorrhage.
- Vertebrobasilar insufficiency. – in posterior circular problems
(vertebrobasilar), less from anterior (cerebral) circ.
• Postural (orthostatic) hypotension:
- Diabetes, hypoadrenalism (Addison’s).
- Parkinson’s disease and autonomic failure.
- Drugs: antihypertensives, diuretics, nitrates.
- Cough, micturition or defecation syncope.
- Hypoglycemia (relative).
o DIAGNOSIS:
▪ Priority: Blood glucose test strip and ECG.
▪ Send blood for FBC, U&Es, cardiac biomarkers, pregnancy test, CXR and CT scan.
o TREATMENT:
▪ Underlying condition.

TIA
o Cerebral circ. Oxford 452
o Origin
▪ 80% carotid origin
▪ 20% vertebrobasilar
o Episodes of sudden transient focal neurological deficit lasting for less than 24 hrs (usually
less than 10 min).
o 12% of patients have a stroke by 1 month (often within 1-7 days).
o types
▪ Anterior
• usually carotid artery or middle cerebral artery
▪ Posterior
• Vertebral, PICA, basilar
o CAUSES:
▪ Embolic:
• Cardiac: Post MI, AF, mitral stenosis, valve prosthesis.
• Extracranial vessels: Carotid stenosis, narrowed vertebral artery.
▪ Reduced cerebral perfusion:
• Hypotension: Hypovolemia, drugs or cardiac arrhythmia.
• Hypertension: Hypertensive encephalopathy.
• Hypercoagulable states: Protein C, S or antithrombin III deficiency.
• Vasculitis: TA, SLE, PAN.
▪ Lack of nutrients:
• Anemia
• Hypoglycemia
o CLINICAL FEATURES:
▪ Anterior - Carotid artery dysfunction – unilateral sympt.
• Hemiparesis.
• Hemianesthesia.
• Homonymous hemianopia.
• Dysphasia.
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• Dysarthria.
• Amaurosis fugax (Transitory monocular blindness).
▪ Posterior - Vertebrobasilar territory dysfunction:
• Bilateral limb paresis.
• Crossed sensory symptoms.
• Diplopia
• Bilateral blurred vision
• 3rd cranial N palsy due to Posterior communicating artery aneurysm
(MCQ)
• Bilateral cortical blindness
• homonymous hemianopia?
• Nystagmus
• Ataxia
• Vertigo
• Cranial nerve paralysis (e.g. IX, X, etc.)
• Memory loss
• PICA – lateral medullary syndrome, due to injury to lateral part of
medulla oblongata
- vertigo
- nystagmus
- ataxia
- Horner
- dissociated sensory loss (affecting face and limbs – MCQ: Blue
Book p. 401)
▪ dorsal colum medial leminiscus fibers: Ipsilateral
sensory fibres in posterior columns (for touch,
vibration, posture) – they only cross at pons level ->
from there up all the fibres from other side are
together) + contralateral anterior and lateral column
spinothalamic fibres (pain + temperature) – they cross
at spinal cord level)
• Corticospinal tract – Motor (UMN)
o 80% of fibres cross at medulla
oblongata level--- lateral corticospinal
o 20 % don’t cross--anterior corticospinal
o DIAGNOSIS:
▪ Glucose test strip.
▪ FBC, ESR, coagulation profile, blood sugar, LFT, electrolytes and lipid profile.
▪ ECG and CXR.
▪ URGENT CT BRAIN to differentiate
• hemorrhage from
• infarction and to look for structural non-vascular lesion.
• CT aspect:
- Infarction – black
- Hemorrhage – white
- Calcification – very white
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• Carotid Doppler: for a suspected carotid territory ischemic event as soon

as possible (atheromatous plaques in neck vessels).
o Mx
▪ ADMISSION if:
• ECG is abnormal.
• TIAs are recurring over a period of hrs or progress in severity & intensity.
• Significant systemic disorder suspected.
• Diastolic BP over 110 mmHg.
▪ Low-dose aspirin 300 mg immediately (all TIAs are ischemic so we can give
them aspirin)
• Then 75-150 mg once daily if complete recovery has occurred.
▪ or Warfarin
• Indications: Cardiac emboli (AF)
▪ if still having TIAs with aspirin or warfarin, add Clopidogrel
▪ Refer to Medical or Neurology outpatients within 7 days.
▪ Pt can present with consequences of TIAs (head injury, Colles’ fracture). Do
not fail to investigate true precipitating event (the TIA).
▪ Carotid endarterectomy: If > 70% stenosis.
Stroke
o Due to a vascular disturbance producing a focal neurological deficit > 24 hours.
o location
▪ right handed => dominant hemishpere is left
▪ can’t speak = left parietal lobe affected
o Causes:
▪ Cerebral ischaemia: 80%.
• Cerebral thrombosis from atherosclerosis, HTN or rarely arteritis.
• Cerebral embolism from AF, post MI mitral stenosis, atheromatous
plaques in neck vessels.
• Hypotension causing cerebral hypoperfusion.
▪ Cerebral hemorrhage: 20%
• Intracerebral hemorrhage associated with hypertension or rarely
intracranial tumour and bleeding disorders including anticoagulation.
▪ Subarachnoid hemorrhage from ruptured berry aneurysm or AV malformation.
o RISK FACTORS:
▪ I – Hypertension – 4-6 x incr.
▪ II - Hyperlipidemia.
▪ Smoking.
▪ DM.
▪ Heart disease (Post MI, Valvular, Ischemic, AF).
▪ Past TIA/ stroke.
▪ Peripheral vascular disease.
o DIAGNOSIS:
▪ Presentation may give a clue to aetiology.
• Cerebral thrombosis: often preceded by a TIA and the neurological
deficit usually progresses gradually (headache and loss of consciousness
are uncommon).
• Cerebral embolism: Sudden, complete neurological deficit.
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• Intracerebral haemorrhage: Sudden onset of headache (suggests

haemorrhage), vomiting, stupor, coma with rapidly progressive
neurological deficit.
• Subarachnoid haemorrhage: Sudden ‘worst headache ever’ associated
with meningism, confusion and lethargy.
• Lacunar infarct
- 25% of all ischemic strokes
- caused by occlusion of a single small deep penetrating artery that
arises directly from constituents of Circle of Willis, cerebellar
arteries, and basilar artery. The corresponding lesions occur in
deep nuclei of brain (37% putamen, 14% thalamus and 10%
caudate) as well as pons (16%) or posterior limb of internal
capsule (10%).
- types (Awad) – 5 syndromes:
▪ 1. Contralat. pure motor (hemiparesis) –MC - 33-50%
▪ 2. Ataxic contralateral hemiparesis – second MC
▪ 3. Contralat. pure sensory
▪ 4. Sensory-motor
▪ 5. Clumsy hands + dysarthria
- Sx (Maria)
▪ isolated hemipareses.
▪ isolated unilat. sensory deficit
▪ isolated unilat ataxia
▪ isolated unilat. dystonia
▪ isolated unilat. parkinsonism
▪ isolated dysarthria
▪ dysarthria + hemiparesis partic. of face, tongue and
hand
- Capsular warning syndrome:
▪ TIA that usually precedes pure motor type of lacunar
infarction in HTN + DM
▪ FBC, ESR, coagulation profile, ELFTs and blood sugar
▪ ECG and CXR
▪ 1. Urgent CT: This may initially be normal with a cerebral infarct.
o Mx
▪ MANAGEMENT:
• If glucose is low give 50% dextrose 50 mL IV.
• If pt is unconscious secure airway, consider endotracheal intubation if
respiratory depression.
• Oxygen: aim for O2 saturation above 94%.
• Avoid to treat acutely (first 24-48 hrs) raised BP unless aortic dissection
or hypertensive encephalopathy.
- lower it gradually – risk of cerebral hypoperfusion
▪ cautious use of oral drugs for BP > 220/110
▪ Preferably: ACE inh.
- B P is often elevated because of stroke (90% of pts with stroke)
• Refer to Stroke unit. – reduces mortality by 20%
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• 2. Antiplatelet agents: Once hemorrhagic stroke is excluded (with CT

scan) give Aspirin 300 mg. – if allergic, Clopidogrel
• or 2. Warfarin, if:
- > 60 yrs
- risk factors
▪ DM, AF
- Vertebrobasilar stroke (not Carotid)
- Recurrent TIA or stroke and patient already on aspirin
• Thrombolysis: Onset of symptoms < 4.5 hrs, no contraindications.
Alteplase 0.9 mg/ kg over 1 hr.
- rarely used
- can convert an ischemic stroke into a hemorrhagic stroke.
Brain hemorrhage
- EPIDURAL/ EXTRADURAL HAEMATOMA:
o sudden
o in MVA
o Neurosurgical emergency if mass effect.
o Arterial bleeding (middle meningeal artery) between skull and dura matter.
o ‘Lucid interval’ of consciousness before CNS deterioration (unconsciousness).
o Imaging: lens shaped (biconvex) collection of blood, crosses the mid-line.
o Rx
▪ surgery – burr hole

-
- SUBDURAL HAEMATOMA:
o Neurosurgical emergency if mass effect.
o MC (20-40%) venous bleeding, slow deterioration.
o in elderly people
o Between dura matter and arachnoid membrane.
o Imaging: Sickle shaped collection of blood. It will NOT cross the mid-line

-
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- SAH
o massive pain (worse pain ever)
o Diffuse layering of blood below arachnoid membrane.
o Does not cause mass effect, predisposes to vasospasm.
o PICA aneurysms: Intraventricular haemorrhage.

o
o Causes
▪ Head injury.
▪ Ruptured aneurysm.
• in polycystic kidney dis. - AD
▪ HTN.
▪ Coarctation of aorta, anticoagulants
▪ AV malformation.
▪ Coagulopathy or vasculitis.
o Sx
▪ Sudden, severe ‘worst headache ever’
▪ Lethargy, nausea, vomiting, meningism
▪ A 3rd N (Oculomotor) palsy suggests bleeding from posterior communicating
artery aneurysm.
o DIAGNOSIS:
▪ Arrange a CT scan urgently to confirm diagnosis (99% caught - Amit)
▪ Lumbar puncture (1%): If CT scan is negative or unavailable (Xanthochromia =
blood in CSF)
o MANAGEMENT:
▪ O2
▪ Prevent main Cx = Vasospasm
• Nimodipine (if BP is stable) – to prevent vasospasm & Subsequent
ischemic stroke!!
• 3 H therapy:
- control HTN
- hypervolemia – overload patient
- hemodilution – thin blood
▪ Refer to neurosurgical unit.
▪ Lorazepam 0.07mg/kg, diazepam 0.2mg/kg or midazolam 0.1mg/kg for seizures
or severe agitation.
▪ Paracetamol 500 mg and Codeine phosphate 8 mg two tablets orally.
Meningitis
o CAUSES:
213

▪ Meningococcus
▪ Streptococcus pneumoniae.
▪ Listeria monocytogenes (infants under 3 months, adults over 55 yrs,
immunosuppression)
▪ Viruses.
▪ Cryptococcus neoformans.
▪ TB
o CLINICAL FEATURES:
▪ Prodromal malaise.
▪ Generalized headache
▪ Fever, vomiting
• TRIAD: fever + vomiting + headache
▪ Altered mental status with irritability and drowsiness (lethargy).
▪ Confusion, coma.
▪ Photophobia.
▪ Neck stiffness ----- Sign of meningial irritation – (also in SAH)
▪ Localized cranial nerve palsies or seizures may occur
o Always consider meningitis in:
▪ Confused elderly.
▪ Sick neonate.
▪ Generalized convulsive status epilepticus.
▪ Coma of unknown cause.
o Meningococeal septicemia
▪ early signs
• Muscle pain: Legs.
• Abnormal skin colour: Pallor or mottling.
• Cold hands and feet.
• Rigors, vomiting, headache.
▪ late signs
• Petechial rash (non-blanching).
• Impaired consciousness.
• Meningism.
o DIAGNOSIS:
▪ Blood cultures
▪ CT scan: If focal neurological signs, especially if signs of incr. ICP
▪ LP: If there are no focal neurological signs and no ↑ICP (CI if ↑ ICP is
suspected) – to confirm diagnosis.
• CSF findings (table – Jay’s notes)
- Bacterial meningitis: WBC - neutrophils incr. (85%), protein
incr. (1 – normal 0.15-0.4), Glucose decr.
- Viral – lymphocytes incr., normal glucose
- TB – Lymphocytes incr., Glucose decr.
- GBS - Prot. incr., cells normal (WBC are not incr. – 90%,
mononuclear cells incr. – 10%)
o Rx
▪ O2 and fluids.
▪ Ceftriaxone (3rd generation) 2 g IV
214

• ± benzylpenicillin 2.4 g IV (ampicillin for Listeria) in immuno-

compromised or Listeria
▪ if penicillin/ cephalosporin hypersensitivity:
• Vancomycin + Ciprofloxaxin
▪ AS SOON AS THE DIAGNOSIS IS SUSPECTED!
▪ + prophylaxis in contacts: ciprofloxacin or rifampicin
▪ Dexamethasone 10 mg IV if bacterial meningitis is strongly suspected (↓
cerebral edema)!
Headaches/migraine
- Headache – see printout from Jay
o Consider the serious or life-threatening diagnoses first:
▪ Meningitis.
▪ Subarachnoid haemorrhage.
▪ SOL.
▪ Temporal arteritis.
▪ Acute narrow-angle glaucoma.
▪ Hypertensive encephalopathy.
o The majority however will be:
▪ Migraine
▪ Tension or muscle contraction headache
▪ Cluster headache
▪ Post-traumatic headache
▪ Disease in other cranial structures
- Migraine
o with family Hx!!
o 5-10% of children
o a. Common – without aura
▪ Hx of at least 5 attakcs
▪ Lasts 4-72 hrs if untreated
▪ Relieved by sleep
▪ Dx
• Have at least 2 of the following headache characteristics
- Unilateral usually
- Pulsating or throbbing
- Moderate to severe
- Aggravated by movement
- Blurred vision in both eyes
• have at least 1 of these associated symptoms:
- nausea and/or vomiting
- photophobia
- phonophobia
o b. Classic – with aura
▪ less common
▪ similar to common migraine plus a history of at least 2 attacks that:
• have a typical aura: reversible visual, sensory or speech symptoms, but
not motor
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• visual: uni or bilateral flashing lights, zigzag lines (teichopsia), central

scotoma
• symptoms develop over 5 minutes but less than 60 mins.
▪ headache precedes, accompanies or follows the aura within 60 mins, although
up to 40% can have aura with no headache
▪ less typical aura – very rare
• Hemiplegia – from which patient recovers completely
• Ophtalmoplegia
• Basilar: ataxia, vertigo, tinnitus, nystagus, diplopia, confusion
o Mx
▪ Darkened room
▪ O2 by facemask
▪ Oral analgesic: Aspirin, Ibuprofen, paracetamol and codeine
▪ Antiemetic: Metoclopramide 10-20 ml IV
▪ if NSAIDs didn’t resolve headache:
• Triptan - Sumatriptan 6 mg SC
- CI
▪ Known coronary artery disease, previous AMI
▪ Children – only:
• Paracetamol
• NSAIDs
▪ Avoid precip factors:
• fatigue, alcohol, caffeine, hunger, chocolate
- Tension headache
o Women & assoc. with stress but without prodrome
o pain comes gradually
o never lasts > 1 day
o bilateral dull and band-like
o mild to moderate
o pain in the morning, gets worse during the day
o mild nausea associated vomiting is rare
o headaches often become chronic
o Mx
▪ Paracetamol + codeine
▪ Reassurance
- Cluster headache
o Rare and common in men
o provoked by alcohol
o 2-3 hrs after falling asleep
o attacks are shorter in duration: 15 min – 3 hrs
o headache is centred around orbit, the pain recurring in separate bouts
o NO VOMITING!
o assoc. with unilat rhinorrhoea, lacrimation, conjunctival congestion
o Mx
▪ acute
• O2 100% (lower conc. are ineffective) – up to 15 min.
- if no improv., after 15 min. stop O2 (can be toxic)
216

• Sumatriptan 6mg SC
•
Dihydroergotamine 1 mg IM
• Lignocaine
▪ Bridging Rx
• often needed while preventive Rx is commenced
• C/S to produce rapid suppresion of attacks (within 24-48 hrs)
- Prednisolone oral 50 mg OD for 7-10 dys then taper over 3 wks
• may recur when steroids are tapered so preventive drug must be
initiated in parallel
▪ Preventive Rx
• Verapamil 160 mg orally daily or
• Methylsergide 1 mg orally daily or
• Lithium 250 mg orally twice
Raised ICP
o signs of raised ICP
▪ deteriorating/ LOC
▪ deteriorating resp. pattern
▪ HTN with bradycardia
▪ progressive headache, worse when waking up in morning
▪ ataxia & vomiting
▪ lateralizing signs (cranial n. paralysis) – tentorial herniation
• 3rd n. palsy
- superior eyelid drop = ptosis
- dilated pupils = mydriasis
- diplopia - eye looking “down and out”
• 4th n. palsy
- diplopia in downward gaze
• 6th n. palsy (lateral rectus m.)
- diplopia – on lateral gaze
• 9th n.
- taste absent on post. 1/3rd of tongue
- Absent gag reflex on side of lesion
▪ Seizures
▪ Papilloedema – late sign

▪ Raised intracranial pressure = drowsiness + vomiting + seizure

Brain tumors
o Children
▪ predom. in the post. fossa
▪ midline cerebellar mass = Medulloblastoma----Infratentorial
• MC malignant brain tumour
• Children
• Obstructs CSF blood flow => headache
o Neurofibromas---------Supratentorial
▪ neurofibromatosis type I
o Meningioma – very slow (slowest)-----Supratentorial
217

▪ usually benign
▪ seizures for 3 years, then suddenly worsening (hemiparesis, etc.)
▪ more common
o Glioblastoma multiforme – much faster
▪ seizures + hemiparesis at the same time
▪ MC malignant and most aggressive tumor
▪ adults
o Astrocytoma - less aggressive
o oligodendroglioma
o ependymoma
Coma and confusion
- Glasgow Coma Scale (GCS)
o Eye 4
▪ 1 - No response to pain
▪ 2 – Opens eye to pain
▪ 3 – Opens eyes to verbal command
▪ 4 – Spontaneous eye opening
o Mouth (Verbal command) 5
▪ 1 None
▪ 2 – Incomprehensive speech
▪ 3 – Inapropriate speech (rudeness, responds with something unrelated to the Q)
▪ 4 – Confused conversation (doesn’t know where he is)
▪ 5 - Oriented
o Hand (motor) 6
▪ 1 No response
▪ 2 (abnormal) extension response to pain (decerebrated – extended neck,
extended and internally rotated arms, extended legs)
▪ 3 (abnormal) flexion response to pain (decorticated – mummy position: flexed
arms, extended legs)
▪ 4 Withdrawing to pain
▪ 5 Localizes pain
▪ 6 Obeys commands
o Values
▪ GCS ≥ 13 -- Mild
▪ GCS 9-12 -- Moderate
▪ GCS ≤ 8 -- Severe
• Intubate
▪ GCS > 8 – Nasogastric (avoid in base of skull fractures) or orogastric tube
- Coma
o GCS ≤ 8
o Types
▪ Metabolic.: Reactive pupils + low GCS
• causes: METABOLIC
- major organ failure
- electrolyte or endocrine disorder
- toxins or temperature (hypothermia)
- acid disorder
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- base disorder
- O2 - hypoxia
- lactate
- insulin or inf.
- cardiac output decr.
▪ Primary CNS problem: Unreactive pupils + low GCS
- Coma of unknown cause:
o give TONG
▪ Thiamine (B1)
▪ O2
▪ Naloxone
▪ Glucose
- Head injury
o Cushing’s Triad – in advanced states of incr. ICP (brain herniation is imminent!)
▪ irregular resp. (resp. depression)
▪ Bradycardia
▪ HT (incr. systolic, decr. diastolic)
o level of consciousness – Most important
- Confusion
o Postop. confusion and disorientation = Acute delirium
▪ causes
• MC = hypoxia
- due to:
▪ atelectasis
▪ analgesics
▪ anesthetic from surgery
▪ Mx/ Dx – Pulse Oximetry
o Other causes
▪ Sepsis
• MC cause of confusion in elderly – UTI
▪ Alcohol withdrawal
▪ hyponatraemia, hypoglycemia
▪ arrhythmias
▪ hypotension
o Confused elderly person
▪ Investigation
• Urine microscopy
• Blood culture
• FBE+ ESR
• Blood glucose
• Urea, creat. and elctrolytes
• Ca and PO4
• TFT
• LFT
• serum B12 and folic acid
• ECG, troponin
• Chest X-ray
219

• CT brain
• Syphilis serology
• ABG
- Brain lobes function.
o Parietal
▪ types
• Dominant
- simple arithmetical calculations (acalculia)
- writing (agraphia)
- right/ left orientation + touch his right ear with his left hand (left-
right disorientation)
- name his fingers (finger agnosia)
• Non-dom.
- recognize digits and letters written in his palm (=graphestesia)
- copy an object that is drawn: house, flower, clock, 2 pentagons
that are overlapping (constructional apraxia)
- recognize shape of objects – astrognosis, tactile agnosia
o Temporal lobe
▪ Memory
• Short term – first affected in Alzheimer
• Long term
o Frontal lobe
▪ Grasp reflex
▪ Verbal fluency – say 7-15 words that start with a certain letter
▪ Interpretation of proverbs
▪ Similarities and differences between objects, people, etc.
▪ Motor sequencing: fist-edge-palm - 5 times
o Occipital lobe
▪ Visual field – examination
- Horner syndrome:
o Due to lesion or compression of one side of the cervical or thoracic sympathetic chain,
which generates symptoms on the ipsilateral side of the body.
o symptoms:
▪ Triad:
• Miosis
• Partial (palpebral) ptosis
• Loss of hemifacial sweating
▪ (PAMELa): Ptosis, Anhydrosis, Miosis, Enophthalmos & Loss of ciliospinal reflex
o causes:
▪ 1. Tumors - often bronchogenic carcinoma (Pancoast tumor) of apex of lung
• T1 compression: affects small muscles of hand (can’t oppose thumb
against other fingers) + sensitivity affected on inner arm (above elbow)
▪ 2. PICA
▪ Syringomyelia
▪ Cluster headache - combination termed Horton's headache [6]
▪ Trauma - base of neck, usually blunt trauma, sometimes surgery.
▪ Aortic aneurysm, thoracic
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▪ Dissecting aortic aneurysm

▪ Carotid artery dissection
▪ Cervical rib traction on stellate ganglion
▪ Sympathectomy for axillary or palmar hyperhidrosis
▪ Nerve blocks, such as cervical plexus block, stellate ganglion or interscalene
block
- Multiple Sclerosis (40-50 yrs female)
o UMN lesion (no wasting of hand muscles as in LMN) MCQ
o white matter involved
o usually affects
▪ Optic nerves
▪ Cerebellum
▪ Brain stem
▪ Spinal cord
o Sx
▪ fatigue
▪ Attacks and remissions
▪ motor weakness, spasticity
▪ Sensation: numbness, pins and needles, pain
▪ Pain: trigeminal neuralgia, dysarthria
▪ Bladder: urge incontinence
▪ GI: swallowing disorder, constipation
▪ Sexual dysfunction – impotence
▪ Progressive visual dysfc. – Diplopia, nystagmus, optic neuritis (blurred vision)
▪ vertigo
▪ decr. cognition, decr. memory, dementia
▪ depression, mania, odd laugther
▪ cranial n. lesion, epilepsia and aphasia – rare
▪ MCQs:
• 40 yr woman, blurred vision and pain on movt. of eye, few days later
developed some sensory loss of right hand
• several attacks of severe pain on the left cheek and left mandibular
area + loss of sensation in those areas = MS
• trigeminal neuralgia + sensory loss (+ young woman) = MS
o Dx
▪ brain MRI with caracteristic pattern - white spots = Demyelination plaques
around the ventricles “Dawson fingers’
- Syringomyelia (a cavity formation in spinal cord at cervical level)
o Upper limb
▪ muscle atrophy where all muscles of both hand are affected: interosseous +
thenar (and hypothenar) muscles affected.
▪ pain and temperature sensation impairment (sensory dissociation)
▪ can be initially asymetrical (often), then symmetrical.
o Lower limb - UMN
- Tabes dorsalis
o LMN
o late complic. of untreated syphilis
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o degen. of the posterior (dorsal) column of the spinal cord, which carry information that
help maintain a person's sense of position (proprioception), vibration, and discriminative
touch. Triad: Unsteadiness of gait + urin. Retention + lightining pains.
o Sympt. start after decades
o Rx
▪ Penicillin
- GB Syndrome
o Acute inflam. neuropathy (autoimmune) (AB destroy the myelin) of peripheral nerves,
Triggered by an infection
▪ URTI
▪ dig. – Campylobacter
o inquire about SLE, HIV, Vaccination
o Sx
▪ Progressive ascending bilat. paralysis: Legs -> Arm –> Face
▪ Hypo- to areflexia
▪ Cranial n. palsies – bulbar lesions (I, II and VIII are never affected)
▪ Paresthesias, sensory nerve loss
▪ Dysautonomia
• Tachycardia/ bradycardia
• hT/ HT
• Urinary retention
o Dx
▪ Immune stimmulus should be detected
• Monospot test - EBV
• Cold agglutinins
- CMV
- HIV
▪ 1. to confirm - CSF
• Protein ↑
• Cells normal
- WBC are not incr. – 90%
- Mononuclear cells incr. – 10%
▪ 2. Nerve conduction studies
• + EMG
o Mx
▪ Monitor resp. fc. with Forced Vital Capacity
• if FVC < 1 L -> assisted resp. (risk of resp. failure) – 30%
▪ Physiotherapy
• prevent contractures of the muscles
▪ plasmapheresis
▪ IV gamaglob. -> ↓the recovery time
▪ Steroids are NOT beneficial
- Botulism – flaccid type of paralysis, descending
- Myasthenia gravis
o autoimmune dis. which affects muscle strength
o assoc. with
▪ thymic tumours
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▪ other autoimmune dis.: RA, SLE, etc.

o Sx
▪ fluctuating symp. and variable distribution of muscle weakness
• from occasional mild ptosis to fulminant quadri-plegia and resp. arrest
- ptosis (60%) and diplopia
- weakness of chewing, swallowing, speech
- limbs
▪ painless fatigue with exercise
▪ “thinker” – hand used to hold the mouth shut and head up
o Dx
▪ ↑ serum anti-acetylcholine receptor antibodies
• some patients don’t have anti-cholinergic AB
▪ Tensilon (edrophonium) test (acetylcholinesterase inh.) – after admin. the
sympt. Ameliorate (muscle strength improves)
▪ CT scan, chest x-ray to detect thymoma
o Rx
▪ thymectomy recommeded for
• thymoma
• < 50 yrs
• not controlled by drugs
▪ plasmapheresis – in acute crisis
▪ anticholinesterase drugs: pyridostigmine, neostigmine
▪ C/S
- Progressive weakness over last 2 months + spastic paraparesis
o Multiple sclerosis + eye involvement
o Tabes dorsalis + bladder involvement
o Motor neuron dis. – would have LMN signs (flaccid paralysis)
- Basal ganglion lesion
o Chorea
o Tremor
o Rigidity
o Bradykinesia
o NOT ataxia
- Plantar reflex
o Normal - flexion
o Pathological – extension = Babinski’s sign
▪ normal in infants up to 2 yrs
▪ causes
• Spinal = UMN sign due to lesion of corticospinal tract
• Subdural hematoma (can’t be caused by alcoholic encephalopathy,
wernicke, korsakoff, hepatic encephalopathy)
- Hemiparesis of right side of body (right handed) + no dysphagia = HTN vascular disease of
vessels of internal capsule
- Transient global amnesia
o middle aged man with an 8-hr period of amnesia following physical exercise
- Doll’s reflex positive = Brain stem damage. Normally eyes dont follow head movements. In
brain stem injury eyes follow the head movements --- +ve Doll’s Reflex.
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- Sydenham chorea
o in Rheumatic fever + SLE
o invol. dancing moments, patient is very emotional, hypotonia
▪ rapid, uncoordinated jerking movements affecting primarily face, hands & feet
- Huntington’s disease
o AD – mutation on chromosome 4
o causes neuronal loss in frontal lobes and other parts of brain
o movement disorder (Chorea) + behaviour changes + dementia
o progression in generation - earlier onset of disease in descendents
- CT brain
o indications
▪ loss of consciousness (LOC)
▪ post traumatic amnesia
▪ vomiting or raised ICP
▪ focal neurol. sign
▪ otorrhea, rhinorhea
▪ fits, seizures
▪ penetrating wounds
▪ on warfarin
o careful in children -> incr. risk of brain tumor
- MRI – only for spine or posterior cranial fossa (brain)
- acute disseminated encephalomyelitis or postinfectious encephalomyelitis, a demyelinating
disease of brain and spinal cord, possibly triggered by vaccination or viral infection
- Cerebral palsy
o Static, non-progressive
▪ Hypoxia -> ischemic injury -> hypoxia disappears, injury stops progressing
o cause
▪ 80% antenatal cause
• Maternal inf. – chorioamnionitis
• Congenital inf. – TORCH
• Prematurity - periventricularmalacia
▪ 10% intrapartum cause (birth asphyxia)
▪ 10% postpartum cause (asphyxia, meningitis, etc.)
o Sx
▪ problem in muscle tone (usually spasticity – biplegia MC in preterm,
quadriplegia in term), posture, movement (can’t walk properly)
▪ epilepsy – 30%
▪ intellectual disability
▪ impaired vision
▪ impaired hearing
Dermatology - OK
o Description
▪ general outlook of patient
▪ location and pattern of lesions
▪ morphology of lesions
• well defined/ poorly defined
• mono/poly morphous
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• red/ salmon pink/ etc.

• scaly (epidermal lesion)
• ABCDE
- asymmetry
- border
- color
- dimension
- extraordinary (different), evolving
o Skin layers
▪ epidermis
▪ dermis
▪ basement membrane
▪ fat
- Wood’s lamp
o UV in dark room
o Color
▪ Green or bright yellow – Tinea capitis (50% of cases)
▪ Coral pink – Erythrasma
▪ Pink gold – Pityriasis versicolor (hypopigmentation)
▪ Yellowish green – Pseudo monas species

Acute / infectious skin eruptions

- Pityriasis rosea (1337 JM 6th )
o Unknown cause (virus?)
o Salmon pink or copper colored scaly eruption following skin cleavage lines “Christmas
tree pattern” seen in young adults.
o Preceeding herald patch
o Umbilical sparing
o Rx – None: Self limiting
- Syphilis (Treponema pallidum)
o Sx
▪ Primary (occurs at source of infection)
• Painless single ulcer = Chancre
• on penis, vagina, rectum
• heals spontaneously after 4-6 wks
▪ Secondary – 6-8 wks after primary inf.
• Maculopapular rash with various aspects on whole body
- rash on palms and soles
- excoriating lesions around anus
• Tonsilar exudates
• Generalized lymphadenopathy
▪ Tertiary – 1-10 yrs after primary inf.
• Gummas (granulomas)
• Tabes dorsalis
• Aortic aneurysm, aortic regurgitation
o least likely to pass to fetus during birth
o Dx – Murtagh 1133
225

▪ Screening: VDRL, Rapid Plasma Reagin - nonspecific

▪ Definitive Dx:
• Treponema pallidum hemagglutination assay (TPHA)
• Fluorescent Treponemal Antibody Absorption (FTA-ABS)
• TP immobilisation test (TPI)
o Rx
▪ IM Penicillin
▪ if hypersensitivity: doxycycline, erythromycin
- Herpes
o Sx – Painful vesicles
▪ or multiple ulcers on oral, mucus, labia and cervix + flu-like sympt.
▪ painful vesicular rash on the penis in 33 yrs man
• cause – HSV2
o HSV 1 (above waist) in first episode and 2 (below waist) recurrent
▪ develop a permanent latency in our body in sensory nerve ganglia
▪ dermatomal distribution
▪ they flare up during immune deficiency, etc.
• sometimes with prodromal symptoms
▪ HSV1 – more frequent in present
▪ Gingivo-stomatitis – in children
• Rx
- Sympt. – Oral lignocain gel
- Severe inf., immunosupressed, eczema herpeticum – Acyclovir IV
or P.O.
• Cx
- Encephalitis
- Eczema herpeticum
- Disseminated HSV inf. in neonates
▪ Keratoconjunctivitis -> can lead to blindness
o HSV2 – more frequent in past
▪ MC cause of genital ulceration in Aus.
▪ almost always aquired sexually
▪ vaginal, anal, oral sex
▪ condoms ↓risk of transmission
▪ transmission risk proportional with number of partners
▪ evol:
• inf. starts at point of entry of virus
- Man: glans penis, penile shaft
- Woman: vulva, vaginal mucose
• incubation in primary herpes: 3-6 days
• primary inf. is usually asympt.
• evol.
- Initially - tingling & burning sensation over affected area ->
vesicular rash -> small red painful ulcers -> heal over 2 wks
▪ Assoc. sympt. – Shooting pain in buttocks and legs
▪ Rx
• Topical
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- Acyclovir
- Silver nitrate
• Oral acyclovir, famcyclovir, etc.
- only within 72 hrs of rash
- 5 days
- doesn’t cure but shortens the episode
• Analgesia
- topical – lignocaine, povidone iodine
• Ice packs
• Wear loose clothing
▪ Cx
• Postherpetic neuralgia
- Rx - amytriptiline
o if recurrent HSV, do HIV testing
- HIV – Murtagh 259
o least risk of inf. = hemophiliacs
o after travel to Thailand
o Stages:
▪ Primary HIV inf. = Erythematous maculopapular rash all over body
• Mononucleosis-like inf., with Splenomegaly and lymphadenopathy
• MCQ: fever and generalized rash erythematous maculopapular, all over
the body, mainly face and trunk, non itchy, no Hx of allergy or drugs, in
30 yr old man, fashion consultant, onset 2 days ago, splenomegaly,
lymphadenopathy. In sexual rship with another man for 2 yrs, without
condoms.
▪ Chronic HIV inf.
• 2 wks – 20 yrs.
• chronic diarrhoea, axillary & inguinal lymphadenopathy, failure to
thrive
▪ AIDS
o HIV antibody testing should not be performed routinely on pts but only after obtaining
their informed consent and after pretest counselling
o Dx
▪ Screening – ELISA:
• Positive - repeat in 12 wks
• Unprotected intercourse + negative – repeat in 12 wks
▪ Confirmation – Western blot (ELISA can be positive in EBV inf.)
▪ evaluate with: Viral load + CD4
o Cx
▪ CMV retinitis
▪ Pneumocysitis carinii pneumonia
▪ Candida inf. (Esophagitis)
▪ cryptosporidiosis – diarrhoea
▪ Cryptococcus neoformans = fungs opportunistic inf. in immunsuppressed (HIV,
kidney transplant, TB), complicated with cryptococcal meningitis
• CSF findings – like in viral meningitis
- Rx – Amphotericin B IV
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o Mx
▪ CD4 < 200 - prophylaxis
- Scabies (scabie, riie)
o elderly in retirement places, homeless
o Mite - Sarcoptes scabiei
o Erythematous papular rash, intensely itchy -> scratch marks
o itch worse at night or when the body is worm (after shower)
o wrists, hands and web spaces (between fingers), male genitalia, elbows, feet, axilla,
ankles, nipples
o Norwegian scabies – crusted form, with millions of mites
▪ nursing homes
▪ AIDS
o transm.
▪ skin to skin
▪ clothes, bed sheets
▪ sexual contact
o MCQ: itchy rash on skin of 19 yr woman
o Dx
▪ clinical
▪ confirmed: Scrapings seen under microscopy
o Mx
▪ Permethrin cream 5% or
▪ Benzyl benzoate 25% emulsion
• apply all over body for whole night, wash in morning
▪ avoid hot bath or scrubbing body
▪ treat everybody in house
▪ wash the clothing and bedding in hot water and expose to sun

- MCQ: Pt wid scabies treated wid permethrin. After 1 month symp again developed. What next tt
option ?
a) repeat permethrin
b) corticosteroids
- Re treat the patient again after 1-2 weeks
- Prolonged itching after scabies is normal and usually requires NO ttt or cortisone
- Head lice (paduchi)
o Pediculus humanus capitis
o white spots in hair
▪ unlike dandruff, the white spots can’t be brushed off
o Rx
▪ Pyrethrins foam/ shampoo
▪ Permethrin
- Fleas (purici)
o itchy erythematous maculopapular lesions, grouped in clusters
o on arms, forearms, leg, waist
- Bed bugs
o 3 or more bites along superficial blood vessels – maculopapular red lesions
o extremely itchy
228

- exanthematous dis.
DISEASE INCUBATION PRODROME RASH OTHER FEATURES &
PERIOD INFECTIVITY
(DAYS)

Chickenpox 10-20 None Macules, papules, Infective until vesicles are crusted
(Varicella) vesicles & pustules of over
different ages
Measles 9-14 Cold, cough, Red, confluent, Koplik’s spots, may be quite ill
Paramyxovirus conjunctivitis maculopapular
Rubella 14-21 None Discrete ink, Occipital & preauricular
(German maculopapular lymphadenopathy. High fever.
measles or 3 Fetal abnormality
day measles)

Mononucle- 5-14 Fever, Transient Tonsillar exudate, cervical

osis inf. malaise, sore maculopapular, itchy lymphadenopathy,
EBV throat drug rash with hepatosplenomegaly, infective
ampicillin! for many months by close
physical contact
Erythema 7-10 Fever, malaise Red slapped cheeks, Transient Arthralgia. Fetal
infectiosum Parvovirus diffuse maculopapular abnormality
B19
Scarlet 2-5 Sore throat, Red, punctuate papules Unwell, strawberry tongue.
Fever fever,
vomiting
o Chickenpox (Varicela) – Varicella zoster virus,
▪ Vesicular skin rash mainly on body and head rather than at periphery and
become itchy, raw pockmarks, which mostly heal without scarring.
▪ Macules, papules, vesicles & pustules of different ages. Intial crops crusting
while others still appearing. Child mildy unwell.
▪ Very contagious (exclusion from school until vesicles are crusted over)
▪ later it reactivates and causes Shingles (zona zoster)
o Measles or rubeola (pojar, rujeola) – from a paramyxovirus (also causes measles)
▪ generalized maculopapular, erythematous rash - starts on head before
spreading to cover most of body, often causing itching. The rash is said to
"stain", changing colour from red to dark brown, before disappearing.
• Koplik spots are a prodromic viral exanthem of measles manifesting on
1st day of rash. They are characterized as clustered white lesions on
buccal mucosa near each Stenson's duct and are pathognomonic for
measles. The textbook description of Koplik spots is ulcerated mucosal
lesions marked by necrosis, neutrophilic exudate and neovascularization.
They are described as appearing like "grains of salt on a wet
background"
o Rubella = German measles - from rubella virus, 3rd syndrome
▪ Mild disease
229

▪ rash (exanthem) on face which spreads to trunk, limbs and usually fades after 3
days (known as 3-day measles). The facial rash usually clears as it spreads to
other parts of the body. The rash of German measles is typically pink or light
red. The rash causes itching and often lasts for about 3 days.
▪ Other symptoms include low grade fever, swollen glands (sub occipital &
posterior cervical lymphadenopathy), joint pains, headache and conjunctivitis.
▪ if mother is infected within first 20 wks of pregnancy, child may be born with
congenital rubella syndrome, which entails a range of serious incurable illnesses.
o Infectious mononucleosis (kissing disease, glandular fever) - from Epstein Barr Virus
▪ Sx (MCQ 2077 p70)
• Triad = Sore throat + fever + lymphadenopathy
• Maculopapular rash – 5%
- but 90-100% of pts have prescribed ampicillin or amoxycillin,
develop an extensive rash, with a purplish tinge!!
• Sore throat, pharyngitis (MC), tonsilitis, petechiae of palate. MCQ
• fever, fatigue, weight loss, malaise, loss of appetite.
• lymphadenopathy
• Splenomegaly – 50%
• Hepatitis, jaundice, hepatomegaly – 5-10 %
• Hemolysis
• Resembles acute HIV, CMV and toxoplasmosis inf.
▪ Dx
• FBE: lymphocytosis (50%) with > 10% atypical lymphocytes (incr. in
bands – immature lymphocytes) (atypical lymphocytes are incr.)
• Confirmed by Monospot or Paul-Bunnell test (for heterophil AB): Only
positive in 70% in first wk. That why repeated.
- False pos. in hepatitis, Hodgkin’s lymphoma, acute leukemia
• EBV IgM – better than Paul-Bunnell test – Murtagh 805
▪ Cx
• Splenic rupture (feels faint, collapses)
• Chronic fatigue syndrome (myalgic encephalomyelitis, chronic Epstein-
Barr syndrome, chronic neuromuscular viral syndrome)
- > 6 months
- extreme exhaustion, headache, muscle ache, poor concentration
and memory, hypersomnia, arthralgia, tender swollen lymph
glands, subjective feeling of fever, sore throat
▪ Rx
• rest, reassurance, psychological support
▪ Rx
• Bed rest
• Symptomatic treatment.
o Viral exanthema (4th syndrome, Duke’s dis.)
▪ caused by various viruses (enterov.)
▪ rubella-like rash, confined to the trunk
• no. of skin rashes:
- Measles
- Scarlet fever
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- Rubella---- 3 day measles

- Duke's disease
- Erythema infectiosum
- Roseola
o Erythema infectiosum (5th syndrome, Slapped cheek syndrome)
▪ Parvovirus B19
▪ Macular rash on cheeks first, then maculopapular rash on limbs
▪ Causes fetal abnormality and termiantion of pregnancy should be offered.
o Roseola infantum (6th syndrome, exanthema subitum, 3 day fever)
▪ HSV-6
▪ 6-18 mths
▪ kids
• high fever -> goes away after 3 days -> then rash mainly on trunk,
usually spares face and limbs
• Dx – Serology
• Rx - Symptomatic
▪ adult – when coming in contact with kids
• arthralgia
- Rx – symptomatic (viral dis.)
• pregnant lady -> risk only if inf. during first trimester (even then rarely)
- check serology
• sickle cell disease – can precipitate:
- aplastic crisis
- sickle cell crisis
o Mx
▪ Ask about recent known contacts: Pregnant person
• If contact with a pregnant person: Serology for antibody
▪ Exclusion from school (least time from onset of rash or sympt.)
• Scarlet fever – 24 hrs (after starting A/B)
• Measles, Pertussis, Rubella – 5 days
• Chickenpox, Hep. A – 7 days
• Mumps – 9 days
• 5th disease, 6th dis., Inf. mono., Hep. B, Hep. C and Molluscum
contagiosum (MCQ) - Nil
▪ infection – isolation of patient until non-infectious 7 – 15 days
- Shingles (Herpes Zoster)
o caused by reactivation of Varicella zoster v.
▪ sometimes reveals an underlying immunosupression: malignancy – leukemia,
lymphoma, etc.
o acquired through primary inf. with Chickenpox –> dorsal root ganglia
o > 50 yrs
o Sequale - postherpetic neuralgia
o radicular pain then unilat. patchy rash in 1-2 contiguous dermatoms then crusted lesions
-> not infectious anymore
o localisation
▪ Trigeminal – 15%
• Opthtalmic branch – 50%
231

- tip of nose, eyes (conjunctiva, cornea)

• Maxillary, mandibular branches
- oral, palatal, pharyngeal
▪ Ramsay-Hunt syndrome
o Cx
▪ Postherpetic neuralgia
• Ophtalmic. area involved
• 70-80% resolves within 1 yr
- 20-30% - may persist for years
• Rx
- Oral
▪ If presents within 24-48hrs valacyclovir or famicyclovir
▪ Amytriptiline – Murtagh, (if presests later)
▪ Carbamazepine – less SE
▪ Gabapentin
- Topical
▪ Capsacin
▪ Lignocaine
- Nerve blocks
- Excision of painful skin scar
o MCQ: painful rash on trunk of child care worker, started with burning pain then rash, lost
6 kg in 2 mths
o Rx
▪ symptomatic: Calamine lotion or cold compressions
▪ within 72 hrs of rash start = Acyclovir, Famcyclovir
• after -> analgesics
▪ investigate what caused immunosupression
- Cellulitis and erysipelas
o after local trauma
o causes
▪ I – Strept. pyogenes (GAS)!!
▪ II – Staph. aureus
o Rx
▪ Strepto. and staph. aureus
• Severe: Flucloxacillin IV 10 days
- then oral Cefalexin for 4-6 weeks! (blue book MCQ 3.177)
• Less severe: flucloxacillin p.o.
▪ in DM
• Penicillin + Metronidazole + Gentamycin (empirical) (Alena)
• Afhsan?
- mild to moderate
▪ Augmentin + cephalexin + metronidazol
• if sensitive to penicilin:
o ciprofloxacin + clindamycin
- severe
▪ add penicilin
232

- Mumps or epidemic parotitis (oreion) – from mumps virus (a paramyxovirus)

o Painful swelling of salivary glands
▪ Parotids – uni- or bilat. (first one then 1-2 days later the other one)
▪ Submand. and sublingual glands are less commonly involved
o Cx
▪ Orchitis – 25% of postpubertal males
• sterility – rare
▪ Aseptic meningitis – common but benign
▪ Abd. pain – transient
- Whooping cough------Bordetella pertussis
o < 2 yrs
o Stages
▪ Catharrhal – 7-14 days
• anorexia, rhinorrhoea, conjunctivitis/ lacrimation, dry cough
▪ Paroxysmal stage - will persist for 4 wks!!
• 1. severe coughing mainly at night
• 2. with inspiratory “whoop”
• 3. vomiting at the end of coughing bout
▪ Convalescent stage – less severe coughing
o Rx
▪ Clarythromycin/ erythromycin
▪ give A/B to family as well
o Immunization – with vaccine
- Hand, foot and mouth dis. ------ Coxsackie v. (enterovirus)
o on hands, palms, soles
o rash with macules -> vesicles -> ulcers (especially on mouth)
o Exclusion from school only after rash has cruted (dried up)
Strepto pathology
- Tonsilitis
o causes
▪ Viral - MC
• redness with pain
▪ Bacterial
• 15 – 30%: Group A streptococcal (GAS) pharyngitis.
- Bacterial causes for sore throat other than GAS are rare.
▪ e.g. EBV
• Sx
- Exudate
- High fever
- Painful lymphadenepathy
o Cx
▪ Scarlet fever
▪ Rheumatic fever
▪ Retropharyngeal abscess
▪ GN
o Rx
▪ < 4 yrs – Probably viral – no A/B
233

▪ > 4 yrs :
• if EBV – no A/B
• if GAS
- if GAS:
▪ Penicillin
▪ if allergic, erythromycin
- Scarlet fever (Scarlatina)
o children, aboriginals (Strepto. inf. in general)
o GA Strepto. pyogenes which produces erythrogenic toxin (exotoxin)
o Sx
▪ prodromal sympt.: fever, sore throat, malaise, then
▪ rash appears on 2nd day, sand-paper like under touch, blanches on pressure,
spares face, palms and soles
• is worse in skin folds. These Pastia lines (where rash runs together in
armpits and groin) appear and can persist after rash is gone.
▪ Circumoral pallor
▪ Strawberry tongue
▪ recovers in 5 days – fine desquam. on recovery
o Dx
▪ PR interval can be prolonged -> may be evolving towards rheumatic fever
o Cx
▪ Rheumatic fever
▪ GN
▪ Erythema nodosum
o Rx
▪ Phenoxymethylpenicillin 250-500 mg orally q.d.s. for 10 days
- Rheumatic fever
o after a Streptococcus group A (S. pyogenes) inf.: tonsilitis, scarlet fever
o indigenous population
o Sx
▪ acute onset with fever, joint pains, malaise
▪ flitting arthralgia mainly in leg (knees, ankles) and arms (elbows, wrists)
• one joint settles as the other one gets affected
o Dx
▪ 2 or more major Jones criteria
▪ 1 major + 2 or more minor Jones criteria
▪ Major criteria:
• polyarthritis
• carditis
- MC affected = mitral valve
- can lead to congestive heart failure
• Sydenham’s chorea
• subcut. nodules
• erythema marginatum
▪ Minor criteria
• arthralgia
• ECG – prolonged PR interval
234

• previous RF or rheumatic heart disease

• fever ≥ 38o C
• raised ESR > 30 mm/hr or CRP > 30 mg/L
• + raised ASO titre, incr. DNAse B titre, positive throat swab for strepto,
Hx of scarlet fever.
o Rx – Penicillin
▪ Benzathin penicillin IM or Phenoxymethyl penicillin PO
- Impetigo (school sores) Exclusion from school until crusted ( 2 days of AB) MCQ
o Types
▪ Vesico-pustular, with honey-colored crusts
• Staph. aureus, Strepto. pyogenes
▪ Bullous impetigo
• < 2 yrs
• Staph. aureus
• with blisters
▪ Ecthyma – more serious form, penetrating deeper, in the dermis
• scars after the ulcers heal
o Rx
▪ Topical antiseptic – bactroban (Mupirocin)
▪ if extensive, systemic A/B
• Flucloxacilin
• Cephalexin
Lumps and pigmented lesions
- Skin CA
o prevention
▪ most important: avoid sun exposure between 10 am – 4 pm
▪ wear sunglasses and a hat
▪ use sunscreen
▪ wear long sleeves
o Non-melanotic
▪ SCC
• 2nd MC skin CA
• from keratinocytes of epidermis
• cause
- Sunlight
- for mouth SCCs - the 4 S’s:
▪ smoking
▪ spirits
▪ spices
• Betel nuts – used as mouth freshner in Asia; risk
factor for SCC
• Pan
▪ syphilis
• Only in sun-exposed areas
- hands, forearms
- ant. thighs
- head
235

▪ bald head
▪ including lips (lower)
• BCC and melanoma rarely on lip
- neck
- + oral cavity, tongue, tonsil, genitalia
• more keratotic and more scaly
• MCQ: lesion on lip of 35 yrs son (SCC)
• Squamous - upper layer of skin
• although they metastasise to lymph nodes, there is no evidence that
prophylactic lymph node dissection is beneficial
• initially firm thickening of skin --> hard nodules --> ulcerate!
• Premalignant lesions
- Solar keratosis = Actinic keratosis JM1365
▪ mildest lesion caused by exposure to sun
▪ with atypical cells
▪ on areas most exposed to sun
▪ back of hands – very common
▪ involves epidermis and dermis
▪ scaly lesion with hyperemic basis that bleed easily with
trauma
• Auzpitz sign – bleeding when scratching it
▪ Rx
• Cryotherapy – liquid nitrogen
• Excision
▪ if left untreated, 15-20% progress to SCC
- Burns - burn scars
- Chronic ulcers
- Leucoplakia
▪ with dysplasia
▪ non-smoker
▪ white patch, hard to take off
- Bowen’s dis. = SCC in situ (slow growing intra-epidermal CA)
▪ scaly red plaque with clearly defined margins
▪ not much related to solar damage
▪ lower legs of females
▪ Rx
•
• Depth
- in situ – Bowen
- invasive
• Rx (Q 18 block 2 bridging course) MCQ
- Surgical excision in depth and laterally.
▪ 4-5 mm margin if diameter < 1 cm
▪ > 5 (10) mm margin if diameter > 1 cm
▪ BCC (not causing keratin scaling MCQ)
• MC skin CA in Aus.
• 80% males
236

• ↑in fair skinned people

• MCQ: how will u assess the prognosis of bcc?
a) thickness of lesion
b) colour of the lesion
c) remnant of cancer at the margins MCQ
d) width of the lesion
e) site of the lesion
• MC on sun exposed areas are also seen in non exposed areas
- mask areas on face (sparing lips)
- neck
- upper trunk
- + limbs
• grows very slowly
• not associated with keratin scaling
• lesion type
- pearly papule or nodule – more obvious if we pull edges of skin
around the tumor
▪ with teleangiectasis
- if it ulcerates = rodent ulcer
- sclerosing – deeper in the skin
- superficial
• MCQ: BCC - on cheek of 50 yr old man, firm nodule, growing slowly,
recently an ulcer in middle with little bleeding.
• cell type
- nodular
- pigmented
- morphic
- cystic
• never metastasizes
- local spread only
• Rx
- local excision with adequate margins (3 mm) in depth and
laterally.
- radiotherapy – if surgery is CI (elderly frail people)
▪ not for lesions next to cartilage (radionecrosis of
cartilage)
- photodynamic therapy
- Imiquimod – topical agent, reduces size
- Moh’s surgery –an excellent therapy for any recurrent tumor
MCQ
- + avoid cryotherapy
- + no more sunbathing!
• SCC vs. BCC
- Ulceration, keratin scales and metastasis to LN - MC in SCC
- Pearly edge = Telangiectasia = BCC = Never metastasizes (local
spread only)
237

- SCC (only in sun exposed areas)= BCC in both exposed and non
exposed areas.
- ear
▪ outer helix – SCC
▪ inner helix - BCC
o Melanotic
▪ Malignant melanoma
• MCQ: pigment mole on trunk of a 30 yr old woman; dark spot was there
for many year (many born with it) but in last few months spot has
become darker

Risk factors (MCQ)

• History of previous melanoma (fivefold)
• Presence of many moles (50 or more), especially atypical dysplastic naevi
• Family history (one or more members)
• History of many sunburns (MCQ) in childhood
• Sun sensitive skin/ fair complexion and male sex
• 30-50 yrs
• location – anywhere on body but MC on:
- lower limbs – women
- upper back - men
• Superficial lesions stay unchaged for many years.
• Stages:
- suspicious lesion – with dysplastic changes inside it (getting
darker) = Dysplastic melanocytic naevi
▪ if lesion > 5 mm, irregular moles
- the presence of change in appearance and irritative sympt. (itch)
in a previously stable pigmented naevus should raise concerns
about malignant change suggesting dysplastic naevus
▪ lesion with irregular borders, irreg. pigmentation, with
background redness, with variable colors (brown, pink,
black).
- melanoma
• most aggressive tumour
• 30% arise from preexisting melanocytic naevi
- rest – from normal skin
• prognostic factors – poor in:
- ↑ depth/ thickness – most important prognostic factor (>
0.7mm poor prognosis)
- deeper skin level
- site: head, neck, trunk – poorer prognosis
- male ---poor prognosis
- > 50 yr
- amelanocytic melanoma
- ulceration
• types
- Lentigo melanoma – Hutchinson’s freckle – 7.5% (JM 1380)
238

▪ mainly in elderly
▪ slow growing intra-epidermal
▪ mainly on sun exposed area
▪ Rx - excision
- Superficial spreading
▪ MC type – 70%
▪ with strking color variation
• multiple or unusual colors – poorer prognosis
▪ grows horizontally (not vertical)
▪ Rx - excision
- Nodular – 20% (called so bc its elevated and looks nodular)
▪ vertical spread but no radial growth
▪ easy to misdiagnose (DD pigmented BCC)
• but variable colors, irregular borders
▪ blueberry appearance
▪ most dangerous
▪ EFG mnemonic:
• elevated
• firm
• growing for more than 1 month
- Acral lentiginous – 2.5%
▪ MC in palms and soles and distal phalanges
▪ poor progn.
▪ MC in dark skinned people
▪ macule -> then a nodule surrounded by a pigmented
halo
- Amelanocytic
▪ skin colored
▪ poor progn. – diagn. too late
• can involve lymph nodes – satellite nodules = late sign
• Metastases
- lungs
- liver
- brain
- small bowel -> can cause intussusception
• Dx
- ABCDE
▪ asymmetry
▪ border is irregular
▪ color – blue-black +/or variety of colors
▪ diameter – when 1st seen usually at least 7 mm in diam
▪ elevation – indicates invasion
• Rx
- Suspicious lesion MCQ
▪ local excision biopsy – 2-3 mm till mid fat layer –> send
to histopathol.
• if malignant melanoma:
239

o if in situ or lentigo – re-excise with 5

mm margin
o if < 1.5 mm depth – re-excise with 1 cm
margin
o if > 1.5 mm depth – re-excise with 2
cm margin
• if benign naevus, dysplastic naevus,
dermatofibroma, pigmented BCC
o no further surgery (MCQ)
o Rx for all skin CAs
▪ surgery
▪ radiotherapy
▪ curettage and cautering
▪ cremes for superficial BCC—Imiquimod --- ↓ size
▪ Photodynamic therapy for superficial BCC
- Naevi
o spider naevi
▪ red central spot surrounded by flaring telangiectasia
• pressure on central spot => it blanches
o benign melanocytic dermal naevus (mole)
▪ light to dark brown
▪ hairy – almost always benign
o congenital melanocytic naevi
▪ present at birth
▪ risk of malignant change (MC in larger ones)
o common acquired naevi
▪ types:
• junctional naevus
- circular macules
- mole found in junction (border) between epidermis and dermis
layers of skin
- may be pigmented and slightly raised
- have a higher risk of developing into malignant melanoma
• compound
- slightly raised, dome shaped
- a bit in the epidermis, predom. in the dermis
- very rarely undergo malignant change
• intradermal
- totally benign
- Keratoacanthoma ---- Benign (JM 1366)
o on sun-exposed skin
o raised crater with ulcer in centre and plaque of keratin (plug)
o might be confused with SCC in early stages
▪ especially if on lip or ear
▪ often with an ulceration
o grows fast then after a few wks they start shrinking and go away in 4-6 mths
o Dx: Rapid dev. + site of lesion
240

o Rx
▪ excision + biopsy, because it looks a lot like SCC (to exclude SCC)
o Seborrheic keratosis (senile wart) --- Benign (JM 1364)
o waxy texure, painted on appearance
o very superficial, epidermis only
o like a sultana pressed on the skin
o usually multiple
o can be raised (stucco – on lower legs) or plaque like lesion with waxy texture
o hemosiderin causes brownish spots on it
o Rx
▪ excision – only if asked for, for cosmetic lesions
- Molluscum contagiosum – on whole body (JM 1363)
o Self limiting, Pox Virus
o Single or multiple lesions: vesicular papules with central umbilication.
▪ on any part of body
o Kissing lesion: Spread to areas of skin contact, e.g., from chest wall to upper arm.
o No systemic symptoms
Advice to parents
• Give the child a shower instead of a bath (the child can spread the virus to other parts of the body).
• Don’t share baths.
• Wash and dry bath toys after use.
• After showers/baths/swimming, dry areas with molluscum last and don’t share/re-use towels.
• Wash hands after touching molluscum.
• Don’t exclude children from school or playing together. MCQ
• If swimming (Avoid swimming in public pool MCQ) , reasonable precautions include
covering the lesions with waterproof tape and having personal kick-boards.
o Mx
▪ Difficult to treat
▪ Reassurance: will resolve within 1 year with no scarring (MCQ)
▪ Pin pricking – if only a few lesions
▪ Cryotherapy – variable success
- Skin infection after trauma
o Staph. Aureus not Strep pyogenes (MCQ)
o Clostridium perfringes
o Pseudomonas aeruginosa - anaerobes
- Longstanding subcutaneous swelling
o Lipoma – diagn. diff. with epidermoid cyst
▪ common benign tumor of mature fat cells in the subcut. tissue
▪ Sx
• soft, well defined, lobulated, painless, rubbery in consistency, freely
mobile
- except trunk and back – attached to skin
• may be one/ many
• any site – MC limbs (arm) and trunk
▪ family Hx.
▪ pain + tender = angiolipoma
▪ Sx
241

• reassurance (benign)
• removal – for cosmetic reasons
- recurrance is common if incompletely removed
o Ganglion (cyst)
▪ wrist
▪ deeply placed subcutaneous lump around joints or tendon sheets
▪ more proeminent on tendon contraction or joint movement.
▪ do not communicate with adjacent joint (only to one they are located on)
▪ Rx
• Aspiration – if cystic
o Bursae
▪ cystic sacs between skin and underlying bony prominences
• inf. => bursitis (e.g. olecranon)
o Epidermoid (Sebaceous, Keratinous) cyst (JM 1360)
▪ any age, any site
• MC – back
▪ traumatic origin
▪ filled with a fatty, white, semi-solid material called sebum
▪ sometimes associated with hereditary syndrome – e.g. Gardner Syndrome
▪ when infected = Cock’s peculiar tumor (on head)
• resemble SCC
▪ central punctum with keratin – attached to skin
▪ Rx
• No inf.
- enucleation
• inf.
- incision + drainage
- Dermoid cyst = congenital inclusion cyst
o true hamartomatous cyst
o in ovaries, cranium, spine
o thin wall cyst
o with fatty material and occasionally hair, even teeth
o at any age
o on face, around the eyes – attached to underlying periosteum
o Rx – excision
- Warts (over growth of skin) JM 1361
o caused by HPV
o types:
▪ common warts – HPV 2, 4
• fingers, elbows, knees
▪ plane warts – along scratch lines
▪ filiform warts – face, neck
▪ digitate warts - scalp
▪ plantar warts – HPV 1, 2, 3, 4
▪ anogenital warts – HPV 6, 11
• Condyloma accuminata (MCQ Rx in pregnancy)
- Rx Podophyllotoxin if fails… Cryotherapy, laser, electrocautry
242

- Rx of choice in pregnancy………… Cryotherapy MCQ

- If cryotherapy fails in pregnancy… Leave it alone. MCQ
- Neurofibromatosis – AD
o tumor of fibrous tissue covering nerves
o Type 1 (Von Recklinghausen’s dis.) --- Chromose 17
▪ ≥ 6 café au lait spots
▪ freckling in axillary and inguinal regions
• (Dx diff: DM – freckles in axilla)
▪ HTN (assoc. with Phaeochromocytoma)
▪ associated CNS tumors
• Optic nerve glioma
• Supratentorial neurofibromas
▪ + eye features: Iris hamartoma = Lische nodules
▪ learning difficulties, cognitive impairment
▪ musculoskeletal problems
o Type 2 --- Chromosme 22
▪ Bilateral acoustic Schwanomas/ neuromas -> deafness
▪ tendency to astrocytoma or glioma
▪ ↑ tendency to epilepsy
o Dx – Clinical
o Rx
▪ Surgical excision
▪ Referral to neurofibromatosis clinics
▪ Yearly exam.
- Xanthomas
o MC form = Xanthelasma (around eyelids)
▪ soft yellow plaque found at inner canthus of palpebral fissure
o when area of skin becomes infiltrated by lipid filled macrophages
o in dyslipidemias
- Dermatofibroma
o very common red skin nodule
o from abnormal scar reaction (reaction to an insect bite)
o typically occurs on leg of young female
o could be itchy and tender
- mycosis fungoides – rare type of lymphoma
o not responding to treatment, e.g. C/S
- pyogenic granuloma
o infected, fast growing, pink granulation tissue
o exophytic growth
o bleeds very easily on contact
o arise mainly in response to minor trauma
o Rx
▪ excision and curettage of area and underlying granulation tissue
- Granuloma annularis – Murtagh 1205
o DM, thyroid dis., SLE + normal people
o assoc. with minor trauma and DM
o papules arranged in annular fashion
243

o children, young adults

o usually on dorsum or side of finger, back of hands, elbows and knees
o Mx – check urine and blood for DM assoc.
o Rx
▪ reassurance – they usually subside in 1 yr
▪ topic C/S
▪ if ineffective, intradermal inj. of triamcinolone
Fixed drug Eruption: Decsribes a cutaneous drug reaction characterized by appearance of
recurrent skin lesion at same site each time responsible drug is started. eg. Trimethoprim and co
trimoxazole.
Common skin conditions
- Urticaria (hives)
o mainly affects dermis
o very itchy
o by duration
▪ acute
▪ chronic
o by lesion
▪ diffuse wheal-like
▪ papular (hives)
o causes
▪ allergies
• dyes
• drugs
• foods
▪ infection
▪ drugs
▪ foods
▪ SLE
▪ insect stings
o Rx
▪ antihismines
• cyproheptadine
▪ C/S
- Dermatitis/ eczema
o Atopic dermatitis (eczema)
▪ Hx of atopy
▪ location
• infants: cheeks, folds of neck and scalp, extensor surfaces
• chilfood: flexural surfaces (cubital and popliteal fossae), hands, feet
▪ edge less well defined
▪ very itchy
▪ ill defined erythema plaque with yellow-honey crust if inf.
▪ special types
• nummular (discoid) eczema
• pityriasis alba
• lichen simplex chronicus
244

• asteatotic dermatitis (winter itch) – elderly

• cracked (fissured) hands/ fingers/ heels
▪ Rx
•
if inf. treat:
- on the outside, clean it
- on the inside – treat. staph.
▪ Cephalexin
• avoid irritants – fabric, heat, drying of skin, known allergen, soap, baths
not too long or hot
• can be
- dry – avoid dryness -> moisturise with creams
- weeping (with crusts)
• depending on area
- face, genital – go easily 1% hydro cortisone
• other areas – can use more concentrated cortisone
o Peri-oral dermatitis – (JM 1326)
▪ lower face, around mouth and chin
▪ due to cosmetics, pregnancy, OCP, C/S
▪ Rx
• Tetracycline, Doxycycline
• avoid topical C/S
o Contact dermatitis
▪ MCQ: Red painful dry hands in a 30 yr old brick layer, hands have been itchy and
dry for a few mths, getting worse now = cement dermatitis
▪ Dx
• Hx and rash site
• confirmed: patch testing
▪ Mx
• Advise patients that rash will remain as long as exposure persists
• C/S cream to gain initial control
• Severe cases – oral C/S
• in sec. inf. – oral A/B
• + emolients for dry skin
• Avoid soap, wash with soap-free washers
• Stop contact with cement
- or at least apply barrier creams + gloves
o Seborrheic dermatitis – JM fig. 113.4, p. 1163
▪ in reaction to the yeast Pityrosporum ovale
▪ chronic relapsing skin eruptions, with erythema and scales
▪ not itchy
▪ in hear bearing areas: scalp, beard, etc.
▪ types
• of infancy
- nappy area and scalp (craddle cap)
- tough to do diff. Dx between
▪ atopic dermatitis
• after 2 months, severely itchy
245

• starts on face -> elbow flexures -> knee flexures

▪ seb. derm.
• during first 3 months
• non-itchy
• red and yellow greasy scales
- Rx
▪ keep area clean and dry
▪ keep skin exposed to air
▪ Cetaphil lotion
▪ rub skin gently with baby oil
▪ Drugs
• 1st line – Sulphur + salycylic acid or Selenium
sulfide shampoos for 9 days, once a day
• 2nd line – Bethamethasone lotion
• Best results: topical C/S and antifungal cream
(Ketoconazole, clotrimazol, etc.)
▪ most children get cleared by 18 mths
• of adults
- scalp (dandruff), face, genital, perianal
- secondary candidiasis is common in flexures
- prognosis is worst in stress and fatigue
- chronic, recurrent condition
- Rx - similar
▪ shampoos for 9 days
▪ then lotions
▪ NOT oral antifungals (only topical)
- Frost bite
o Localised inflammatory reactions caused by prolonged exposure to cold usually on toes,
fingers, nose, ears.
o Precautions – watch for secondary infections, tetanus, gangrene.
o Physical treatment – elevate affected limb
o Rewarm in water just above body temp.
o Avoid refreezing.
o Surgical debridement.
o Avoid alcohol and smoke
o If blistering - apply warm water compress for 15 mins every 2 hrs.
o Drugs- analgesics.
- Acne – Murtagh 1171
o Classification
▪ Infantile: occurs in first few months of life
▪ Adolescent – MC, usually settles by age of 20, occurring around puberty. It is worse
in males aged 18–19 years and slightly less common in girls.
• premenstrual exacerbations.
▪ Cosmetica – after prolonged use of cosmetics/ skin care products
▪ Oil -- On legs of oil workers
▪ Drug induced – especially C/S
o Drugs that aggravate acne:
246

▪ C/S
▪ chloral hydrate
▪ iodides or bromides
▪ Lithium
▪ Antiepileptics – e.g. Phenytoin
▪ Quinine
▪ OCP
o Response to any Rx occurs after 2 months or later
o types
▪ Mild and moderate
• Rx
- Basic regeimn – 3 months, then review
▪ Benzoyl peroxide – in morning +
▪ Tretinoin or isotretinoin cream at night (causes
photosensitivity)
• only specialist can prescribe it
• causes atrophy of sebaceous glands
• teratogenic –> do a pregnancy test first!
- alternative Rx/ if recalcitrant
▪ topical clindamycin
▪ topical erythromycin
▪ Inflammatory acne (moderate to severe papulopustular) – min. 4 mths (std. 6
mths)
• Rx
- Oral tetracyclin or doxycyclin
- Erythromycin
▪ Severe (nodular/ cystic) or non-responsive
• Rx
- Oral isotretinoin
- Spironolactone – antiandrogenic effect
- Dapsone – antibact. (leprosy), anti-malleric, antiinflam.
- OCP – second line
o additional advice
▪ usually not assoc. with food
• if it does (e.g. chocolate) –> avoid that food
▪ avoid oily and creamy cosmetics
▪ avoid picking and squeezing blackheads
▪ UV/ sun light helps
- Rosacea (JM 1326)
o unknown etiology
o middle aged women
o acneiform lesions on forehead, cheeks, nose, chin - with papules, pustules & erythema
o flushing and blushing precedes the rash
o telangiectasia, erythema
o photosensitivity, hypertrophy of soft tissue on nose
o improved by OCP
o worsened by topical C/S
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o Rx
▪ 1 – Tetracyclin
▪ 1 - Erythromycin
- Dermatitis herpetiformis
o Herpes simplex-like vesicles, erupt at dermatoepidermal junction
o Extremely itchy
o Mainly over extensor surfaces of elbows, knees, trunk, shoulders
o MC assoc. with coeliac disease
o Skin biopsy is diagnostic
o Rx
▪ gluten-free diet
▪ dapsone 100 mg/ day
- Lichen planus (JM 1305)
o Idiopathic inflam. condition found on flexor surface of wrist and hand
o occasionaly triggered by drugs or Hep. C infection
o can affect skin, hair, nails, oral and genital mucosa
o Violaceous polygonal flat topped papules that show lacy white lines (Wickham’s striae)
o can form ulcers
o risk of malignant transformation of oral l.p. needs to be considered, especially in
patients with chronic ulcers and Hx of tobacco use
o Mx
▪ skin eruptions resolve in 6-9 mths, but leave discolored marks and no scarring
▪ moderately potent topical C/S ointment
▪ if not improved, oral prednisolon
- Lichen simplex chronicus: Fibrosis and thickening of skin due to excessive itching caused by
eczema, seborrhic dermatitis, psoriasis and dermatitis a process called lichenificaton.
- Lichen sclerosus (JM 1163)
o Premalignant for SCC of vulva
o Reticular white (sclerotic) lesion in vagina or genital area causing irritation, pruritis,
o Mx
▪ must do biopsy
• if no SCC is Dx – still life long surveillance.
- Nappy rash
o MC cause: simple irritant dermatitis
o itchy – fungus
o non itchy – seborrheic dermatitis
Common causes Uncommon causes Rare causes
Irritant - MC Staph. inf. Tinea
Candidiasis Strep. inf Gluteal granuloma
Seborrheic dermatitis Herpes simples Zinc deficiency
Psoriasis
Atopic dermatitis
o irritant nappy rash
▪ loss of epidermal barrier fc. due to overhydration and exposure to fecal
enzymes
▪ later becomes colonized by candida
o Mx
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▪ advice for mom

• keep area dry
• use highly absorbant single use nappies
• if cloth nappies – change every 2 hrs
• do not use soaps or baby wipes (have antiseptics)
• apply barrier application (cream) after each nappy change
▪ Drugs
• Hydrocortison 1% ointment 2-3 times/ day
• Nystatin
▪ if bacterial inf.
• Fluclox. orally 12.5 mg/ kg x 6 hrly for 7 days.
• Mupirocin 2%
- Tinea corporis – (JM 1328, fig. 123.17)
o Ringworm inf. of body, mainly by tinea rubrum (60%) or microsporum canis
o typical rash – anular, scaly and itchy, with a definite edge and central clearing
o scaly lesion, well circumcised, with elevated margins
o transmitted by contact with infected animals (dogs and cats)
o locations:
▪ tinea corporis of the scalp (Tinea capitis) – only in children
▪ Tinea cruris
• itchy rash in the groin area (scrotum, inner thighs) in young men
- in the same area – Candida intertrigo
• Rx – clotirimazole cream
▪ Tinea pedis – athlete’s foot
o Dx
▪ fungal microscopy and culture confirm it
• recommended before Rx with antifungals
o Rx
▪ terbinafin 1% cream for 1 wk
▪ clotrimazol 1% cream
▪ ketoconazol
▪ bifonazole 1% cream
▪ in hair-bearing areas, palms, soles, nail
• oral Terbinafine, Fluconazole
▪ griseofulvin
- Red, scaly plaques
o Tinea corporis
o Eczema
o Psoriasis
o Connective tissue diseases – SLE
- Pityriasis versicolor
o aka Tinea versicolor
o pink gold with Wood’s lamp
o rash on the upper trunk and proximal extremities
o majority of pityriasis versicolor is caused by Malassezia globosa, although M. furfur is
responsible for a small number of cases
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o These yeasts are normally found on the human skin and only become troublesome under
certain circumstances, such as a warm and humid environment
o Rx
▪ selenium sulphide
▪ clotrimazole, ketoconazole
- Portwine stain
o cavernous haemangiomas
o can have vasc. malformation = Sturge – Weber syndr.
▪ Rx – laser therapy
▪ trigeminal n. affected
- Erythema marginatum – rheumatic fever
- Erythema nodosum (M 259, fig. 30.1)
o acute inflam. immunol. reaction
o resolves in 2-3 wks, with discoloration but no scarring
o tender, bright, red, raised subcut. nodule on shin (usually bilat.) below knee
o can be seen in:
▪ Sarcoidosis
• Dx – chest X-ray
▪ IBD - Crohn
▪ autoimmune dis. – SLE, rheumatoid arthritis, Behcet’s syndrome
▪ inf.: strepto., viral, TB, leprosy, fungus, toxoplasmosis
▪ drug induced – sulphonamide, OCP, tetracyclines, bromides
▪ TB
▪ lepromatosus leprosy
▪ Mycoplasma pn.
▪ lymphoma, leukemia
▪ idiopathic
o Rx
▪ bed rest
▪ RICE and NSAIDS
▪ Prednisolone
- Erythema multiforme (JM 1341)
o very serious condition – can evolve to a Stevens–Johnson syndrome
o mild to severe forms
o causes
▪ HSV
▪ mycoplasma
▪ drugs
• Sulphonamides
• Trimetoprim
• Allopurinol
• NSAIDs
• anticonvulsants: phenytoin, lemotrigin
• nifedipin?
o macules, papules, wheals, vesicles (hands, feet, face, mouth) – lesions with raised edges
and central scar (target appearance)
▪ round to oval triphasic iris-like lesions known as target lesions
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• central purple or dusty area

• surrounded by white oedematous concentric rim
• surrounded by a red halo
o Self-limiting – 2 wks
o Rx
▪ remove cause
- Stevens–Johnson syndrome
o SJS and toxic epidermal necrolysis (TEN) are 2 forms of a life-threatening condition
affecting skin in which cell death causes epidermis to separate from the dermis.
o It is thought to be a hypersensitivity complex affecting skin and mucous membranes.
o Although majority of cases are idiopathic, main class of known causes are medications,
followed by infections and (rarely) cancers.
o causes
▪ Idiopathic ---Majority 50%.
▪ Drugs
• Sulphur drugs - MC
• Penicilin
• Antiepileptics - Phenytoin
▪ inf.
• HSV1 – MC – 33%
• Mycoplasma
▪ Malignancies
• Hodgkin’s
• Myeloma
o immune complex mediated hypersensitivity
▪ severe expression of Erythema Multiforme
▪ also manif. as toxic epidermal necrolysis (TEN) – gravest form
o Rx - supportive
Psoriasis (M 1319) chronic, immune-mediated skin disorder of unknown aetiology
MCQ – 30 yrs man with scaly rash on extensor surfaces of elbows and knees, over lower back and scalp,
appeared after a MVA in which he had femur fracture. He remembered that his father used to be
bothered by some chronic rash. The rash got worse over the last month
▪ can also be on flexural surfaces (flexural psoriasis)
▪ other locations
• scalp, sacral area, pustular (palmoplantar)
o peak onset 10-40 yrs
o ↑ epidermal cell proliferation with vasc. prolif. (Auzpitz sign)
o salmon pink lesions with adherent silvery scales
o 2-4% of population
o waxes and wanes in intensity
o can be drug induced
▪ Lithium
▪ β blockers (MCQ 2098 p 78)
▪ Chloroquine
▪ Hydroxychloroquine
o can be precip. by inf., trauma or emotional stress can be familial
o improves with sunlight, worsens with sun burns
251

o can be assoc. with

▪ Psoriatic arthritis:
• Fingers and toes - DIP involvement
• Sacroilitis – like in akylosing spondylosis
• RF neg.
▪ Psoriatic nails: pitted nails
o often involves umbilicus
o types:
▪ plaque – MC
▪ guttate
▪ pustular
▪ flexural
▪ infantile
o Dx
▪ clinical
▪ biopsy
o Rx
▪ there is no complete cure
▪ mild cases – occlusive dressing with:
• 1. Dithranol – antiprolif. agent
• 2. Tars – stains and smells
• 3. Topical C/S
• 4. Keratolytic agents
• 5. Emolients
• 6. Calcipotriol (vit. D derivative)
▪ severe and widespread
• Methotrexate
• Cyclosporine
• Acitretin
• Phototherapy (UV)
• Photochemotherapy - PUVA (psoralen + UV-A)
Hair disorders
- Tinea capitis: only in children
o dermatophyte infection
o from cats and dogs
o patch and scaly, alopecia
o breaking of hair shafts in one location
▪ with small broken hair shafts (not clear)
o Rx
▪ Griseofulvin –oral, up to 6 wks, 10 mg/ kg/ day, max 250 mg
▪ (not amphothericin – only in hospitals – nephrotoxic)
▪ skin - terbinafin cream or imidazol cream
▪ scalp – oral terbinafin (less SE, more effective) or oral griseofulvin
- Alopecia--- 20% familial
o causes
▪ SLE, autoimmune thyroiditis
▪ nutritional
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▪ fungal inf.
▪ …
o types
▪ Areata (Patchy, non scaly) – one or more discrete circular areas of hair loss
• can occur anywhere on body (not just on head)
• triad: patch of complete hair loss + clean scalp + exclamation-mark
hairs
▪ Totalis – involves whole scalp
▪ Universalis – involves eyebrows and eyelids as well
o triggers
▪ severe febrile illness
▪ severe emotional stress
o Dx
▪ FBE – Hb, thyroid, iron, zinc
▪ biopsy of scalp
▪ examine hair under microscope
• exclamation mark sign
▪ pull hair sign
▪ examine nail – psoriasis
▪ where else in body is hair loss: eyebrow, chest, etc.
o Rx
▪ aim: regrowth of hair + pyschological support
▪ initial – potent topical C/S Betamethasone 0.5% – 1 – 2 times/ day
▪ small lesion – intralesional C/S
• triamcinolone acetonide
▪ oral C/S if topical failed
▪ topical dithranol
▪ topical minoxidil
▪ adjuvant
• topical immunotherapy
• UV radiation (PUVA)
▪ drugs – each used for 3-6 months before switching to another one
o prognostic
▪ 33% chance of complete regrowth within 6 mths
▪ 50% chance of complete regrowth within 1 yr
▪ 80% chance the cured people will relapse
- 4 conditions that can be confused with alopecia:
o Tinea capitis
▪ scaly! (not clean skin as in alopecia)
o Trichotillomania
▪ they don’t have clear patches of hair loss, but patches with short/ long hair
▪ Hx of stressor (in family)
o Lichen planus – causes permanent scarring of scalp
o Discoid cutaneous lupus – causes permanent scarring of the scalp
- any hairy lesion on skin = benign until proven otherwise
Nail problems
- Ingrowing toe nail/ onychocryptosis:
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o Very common condition esp in adolescent boys.

o May follow injury or deformity of nail bed.
o Typically located along the lateral edges of great toe nail and represents an imbalance
between the soft tissue of nail fold and growing nail edge.
o It is exacerbated faulty nail trimming , constricting shoes , poor hygiene.
o Prevention
▪ Instruct on correct foot and nail care.
▪ Foot hygiene.
▪ Correct trimming of toe nails-esp leaving the corners project beyond the skin.
▪ Daily stretch the toe nails with the pads of the thumb.
o Treatment- Elliptical excision of the skin.
▪ Wedge resection of region with removal of ingrowing edge of the nail and
lateral extremity of germinal nail bed leaving a nail of lesser width.
▪ Electrocautery of the wedge of tissue.
▪ Phenolisation method.(deep cleaning with the cotton pad soaked in phenol
deep into the nail bed). Put cotton pad beneath the nail bed and allow nail to
grow out of skin fold.
- Paronychia
o infection where the nail and skin meet at the side or the base of a finger or toenail
o can be assoc. with DM
o can be:
▪ acute
• MC Staphylococcal aureus
• Rx
o elevation of nail fold or puncture of the fold
o removal of nail
o if recurrent – , removing the edge of the nail and the
corresponding germianl nail bed
▪ chronic
• secondary inf. with Candida
- Onychomycosis
o Rx – terbinafine – for 3 mths
- Nail problems
o Nail clubbing (convex)
▪ pulm. causes: lung CA, chronic lung supuration (empyema, abscess),
bronchiectasis, cystic fibrosis, TB, fibrosing alveolitis
▪ GIT causes: IBS (Crohn, ulcerative colitis), liver cirrhosis, GIT lymphoma, malabs.
(coeliac dis.)
▪ CV causes: congenital cyanotic heart dis., endocarditis, atrial myxoma,
aneurysms, infected grafts
o Koilonychia (flat or concave)– Iron-deficiency anemia
o Onycholysis (lifting of nail plate)
▪ psoriasis
▪ trauma
▪ fungal
o Pitting of the nail
▪ psoriasis
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o Nail apparatus melanoma

▪ 2-3% of melanomas
▪ longitudinal pigmented streak in the nail
▪ pigmentation of the proximal nail fold
▪ late Dx
▪ poor prognosis
Skin ulcers
- Skin ulcer – Murtagh 1195
o Venous ulcerations (gravitational, stasis, varicose ulcers) - MC
▪ location
• lower 1/3 of leg, above medial or lateral malleolei (gaiter area)
• more on medial side of leg
▪ Hx of trauma, venous insuffic. or DVT
▪ always sec. to deep venous thrombophlebitis
• Assoc. chronic venous HTN causes trophic changes:
- hyperpigmentation
- fibrotic thickening
- induration
- eczema and finally ulcers
▪ ulcers usually shallow but can reach to periosteum
▪ sometimes you can find granulation floor
▪ slow to heal
▪ not tender but can be painful
• pain is relieved by raising leg
▪ Sx
• Warm and wet leg, blue skin
• varicosities, varicose dermatitis
• edema
• ragged edge
• often superficial
• dermatitis
• hyperpigmentation
• “atropie blanche”
• ABI > 0.9 (normal 0.9 -1.2)
o Arterial Ulcer
▪ Distal
• below ankles:
- tips of toes
- point of heel
- pressure points
▪ heels
▪ head of first metatarsal
▪ malleoli
▪ punched out
▪ dry often deep and cold leg
▪ painful
▪ skin atrophy around
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▪ no edema
▪ less granulation tissue
▪ loss of hair
▪ ABI (Ankle brachial index) < 0.5-0.8
▪ Hx of arterial disease, smoking, DM
o Rx
▪ we need patient’s compliance
▪ promote clean granulation tissue
▪ appropriate cleansing and dressing
• avoid antiseptics and soaps
• just wash with NS
• use intrasite gel and Benzoyl peroxide
• occlusive bandages with Zinc oxide
▪ in infection or cellulitis - A/B
▪ compression banding is mainstay of Rx
• from base of toe (toe not included) to just below knee
• depending on ABI
- ABI < 0.8 – caution
▪ mild compression for 0.6-0.8
▪ Bed rest, elevation above heart level
▪ RICE:
• Rest Ice Compression Elevation
▪ encourage early mobilization and good nutrition
▪ if edema elevate leg + diuretics
• ulcers will not heal in edema
▪ treat varicose veins
▪ Unna`s boots - compression stockings + unna`s paste = 15% Zinc oxide
o + Metabolic Ulcer
▪ DM – (Neuropathic) = Trophic ulcer
• Due to diabetic neuropathy causing loss of sensation which follows an
injury of which pt is unaware.
• Deep punched out lesions over pressure points.
• MC site – ball of foot under 1st metatarsal head. Sometimes heel may
also be affected.
• Ulcers may extend to bones and joints.
• Prone to secondary infections.
• Rx
- control diabetics.
- infection with appropriate antibiotics.
▪ (IV Flucloxacillin + IV Gentamycin + IV Metranidazole)
- Sensory loss: Gloves and stockings
- Dx to confirm cause – Arterial Doppler
o + Pyoderma gangrenosum
▪ deep ulcers, usually on legs in IBS, RA, multiple myeloma, etc.
▪ oral C/S as Rx of choice in pyoderma gangrenosum (skin manif. in ulcerative
colitis)
o Infections. – Smelly discharge
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▪ Bact. gram +, -, anaerobs (deeper)

▪ Syphillis
▪ Deep, chronic
• Atypical mycobacterium
▪ Deep fungi
Infectious diseases - OK
TB
o Triad: Malaise + cough + wt. loss ± erythema nodosum
▪ Primary TB
• Sx – cough, hemoptysis, sweating , fever, malaise, anorexia
- Murtagh – in most cases asympt.
• X Ray: infiltrates in middle and lower zones + hilar lymph nodes
(unilat.) known as Ghon Complex
▪ Latent TB - MC
• Mantoux test – positive
• no clinical features
• usually no X Ray changes
• 10% (if weak immune system) will progress (progressive primary TB) to
reactivation =>
▪ Active secondary TB, within first 2 yrs of exposure
• clinical
- constit. – fatigue, night sweats, wt. loss
- site dependent sympt.
▪ Pulmonary TB – MC
• Sx
o chronic productive cough
o +/- hemoptysis
• X Ray
o infiltration and cavitations in upper
lobes (apical area)
o No hilar lymphadenopathy
o pleural effusion
o past. inf. - apical calcif. and scarring –
can still have surviving bact.
▪ Miliary TB
• X Ray: multiple small bilat. seed-like lesions
▪ Extrapulm TB
• Pericarditis, peritonitis, meningitis,
osteomyelitis, epididymitis or tubal TB
o MCQ: Constrictive pericarditis with
previous TB exposure (ventricular
failure, edema, JVP extremely high, abd.
distension)
▪ X Ray - infiltr. in apical lobes +
pleural effusion
o
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o Dx
▪ Mantoux test:
• delayed hypersensitivity test
- evaluated after 72 hrs
• < 5 mm = negative
- do vaccination!
• 5-10 mm = past vaccination
• > 10 mm = positive
- evidence of inf.
▪ active
▪ inactive – latent TB
▪ chest X Ray
▪ if productive cough
• sputum – acid-fast bacili
- stain – Ziehl Nielson
- culture
▪ TB specific – interferon gama release assay
▪ bronchoscopy and biopsy can be considered
▪ pleural effusion – with monocytes
o Mx
▪ only by specialist! (not by GP)
▪ notifiable dis. -> Dept. of Human Services
▪ contact tracing by Dept. of Human Services
▪ bacterial confirmation and drug susceptibility testing first – only then will be
Rx
▪ no isolation!
o Rx
▪ Active TB (RIPE)
• 4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2 mths
• then 2 drugs (rifampicin and isoniazid) for 4 mths
- total 6 mths
▪ Latent TB (Mantoux positive, no sympt., no X Ray features)
• when active TB is excluded: isoniazid mono-therapy for 6-9 mths
• treat only specific groups:
- recent TB converters (Mantoux test neg., recently – within last 2
yrs - became pos.)
- children, adolescents
- close contact with patient smear-TB positive
- patient with HIV, DM uncontrolled, CRF, Ch liver Failure
- overseas trained people (immigrants)
▪ Pregnant (IRE)
• start Rx ASAP
- pyrazinamide not recommended
- isoniazid, rifampicin, ethambutol – 9months
▪ don’t cross placenta
▪ no teratogenic effect
▪ minimal conc. in milk – breast feeding is NOT CI
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▪ Isoniazid resistant TB
• Streptomycin or Amikacin instead of isoniazide
Diarrhoea and traveller’s disease
Food poisoning
- Diarrhoea – Murtagh 470, Oxford 390
o Staph. aureus - 1-6 hrs
o Vibrio cholera – 2 hrs – 5 days
▪ Rx – Doxycycline
• Pregnant: Amoxycillin
o Clostridium perfringes – 8-24 hrs
o Clostridium botulinum – 12-36 hrs
▪ Honey, canned food
▪ Botulism – descending paralysis
o Salmonella – 12-48 hrs
▪ can return to work after 3 consecutive weekly negative stool cultures
▪ usually no A/B if not inflammatory (no blood, no fever) – just observe, give fluids
▪ if severe: ciprofloxacin
o E. coli – 12-72 hrs
▪ Rx – in moderate/ severe cases: Norfloxacin, Ciprofloxacin
o Shigella – 2-3 days
▪ Bacillary dysentery: blood in stool, fever
▪ Rx – moderate to severe: cotrimoxazole., norfloxacin
o Campylobacter – 2-5 days
▪ Rx – if prolonged: norfloxacin
o Giardia lamblia – 3-25 days
▪ MC non-viral gastroenteritis
▪ profuse watery diarrhoea, foul smelling with undigested food
• no mucous, no blood, no fever
▪ steatorrhoea, malabs. syndrome
▪ abd. distension, cramps
▪ wt. loss, FTT
▪ after camping
▪ Dx – stool microscopy
▪ Rx – tinidazole, metronidazole
o Entamoeba hystolytica – 1-4 weeks
▪ amoebiasis
• dysentery (blood, mucous in stool)
• Rx - metronidazole
o Clostridium difficile – 1-7 days
▪ Pseudomembranous colitis
• after antibiotics (Clindamycin, Cephalosporins, Penicillin based AB, like
amoxycilin)
• bloody diarrhoea, GI perforation, toxic megacolon
• Rx:
o Stop A/B
o Metronidazole
o Vancomycin
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o Rotavirus – 1-7 days

Traveller’s disease
- Traveller’s diarrhoea (after visiting developing countries)
o 1. E. coli – 12-72 hrs
o 2. campylobacter – 2-5 days
o 3. yersinia & pseudomonas aer.
o Giardia – 1-4 weeks
- Travaller’s dis. (Alena)
o travelling to an area with sleeping sickness – Rx – give him vaccine
o after travel
▪ Sympt. within 2 wks in most diseases
▪ Sympt. > 2 wks -> only HIV
o if GIT symptoms
▪ Dx
• 1 - stool microscopy
• 2 - stool culture
o Traveller’s diarrhea:
▪ Acute (not persistent)
• E. coli - MC
• 6-12 hrs after food intake
• lasts for 2-3 days
• watery stool ± vomiting
• Mx
- Rehydration in mild cases
- A/B only in moderate and severe cases
▪ Norfloxacin, ciprofloxacin, azithromycin
▪ Persistent diarrhoea
• Giardiasis (symptoms 3-25 days after infection)
- no mucous, no blood, no fever
- Mx - metronidazol
• Amoebiasis
- mucus and blood
- Mx - metronidazol
▪ Typhoid fever
• Salmonella typhi
• incub 3-21 days
• spread: Feco –oral Route
• Sx
- Triad: stepladder fever (gradually increases over 4 days) + abd.
pain + bradycardia
- insidious onset, headache, dry cough, fever, abd. pain, pea-soup
diarrhoea or constipation
- high fever with relative bradycardia (usually fever causes
tahycardia)
- abd. pain, splenomegaly
- rose spots on trunk (40%) – late sympt.
- CNS signs: confusion, lethargy, coma, meningism = Toxic state
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- Dx
▪ First 10 days ---- Blood culture
• Serology
▪ Later – urine/ stool
- Cx
▪ GIT bleeding
▪ GIT perforation
- Rx
▪ Ciprofloxacin
▪ if fever, rigors – MC = Malaria
• Malaria = returned traveller (most of them within 2 months of return) +
fever. P. Falciparum is most severe form having incubation period 2 wks.
P vivax has a long incubation period.
- return from Vietnam
- Sx
▪ Triad: fever + chills + headache
▪ abrupt onset with high fever, chills, rigors, sweating,
headache, abd. pain
▪ atypical presentation: diarrhea, abd. pain, cough,
vomiting, jaundice
▪ arrhythmia
▪ huge hepatomegaly, splenomegaly
- Dx
▪ thick and thin films (from blood)
▪ FBE: monocytosis + thrombocytopenia, Normocytic/
normochromic anemia
▪ Cerebral malaria: Periventricular changes on CT scan
- Rx
▪ admit
▪ supportive
▪ antimalarial drugs
• P. vivax, P. ovale, P. malaria – Chloroquine +
primaquine
• Chloroquine-resistant malaria -> artimisinin,
artemether, mefloquine
o artimisinin also for pregnancy & kids
• Uncomplicated P. falciparum - quinine +
doxycycline or mefloquine
• complicated P. falciparum (severe) – quinine IV
Chemoprophylaxis:
A. Doxycycline: from 2 days before travel until 2
weeks after return
B.Chloroquine: from 1 week before travel and
continued for 4 weeks after leaving endemic area

- Prophylaxis (murtagh 116)

▪ avoid mosquito bites:
261

• keep away from rural areas after dusk

• sleep in rooms with mosquito nets
• use insect repellent
• wear long sleeves and trousers
• avoid using perfumes – attract mosquitos
▪ take antimalarial medicines regularly
• Non-pregnant
o chloroquine sensitive area ->
chloroquine
o chloroquine resistant area ->
mefloquine or doxycycline or proguanil
o multidrug resistant area (Thailand,
Cambodia, Myanmar) -> Doxycycline ±
chloroquine
• Pregnant
o 1st trimester Chloroquine & Proguanil
o 2nd & 3rd trimester mefloquine.
o other traveller’s dis. w/o diarrhoea
▪ hepatitis A, E
▪ Dengue fever – M 123, 260
• Triad: fever + severe aching (muscle ache/ body ache/ pain on
movement of eyes) + rash
• endemic in Queensland
• flavi virus, part of arbovirus
• mosquito transmission
• transm. - female Aedes mosquito
• children get least severe illness
• pain
- starts with pain behind eye
- severe backache—bone breaking fever
• charact. maculopapular rash – starts from limb - > trunk
• fever, malaise, nausea
• Dx
- IgM serology
- leucopenia with thrombocytopenia
• Rx – symptomatic
• convalescence – severe fatigue and depression (suicidal risk)
• no vaccination
▪ Ross River fever ---Alpha Virus
• from Queensland with fever = Ross River fever
• mosquito borne
• fever + polyarthralgia + rash + from Queensland
▪ Yellow fever (bradycardia like in typhoid + jaundice like in malaria)
• Triad: fever + bradycardia + jaundice
• Africa, South America
▪ West Nile River encephalitis
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• transm. by mosquitos – mosquito nets, repellants

• viral disease
• more common in US
o Immunisations
▪ Compulsory
• Yellow fever
• Menigococcus
▪ Voluntary
• Hep. A, B, E
• Typhoid
• Cholera
• Japanese B encephalitis
- triad: febrile illness + vomiting + stupor
• Rabies
• Typhus
• Plague
- Zoonoses
o Brucellosis (undulant fever, Malta fever)
▪ from cattle
▪ Triad: malaise + headache + undullant fever
▪ Cx – chronic fatigue syndrome
o Q fever – Coxiella Burnetti (MCQ 3174 P285)
▪ in cattle (and sheep) handlers and farmers
▪ abattoir workers
▪ Triad: fever + headache + prostration
▪ sudden onset with fever, rigors, myalgia
▪ pneumonia, hepatitis, endocarditis – sometimes
▪ Dx - Serum antibody level (MCQ )
▪ Rx – Doxycycline
▪ Vaccine
o Leptospirosis:
▪ in abatoir workers, veterinarians, sewage workers, farmers
▪ Sx
• Triad: abrupt fever + headache + conjunctivitis
• undulant fever?
• abrupt headache
• severe myalgia
• jaundice
• petechial rash on skin
• liver and spleen enlarged
- HIV
o chronic diarrhoea, axillary and inguinal lymphadenopathy, failure to thrive
- Diarrhoea
o hyponatremic – can cause seizures but less often
o hypernatremic – with less dehydration but more often seizures
263

Other infectious diseases

- Ischaemic colitis
o in elderly
o Perfusion problems e.g. after thrombosis
- Gas gangrene (is an emergency)
o also known as "Clostridial myonecrosis"
o bacterial infection that produces gas within tissues in gangrene.
o deadly form of gangrene usually caused by Clostridium perfringes bacteria.
o sudden onset of pain + swelling in contaminated wound + brown exudate + dusky
decoloration of skin + gas in tissue on palpation and X Ray + toxemia + shock & circ.
failure
o Dx
▪ initial Dx is based on patient’s Sx and exam. findings
▪ finding bubbles in muscle tissue on X Ray increases suspicion
▪ exam. of secretion from wound swab under microscope may reveal Clostridium
▪ culture from swab will confirm it
o Rx
▪ Wound debridement
▪ A/B
▪ Hyperbaric O2
▪ Anticlostridium immunglobulins
- Meningococcal septicemia
o Rx
▪ GP
• Benzyl penicillin -> send to tertiary hospital
- Blood cultures -> ceftriaxone
▪ ED
• Ceftriaxone
• Cefotaxine
o Prophylaxis
▪ Rifampicine – in close contacts of patient
- Hemolytic uremic syndrome vs. DIC
o Cause: after camping + E. coli for both
o DIC: Bleeding from venopuncture sites, hematuria, incr. bruising
o HUS: Hemolysis (low Hb), kidney involv. (high urea, high creat.), unconj. bilirubin incr.,
pallor, hematuria, hemoglobinuria, incr. in uric acid.
- Tetanus – Murtagh 1384
o DPT – 3 shots required: 1st and 2nd 4wks apart and 3rd after 12 months
Time since vaccination Type of wound Tetanus toxoid Tetanus immunoglobulin
Hx of 3 or more doses of tetanus toxoid (or DPT)
< 5 yrs All wounds No No
5-10 yrs Clean minor wounds No No
All other wounds Yes No
> 10 yrs All wounds Yes No
Uncertain vaccination Hx, not vaccinated or < 3 doses of tetanus toxoid (or DPT)
Clean minor wounds Yes No
264

All other wounds (+ A/B) Yes Yes

- Trachoma:
o MC inf. cause of blindness in aboriginals
o direct transm.
o Chlamydia trachomatis
o 5 stages: FISTO
▪ 1. follicles > 5
▪ 2. inflam.
▪ 3. scarring
▪ 4. trichiasis (inversion or eversion of eyelashes)
▪ 5. opacity of cornea
o Mx: SAFE
▪ Surgery
▪ A/B
• Non-pregnant woman, child – Azythromycin
• Pregnant woman, child < 6 kg – Erythromycin or Roxythromycin
▪ Facial cleanliness
▪ Environmental upgrade: sanitation, hygiene
Hematology - OK
Leukemias
- Multiple myeloma (MM)
o cancer of plasma cells, a type of WBC normally responsible for production of antibodies.
o elderly – 60 yrs
o Sx
▪ Triad: weakness + back pain + weight loss
▪ CRAB: calcium incr., renal failure, anemia, bone lesions
▪ Osteoporosis, back pain (> 80%), bone pain and tenderness
• ↑ pathological bone fractures (MCQ)
▪ weakness, tiredness and recurrent inf.
▪ CRF
▪ hyperviscos. syndrome – clots in brain, dementia, etc.
o Dx
▪ Normocytic anemia
▪ Next examination: Protein electrophoresis in serum and urine -> ↑ level of
abnormal globulins
• Serum – M (monoclonal protein) spike in IgG zone
• Urine - Bence-Jones protein (composed of free light chains)
▪ ALP is normal, unless fractures present
▪ very high ESR
▪ ↑ Ca, normal phosphate
▪ Best examination: Bone marrow aspiration to confirm Dx: increased plasma
cells, replacing bone marrow
▪ X Ray: “Punched out osteoclastic lesions on skull.”
o Rx
▪ Chemotherapy
▪ Medial survival = 3 yrs
- Leukemias
265

ALL AML CLL CML

2-10 yrs + 55-60 yrs 65 yrs (older) 40-60 yrs (younger)
2nd peak at 40 yrs MC type of leukemia
Triad: Malaise + pallor Triad: malaise + pallor Triad: fatigue + wt. Triad: fatigue + night
+ bone pain. + oral problems loss + sweats + abd. fullness
Lymphadenopathy, Gum hypertrophy, lymphadenopathy Massive
hepato-splenomegaly gingival bleeding Enlarged rubbery splenomegaly (due to
Testic. and CNS involv. CNS involv. at lymph nodes (only in bleeding disorders)
Pancytopenia with presentation is rare lymphoid line CA, not Gout features (purine
circulatory blast cells Pancytopenia with in myloid line CA) in destruction)
Pallor of normocytic circulatory blast cells. neck, axilla, groin Priapism
anemia. Susceptibility Pallor of normocytic Hepatosplenomegaly Blast crisis = final
to infection. Bruising, anemia Susceptibility (50%) stage -> behaves like
petechiae due to ↓ to infection Bruising, Mild anemia an acute leukemia,
Platelets. MCQ: ALL petechiae due to decr. with rapid
post chemotherapy –> platelets progression and short
fever & pancytopenia – survival
> admit patient.
Blasts (lymphoblasts) Blasts (myeloblasts) Lymphocytosis > Philadelphia
Positive for TDT AUER rods Positive for 15x109/ L mature Chromosome t(9:22)
myeloperoxidase and (BCR/ABL fusion
Sudan dye gene) WBC very ↑ >
100 x 109/L
Left shift (immature)
Chemotherapy Chemotherapy Chemotherapy – Chemotherapy -
(Vincristine, Aspargine, Complic. of chemo: Chlorambucil Imatinib
Daunorubicin) If CNS 1. Infection Radiotherapy – to Stem cell transplant
involv. –> intrethecal 2. Tumor lysis de-bulk swollen
methotrexate.Treat syndrome (↑serum lymph nodes
aggressively any inf. (IV urea level, acute renal Splenectomy
A/B) Relapses – bone failure) Relapses –
marrow/ stem cell bone marrow/ stem
transplant cell transplant
- Hodgkin vs. non-Hodgkin Lymphoma
Hodgkin Non-Hodgkin (more common 90%)
Reed-Sternberg cells (50% infected with EBV) No R-S cells
2 Peaks: young adults (15-35), elderly (> 55)
Rubbery painless lymph nodes (esp cervical 60-70%, More than 1 region of lymph nodes
axillary, inguinal, para-aortic, mediastinal) -> may involved (2-3) + extranodal tissues
later become matted (agglutinate to form a mass) involved:
Triad: Malaise + Drenching night sweats + pruritus Waldeyer’s ring – Peritonsilitis
Cyclical fever. Burkitt’s lymphoma – Characteristic jaw
Pain in enlarged lymph nodes after drinking alcohol lymphadenopathy (assoc. with EBV or
Splenomegaly (a lymph node) Hepatomegaly HIV). Skin tumor – Cutaneous T cell
Scenarios: lymphoma = Sezary syndrome
1. One tonsil enlarged, no fever, no pain Hepatosplenomegaly
2. tonsil enlarged
266

- Young, non-smoker = Lymphoma MCQ

- 1 Tonsil enlarged, smoker, ulcer on tonsil = SCC
Dx Dx
1st Step: FNAC - Cytology 1st Step: FNAC - Cytology
2nd and best: lymph node excisional biopsy - histology 2nd and best: lymph node excisional
Blood: Hypochromic anemia, ↑WBC, Platelets N or ↓ Biopsy – histology. Blood: Pancytopenia
Rx – Chemotherapy ± Radiotherapy Rx – Chemotherapy ± Radiotherapy
Prognosis: More aggressive than Hodgkins
1. Lymphocytes predom. – best prognosis Poorer prognosis
2. Nodular sclerosis
3. Mixed cellularity
4. Lymphocyte depletion
- Stem cell
o Lymphoid stem cell
▪ Lymphoid blast
• Lymphocyte
o Myeloid stem cell
▪ Myeloid blast
• RBC
• WBC
• Platelets
- Types of leukemia:
o Acute leukemia – Problem at blast (immature) level
o Chronic leukemia – Problem at mature cells level
Other hematological problems
- Myelofibrosis (oxford 350)
o Replacement of bone marrow with fibrotic tissue
o > 50 yrs
o Sx
▪ Constitutional sympt.: Night sweats, wt. loss, loss of appetite
▪ Abd. discomfort – Hepato-splenomegaly
o Dx
▪ decr. WBC => recurrent inf.
▪ decr. platelets => bleeding
▪ leucoerythroblastic anemia (immature mylocytes in field)
▪ tear drop RBCs
▪ confirm diagn. = Bone marrow biopsy
o Sx
▪ Supportive
▪ Young patient – Bone marrow transplant
▪ Prognosis – 4-5 yrs
Polycythemia vera- a malignant proliferation of RBCs, WBCs and platelets.
o Sx
▪ Itching after hot baths
▪ gouty arthritis
▪ peptic ulcer
▪ erythromyelgia
267

• Rx - aspirin
o Cx
▪ Thrombosis, due to blood thickening: MI, stroke, DVT, Budd-Chiari syndrome
o Dx criteria
▪ Major criteria
• incr. red cell mass
- Man 36ml/ kg
- Woman 32 ml/ kg
• SaO2 92%
• Splenomegaly – 60% - most characteristic
▪ Minor
• Platelets > 400,000
• WBC > 1200
• leucocyte Al PO4 > 1000 ?
• serum B12 > 900 micrograms/ ml ?
• unbound B12 > 2200
o Rx
▪ Venesection
- Ig stuff
o Ig that crosses placenta = IgG
o Ig related to Grave’s disease = IgG

Coagulation problems
INR, PT (extrinsic APTT (intrinsic & common Platelets Bleeding time
pathway) pathways)
DIC Incr. Incr. Decr. Incr.
Heparin Incr. Incr. N N
Warfarin, Vit. K def. Incr. Incr. N N
Hemophillia A N Incr. N N
Von Willebrand N Incr. N Incr.
Thrombocytopenia N N Decr. Incr.
HSP (vasculitis) N N N N
- DIC
o Sx
▪ Bleeding from venopuncture sites, hematuria, ↑bruising
o Dx
▪ ↓Platelets & fibrinogen
▪ incr. D-dimer = incr. fibrin degradation products
▪ + schizocytes = fragmented RBCs
o Rx
▪ fresh frozen plasma
▪ IV heparin – to stop clotting in peripheral vessels
- Bleeding problems
o Haemophilia – X-linked recessive (only in boys)
▪ A
• Fact. VIII deficiency, more common
268

• Sx
- Triad: spontaneous hemarthrosis + muscle bleeds + delayed
bleeding
- spontaneous hemarthrosis, MC in knees, ankles and elbows =
pathognomonic
- many are seropos. for HIV, HBV, HCV – transmission through
factor VIII
▪ Low platelet count – suspicion of HIV-assoc. ITP
• Rx
- Avoid aspirin
- Cryoprecipitate (contains fact. VIII and vWF)
- Fact. VIII concentrates
▪ B (Christmas dis.)
• fact. IX (Christmas factor) deficiency, less common
• Rx
- recombinant fact. IX concentrates
o von Willebrand disease --- AD
▪ Def. of von Willebrand factor => affects
• transport of fact. VIII
• platelet adhesion to each other and to vessel walls
▪ MCQ: in girls, but actually equal in both genders
▪ MC bleeding disorder (1%)
▪ mild, with excellent prognosis
▪ bleeding tendency aggravated by aspirin
▪ Sx
• Triad: ↑bleeding 1. Incision, 2. Dental, 3. Mucosal
• Man
- epistaxis
- hemarthrosis (rare)
• Female MCQ 2051 p 132
- long and intense first period (menarche) = menorrhagia
- epistaxis
- hemarthrosis (rare)
▪ Dx
• Prolonged Bleeding time
• Prolonged APTT
▪ Rx
• avoid aspirin!
• before dental or surgical procedures + to stop existing bleeding use:
- Desmopressin acetate (DDAVP –↑release of vWF from vessel
walls)
- Fact. VIII concentrate
- Tranexamic acid - antifibrinolytic
- Cryoprecipitate (fact. VIII + vWF+ other factors)
o Petechiae/ purpura/ ecchymosis:
▪ Vascular
• HSP
269

- Non-thrombocytopenic purpura
• Severe inf. – severe angitis, usually followed by DIC
- Meningococcemia
- Other septicemias
• Simple purpura (easy bruising syndrome)
- in young women
▪ bruising with minor trauma + heavy periods
▪ Platelet disorders - platelets < 50 x 109/L
• Immune thrombocytopenic purpura (ITP) = Isolated thrombocytopenia
- Autoimmune disease where IgG autoantibodies against platelets
sesnitise them for destruction. NO SPLENOMEGALY.
- Types:
▪ Acute thrombocytopenia of childhood
• child well otherwise
• viral inf. in recent Hx or drugs
• cross-reacting AB against platelets
• Dx
o BMA: Megakariocytes increased
(compensatory)
• Rx of bleeding
o C/S initially which reduce clearance of
sensitised platelets.
o IV gamma globulins: if there is an
inadequate response to C/S.
o Splenectomy
o Azathioprine: If C/S and splenectomy
have failed.
• Prognosis
o 90% self-limiting in 6 months
o 10% pass into chronic ITP
▪ Chronic ITP
• autoimmune disorder
• adult women
• Rx
o Prednisolone
o Azathioprine, methotrexate
o Splenectomy – in some pts (but risk of
subsequent severe inf., e.g. with
streptococcus pneumonia)
▪ avoided in children
- Sx
▪ Triad: Bruising + Oral bleeding + Epistaxis
▪ No splenomegaly (rare)
- Dx
▪ exclude ALL/ AML
▪ FBE:
• Platelets significantly decr.
270

• All else normal

• Thrombotic thrombocytopenic purpura (TTP)
- assoc. with hemolytic uremic syndrome (HUS)
▪ after E. coli or Shigella inf. (camping)
▪ hemolysis (low Hb) hemoglobinuria & hematuria,
kidney involv. (high urea & creat.), unconj. bilirubin
incr., palor, ↑Uric acid
- Sx
▪ HUS
• hemol. anemia
• ARF
▪ fever (non-inf.)
▪ fluctuating CNS signs
▪ thrombocytopenia
- Rx
▪ Plasma exchange
▪ FFP
▪ Platelets
• SLE – autoimmune purpura ē Splenomegaly MCQ 2054 p133
• Portal HTN –> Splenomegaly -> ↓ platelets
o Splenectomy
▪ indic.
• chronic ITP
• heredit. Spherocytosis (HS)
• hypersplenism
• trauma
• lymphoma
▪ who will benefit more from splenectomy: chronic ITP
▪ risks
• short term
- Thrombocytosis
- risk of thrombembolism
• long term
- severe inf. with strepto. pn. in first 2 yrs
▪ Rx – start A/ B ASAP: Penicillin, amoxycillin
▪ Prophylaxis
• Pneumococcal vacc. 2-3 wks pre-op. + repeat every 5 yrs
• Meningococcal vacc. – every 5 yrs.
• H. influenza B – Hib – once (if not immunized)
• MCQ: after 2 yrs, URTI –> Rx - A/B (Penicillin)
o Bleeding
▪ from everywhere – DIC
▪ Hemarthrosis – Hemophilia
▪ Petechial rash, bruising, no splenomegaly – ITP
o Epistaxis
▪ causes
• HT - MC
271

• Local
- cocaine abuse
- chronic rhinitis, chronic sinusitis
- ulcers in nasal cav.
- perforation of nasal septum
- nasal polyps
• Bleeding disorders: von Willebrand dis., etc.
- Thrombophilia – Murtagh 1367
o primary tendency to coagulopathy
o types
▪ inherited
• fact. V Leiden gene mutation
• prot. C deffic.
• prot. S deffic.
• prothrombin gene mutation
• antithrombin deffic.
▪ acquired
• anti-phospholip. AB
• lupus anticoagulant
• incr. homocystein
o thrombophilia screening – all the factors above:
▪ fact. V Leiden
▪ prot. C
▪ prot. S
▪ prothrombin
▪ antithrombin
▪ antiphosphopholipid AB
▪ lupus anticoag.
▪ homocystein
▪ + anthrombin C AB?
▪ + antiocardiolipin AB?
o indic. for investig.
▪ recurrent thrombosis
▪ venous thromboembolism < 40 yrs
▪ arterial thrombosis < 30
▪ skin necrosis on warfarin
▪ recurrent fetal loss
▪ familial thromboembolism
o MCQ:
▪ daugther asking for OCP, mother had DVT
▪ woman with DVT wants to get pregnant
• -> do thrombophilia screen
Anemia
- Iron studies – Murtagh table p. 146
o 1. Serum iron
o 2. Transferrin (major iron carrying protein in blood)
▪ Transferrin conc. = TIBC (total iron-binding capacity)
272

▪ Level rises in iron deficiency

▪ Low iron + incr. TIBC = Iron deficiency
o 3. Tranferrin saturation = Serum iron/ TIBC x 100 (taken as %)
▪ very incr. in hemochromatosis > 60%
o 4. Serum ferritin (an intracellular prtein for iron storage)
▪ reflects iron stores in body (single most reliable indicator of Fe def. anemia)
▪ decr. values even before serum iron gets decr.
Serum Fe TIBC % Transferrin saturation Ferritin
Iron deficiency Decr. N or incr. Decr. Very decr.
Anemia of chronic dis. Decr. N or decr. Decr. N or incr.
Thalassaemia, N or incr. N N or incr. Incr.
Sideroblastic anemia
Hemochromatosis Incr. Decr. Very incr. Very incr.
- Anemia – Murtagh 212
Iron defic. B12 defic. Folate defic. Chronic dis. Hemolytic anemia
MCV (N80-95fl) < 80 > 98 > 98 N or < 80 N
Iron Decr. N or decr. Incr.
TIBC Incr. Decr. Decr.
Transferrin sat Decr. Decr. Incr.
Ferritin ↓(most Incr. Incr.
characteric)
Other findings ↑urobilinogen,↑
reticulocytes, ↑ Fe
absorp,↓RBC survival
- Anemia:
o Sx
▪ Triad: fatigue + palpitations + exertional dyspnea
▪ headache, faintness/ dizziness
▪ angina on effort (Stable)
o Types:
▪ Microcytic anemia - MCV < 80 fl
- Fe deficiency anemia
▪ causes
• Chronic blood losses: Menorrhagia, GIT bleeding,
malignancy (occult blood losses – Colon CA)
• ↑demands: Prematurity, multiple pregnancies,
adolescence, pregnancy
o Fe stores in
▪ term baby for– 6-8 mths
▪ premature baby for – 6 weeks
• Malabs.: Celiac, post gastrectomy
• Inadequate intake: drinking a lot of cow’s milk
▪ High risk
• children:
o Prevention < 6 months, premature and
low wt.
273

o 1. Toddlers 6-36 mths with a diet high

in cow’s milk & low in iron: highest risk
o exclusively breastfed > 6 mths
o delayed introduction of solids
o lack of Vit. C
• 2. Adolescents
• adults
o 3. Women of child-bearing age
▪ Prevention
• avoid cow’s milk in first 12 mths
• avoid excessive cow’s milk in first 24 mths
• introduce Fe-containing solids early at 4-5 mth
▪ Rx
• correct the cause
• Fe-rich foods
• Fe supplements
o types:
▪ Oral – 6 months (to replenish
stores)
▪ Parenteral (SE – allergic reaction)
o anemia responds in 2 wks and is corrected
after 2 months
- Hemoglobinopathy
▪ Thalassemia- (Alpha and Beta) AR
• incr. prevalence
o Alpha - Asia
o Beta – Mediterranean (Greek) basin,
Middle east, north & central India, South
East Asia (China)
• Alpha - deletion of 1-4 genes for 2 alpha chains
o 4 genes – Major alpha thalassemia (no
alpha chains; hydrops fetalis)
o 3 genes – Haemoglobin H dis. (mild to
moderate anemia; HbH on electrophoresis)
o 1-2 genes – Symptomless carrier
• Beta – 2 genes
o 1 gene mutated -minor/ heterozygous/ trait
▪ usually asympt.
o 2 genes mutated- major/ homozygous –
▪ very severe hemolytic anemia
▪ triad: pallor + hepatosplenomegaly
+ jaundice
▪ neonatal jaundice
▪ Dx
• HbA2 (no alpha chains) incr. (> N =2%)
o > 3.5 = trait
• Hb F (fetal)
274

• Blood film: (Hb electrophoresis)

o microcytic, hypochromic anemia
o target cells MCQ
o nucleated red cells
o reticulocytosis
o Basophilic stippling - erythrocytes
display small dots at periphery. These
dots represent accumulations of rRNA
and are always pathological.
• Rx (in major)
o transfusions
o desferroxamine (iron chelation agent)
o folic acid
o splenectomy
▪ HbE syndrome
• South-East Asia (like thalassemia)
▪ HbC syndrome
▪ and various other unstable Hb diseases
- Sideroblastic anemia
▪abnormal production of ringed sideroblasts, caused either
genetically or indirectly as part of myelodysplastic
syndrome which can evolve into hematological
malignancies (esp. acute myelogenous leukemia).
▪ Body has iron available but can’t incorporate it into Hb.
Failure to completely form heme molecules, whose
biosynthesis takes place partly in mitochondrion. This leads
to deposits of Fe in mitochondria that form a ring around
nucleus of developing RBC.
▪ types:
• Hereditary sideroblastic anemia.
• Acquired sideroblastic anemia, including Pb toxicity.
• Reversible sideroblastic anemia.
- Anemia of chronic disease (MC presenting as normocytic anemia)
▪ Macrocytic anemia – MCV > 98 fl
• with Megaloblastic changes:
- Defic. of Vitamin B12
▪ body stores: 3-5 mg
▪ causes:
• vegans/ vegetarians > 3 yrs
• Macrocytic anemia can also be caused by
removal of functional portion of stomach, such
as during gastric bypass surgery, leading to
reduced vit. B12/ folate absorption.
• Pernicious anemia is caused by a lack of
intrinsic factor which is required to absorb Vit.
B12. A lack of intrinsic factor may arise from:
275

o an autoimmune condition targeting

parietal cells (atrophic gastritis) that
produce IF or
o Antibodies against intrinsic factor itself
(anti intrinsic and antiparietal cell
antibodies). These lead to poor
absorption of Vit. B12.
o Dx - hypersegmented polymorphs?
• Terminal ileum pathology (where B12 is
absorbed): Crohn, ileitis, tapeworm
• blind intest. loop syndrome
• H. pylori inf.
• H2 receptor blockers, PPI
• other drugs: OCP, metformin
• chronic alcoholism
• HIV
• incr. demands
▪ Sx
• anemia
• neurol. problems
o subacute combined degen. of sp. cord
o polyneuritis
o atrophic glossitis
▪ Dx
• Schilling test
▪ Rx
• Vit. B12 IM
- Defic. of Folic acid (or both).
▪ not stored in body
▪ daily requirements: 5-10 µgms/ day
▪ No neurological symptoms, while B12 defic. cause.
▪ causes:
• ↓intake: old age, poverty, malnutrition,
alcoholism
• malabs.
• drugs: Phenytoin
• ↑ demands in pregnancy – pernicious anemia
of pregnancy
o MC cause of anemia in pregnancy
▪ Rx
• Folate P.O.
- Drugs:
▪ Cytotoxic: Methotrexate, zidovudine, azathioprin, 5-
fluorouracil
▪ anticonvulsants: Phenytoin, phenobarbitone
▪ A/B: Co-trimoxazole, pyrimethamine
• without megaloblastic changes:
276

- Alcoholism commonly causes a macrocytosis, although not

specifically anemia.
▪ first indication of alcohol abuse
- Other types of Liver Disease can also cause macrocytosis.
- Myelodysplastic disorders (sideroblastic anemia)
▪ Cx
• inf.
• hemorrhage
• leukemia (CML)
- Hypothyr. (usually normocytic)
▪ Normocytic anemia - overall Hb levels are always ↓, but RBC size (Mean
corpuscular volume) remains normal.
• 1. Acute blood loss
- causes
▪ hematemesis
▪ malena
- Dx – Reticulocytes incr.
• 2. Hemolytic anemia
- Dx
▪ ↑ unconjugated bilirubin
▪ reticulocytosis (polychromasia, a non specific feature)
▪ ↓ haptoglobin (Key finding)
• In blood plasma, haptoglobin (a protein) binds
free Hb released from erythrocytes during
hemolysis. The haptoglobin-Hb complex will
then be removed by reticuloendothelial system
(mostly spleen).
• In clinical settings, haptoglobulin level is used to
screen for intravascular hemolytic anemia.
o In intravascular hemolysis free Hb will
be released into circulation and hence
haptoglobin will bind Hb. This causes a
↓ in Hp levels.
o Conversely, in extravascular hemolysis
the reticuloendothelial system,
especially splenic monocytes,
phagocytose the erythrocytes and Hb is
not released into circulation and hence
haptoglobin levels are normal.
- types
▪ Congenital:
• Hereditary Spherocytosis (favism) AD
o Cause Parvovirus (MCQ)
o Spherocytes -> get stuck in spleen ->
splenomegaly
o Dx
▪ Clinical
277

▪ ↑ MCHC
▪ Osmotic fragility test
o Rx
▪ Phototherapy or exchange
transfusion – if kernicterus +
folic acid to prevent
megaloblastic crisis
▪ Splenectomy
• Hereditary eliptocytosis
• Thalassemia: microcytic hypochromic anemia
• Sickle cell anemia
• Defic. of G6PD
o X- linked recessive – in boys only
o African (Sudanese), Mediteranean,
Asian
o causes episodic H. anemia due to ↓
capac. of RBC to deal with oxidative
stress; precip. by
▪ inf.
▪ antioxidant drugs:
Sulphonamides, antimalarial,
nitrofurantoin, Vit. C Vit. K,
traditional medicine, high dose
aspirin, naphthalene,
cotrimoxazole
▪ broad b eans (favism)
o Neonatal jaundice
o Dx
▪ Beutler fluorescent spot test
▪ Heinz bodies (bill cell) –
Denatured Hb within RBC
▪ Peripheral smear: Bite cells
▪ sometimes with spherocytes
o no Rx
• defic. of pyruvate kinase
▪ Acquired
• ABO/ Rh immunis.
• Drug toxicity
o A/B: antimalarials, sulphamethoxazole
o Anti-inflammatory
o Penicillin, methyldopa
• Infections:
o Mycoplasma
o malaria
• DIC
• Auto immune:
o cause
278

▪ Idiopathic - 50%
▪ Non-Hodgkin lymphomas
▪ SLE
o action
▪ cold agglutinin dis. - IgM
▪ act at body temp. – Ig G -
autoimmune hemol. anemia
o Dx – direct Coomb’s test +
• 3. Anemia of chronic disease and malignancy
- enough iron, but intercellular iron transport within bone marrow
is suppressed in inflam. => erythropoiesis is suppressed
- MCQ: boy who looks pale and has chronic diarrhea.
• 4. Chronic kidney disease – defic. of erythropoietin
- Rx – adm. of erythropoietin
• 5. Endocrine disorders: hypothyroidism (can be macrocytic as well)
- with bradycardia, fatigue, constipation, lymphocytosis
• 6. Bone marrow replacement
- metast.
- myelofibrosis
- ALL, AML, CML, CLL, lymphoma
- Aplastic anemia
o destruction of hematopoesis and bone marrow stem cells
o pancytopenia + hypocellularity in bone marrow
o types
▪ Congenital – Fanconi
▪ Acquired
• idiopathic – MC
• immune
• post-viral inf.
- Parvovirus B19
- HBV
- Epstein-Barr
- HIV
o Sx
▪ no splenomegaly
▪ no hepatomegaly
▪ no lymphadenopathy
o Rx
▪ supportive
▪ RBCs, platelets transfusion
▪ A/B
▪ immunosuppresion – if immune cause
▪ Bone marrow transplant
Digestive system - OK
Jaundice and other biliary problems
- Murtagh – table P 622
- Bilirubin metabolism: MCQ 2079 P 71
279

o Old erythrocytes -> destroyed in spleen -> heme is converted to unconjugated billirubin-
> sent to liver -> conjugated bilirubin -> eliminated through bile -> some is metabolized
in large intestine to urobilinogen (-> stercobilinogen -> stercobilin, gives feces brown
color) -> some of urobilinogen is reabsorbed and eliminated through urine (along with
an oxidized version, urobilin).
o Pathology:
▪ liver problems + biliary obstruction = some of conjugated bilirubin leaks out
from hepatocytes in blood and is excreted in urine as bilirubin -> dark urine.
▪ Hemolytic anemia - ↑ unconjugated bilirubin in blood -> ↑urobilinogen in urine
• high ratio of unconjugated to conjugated bilirubin in serum.
Hemolytic Hepatic Obstructive
Function test Pre-hepatic Jaundice Hepatic Jaundice Post-hepatic Jaundice
Total bilirubin Normal/ Increased Increased
Conjugated bilirubin Increased ↑
Unconjugated bilirubin Increased Normal/ Increased Normal
Urobilinogen Normal/ Increased Decreased/ Negative
Normal Dark (urobilinogen + Dark (conjugated bilirubin)
Urine Color
(urobilinogen) conjugated bilirubin) Absence of urobilinogen
Stool Color Normal Pale
Alkaline phosphatase
Increased
levels
Normal
Alanine & Aspartate
Increased
transferase levels
Conjugated Bilirubin in Urine Absent Present
- Jaundice
o Blirubin > 17 µmol/L
o Clinical jaundice > 50 µmol/ L
- Hyperbilirubinemia:
o Unconjugated
▪ Hemolytic jaundice (Prehepatic) – starts after 4-6 mths
• Spherocytosis
• G6PD deficit, (X linked recessive), Dx by Heinz bodies
• Drugs – Methyldopa, penicillin
• Sickle cell anemia
- Dickle cell crisis
▪ sickle cells get plucked inside capillaries & cause infarcts
▪ precip. by
• infection
• cold weather
• hypoxia
• dehydration
• acidosis
• surgery
▪ types:
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• Vaso-occlusive
• Splenic sequestration
o => infarction
o severe pain in LUQ
o Rx
▪ O2 + hydration
• aplastic
• hemolytic
▪ Cx
• unequal digits (infarction in bones)
▪ Dx
• Hb electrophoresis (HbS)
• Howell-Jolly bodies = Basophilic nuclear
remnants (clusters of DNA) in circulating
erythrocytes
o Post-splenectomy
o Sickle cell – causes autosplenectomy
o Celiac dis. – splenic atrophy
o Spleen radiation therapy - Hodgkin
o + myelodysplasia
o + megaloblastic anemia, B12 defic.
o + severe hemolytic anemia
▪ Rx
• pneumococcal vaccine
• oral penicillin till 5 yrs
• ± splenectomy
▪ ineffective erythropoiesis - megaloblastic anemia
▪ Polycytemia vera
• incr. RBC, WBC and platelets + Splenomegaly
• incr. viscosity, arterial and venous thrombosis, visual blurring (TIA)
• gross retardation at delivery
▪ MC = Gilbert’s syndrome ---- AD - 3-5%
• Defic. of glucuronyl transferase -> ↑ Unconjugated bilirubin
• No evidence of hemolysis (fatigue, tachycardia , dyspnoea, pallor)
• all other fc. test are normal (Normal LFTs except for ↑ unconjugated
bilirubin).
• jaundice when
- under stress
- fasting
- sick (cold) etc.
• Dx
- fasting bilirubin
- bilirubin after nicotinic acid
- liver biopsy - normal
• no Rx required
▪ drugs:
• A/B
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- flucloxacillin
- amoxyclave
- erythromycin
- rifampicin
• radiographic agent
▪ Crigler Najjar syndrome --- AR (very rare)
• types
- I
▪ Uridine diphospho- glucuronyl transferase absent
▪ unconj. bilir. > 340 µmol/ L -> kernicterus, unless
treated
▪ Rx
• Phenobarbital doesn’t help
• Phototherapy, exchange transfusion, etc.
- II
▪ UDP-G decr.
▪ Unconj. bilirubin < 340 µmol/L
▪ Rx
• Phenobarbital helps
▪ Hypothyroidism
• Rx - thyroxine
▪ ABO/ Rh hemolysis
▪ Breast milk jaundice
▪ Physiological
o Conjugated
▪ familial disorders
• Rotor syndrome—AR - rare
- non-itching jaundice
- liver cells are not pigmented
- no Rx is required
• Dubin Johnson syndrome---- AR
- inability of hepatocytes to secrete conjugated bilirubin into bile
- liver is pigmented black
- no Rx is required
▪ Hepatitis
• both direct and indirect bilir. ↑
• FTT, dark urine, pale stools
▪ drug induced
• Chlorpromazine
• OCP
▪ Primary biliary sclerosis
▪ Biliary atresia
• after first week
• stools are white
• AST/ ALT incr.
• chronic cholestatic jaundice
▪ Neonatal sepsis
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▪ Galactosemia
▪ Postop. jaundice
▪ Intraductal problems/ Obstructive Jaundice
• Gall stones/ CBD stones
• Biliary strictures
• Infection
• Malignancy – cholangiocarcinoma
▪ Extraduct problems
• Pancreatic CA
• pancreatitis
- Jaundice
o in newborn: (1g= 18mmol)
▪ Kernicterus if bilirubin > 340 µmol/ L
▪ Rx
• > 285 µmol/L -> Phototherapy
• > 360 µmol/L -> consider exchange transfusion
▪ types
• 1st 24 hrs – Pathological
- ABO incompatibility – MC
▪ Mother is group O, child is A or B
▪ direct Coomb’s test +
▪ w/ spherocytes
• DD: day 1 – ↑Unconjugated bilirubin + ↑
spherocytes + family Hx of spherocytosis =
Spherocytosis
▪ Rx
• Phototherapy immediately
- Rh incompatibility – more severe
▪ direct Coombs test +
▪ w/o spherocytes
• > 24 hrs
- Physiological jaundice – MC cause of jaundice in newborn (50%
of term babies and 80% of prematures develop jaundice in 1st wk
▪ due to immature liver enzymes
▪ starts at 2-3 days, max by day 3-5, finishes in 1-2 wks
(less than 2 wks)
▪ not very severe
▪ Rx - Phototherapy
- Breast milk jaundice (↑unconjugated bilirubin)
▪ Starts on day 4-7, lasts up to 6 wks
▪ Hormones secreted through milk are inhibiting UDP-G
▪ Child normal, feeding normal, liver enzymes normal
▪ Dx – by suspending breast feeding for 24-48 hrs =>
serum bilirubin falls = Breast milk jaundice
▪ Mx – Continue breastfeeding
- Hypothyroidism
- Neonatal sepsis
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▪ lethargic baby + jaundice + hepatosplenomegaly at end

of 1st wk
▪ Dx
• Both direct and indirect bilirubin are ↑
▪ Mx
• 1st Step: Blood culture
• A/B
- Conjugated bilirubin
▪ Neonatal hepatitis
▪ Biliary atresia: Presents on 4th day, Dx USG
▪ Galactosemia
▪ Check bilirubin in
• day 1 jaundice (ABO)
• jaundice that persists > 14 days
- Biliary problems
o 1st test - U/S: look for 3 things
▪ Dilatation of CBD – most important thing to look for
▪ Stones
▪ Gall bladder – cholecystitis?
AST/ALT ALP (obstr. GGT (alcohol +
+ bone dis.) drugs + obstr.)
Cholecystitis: + fever, Murphy’s positive, N N N
U/S thick gall bladder walls
Cholelithiasis + RUQ pain, nausea, vomiting, N N N
no fever
Murphy’s negative, U/S gall bladder stones
Hepatitis very↑ Incr. Incr.
Cholangitis N or Very incr. Very incr.
(Rx – ERCP) incr.
o Congenital hepatic fibrosis – less likely with jaundice
Biliary atresia (progressive Neonatal hepatitis:
sclerosing cholangitis) - Infective (TORCH)
- Idiopathic
- Metabolic (AR)-galactosemia, Wilson, alpha 1 antitripsine
Assoc. with other anomalies Depends on conc.
No family Hx Family Hx
Term babies ↑AST/ALT Pre-term
Persistent pale stools Normal color stools
U/S gall bladder not visible Gall bladder visible
- Biliary problems
o female + pain in RUQ radiating to back after eating fatty foods + stones on USG =
cholelithiasis ē biliary colic
o same + fever = Cholecystitis
o jaundice + stones in CBD + pain = Choledocholithiasis
▪ pale stools, dark urine
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▪ Dx
• 1 – USG
• ERCP
• MRCP – the best
o Acute cholangitis = (obstructive) jaundice + fever, chills, rigor + abd pain
▪ Charcot triad:
• fever, chills
• jaundice
• severe pain
▪ Dx
• 1 – USG
• ERCP
• MRCP – the best, less invasive
▪ Rx
• IV fluids
• A/B: Ceftriaxone, penicillin, aminoglycosides
• ERCP surgery – Gold standard
- Biliary lithiasis
o Sx
▪ Biliary pain:
• Severe, constant pain that can last for hrs.
• History of episodes of similar pain.
• Epigastric
- referred to scapula
• If cholecystitis develops, pain typically shifts to right upper quadrant
and becomes more severe. + tenderness, guarding (Murphy’s sign +)
▪ The patient may be jaundiced if CBD is obstructed.
▪ Look for right upper quadrant tenderness.
o DIAGNOSIS:
▪ FBC
▪ U&E
▪ LFTs
▪ Lipase/ amylase
▪ Request an upper abdominal USG
• if equivocal/ technically inadequate (obese woman) => HIDA (Tc-IDA)
scan of GB (contrast injected in blood -> liver -> secreted in bile)
▪ Dilatation of CBD
• best seen with:
- I – MRCP
- II – ERCP
o MANAGEMENT:
▪ PAIN relief: Morphine 0.1 mg/ kg IV with metoclopramide 10 mg IV
▪ Advise patients to eat a low fat diet.
▪ Refer patient to Surgical OPD for follow-up.
o Cx
▪ 1. Cholecystitis = MC
▪ 2. Choledocholithiasis and jaundice
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▪ 3. Pancreatitis
▪ 4. Ileus
- Acute cholecystitis
o Acute, CONSTANT right upper quadrant pain.
▪ Referred to scapula
o Associated with fever, anorexia, nausea and vomiting.
▪ no jaundice
o SIGNS: Localized tenderness with involuntary guarding and rebound tenderness.
▪ Murphy’s sign
o DIAGNOSIS AND MANAGEMENT:
▪ FBC, U&E, blood sugar, LFTs, lipase/ amylase and blood culture.
• ↑ CRP, ESR
▪ USG: thick walls
▪ Gentamicin, ampicillin.
▪ Refer to Surgical team for bed rest, analgesia, antibiotics and cholecystectomy.
• surgery not in acute cholecystits or cholangitis, but after treating inf.
Liver pathology
- types of hepatitis – table Murtagh p. 625
- Liver enzimes, ALP, etc. in various hepatic dis. – table Murtagh p. 622
- Hepatitis B – printout with the table
HbsAg Anti HBs HbeAg Anti Hbe AntiHBc HBV ALT, AST
DNA
Acute HBV + - + - IgM + Highly
Highly infective incr.
Chronic HBV + - + - IgG + Highly
highly infective incr.
Chronic HBV + - - + IgG Incr.
low infective
Recovery + IgG
Immunization +
o Serology guidelines
▪ HbsAg = Persistent inf. highly infectious (carrier state)
▪ anti-HBs = Past inf. and immunity (sole marker after HBV vaccination)
▪ HbeAg = highly infectious
▪ HBV DNA = circulating and replicating virus
▪ anti-Hbe = low titre of HBV (low infectivity)
▪ anti-HBc IgM = Recent inf.
▪ anti-HBc IgG = Past inf.
▪ HBcAg = O nly found in liver (biopsy), not in blood
o Transmission
▪ blood
▪ sex
• also at risk – sexually active homosexual male
▪ saliva
▪ MC Vertical - perinatal transmission mother to fetus – Asia (Chinese South
Asia) MCQ
▪ lowest risk = scientist in a pathol lab
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o Rx
▪ Alpha interferon
▪ Lamivudine: drug of choice after 12 months treatment normalisation of liver
enzymes.
▪ Liver transplant – recurrance of HBV
o Cx
▪ Chronic hepatitis 5-10%
• Cirrhosis - 15-40%
- 6-15% in 5 yrs -> CA - risk factor for hepatocellular CA (90-100x
or 223x incr. risk)
- 20-23% in 5 yrs -> liver failure
▪ Rx – liver transplant
o Prophylaxis
▪ normal human immunglobulin – in people who sustained a needlestick injury
with blood products from a confirmed HBV donor
▪ Hep. B vaccine
• can be admin. to chronic carriers without harm
• types
- recombinant
- plasma-derived
- Hepatitis C
o MC type of infective hepatitis in Aus.
o in
▪ IV drug users and tatooing - most frequent
▪ post-transfusion
▪ hemophilia
▪ hemodialisys
▪ sex and vertical - uncommon
o Cx
▪ 60-80% chronic hepatitis = MC cause of chronic hepatitis
• Cirrhosis 10-25% in 20-30 yrs
- CA
- liver failure
o RX (No vaccine available)
▪ Ribavirin
▪ Alpha interferon
- Hepatitis A (feco-oral route)
o mild, but can cause fulminant hepatitis as well
o excretion of virus in feces diminishes at the onset of clinical dis.
o Sx
▪ jaundice – more common in childrent than in adults
o Px
▪ Gamma-globulin – within 2 wks of exposure decr. the attack rate
▪ Hep A Vaccine
- Chronic liver disease
o Sx
▪ Ascites
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• central abd. resonance and dullness around it and on flanks

• min. 250 ml in order to be detected clinically
• Rx
- Bed rest
- < 1.5 L of fluids/ day
▪ measure body wt. daily
- Spironolactone 100 mg (up to 400 mg)/ day
▪ add furosemide if response is inadequate
- Paracentesis + albumin infusion
▪ Bilateral parotid gland enlargement
▪ Pigmentation of skin
▪ telangiectasis
▪ palmar erythema
▪ easy bruising
▪ spider naevi
▪ muscle wasting
▪ testicular atrophy
▪ gynecomastia
▪ asterixis (hepatic flap)
▪ lymphadenopathy
▪ NO peripheral neuropathy
o Dx
▪ Smooth muscle autoantibodies
o poor prognosis factors – Child-Pugh classif. of severity
▪ 1. Encephalopathy resistant to Rx
▪ 2. Ascitis resitant to Rx
▪ 3. ↑ bilirubin
▪ 4. Low serum albumin
▪ 5. Incr. INR
o Cx
▪ Portal HTN
• portal pressure gradient (difference in pressure bw portal and hepatic
veins) of 5 mm Hg or greater
• types
- Prehepatic
▪ portal vein thrombosis
▪ congenital atresia
- Intrahepatic.
▪ congenit. fibrosis
▪ Primary biliary stenosis -> primary biliary cirrhosis
▪ Hemochromatosis
▪ other infiltrates:
• Sarcoidosis
• Wilson’s dis.
▪ chronic viral inf. – HBV, HCV, HDV
▪ Alcohol
- Posthepatic
288

▪ Budd-Chiari = hepatic v thrombosis (or

thrombophlebitis)
• can be sec. to polycythemia vera
• Cx – cirrhosis, ascitis
▪ IVC thrombosis
▪ constrictive pericarditis
• Sx
- Ascites (free fluid in the peritoneal cavity)
- Hepatic encephalopathy
- ↑ risk of spontaneous bacterial peritonitis (SBP)
- ↑ risk of hepatorenal syndrome
- Splenomegaly with consequent sequestration therein of RBC,
WBC and platelets, together leading to mild pancytopenia.
- Portocaval anastomoses (esophageal, gastric & anorectal varices
[not to be confused as hemorrhoids] caput medusae – radiate
centrifugally from umbilicus), with esophageal varices and gastric
varices posing an ongoing risk of life-threatening hemorrhage with
hematemesis or malena.
• Rx
- Prophylaxis of varices
▪ endoscopic banding
▪ Portosystemic shunt – TIPS (transjugular intrahepatic
portosystemic shunt)
• but ↑ risk of hepatic encephalopathy and it
dosn’t improve mortality rate
- Management of ascites
▪ It should be gradual to avoid sudden changes in
systemic volume status which can precipitate hepatic
encephalopathy, renal failure and death. Management
includes salt restriction, diuretics (spironolactone),
paracentensis, TIPS and peritoneovenous shunt.
- Control of hepatic encephalopathy
▪ ↓ dietary protein, followed by lactulose and use of oral
antibiotics.
- Non-alcoholic fatty liver disease (NAFLD)
o is one cause of fatty liver changes, when fat is deposited (steatosis) in liver when this is
not due to excessive alcohol use.
o is related to insulin resistance and metabolic syndrome and may respond to treatments
originally developed for other insulin-resistant states (e.g. DM type II), such as weight loss,
metformin and thiazolidinediones.
o Non-alcoholic steatohepatitis (NASH) is the most extreme form of NAFLD, which is
regarded as a major cause of cirrhosis of liver of unknown cause.
-
o massive enlargement
▪ in metastases – not enlarged
o Dx
▪ tumoral markers
289

• alphafeto protein (AFP)

Pancreatic pathology
- Acute pancreatitis
o past Hx of gall stones, alcoholism
o previous attacks
o risk factors: GET SMASHED
▪ Gall stones
▪ Ethanol
▪ Trauma
▪ Steroids
▪ Mumps
▪ Autoimmune
▪ Scorpion, snake bites
▪ Hypercalcemia, hyperlipidemia, hypertriglyceridemia, hypothermia
▪ ERCP, emboli
▪ Drugs (azathioprine), duodenal ulcers
o Sx
▪ first sympt = severe and constant pain in epigastrium region, radiating to back
• pain may be partly relieved by sitting up and leaning forwards.
▪ nausea and vomiting
▪ fever, tachycardia, pale, sweating, anxious (shock)
▪ reduced or absent bowel sounds, abd. distension
▪ Cullen sign – periumbilical echymosis (discoloration)
▪ Bluish discoloration in the loins (Grey Turner’s sign): Uncommon and develops
after several days.
o Dx
▪ I - FBE
• Amylase – early, at least 3x > normal level
- Inaccurate ↑ in people with hyperlipidemia!
• Serum lipase – most reliable
▪ if jaundice, high bilirubin, severe pancreatitis, suspicion of stone
• II = ERCP – Dx and Rx
• MRCP – more acurate, non invasive
▪ if no jaundice, mild pancreatitis
• II = abd CT - best
- if stone => do III. ERCP
▪ U/S to identify Gall stones
▪ X Ray
• exclude intraperit. gas as a result of visceral perforation
- usually normal or showing ileus
• exclude basal pneumonia
▪ LFT
▪ CRP incr., leucocytosis
▪ glucose incr., Ca decr.
o Rx
▪ Admission
▪ hydration:
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• needle-by-mouth (nothing by mouth) = iv fluids

▪ analgezics – morphine
▪ antiemetics – Metoclopramide, Prochlorperazine
▪ Ca gluconate (if Ca decr.) – slow IV
o mortality > 20%
o Complic
▪ early
• shock
• acute renal failure
▪ severe dehydration => renal failure (hypovolemia)
• DIC
• sepsis
• hypocalcemia, hyperglycemia
• resp. problems
- atelectasis
- pneumonia
- pleural effusion
▪ late
• Pseudocyst
- no epithelial lining: Wall = granulation tissue-> fibroid wall
- complic. of acute or chronic pancreatitis
- doesn’t move with resp. (retroperit.)
- Size of cyst
▪ < 6 cm – small, usually asympt., will resolve on its own
▪ > 6 cm – large, symptomatic, can cause gastric outlet
obstr. or compression of bile ducts
• Palpable, painful
• Mx – if stomach obstr. or bile ducts drainage,
even if < 6 weeks, do drainage into stomach,
duodenum or jejunum
o laparoscopic or laparotomy (depending
on size and surgeon)
- Age of cyst
▪ < 6 wks – fragile wall (only granulation tissue), can
break
• Mx – wait, will probably disappear on its own
▪ > 6 wks – mature, with fibroid capsule, stronger,
resistant wall
• Mx – no matter the size, do drainage
- Dx
▪ best investig: CT scan
• abscess
• pressure on surrounding organs (if inflamed)→ obstruct.
• hemorrhage/ rupture
• Portal V thrombosis
- Chronic pancreatitis
o MC assoc. with alcoholism
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o Sx
▪ pain
o Dx
▪ amylase is N or slightly incr.
▪ some have calcification
o if associated DM -> Rx with low doses of insulin
- Dilatation of gall/ bile ducts
o Dx
▪ first – USG
▪ ERCP - best
▪ MRCP – even better – if available
- Pancreatic CA
o head of pancreas
▪ men
▪ Sx
• Triad: anorexia + wt. loss + jaundice ± epigastric pain
• distended gall bladder, which moves with respiration
• jaundice, pale stools, dark urine (Obstr. jaundice)
• Wt. loss
▪ Dx
• U/S: distended intra and extrahepatic bile ducts
- pancr. duct might be dilated as well
• Urine: conj. bilirubin, no urobilinogen.
• Blood: AST/ALT moderately elevated, incr. total and conj. bilirubin, incr.
ALP

Abdominal pain
o Pancreatitis – Hx of alcoholism or biliary stones
▪ fever + epigastric pain + radiating to back
▪ no abd. signs except for
• Cullen sign
• Gray Turner sign
o Hemorroids – small amounts of painless rectal bleeding
o Anal fissure – small amounts of painFULL rectal bleeding
o Rectal CA – tenesmus + rectal bleeding + alternate bowel habits + wt. loss
o pregnant woman with lower abd pain
▪ I trim – ectopic
▪ II trim – ovarian torsion/ twisted ovarian cyst
▪ III trim – red degeneration of fibroid
o a few wks Hx of postprandial pain = Mesenteric ischemia
Acute mesenteric ischemia Chronic mesenteric ischemia
Hx of atherosclerosis/ AF (irregular pulse)/ digoxin After eating -> abd. pain
Acute abd. pain + tenderness + no bowel sounds
Blood stained stool
o Acute mesenteric ischemia = acute abd. pain + tenderness + irregular pulse + no
bowel sounds = Mesenteric infarction (Afshan)
▪ CAUSES:
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• Mesenteric arterial embolism (often associated with AF).

• Mesenteric arterial thrombosis.
• Decreased mesenteric blood flow (hypotension).
• Mesenteric venous thrombosis.
▪ CLINICAL FEATURES:
• Middle-aged or ELDERLY pt.
• History of vascular disease elsewhere.
• Sudden onset of severe diffuse abdominal pain.
• Severity of pain far exceeds the associated physical signs.
• Associated with vomiting and bloody diarrhoea.
• Abdominal examination: Distension, generalized tenderness, absent
bowel sounds.
• diffuse tenderness and rebound tenderness (diffuse peritonitis)
• maybe - a few wks Hx of postprandial pain = Mesenteric ischemia
• Rectal examination: Fresh rectal blood.
• MCQ: Rx of digoxin (and thiazide) + acute abd. pain + tenderness +
irregular pulse = hypokalemia (with bowel sounds present; no bowel
sounds + PR – dark, blood stained material = Acute mesenteric
ischemia)
▪ Dx
• Angiography to confirm diagnosis
• Metabolic acidosis
• Serum LDH (MCQ)
▪ MANAGEMENT:
• IV infusion of N. saline.
• Refer to Surgical team.
• Poor prognosis.
o Rectus sheath hematoma – common in pregnancy + pain after bouts of cough
▪ rupture of abdominal rectus sheath
• elderly
• Hx of
- coughing due to URTI, TB, bronchitis, asthma
- anticoag therapy
- trauma
- labor
- vigorous and coordinated rectus muscle contr. due to Valsalva
manouvers, coughing, sneezing, straining from constipation,
intercourse
• Sx - severe, sudden, acute abd. pain, guarding and abd. rigidity (due to
bleeding inside peritoneal cavity)
• can cause intest. obstruction
• periumb. echymosis = Cullen sign (same as in acute pancreatitis)
• Dx
- CT
- USG in pregnant lady
• Mx
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- surgery

Dysphagia and oesophageal pathology

o Esophageal rupture (Boerhaave syndrome)
▪ sudden chest pain after prolonged excessive vomiting in alcoholics
• forceful vomiting against a closed epiglottis (trying to withold vomiting)
▪ shock, hT
▪ pleural collection: breath sounds absent on a hemithorax
▪ + subcut. emphysema, pneumo-mediastinum, pneumothorax
▪ Dx
• CT
• then endoscopy – not prior, since it might cause an incomplete tear to
become complete
- Dysphagia
o Esophagitis
▪ causes
• Candida (monilial esoph.)
• reflux
- Rx
▪ PPI – the best
▪ H2- receptor blocker
▪ prokinetic
▪ antacid
▪ lifestyle measures
o Myasthenia gravis
o Plummer-Vinson syndrome = syderopenic dysphagia
▪ dysphagia (esophageal webs) + iron-deficiency anemia + glossitis
▪ risk factor for esophageal SCC CA
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o Parkinson
o Peptic stricture
▪ lower 3rd of esoph.
▪ Cx of reflux oesophagitis
▪ rare today with current treatments
▪ Dx
• Barium swallow
• Endoscopy
▪ Rx
• dilate stricture
• treat reflux
o Globus hystericus = lump in the throat
▪
o Pharyngeal pouch (Zenker’s diverticulum)
▪ post. pharyngeal diverticulum, pushing the esophagus
▪ elderly
▪ Sx
• dysphagia, food regurgitation, gurgling in neck
• coughing immediately after eating (food regurgitated in airways)
• halitosis
• no pain
o Esophageal diverticulum
▪ usually sec. to an underlying motility problems -> sympt. due to primary pbm
▪ hiatal hernia
o Achalasia
▪ Failure of relaxation of lower oesophageal sphincter + ↑muscle tone
▪ women, 30-40 yrs
▪ Sx
• dysphagia for liquids and solids organic, mechanical causes usually have
dysphagia only for solids!)
- if severe: has more difficulty in swallowing liquids than solids
- usually not progressive!
• wt. loss
• regurgitation
- at night
- when lying down
• chest pain, hiccups, aspir. pneumonia
▪ Dx
• 1. Plain X Ray
- air-fluid level behind heart
- absence of gastric air bubble
• 2. Barium swallow
- distended esoph. - S-shaped + narrowing of contarst in barium
swallow = “rat-tail” (not charact.) + fluid level
• 3. Manometry - high tension at lower end of esophagus
• 4. Endoscopy – exclude CA
▪ Cx
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• Stricture
• Esophageal CA
▪ Rx
• Botox inj. – Short term relief
• Drugs:
- Nitrates—relaxes lower esoph. sphincter
- Ca channel blockers
• Pneumatic dilatation – may recur
• Laparoscopic cardiomyotomy (Heller’s myotomy) – the best
o Esophageal CA
▪ Barrett’s esophagus = Premalignant lesion for adeno CA of esoph. = metaplasia
with columnar-lined epithelium in lower 3rd of esophagus + ulcer inside +
stricture (blue book MCQ 3.106) P 250
• due to prolonged reflux
▪ types
• SCC CA
• Adeno CA
▪ Sx
• Triad: fatigue + gradual dysphagia + wt. loss
• severe dysphagia at beginning of meal + painful swallowing + severe
wt. loss
- gradual (increasing) dysphagia initially for solids, then for liquids
• dysphagia + hoarseness of voice = Esoph. CA
▪ Dx
• Barium swallow – apple core
• Endoscopy: narrowing of esophagus + ulcer
- + Biopsy
▪ if initially negative (especially with premalignant
lesion), repeat (MCQ)
Upper GI hemorrhage
o Mortality: 5-10% related to age over 60 years, comorbid disease, shock and coagulopathy.
o CAUSES:
▪ Peptic ulceration: Over 40% of cases.
• 1. Duodenal Ulcer.
• Gastric Ulcer (less common).
▪ Gastric erosions or gastritis.
• Post-alcohol.
• Drug-induced (Salicylates, NSAIDs, steroids).
▪ Mallory-Weiss tear (partial esophageal tear following vomiting or retching).
• bouts of protracted vomiting or cough -> blood
- tear of mucosa at gastroesophagal junction
- self limiting
- Dx – esophagoscopy
▪ 2. Bleeding esophageal or gastric varices associated with portal HTN
• MC in alcoholic cirrhosis
▪ Reflux esophagitis.
▪ Others: Gastric neoplasm, coagulation disorders.
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o PRESENTATIONS:
▪ Hematemesis:
• Fresh red blood.
• Altered blood ‘coffee grounds’.
▪ Melaena.
▪ Collapse and shock.
▪ Syncope and postural hypotension.
▪ Hematochezia (bright red rectal bleeding).
▪ Signs of CLD: Jaundice, bruising, palmar erythema, clubbing, gynecomastia,
spider naevi, hepatomegaly and encephalopathy.
▪ Signs of portal HTN: Splenomegaly and ascites.
o MANAGEMENT: General
▪ High-dose oxygen.
▪ Fluid replacement.
▪ Cross-matched blood if patient is shocked or bleeding is continuing.
▪ Disease specific:
• Peptic ulcer: PPI
- Omeprazole 40-80mg IV followed by and infusion at 8 mg/h.
• Varices: Octreotide 50µg IV(↓portal vessel pressures in bleeding varices)
▪ Urgent endoscopy: to differentiate the cause of bleeding +
• allow injection therapy or banding for varices.
• adrenaline injection in ulcer’s edges
▪ Sangstaken-Blackmore tube
• with 2 balloons
• after being introduced and inflated, it has to be checked every 2 hrs
- did it stop bleeding?
- prevent mucosal ischemia
- Stomach CA
o Risc factors
▪ gastric resection > 25 yrs before (CA on gastric stump)
▪ ↑age (> 40 yrs)
▪ smoking
▪ blood group A
▪ atrophic gastritis
o Male 3:1
o Metastases
▪ left supraclavicular node
▪ ovary – Krukenberg tumor
▪ liver
o Sx
▪ Triad: anorexia + dyspepsia + wt. loss
o Rx - Gastrectomy
▪ Cx
• Dumping syndrome
- types
▪ Early
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• after thick liquids -> fall in BP, abd. distension,

pallor, sweating, diarrhoea
• cause: stomach content is dumped in small
intest. -> blood is attracted in small bowel to
deal with all this food => low BP
• usually disappears on its own
▪ Late
• a lot of insulin is released -> hypoglycemia
- Rx
▪ ↓ carbohydrates in food
▪ avoid very hot or cold foods
▪ add more fiber to diet
▪ surgery – take a loop of small bowel and reverse it ->
its peristaltis (in opposite direction to the rest of the
intestine) will slow down the progression of food
- Gastro-esophageal reflux
o frequent in babies
o usually ceases after solids are introduced in diet
o Cx
▪ Barrett esoph.
▪ esoph. stricture
▪ esophagitis
o Rx
▪ more frequent small feeds
▪ thickening agents
- Functional (non-ulcer) dyspepsia
o ulcer-like
o dysmotility-like
- Gastritis
o burn -> stress -> acute erosive gastritis
o alcohol -> gastric erosions
o after NSAIDs
▪ nonerosive gastritis
▪ superficial gastritis
- Peptic ulcer disease:
o DU:GU = 4:1
o male
o O blood group
o > 2/3 – due to H. pylori
o aspirin, NSAIDs, prednisolone -> GU
o Sx
▪ Burning pain in epigastrium.
• Duodenum
- made worse by fasting (food left the stomach, arrived in
duodenum)
- Relieved to a degree by food or antacids.
• Stomach
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- made worse by food

• Typically episodic.
o Dx
▪ Endoscopy – gold standard
▪ Barium swallow
▪ Serum gastrin – in multiple ulcers
• Zollinger-Ellison syndrome: Gastrinoma (tumor of pancreas or
duodenum) + acid hypersecretion + multiple severe peptic ulcerations in
stomach/ duodenum/ small bowel.
▪ for H. pylori
• biopsy
- + urea breath test -> preferred
- histology – spirochete-like organisms
• serology
• follow up – C13 urea breath test
o Rx
▪ types of drugs
• antacids – neutralize acid secretion
- carbonate: Alka-Seltzer, Maalox tablets, Pepto-Bismol children,
Tums, Rolaids
- Al hydroxide: Maalox liquid, Gaviscon
- Mag hyrdoxide: milk of magnesia, Rolaids
- Bismuth subsalicylate (Pepto-Bismol), bismuth subcitrate (De-Nol)
- Sucralfate
• ↓ acid secretion
- H2-receptor antagonists – Oral use for 8 wks
▪ cimetidine
▪ famotidine
▪ ranitidine
▪ nizatadine
- PPI – for 4 wks
▪ omeprazole
▪ lansoprazole
▪ pantoprazole
• Prostaglandine analogue (to prevent ulcers caused by NSAIDs):
- Misoprostol (also induces labor – abortion)
▪ Tripple therapy
• options – all for 7 days
- 1st line: PPI + clarythromycin + amoxycilin
- 2nd line: PPI + metronidazole + amoxycilin
- 3rd line or if sensitive to penicilin: PPI + clarythromycin +
metronidazole
• > 90% success in 2 wks
• follow up with urea breath test after 6 wks (3 mths?)
• stop PPI at least 2 wks before test, otherwise false negative test
▪ Surgery
• indic.
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- failed Rx after 1 yr
- complic.
▪ uncontrollable bleeding
▪ perforation
▪ pyloric stenosis
- suspicion of malignity in GU
- recurrent ulcer after previous surgery
- + elderly – tolerate less well the blood loss
• types
- GU
▪ partial gastrectomy +
• Billroth I (gastroduodenostomy)
• Billroth II (gastrojejunostomy)
- DU
▪ Vagotomy
• truncal
• highly selective
- Apendicitis
o CLINICAL FEATURES:
▪ Anorexia, nausea, vomiting, diarrhoea or constipation.
▪ Low-grade pyrexia.
▪ Localized abdominal pain: Epigatrium, periumbilical region, RIF.
▪ Tenderness and guarding in RIF.
▪ Rectal examination: To help diagnose a retrocecal or pelvic appendix.
o Typical march of symptoms (J.B Murphy):
▪ Prodromal mild bowel upset.
▪ Development of abdominal pain, which progressively worsens.
▪ Anorexia (key word), nausea, vomiting.
▪ Moderate (not high) fever.
▪ Signs of focal peritonitis over inflammed appendix.
o DIAGNOSIS:
▪ Physical examination: Abdominal auscultation, palpation, percussion.
▪ FBC and Urinalysis: Leukocytosis, rule out UTI.
▪ Pregnancy test: Female adolescents.
▪ USG: Female (doubt and no peritonitis).
▪ CT: For doubtful cases only.
o MANAGEMENT:
▪ Normal saline infusion.
▪ Give gentamicin 5 mg/kg IV, ampicillin 1 g IV and metronidazole 500 mg IV if
rupture is suspected with peritonitis.
▪ Refer to Surgical team.
- Meckel’s diverticulum: (MC presentation is asymptomatic anomaly noted during surgery for
another cause)
o most frequent malformation of gastrointestinal tract
o rule of 2s
▪ 2% population
▪ 2 inches in length
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▪ 2% are symptomatic
• usually discovered during abd. surgery for a different problem
▪ 2 feet from ileo-cecal valve (distal ileum)
▪ age group – 2 yrs
▪ male:female = 2:1
▪ 2 types of ectopic tissue:
• gastric
• pancreatic
o Sx
▪ painless rectal bleeding (not mixed with feces), malena or blood loss anemia
▪ acute/ chronic bleeding
▪ umbilicus fistula
o Dx – Tc99m pertechnetate scan, laparotomy
o Cx
▪ intestinal obstruction
o Rx – surgical resection
- Diverticular disorder (large bleeding not accompanied by fecal mater)
o 90% in descending colon
o due to lack of fibres
o over 40 yrs
o 1/3 people > 60 yrs
o Sx
▪ usually asympt. = diverticulosis
• sometimes - irregular bowel habits, constipation
▪ diverticulits – sympt. (< 10% of people with diverticulosis)
• This follows inflammation of one or more colonic diverticulae.
• LOWER abdominal pain radiating to left iliac fossa + tenderness in LIF
• can occur anywhere (e.g. small bowel)
• Bloody diarrhea
• Sometimes with sudden PROFUSE rectal bleeding (without feces).
• Sx
- triad: acute pain + left-sided irradiation + fever
- Low-grade fever.
- Abdominal tenderness in LIF
- pain increased with walking and change of position
- Guarding on LIF with a palpable mass.
• Complications:
- Perforation.
- Paracolic abscess
- Severe bleeding (elderly).
- Fistula formation (Colovesical fistula + vagina, small bowel).
MCQ 2045 P128.
- Bowel obstruction.
• DIAGNOSIS
- Request an erect CXR if perforation is suspected.
- USG, CT scan – detect fistula or perforation
- Sigmoidscopy
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• Rx
- Commence an IV infusion to treat dehydration or shock.
- Analgesia.
- Antibiotics: Gentamicin, ampicillin and metronidazole.
- Refer to surgical team.
- Profuse rectal bleeding
o diverticular Disease
o angiodysplasia
o ulcerated CA
o IBD
o ischemic colitis
Inflammatory bowel disease (IBD)
Ulcerative colitis Crohn (terminal ileitis) disease
Main Sx Long history of bouts of diarrhea + blood Triad: colicky abd. pain + diarrhoea +
in young adult (15-40 yrs) fever Recurrent diarrhea (with blood
May present as a fulminating attack. and mucus in stools) in a young person
(20-40 yrs) + abd. Pain.
Fever, tachycardia and hypotension. Malaise, wt. Loss. May present acutely
Risk factors: family Hx, previous attacks, with obstruction, perforation or RIF
low-fibre diet pain. CAN MIMIC acute appendicitis.
Site Colon only (begins in rectum, continues All GIT, mouth to anus (terminal ileus),
proximally) lead pipe deformity repeated perianal lesions (abscesses,
fistulas), mouth ulcers – caused from
granulomas (granulomas in Crohn - non-
caseating - and TB - caseating)
½ ileocolic, ¼ - small bowel only, ¼-
colon only
Rectal Rectum always involved Lump in right iliac fossa + rectal changes
(e.g. fistula)
Systemic Wt. loss, fever, lethargy are UNCOMMON Wt. loss, fever, lethargy, etc.
Sx
Lesions The whole colon involvemt but superficial Skip lesions but affecting whole width
mucosal only of intestinal wall. Fine granular mucosa
FBE ESR Incr.
Dx Extensive mucosal ulceration may leave X Ray: Free air associated with
normal mucosal islands (pseudo-polyps) perforation may be seen.
visible on plain film. Stenotic regions are best visualized with
Dilation of the transverse colon > 6 cm Ba follow-through studies or on
indicates presence of toxic megacolon. colonoscopy.
Sigmoidoscopy: granular red proctitis, Sigmoidscopy: Cobblestone appearance
with contact bleeding (patchy mucosal edema) Aphthous
1st Step: Stool culture - exclude a ulceration
gastrointest. Infection Colonoscopy – Dx diff. with UC
CA Colon CA more often, > 7 yrs (colon CA more rare)
100 x incr. risk for adenoCA in affected
portion (terminal ileum)
Extrainte Arthritis, ankylosing spondylitis, sclerosing Arthritis, ankylosing spondylitis,
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st. Sx cholangitis, episcleritis, uveitis, erythema episcleritis, Uveitis, pyoderma

nodosum, pyoderma gangrenosum, gangrenosum, erythema nodosum
recurrent optic neuritis, Vit. B 12 defic. (if
terminal ileum is involved by “backwash
ileitis”, bronchiectasis
Cx Toxic megacolon (Rx – emmergency Fistula, abscess, stricture
surgery) Incr. risk of biliary and renal calculi
Rx Drugs: Drugs:
1. Sulfasalazine (mainstay), mesalazine – Sulfasalazine (mainstay), mesalazine –
more used for UC more used for UC (less useful in Crohn)
C/S – for acute flares C/S – for acute flares
Immunomodef. drugs: Azathioprine, A/B
cyclosporin, methotrexate Immunomodef. drugs: 1. Azathioprine,
Surgery – cured by removal of colon cyclosporin, methotrexate
Surgery – for complications; recurrence
after removal of affected part (50%)
Prognosis Less favorable than for UC
Intestinal obstruction
o triads
▪
with (and without?) Hx of surgery – Adhesions
▪
absolute constipation + without bowel sounds = Obstruction
▪
elder came with PAIN + constipation + abd. distension + bowel sounds present
= Pseudoobstruction = hypokalemia
▪ absolute constipation + with bowel sounds present ± no X Ray given = MC
cause is fecal impaction
▪ MC cause of diarrhoea in a bed-ridden pt = fecal impaction
▪ debut:
• Small bowel obstr. – Pain
• Large bowel obstr. – Constipation, abd. distention
▪ if X Ray:
• Sigmoid volvulus (Inverted U- shaped Loop)
• multiple gas shadows/ haustration
- with Hx of surgery = Adhesions
- without Hx of surgery = Indirect inguinal hernia
o MC cause in Aus.
▪ Small bowel:
• Adhesions (if Hx of surgery)
• Obstructed groin hernia (Indirect)
• Gallstone ileus – with Hx of cholelithiasis + cholecystoduodenal fistula
- with free air in biliary tree on X Ray
▪ Large bowel:
• CA: Large bowel gaseous dilatation with cut off at sigmoid colon
without rectal gas.
• Volvulus
- MC in
▪ Neonates (malrotations)
▪ Young paralized people, bed-ridden
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▪ Bed-ridden elderly people, nursing home pts, chronic

constipation -> stretching -> twisting.
- Dx
▪ X Ray: inverted U, pointing up and right (sigmoid loop)
- Rx
▪ Endoscopic – passing tube beyond the kink
• Fecal impaction
- Dx
▪ X Ray: ground glass appearance (colon stuffed with
solid feces)
- Rx
▪ enemas
▪ manual disimpaction
• Diverticulitis.
• Intussusception.
• Mesenteric Infarction.
• Crohn’s disease.
o Sx
▪ Colicky pain.
• becomes continuous pain in case of strangulation (MCQ)
▪ Periumbilical pain: suggests small bowel origin.
▪ Large bowel obstruction can cause pain anywhere in abdomen.
▪ Strong association with vomiting, constipation and abdominal distention.
▪ Visible peristalsis may be seen.
▪ Tinkling bowel sounds.
▪ Signs of dehydration.
▪ Pain becomes more continuous and generalized if strangulation occurs (MC
with femoral hernia).
▪ Always examine the hernial orifices and perform a rectal examination.

o
o DIAGNOSIS:
▪ Send blood for FBC.
▪ Urea and electrolytes.
▪ Lipase.
▪ Amylase.
▪ Blood sugar levels.
▪ Request erect and supine abdominal X Rays and look for following features:
- SMALL BOWEL OBSTRUCTION - LARGE BOWEL OBSTRUCTION
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- Dilated loops of small bowel. - Dilated large bowel.

- Colon devoid of air. - Peripheral distribution.
- Small bowel is usually central in distribution. - Irregular haustral folds.
- Regular transverse bands extending across - Fecal mass content.
entire diameter of bowel (Valvulae conniventes)
- Multiple fluid levels (>5).
o MANAGEMENT:
▪ Commence an infusion of N saline to correct dehydration from vomiting and
fluid loss into bowel.
• 1. NS before surgery
• 2. Hartmann before surgery
▪ Pass a NG tube.
▪ Analgesia.
▪ Small and large bowel obstr in elderly - gastrografin enema to Dx. diff.
mecanical obstr. (surgery) VS pseudobstr./ perforation.
▪ Refer pt to Surgical team.
- Intestinal pseudo-obstruction (Paralytic ileus)
o Chronic impairment of GI motility
▪ Colon: colonic ileus, Ogilvie syndrome
▪ Small intestine
o Pts affected: mainly elderly and taking tricyclics antidepressants (anticholinergics).
o types
▪ Primary
▪ Sec.
• Scleroderma (esophageal motility is impaired)
• Myxedema
• Amyloidosis
• Muscular dystrophy
• Multiple sclerosis
• Hypokalemia
• Chronic renal failure
• Diabetes mellitus
• Drugs (anticholinergics – in Parkinson, HT medication, opiates)
• After pelvic surgery
• Severe system illness
o Although may involve any part of GI tract, typically presents with colonic distention.
o Dx
▪ X Ray: Gas in bowel all the way to rectum, maximal in cecum (classical
obstruction - no air in rectum).
o Treatment:
▪ Rectal exam. or sigmoidoscopy to attempt deflation
▪ then prokinetics
▪ then colonoscopic decompression
- Perforation of a viscus:
o May occur anywhere in the GI tract.
o Common sites are:
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▪ 1. Peptic ulcer: risk factors.

▪ 2. The appendix.
▪ 3. Colonic diverticulum.
o Can occur de novo.
o CLINICAL FEATURES:
▪ Severe abdominal pain.
▪ Signs of generalized peritonitis with board-like rigidity.
▪ Shock soon supervenes.
o DIAGNOSIS AND MANAGEMENT:
▪ FBC, U&E, blood sugar and lipase/ amylase.
▪ Request an erect CXR:
▪ Look for gas under the diaphragm.
• Seen in over 70% of cases.
o Rx
▪ IV N saline.
▪ Analgesia with morphine 2.5-5 mg.
▪ Pass NG tube.
▪ Commence broad-spectrum antibiotics such as Gentamycin 5 mg/ kg once
daily, Ampicillin 1 g IV q.d.s. and Metronidazole 500 mg IV t.d.s.
▪ Refer the patient immediately to the surgical team.
Colon CA (Stool mixed with blood and mucus in elderly person) MCQ
- colon CA – Murtagh 440
o men > 50 yrs (90% of all cases)
o mortality rate 60%
o incidence
▪ women 1:25 = 0.04
▪ man 1:20 = 0.05
▪ first degree relative - 1:8 = 0.12
o usually arises from an existent adenoma
o 2/3 in descending colon and rectum
o risk factors
▪ Family Hx
▪ Ulcerative colitis
▪ Colonic adenomata
▪ Decr. dietary fibre
▪ Familial
• Familial adenomatous polyposis (FAP)- AD – 100% by 50 yrs
- risk factor for colon CA, duodenal and small bowel CA
- assoc. with retinal pigmentation (need ophthalmo. screening)
- + Gardner’s syndrome = most severe form of FAP
▪ multiple (countless) polyps in colon (predispose to
colon CA) + tum. outside colon (osteoma of skull,
thyroid CA, desmoid tumors of abd. wall, epidermoid
cyst, sebacous cyst, fibroma)
• Lynch Syndrome: Hereditary non-polyposis colorectal CA (HNPCC)
• Rx of FAP: 1.Total colectomy + Ileorectal anastomsis + continuous
endoscopic review of rectal segment.
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2. Total proctocolectomy + ileostomy

▪ other precancerous lesions
• villous adenoma
o Sx:
Right colon Anemia
Dyspepsia
Mass
Left colon Altered bowel movt., Partial obstr.
Pain
Sigmoid Altered bowel movt., Complete obstr.
Rectal bleeding
Rectal Rectal bleeding
Tenesmus (sense of incomplete evacuation)
Mass
▪ triad Murtagh: Rectal bleeding + mucous discharge + change in bowel habits
▪ MCQ: Stool mixed with blood and mucus in elderly person – MC is colon CA
o Screening - new mcq book – p. 101 + Murtagh p. 77 + Alena’s printout
▪ Colon CA screening – Blue book – p.101-102 - > 50 yrs
a. Asymptomatic with no risk factors
a. FOB every 1-2 yrs after 50 yrs or sigmoidocopy.
b. Slightly increased risk (1st or 2nd degree relative ē colon CA after 55 yrs)
a. FOB annualy > 50 yrs or 10 yrs earlier than the family’s earliest
affected relative
b. Sigmoidoscopy every 5 years
c. Moderately increased risk (1. first degree relative with cancer before 55
years or 2. 1st or 2nd degree relatives with colon CA at any age)
a. colonoscopy every 5 years
b. FBO annualy in the intervening years
d. High risk
a. 2 or more 1st or 2nd degree relatives with colon CA < 50 yrs or 3 or
more 1st or 2nd degree relatives with colon CA at at any age
a. Colonoscopy every 2 yrs from 25 yrs
b. Familial adenomatous polyposis (FAP)
a. Annual sigmoidoscopy – from the age of 10
b. Then every 3 years - from the age of 35
c. Lynch Syndrome I: Hereditary nonpolyposis colorectal CA (HNPCC)
autosomal dominant predisposition to colorectal CA
right sided predominance (70% proximal to splenic flexure)
Lynch Syndrome II (HNPCC II) (MCQ) = Colonic Ca + Uretreic CA
same features of Lynch I plus extra-colonic cancers esp.
endometrial carcinoma, carcinoma of ovary
CA of small bowel, stomach, pancreas
transitional cell CA of the ureter and renal pelvis
Dx: Colonoscopy every 1-2 yrs after age of 25
o Dx
▪ Colonoscopy – the best
▪ CT scan – might miss some small tumors
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▪ Not USG
o Duke’s classif.
Stage Extension 5 yr survival
A Mucosa and submucosa 90%
B Muscularis or serosa 75-85%
C Regional lymph nodes 30-40%
D Distant metastases <5%
▪ Duke A – 75% detected with FOB
o Rx
▪ Duke A, B – surgery
• pancolectomy
• paucy surgery
▪ C,D – surgery + radiation
- Peutz-Jehgers – AD = hereditary intestinal polyposis syndr.
o dev. of benign hamartomatous polyps in the GIT -> strong tendency to dev. CA in multiple
sites (breast, liver, pancreas, etc.), while the polyps don’t have malignant tendency
o lowest malignant potential (2%) for colon CA
▪ may undergo malignant transf. into adenocarcinoma
o hyperpigmented (black) macules on the lips and oral mucosa
- Tumors in small bowel – predom. benign
o types
▪ Adenocarcinoma
• 100 x incr. risk in Crohn in the affected portion (distal ileum)
▪ Lymphomas
• terminal ileum
• proximal jejunum – assoc. with celiac dis.
▪ Carcinoids
▪ Familial adenomatous polyposis
• incr. risk of duodenal and small bowel carcinoma
▪ Peutz-Jehgers – hamartomas, may undergo malignant transf. into
adenocarcinoma
- Adenoma with incr. malignant potential (benign tum. of colon)
o villous
o > 2 cm
o multiple
o with dysplasia
- benign villous adenoma
o Sx - clear discharge
o Cx - causing marked electrolyte imbalance = depletion syndrome - prerenal azotemia,
hyponatremia, hypokalemia
Anal pathology
- anal anatomy:
o lower ½ of the anal canal – sensitive, painful
o upper ½ of the anal canal – where the hemorrhoids start from
▪ separated by the dentate line
- Anal fissure
o mid-posterior position (6 o’clock)
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o MC cause of painful rectal bleeding = anal fissure

o Rx
▪ analgezic creams
▪ local nitroglycerine ointment
• SE
- postural hTN
- headaches
▪ Surgery – in recurrent fissure or with fibrosis/ stenosis
▪ Lord’s procedure – 8 finger dilatation of the anus – breaks down all the scar and
inflam. tissue is broken down -> fissure heals
- Perianal abscess and fistula
o blocked anal gland => abscess => fistula – pussy discharge, pain, tenderness
▪ Rx
• Abscess
- Cruciate incision ± A/B
• fistula
- excise the fistulous tract
▪ Cx – fecal incontinance
- Perianal hematoma – lower ½ of the anal canal
o rupture of an external haemorrhoidal vein from horse riding, constipation, homosexuals
o Rx
▪ 1 day – aspirate with wide gauge needle
▪ 1-5 day – incision under local anesthesia (clot already formed),
▪ > 5 days – leave alone except if fever (infected) or severe pain
- Hemorrhoids (bleeding on fecal mater, rather than in faeces)
o 20-50 yrs
o causes:
▪ MC – chronic constipation, lack of dietary fibre
▪ Portal hypertension
o Sx
▪ bleeding with blue red blood (venous blood) on, rather than in, faeces, prolapse,
mucous discharge, itching, incomplete bowel evac.
▪ venous varices starting above the dentate line
▪ Degrees
• I – above dentate line
- only bleeding + itching, mucous leak
• II – prolapse below dentate line – will reduce on its own
- bleeding
• III – prolapse, needs manual reduction
- bleeding
• IV – complicated, can’t be reduced + thrombosis + lots of pain
- strangulated – pain –> refer immediately -> hemorroidectomy
o Mx – Murtagh 361
▪ I degree
• high fiber diet, prevent constipation, laxatives
▪ II-IV? or if profuse bleeding or thrombosed or IV (paul)
• injecting of sclerosing solution -> clotting of hemorroids -> drop off
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- now not so favored

• I. MC -Rubber band ligation (no general anesthesia required) - they clot
and drop off
• II. Cryotherapy
• III. Best – Hemoroidectomy – if severe, recurrent, strangulated
- post-op hot sitz baths – relaxes the spasm of the sphincter
- analgezic - Pethidine
▪ don’t give morphine – causes smooth muscle spasm
- Pilonidal sinus:
o abscess midline, in the natal cleft
o more frequent in Greeks (hairy backs)
o due to hair strand which goes out then goes back in the skin
o in drivers in the army (non-padded car seats)
o Rx
▪ acute – incision & drainage (incision and leave open, not incision and stitch)
• Karydakis – big incision
▪ chronic - excise the abscess
• flatten out the natal cleft
- Chronic constipation in elderly
o Mx
▪ 1st line - Ispagula husk (bulking agent)
▪ 2nd line - lactulose syrup
▪ 3rd line – glycerine suppository
▪ peristaltic stimulants
• docusate (Coloxyl) with senna
• bisacodyl (Durolax)
• Movicol
• Shaw’s cocktail for severe cases
▪ Bulk forming agents
Scrotal swellings and hernias - OK
- Testis size
o 3.5-5.5 cm long
▪ Klinefelter ≤ 2 cm
o 2-3.5cm wide
- Testic. CA – Murtagh 1987
o 15-40 yrs
o Sx
▪ painless lump (15% painful – in late stages usually)
▪ loss of testicular sensation
o Risk factors
▪ Undescended testis (cryptorhidism) – 5x the risk
▪ Orchidopexy
▪ Testic. atrophy
o all solid scrotal lumps are malignant until proven otherwise!
o types
▪ seminoma
• 40%
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• slow growth
• better prognosis: stage 1 - 98% 5 year survival rate
• 90% diagnosed at stage I
• lymphatic spread
- -> retroperit. lymphnodes -> mediastinal -> left cervical with
worst prognosis (eval. with CT)
• tumor markers - normal
- purple book: raised in a large proportion of seminomas?
• sensitive to radiotherapy
• non-sensitive to chemotherapy
▪ non-seminoma (teratoma)
• 60%
• rapid growth
• poorer prognosis: stage 1 - 75% survival at 5 yrs
• 60% Dx at stage I
• tumor markers – markedly incr.
- 1 - alfa fetoprot.
- 2 - beta HCG
• blood stream metastases to liver and lungs
- + lymph. nodes involv.
• sensitive to chemotherapy
o staging
▪ I – only testis
• orchidectomy
▪ II – paraaortic lymphnodes involved (below diaphragm)
• orchidectomy + lymphnode resection
▪ III – lymphnodes above the diaphragm
• radiotherapy or chemotherapy
▪ IV - lungs, liver metastases
• radiotherapy or chemotherapy
o Dx
▪ 1. USG
▪ 2. tumor markers:
• alfa fetoprot.
• beta HCG
- Alpha-fetoprotein (AFP, a-fetoprotein)
▪ In adults, levels over 500 nanograms/milliliter of AFP
are seen in only three situations: Hepatocellular
carcinoma, Germ cell tumors, and metastatic cancer in
the liver originating from other primary tumors
elsewhere.
- Beta HCG (human chorionic gonadotrophin)
▪ raised in testicular cancer
- Carcinoembryonic antigen (CEA)
▪ serum from individuals with colorectal carcinoma,
gastric carcinoma, pancreatic carcinoma, lung
carcinoma and breast carcinoma, as well as individuals
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with medullary thyroid carcinoma, had higher levels of

CEA than healthy individuals.
- AFP alpha1 feto protein
▪ increased in:
• hepatocellular carcinoma
• liver metastatasis from other cancers
• germ cell tumours (e.g. testicular cancer)
- Beta HCG (human chorionic gonadotropin)
▪ secreted also by some cancers including:
• testicular cancer:
o seminoma
o choriocarcinoma
o germ cell tumors
o teratoma with elements of
choriocarcinoma (this is rare)
• islet cell tumor (pancreas)
• hydatidiform mole
▪ for staging: chest X-ray, CT of chest and abd.
▪ no FNAC
o Rx
▪ 1. Bilat. orchidectomy through an inguinal incision
▪ 2.
• seminoma: + radiotherapy and chemotherapy (cisplatinum) for the
lymphnodes
- MCQ blue book p. 488 - large paraaortic lymphnodes:
▪ orchidectomy + chemoradiotherapy for the lymphnodes
with delayed surgical excision of the residual tumor in
nodes
• teratoma: + chemotherapy for relapses
- + lymphnodes disection of if residual mass after chemotherapy
• sometimes can be cured with radio-chemotherapy even when
metastatic
- scrotal lumps - Murtagh – 1084 + 1090
o painless
Clinical signs Position Palpation Transillu Rx
and setting mination
Hydrocele Any age Confined to Smooth, pear-shaped Yes Aspiration
Primary or sec. scrotum Non tender + inj. of
to tumor, inf., Surrounds the Testis impalpable sclerosant
trauma testis agent
Cyst of Asympt. Behind and Smooth and tense Yes Surgical
epididymis Dragging above testis Multilocular excision
(Spermatoc sensation Testis can be Aspiration
ele) palpated + inj. of
Cyst separate from sclerosant
testis agent
Chronic TB, Chlamydia Behind and Firm swelling No
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epididymo- above testis Hard and craggy

orchitis Testis N - can be
palpated
Varicocele Dragging Usually on left Bag of worms or No
discomfort side grapes
Worse when Along the line Testes smaller
standing of spermatic
cord
Above testis
Carcinoma Young men, 20- In body of Enlarged firm testis No
40 testis Can palpate testis
Painless lump May have
Loss of testic hydrocele
sensation
o painful
Torsion Epididymo-orchitis
Age 5-15 yrs Young adults; STI; elderly; due
to inflam. or instrumentation
Onset Usually sudden, can be gradual Gradual
Pain Very severe Moderate
Assoc. Sympt Vomiting, groin pain, abd. pain Fever, dysuria
Scrotum Very tender, testis is high and transverse Swollen, red, tender, tender
(horizontal).There might be small hydrocele. on PR examination
Investig U/S – can do the diff. Dx with Epididymo- Urine culture and microscopy
orchitis (MCQ) PCR, U/S
Tc 99 scan if available < 45 yrs I - Chlamydia, II -
(Technetium) Gonorhea
>45 yrs I - E. coli – MC overall
Rx Emmergical surgical exploration! Bed rest
Surgery within 6 hrs Analgezics
Prognosis: A/B:
6 hrs good, 85% recovery,10 hrs – 20% STI: ceftriaxone + doxycycline
Opposite testis should be fixed by Instrumentation: amoxyclav or
orchidopexy. (even if not affected yet – prone trimethoprim
to torsion as well).
Causative < 45 yrs I - Chlamydia, II –
agent gonorhea >45 yrs I - E. coli –
MC overall
o Get above swelling = no hernia
o Torsion:
▪ There can be previous episodes of pain = self-resolving torsion
▪ MCQ: Scrotal pain after playing soccer 3 hrs – testic. torsion
o Inguinal swelling
▪ Direct inguinal hernia
• above inguinal ligament, doesn’t go to scrotum
▪ Femoral hernia
• Below inguinal ligament, doesn’t go to scrotum
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• Female, after multiple pregnancies or wt. loss

• MC on right side (60%, 40% left).
o Inguino-scrotal swelling
▪ Indirect inguinal hernia
• cough impulse positive
• you can’t get over the swelling (continues towards abd.)
• disappears when lying down
▪ Varicocele (more advanced -> inguinal area)
• disappears/ gets smaller when lying down
• cough impulse negative
o Scrotal swelling:
▪ 1st test = U/S
▪ no biopsy!
o Varicocele:
▪ varicosity of veins in the pampiniform veins
▪ usually left sided = benign
• because:
- right gonadal vein –> inferior vena cava: right varicocele = tumor
compressing (Malignant- RCC).
- left gonadal vein –> left renal vein –> IVC = Benign
▪ but if old person + sudden varicocele = malignant (MC
renal cell CA)
▪ Dragging discomfort
▪ assoc. subfertility / infertility
▪ not assoc. with hernia
▪ disappears in supine position
▪ Mx
• firm fitting underpants
• leave and review
• Rx if symptomatic or infertility = Ligation
▪ Pelvic/ abd. malignancy suspected if newly diagnosed in males -> 40 yrs -> do
U/S
• if sudden thrombus by tumoral cells – see MCQ 2.079
o Epididymo-orchitis:
▪ MC cause of inf.
• Young – Chlamydia
• Old (50 yrs) – E. coli
▪ risk factors
• Chronic prostatitis leads to acute epididymitis
o Orchitis:
▪Acute – mumps
▪Chronic – TB, etc.
o Hydrocele: (presents as swelling which can’t be felt separately from scrotal lump).
▪ In young pts is considered due to testic. CA until proven otherwise!
▪ In old pts can be safely assumed to be of benign origin.
▪ Testis impalpable, Transillumination +ve
• Dx
314

- U/S
- no aspiration (can spread the CA)
▪ in children
• types
- Bilat – usually disappears at 1 yr
- Unilat – tense
▪ Might persist after 1 yr -> 90% will resolve by 18 mths
▪ > 2 yrs -> refer for surgical intervention.
o Cryptorhidism:
▪ 2-4% at full term
▪ 20% in premature babies
▪ 1% at 1 yr
▪ 2/3 are in superf. inguinal pouch – can be palpated
▪ types
• Undescended
• Retractile – can be manipulated into the scrotum
• Ectopic – 5%
• Ascending
▪ risk for
• 1. Torsion
• 2. Testic. CA (seminoma) – 5-10 x incr. risk
• testic. dysplasia
• infertility
• most assoc. with indirect inguinal hernia??
- Hernias – Murtagh 1081
o types
▪ Inguinal
• Direct
- men
- doesn’t go to scrotum
- doesn’t usually strangulate (least often)
- through the post. wall of the inguinal canal, above the inguinal
ligament, above and lateral to pubic tubercle.
• Indirect
- at external inguinal ring, above and medial to pubic tubercle
- cough impulse +ve
- pain referring to testicle
- disappears when lying down, usually reducible
▪ but can strangulate
- if inguinoscrotal -> you can’t get above swelling (continues
toward abd.)
- Dx – Clinical!
▪ Femoral
• below the inguinal ligament, below and lateral to pubic tubercle
• female, after multiple pregnancies or wt. loss
• often irreducible
• most prone to strangulation. So If diagnosed immediate urgery
315

• MC on right side (60%, 40% left)

▪ Epigastric hernia – swelling in middle, between xiphoid and umbilicus
• = linea alba hernia
• MC content = extraperitoneal fat
▪ Paraumbilical hernia
• = Linea alba hernia around umbilicus
▪ Umbilical
• boys, obese women
• feature of classical cretinism
• usually resolves spontaneously
• strangulation is rare
• strapping doesn’t help
• surgery if not resolved after 3 yrs
▪ Diaphragmatic
• Hiatus hernia
- types
▪ Sliding, esophageal – 95%
▪ Rolling, non-sliding, paraesophageal – 5%
• Cx – Esophageal stricture
- causes
▪ Increased pressure within abdomen caused by:
• Heavy lifting or bending over
• Frequent or hard coughing
• Hard sneezing
• Pregnancy and delivery
• Violent vomiting
• Straining with constipation
• Obesity (extra weight pushes down on
abdomen increasing pressure)
• Use of sitting position for defecation
▪ Heredity
▪ Smoking
▪ Drug use, such as cocaine
▪ Stress
▪ Diaphragm weakness
- Sx
▪ usually asympt.
▪ can mimic any pathology
• dull pains in his or her chest
• shortness of breath (caused by the hernia's
effect on the diaphragm)
• heart palpitations (due to irritation of vagus n).
• Pain and discomfort that a pt experiences are
due to the reflux of gastric acid, air or bile
- Dx
▪ X Ray
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▪ Endoscopy
▪ Manometry
- Rx
▪ Antisecretory drugs
• PPI
• H2 receptor blockers
▪ if severe sympt. – surgery: Nissen fundoplication
• prophylactic AB least needed in fundoplication
o Rx
▪ surgical repair
▪ conservative
• truss to control a small inguinal hernia, with a perineal band to control
slipping
• in
- asympt. patients
- associated medical conditions, with significant operative risk
o Sx
▪ Obstruction – w/o any previous abd surgery -> hernias:
• I - femoral
• II - indirect inguinal
• III - direct inguinal
▪ (Obstruction – w/ previous abd surgery
• adhesions!!)
Renal, urinary and male pathology - OK
- Renal function.
o Plasma urea & creatinine
o Most accurate tests: eGFR (new standard) or creatinine clearance test
- Renal failure
o CRF
▪ Def. = GFR < 60 ml/min/1.73m2 for ≥ mths w/ or w/o evidency of kidney dis.
▪ causes
• MC – DM
• HT
• GN
- MC with IgA nephropathy
• Analgesic nephropathy
• Polycystic kidney dis.
• Reflux nephropathy
• Gout
• Drugs:
- Aminoglycosides: Gentamicin, etc.
- Vancomycin
- Tetracyclines
- Cephalosporins - some
- NSAIDs, COX-2 inhibitors
- ACE inh. and AIIRA antagonists
- Lithium
317

▪ Stages – 1-5, based on eGFR

• 1. > 90 (Normal)
• 2. 60-89 – mild
• 3. 30-59 – moderate
• 4. 15-29 – severe
• 5. < 15 – end-stage kidney failure -> requires dialysis or transplantation
▪ Sx
• triad: a/n/v + fatigue + sallow (yellow-brown) skin
• anorexia/ nausea/ vomiting
• tiredness, lethargy
• polyuria with less concentrated urine (can’t concentrate urine)
• normocytic anemia
- due to defic. of erythropoietin
▪ Rx – erythropoietin
▪ Mx
• restrict protein in sympts. of uremia (vomiting, etc.)
• low sodium and potassium
• best way to measure day to day fluid balance = Wt.
• dialysis
- hemodialysis – 2/3
- peritoneal dialysis – 22%
• kidney transplant
o Acute renal failure: ARF
▪ Triad: extreme malaise + anorexia/ nausea/ vomiting + confusion ± oliguria
▪ types – by the cause:
• Prerenal – ischemic
• Postrenal - obstruction
• Kidney (intrinsic)
- GN
- Acute tubular necrosis: ATN- MC cause
▪ Death of tubular cells that form the tubules that
transport urine to the ureters.
▪ Tubular cells continually replace themselves and if the
cause of ATN is removed then recovery is likely. ATN
presents with ARF and is one of the MC causes of ARF.
▪ ATN is classified as a "renal" (i.e. not pre-renal or post-
renal) cause of ARF.
▪ Classification
• Toxic ATN occurs when the tubular cells are
exposed to a toxic substance (nephrotoxic ATN).
o can be caused by free Hb or myoglobin,
by medication such as antibiotics and
cytostatic drugs, or by intoxication
(ethylene glycol, "anti-freeze",
poisons, organic solvents, heavy
metals)
318

• Ischemic ATN occurs when tubular cells don’t

get enough O2, a condition that they are highly
sensitive and susceptible to, due to their very
high metabolism.
o caused when the kidneys are not
sufficiently perfused for a long period of
time (i.e. renal artery stenosis) or
during shock, dehydration.
Hypoperfusion can also be caused by
embolism of the renal arteries.
▪ Diagnosis
• low osmolality, high Na+ in urine (like plasma)
o Dx diff. from reversible ischemic renal
failure: high osmolality and low
sodium in the urine
• FeNA (fractional excretion of sodium) > 3 and
• The presence of "muddy brown casts" of
epithelial cells found in the urine during
urinalysis is pathognomonic for ATN.
• On histopathology, there is usually
tubulorrhexis, that is, localized necrosis of the
epithelial lining in renal tubules, with focal
rupture or loss of basement membrane.
Proximal tubule cells can shed with variable
viability and not be purely "necrotic".
o Toxic ATN is characterized by proximal
tubular epithelium necrosis (no nuclei,
intense eosinophilic homogeneous
cytoplasm, but preserved shape).
Necrotic cells fall into tubular lumen,
obliterating it and determining ARF.
Basement membrane is intact, so
tubular epithelium regeneration is
possible. Glomeruli are not affected.
o Ischemic ATN specifically causes skip
lesions through the tubules.
- renal dis.
Nephrotic syndr. Post streptococcal/ IgA HSP nephritis
Acute glomerulonephrts nephropathy
(at immediate risk of (Nephritic
death from LVF) syndrome)
HTN No Yes – 90% 50% Yes
Hematuria No Yes Yes Yes
Age 2-6 yrs All ages (5-12 – school 10-35 yrs Any age
age)
Edema +++, Generalized ++ - +
319

Protinuria +++ (>3g/ 24hrs) + and oliguria No proteinuria +

Other Sx Hypoalbuminemia, rash, purpura
normal globulins on extensor
Hyperlipidemia, surfaces, abd
hypercholest. pain, arthritis,
intussusception
Renal fc. Ok not OK OK Not OK
Hx of inf Yes – e.g. 2 wks after 1-2 wks after Acute – 1-2 1-3 wks after
an URTI pharyngitis/ skin inf. days after an URTI
(skin barrier delays inf. or during
onset) inf.
Frequency Less common cause of MC cause of
nephritic syndrome nephritic
syndrome
Rx C/S. Renal biopsy (MCD) AntiHTN + Diuretics None
- Hematuria
o types
▪ Microscopic
• joggers & athletes –dipstick +ve: Normal, transient (after intense effort)
▪ Macroscopic
o causes
▪ trauma
▪ hemolysis
▪ GN – Nephritic syndrome (IgA Nephropathy)
• after a recent inf.
▪ CA causes
• Bladder – 70%
- Dx - cystoscopy
• Kidney – 17%
• Ureter – 7%
• Prostate - 5%
o Timing during urination
▪ at the start – urethral injury, prostatic lesion
▪ terminal – bladder pathology
o Massive hematuria – radiation cystitis (cervical CA)
o Pseudohematuria – red urine but no RBCs
▪ causes:
• Factitious/ malingering (Munchausen, morphine addicts – simulating a
renal stone so they can get morphine)
• Anthrocyanins in food (beetroot, berries)
• free Hb = hemoglobinuria
- Rhabdomyolisis
▪ incr. CK + AST, ALT, LDH, CRP
▪ Dx
• Urine dipstick +ve
• Microscopy – No RBCs
320

o e.g. myositis = SE of statins

▪ statins + fibrates = bad
combination -> risk of
myopathy (simvastatin
myopathy)
▪ even worse with erythromycin
– liver enzyme inhibitor
▪ causes rhabdomyolisis
▪ check serum CK and urine
myoglobin.
▪ myoglobinuria/ hemoglobinuria
(not hematuria) – no RBCs on
microscopy.
• Myoglobin – red-black
- GN
o Sx
▪ I. Nephritic syndrome: Edema + HTN + hematuria
• 1. IgA nephopathy
- Nephritic syndrome
- deposition of IgA AB complexes in the glomeruli
- hematuria in young adults which persists for several days
- after 1-2 days of mucosal inf. (URTI, influenza, tonsilitis, etc.)
- rare
▪ renal failure
- Rx – none
• 2. Poststrepto. GN
- MC in Indigenous, after GBS inf. (tonsilitis) or impetigo
- after 7-10 days
- Sx
▪ triad: discolored urine + periorbital edema + oliguria
▪ lethargic, sick child
▪ hematuria, rapid wt. gain, low urinary output,
periorbital edema, HTN
- Dx
▪ urine: hyalin and RBC casts
▪ strepto tests
• ASO titre – only rises after 2-3 wks – doesn’t
exclude the Dx
• Streptolysin test
• Serum complement III – incr.
- Rx
▪ Admit/ bed rest
▪ Fluid restriction
▪ Low protein, low salt and high carbohydrate diet
▪ if HT – antiHT medication + diuretic
▪ Penicillin if swab showed group A strepto beta hemol.
• 3. thin glomerular basement membrane dis.
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• 4. systemic vasculitis
▪ II. Nehprotic syndrome: edema + hypoalbuminemia +proteinuria
• 1-4 yrs
• Sx
- triad: proteinuria + generalised edema + waxy pallor
- proteinuria + dysmorphic hematuria + RBC casts = glomerular
origin
- proteinuria > 3g/ 24 hrs
- generalized gravitational edema (anasarca), ascites, periorbital
puffness
- hypoalbuminemia < 25g/L
- normal BP, No hematuria
• causes
- 1/3: systemic kidney dis. (DM, HBV, malaria, etc.)
- 2/3 (90%): idiopathic nephrotic syndrome
▪ Dx: kidney biopsy
• Minimal change dis. – MC (85%)
o modest if any hematuria
o responds to C/S!
• focal segmental glomerular sclerosis - FSGS =
GN (10-15%)
o frequent in HIV
o = GN
▪ HT
▪ significant hematuria
▪ RBC casts
o no response to prednisolone!
▪ Mx – renal biopsy to conform
the type of lesion
• membranous nephropathy
o hyaline, granulous casts in urine
• membranoprolif. GN
• Rx
- C/S - prednisolone
▪ -> if they fail -> renal biopsy:
• MC
o minimal change nephritis/dis. in
children or
o membranous glomerulonephritis in
adults?
• CA?
▪ III. asympt.
- Proteinuria
o N: < 100 mg/ 24 hrs
o Pathol. > 300 mg/ 24 hrs (> 150 mg/ 24 hrs in adults)
▪ > 1 g/ 24 hrs – serious problem
▪ ≤ 1 g re-examine
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• orthostatic
• fever
• …
o causes
▪ orthostatic
• 5-10%
• adolescents
• usually self-limiting
- can foreshadow serious kidney dis.
▪ DM – Diabetic microalbuminuria
• first sign of DM nepropathy = Kimmelstiel-Wilson lesion (diabetic
glomerulosclerosis)
- UTI
o types
▪ sterile pyuria
▪ asympt. bacteriuria
• treated only
- if recurrent in pregnancy
- if recurrent after sexual intercourse
▪ acute cystitis
• dysuria, urinary frequency
▪ acute pyelonephritis
• loin pain, fever, rigors, nausea, vomiting
• dysuria, urinary frequency
▪ urethral syndrome
• dysuria and frequency, but nothing in the cultures
• e.g. interstitial cystitis
- continuous pain relieved briefly by bladder emptying
- small hemorrhages on distension of the bladder
o Dx
▪ (MCQ recalls: urine sample
• 0-12 mths: suprapub. (SPA)
• 1-3 yrs: catheter
• > 3 yrs: MSU
▪ URINE COLLECTION:
• > 3-4 yrs
- Midstream specimen (MSU)
- Catheter specimen (CSU)
▪ in women with failed MSU
• < 3-4 yrs
- Suprapubic aspirate collection (SPA): Any growth indicates
infection.
▪ Urinary dipstick test: Only a screening test for UTI.
• leucocytes
• nitrites - bacteria
- but not in all the inf. nitrites are present!! (e.g. some Gram-pos.
cocci don’t produce nitrites)
323

▪ Microscopic exam.
• > 5-10 WBCs/ HPF
- = > 5-10 x 106 WBC/ L
• > 8000 WBC/mL in phase-contrast microscopy
▪ Culture
• MC: E. coli + Staph. saprophyticus > 90%
• > 105/ ml (108/ L) in fresh MSU
o Rx
▪ Acute cystitis:
• AB - TG (Alena)
- 1 – Trimethoprim – not in pregnancy
- 2 – Amoxiclave – also in pregnancy
- 3 – Cefalexin – Drug of choice in pregnancy
- 4 – Nitrofurantoin – also in pregnancy
• duration of Rx
- 5 days in women
▪ 10 days if known urinary tract abnormality
▪ MSU – 3 wks later
▪ + make the urine alkaline with sodium citrotartrate
- 14 days in men
▪ + investigate underlying abnormalities, e.g. prostatitis
▪ Acute pyelonephritis
• same AB – use for 10 days
• ciprofloxacin – if resistance
• severe inf. + septicemia: Amoxycillin + Gentamicin – 14 days
▪ in recurrent UTIs after coitus (in women)
• Rx
- A/B before or after each coitus
▪ trimethoprim
▪ nitrofurantoin
- prophylactic coitus-time A/B: as effective as continuous Rx
▪ Pyelonephritis in pregnancy and puerperium
• 2% of women
• when unilat., MC on right side
• anorexia, nausea, vomiting
• cause - due to dilatation and slower emptying of the urinary tract, due
to high progest. in pregnancy
• MC agent is E.coli
▪ Pregnancy
• Cephalexin 500 mg orally 12 hrls for 10 days – class A
• amoxy + clavulanate (500 + 125 mg) 12 hourly for 10 days
- class B in pregnancy (some teratogenicity)
• nitrofurantoin 50 mg orally 6 hourly for 10 days– class A
▪ Children
• Sx
- Non-specific: fever, irritability, poor feeding and vomiting.
324

- Loin or abdominal pain, frequency and dysuria

- MC cause of confusion in elderly.
• 40% of children with UTI have VUR, 27% have scarred kidneys (reflux
nephropathy) and HTN.
- VUR = abnormal (short) insertion of the ureter in the bladder
- Dx
▪ 1st test = U/S
• < 1 yr: U/S
o ± micturating cystouretrhogram (MCU)
▪ also for Dx of posterior urethral
valve
• > 1ys: U/S
▪ Dimercaptosuccinic acid scintigraph – Gold standard
for Dx of kidney scarring + measurement of differential
kidney fc.
• reserved for children with dilating VUR
- Rx
▪ A/B
• child well
o Trimethoprim 4mg/ kg (150mg max) BD
(only tablets generally available) – first
choice OR
o Co-trimoxazole (200/40 mg in 5 ml) 0.5
ml/ kg (20ml max) BD OR
o Cephalexin 15mg/ kg (500mg max) TDS
o All for 1 wk
• Unwell, age under 6 months: Admission!
o Gentamicin 7.5 mg/kg (240 mg) IV daily
+ Benzyl penicillin 50 mg/kg (3g) IV 6
hrly for children over 1 month of age.
• Avoid: Ciprofloxacin & norfloxacin in children
▪ if urinary reflux/ reflux nephropathy
• MCQ: 23 yrs old with proteinuria, enuresis till
13 yrs, her sister had enuresis as well
• Rx
o Prevention of inf. – continuous AB
o surgery for VUR
- Renal CA
o types
▪ Adenocarcinoma
• triad: loin pain + palpable loin mass + hematuria = Adeno -CA
• metast
- liver
- lungs
- brain
- bones
325

• RCC can present as extrarenal manifestation such as bony metastasis (+

continuous fever) or isolated pulmonary metastasis (Cannon ball).
• Dx – CT scan
• Rx – radical nephrectomy
▪ Nephroblastoma – Wilms’ tumor
- Nephroblastoma (Wilms’ tumor) vs. neuroblastoma
Nephroblastoma (Wilms’t) Neuroblastoma
Renal pathology Pathology in sympathetic system (anywhere in the body –
MC in one of adrenal glands)
Fever Fever
Swelling/ mass in abd. Swelling/ mass in abd.
HTN+ Hematuria – 20% -
Less toxic More toxic, miserable, bony pain don’t allow you to touch
them, periorbital ecchymosis
doesn’t cross mid line crosses the midline
Much regular, smooth, firm Irregular, hard, painful
Assoc. with WAGR syndr., MC CA in kids
Beckwith Weidman syndr. Rx – Surgery, intensive chemo and radio therapy, stem cell
(hemihypertrophy of body) transplant, differentiation agent isotretinoin also called
13-Cis-retinoic acid and frequently immunotherapy.
Curable when localised, poor prognosis if advanced.
• Wilms
- 2-3 yrs
- 10% of CA in kids
- Sx
▪ triad: fever of undetermined origin + abdominal mass
+ malaise
▪ HTN+ hematuria - 20%
▪ abd. pain
▪ malaise
- Dx
▪ U/S
▪ CT
- Rx
▪ Nephrectomy + chemotherapy -> very favourable
prognosis if caught early.
• Urothelial tumors
- papillary tumors of urinary transitional epithelium
- incidence incr. progressively from renal pelvis -> bladder
▪ MC type of bladder CA (90%)
- incr. risk
▪ aniline dye industry workers
▪ smoking
- Sx
▪ hematuria
- Rx
326

▪ remove as much of the uroepithelial tissue as possible

• e.g. tumor in the renal pelvis ->
nephroureterectomy (removes a cuff of
bladder at the vesicoureteric orifice as well)
• bladder tumor – partial or complete
cystectomy
- Urethral rupture
o Rx -Ascending urethrogram
- Horseshoe kidney
o risk factor for renal CA
o Cx
▪ temporary urinary obstr. => atypical renal “colic”, with no hematuria
▪ calculus
▪ UTI
- Colovesical fistula
o recurrent UTI (with E. coli) + pneumaturia
o after pelvic abscess or sigmoid diverticulitis
- Gram-negative bacteraemia: after BPH and instrumentation (cystoscopy)
o high fever (e.g. 40 degrees) + rigors
- Renal stone
o <5 mm – pass pontaneously – 90%
Renal pelvis <2.5 cm ESWL
> 2.5 cm PCNL (percutaneous nephrolithotomy)
Ureter upper ½ < 1 cm ESWL
> 1 cm ESWL / PCNL
Lower upper ½ < 1 cm ESWL
> 1 cm ESWL / Endoscopy / Basket removal
Bladder < 3 cm Transurethral lithotomy
> 3 cm Cystotomy
o 20-40 yrs peak age, male:female=3:1
o Risk factors
▪ decr. fluid intake
▪ drugs:
• Lithium
• Antacids
• C/S
• Allopurinol
• Vit. C,D
o Staghorn stones (only calcium based)
▪ causes
• Hypercalcaemia
• Hyperparathyroidism
• Idiopathic hypercalciuria
• Urinary inf. – bact. form the nucleus for the stone
• NOT - hyperuricemia
o types
327

▪ Calcium oxalate 75%

▪ Magnesium phosphate 20%
▪ Urate and xanthine– may be radiolucent
• do serum uric acid estimation
▪ Cysteine
o Sx
▪ pain from loin to groin, waxing and waning
▪ painful hematuria (painless in CA)
▪ ± proteinuria
▪ ± inf.
o Dx
▪ X Ray - first
▪ abdominal CT w/o contrast – best (gold standard)
• pregnant lady – U/S
▪ U/S to evaluate the kidney – pyelonephrosis?
▪ delayed urografic films – for ureteric calculi
▪ serum calcium – exclude hypercalcemia due to hyperparathyroidism
• 3 estimations – to identify pts with intermittent hypercalcaemia
o Mx
▪ if obstruction – treat it first by stenting
▪ if inf. – treat that secondly?
• blue book: p486 – surgery w/o doing urine culture first
▪ then stone removal
o prevention
▪ incr. fluid intake
▪ decr. Na intake
▪ allopurinol – urate stone
▪ thiazide diuretics – oxalate stones
- Renal artery stenosis
o causes
▪ AS - MC
▪ fibrosing stenosis of renal artery (fibromuscular dysplasia)
• young women
• hereditary
• Sx
- severe HT + hypokalemia = hyperaldosteronism
• Dx
- Doppler U/S – best test
- angiography: beaded appearance
- incr. renin levels => secondary hyperaldosteronism
• Rx
- > 50% - renal artery angioplasty
- <50% - low dose aspirin, lipid lowering drugs
o Dx – Doppler U/S
o Cx – sec. HT
- IVP – rarely done now (AMC)
o for anatomical abnormalities of kidney and urinary tract
328

▪ horshoe kidney
▪ polycystic kidney
• bilat. large kidneys, with multiple cysts
• Sx
- renal pain
- hematuria
- UTI
- progressive renal impairment
▪ hydronephrosis
o trauma of kidney
- 1 kidney smaller than the other
o causes
▪ normal
▪ hypofc. kidney
o Dx. diff
▪ Doppler U/S – blood flow
▪ renal isotope scan – renal fc.
- Urinary retention
o acute – BPH
▪ painful
o chronic
▪ painless
- Acute urinary retention
o PREDISPOSING FACTORS:
▪ Prostatic hypertrophy.
▪ Urethral stricture.
▪ Bladder neck obstruction by fecal loading or pelvic mass
▪ Pelvic neoplasm.
▪ Anticholinergic drugs.
▪ Pregnancy.
▪ Local painful conditions such as genital herpes.
▪ Neurogenic: Multiple sclerosis.
o often precipitated by extreme cold or alcohol
o CLINICAL FEATURES:
▪ Enlarged bladder is easily palpable.
▪ Dull to percussion.
▪ Painful.
o Dx
▪ Rectal examination:
• assess perineal sensation.
• empty any fecal impaction
▪ Examine leg reflexes in all patients. – neurol. cause?
▪ catheterisation to relieve obstruction
▪ if drug induced -> drug withdrawal + catheterisation for 48 h
▪ give a trial of prazosin -> if it works, use it as a long term Rx for BPH
- Urinary ret. in women
o causes
329

▪ spinal tumor
▪ fibroid
▪ vaginal herpes
▪ enlarged retroverted uterus
▪ NOT - HPV
- Urinary schistosomiasis (bilharziasis)
o small trematode flat worm – Schistosoma sp.
o endemic in Egypt
o UTI (cystitis) + terminal haematuria in a male patient from Egypt
▪ + haemospermia
o primary inf. transm. from water - “swimmer’s itch”
o worms live in vesical veins or intestinal veins
o chronic hepatitis, fibrosis, cirrhosis
o Dx - urine microscopy
o Rx - praziquantel
Male pathology
- ED – Murtagh 1120
o causes
▪ psychosocial – young
▪ elderly
• DM
• hyperlip.
- Premature ejaculation
o persistent or recurrent ejaculation before, on or shortly after penetration
▪ time from penetration to ejaculation < 2 min
o MC male sexual dysfc.
o MC cause = performance anxiety
o can be
▪ primary – since beginning of sexual life
▪ sec. – developed later
o Rx
▪ short term
• topical anesthetics
- lignocaine 2.5% + pilocaine 2.5% cream to glans penis ½ hr
before intercourse
▪ long term
• SSRI (fluoxetine, sertraline, paroxetine) + clomipramine => relieve
anxiety
- 3-5 hrs before intercourse
• squeeze technique no longer advised
- Balanitis
o inflam. of glans penis + foreskin
o MC – candida
o children – wet nappies
o adults – immunocompromised people, DM
o Sx
▪ saline bath
330

▪ topical C/S
▪ topical nystatin
▪ topical myconazol
- balanitis xerotic obliterans
o thickening of the foreskin + skin pallor
o Sx
▪ topical C/S
▪ circumcision
- Prostate CA
o 80% at 80 yrs
o risk factors
▪ 1. age > 75 yrs
▪ 2. relative Dx with prostate CA < 60 yrs – most important!
• family Hx is responsible for 5-10% of cases
o MC CA in men
o structure
▪ central/ transitional -> BPH
▪ periph. -> CA
• peripheral -> doesn’t usually give urinary sympt. (like BPH or prostatitis -
central)
o metastases
▪ lymphatic -> pelvic nodes (not groin)
▪ blood
• Osteosclerotic mets in the bones: Pelvis, spine
o CA that doesn’t metastasize to brain = Prostate
o Sx
▪ obstruction
▪ acute retention
▪ back pain
▪ hematuria, uremia – 5%
o Dx
▪ screening – controversial
• PR
- signs of CA:
▪ Hard lump
▪ Asymmetry/ irregular
▪ Induration
▪ Loss of median sulcus
• PSA:
• can be elevated without cancer (e.g. BPH, exercise, infection,
instrumentation, recent ejaculation)
• must be tested with DRE is prostate specific, not prostate cancer specific
• No PSA testing over age 70
- > 10 ng/ mL suggestive of prostate CA
▪ > 20 – most probably advanced CA with mets
- 4-10- prostatitis, benign hypertrophy
- Normal < 4
331

• Serum acid phosphatase – PSA is preferred

• Men considering a PSA should be informed about benefits/ harms of
testing.
• Men with an average risk whowant regular testing after being informed
of the benefits and harms should be offered PSA testing every 2 yrs from
age 50-69. If total PSA concentration is > 3ng/mL then further
investigation (core biopsy) should be offered.
• Men over 70 who have been informed of benefits and harms of testing
and who wish to start or continue regular testing should be informed
that the harms of PSA testing may be greater than benefits of testing in
their age group.
• Men with a father or one brother who has been diagnosed with prostate
cancer has 2.5 – 3 times higher than average risk of developing the
disease. If these men have decided to undergo regular testing after being
informed of the benefits and harms, they should be offered PSA testing
every 2 years from age 45 to 69.
• Men with a father and two or more brothers who have been diagnosed
with prostate cancer have at least 9 to 10 times higher than average risk
of developing the disease. If these men have decided to undergo regular
testing after being informed of the benefits and harms, they should be
offered PSA testing every 2 years from age 40 to 69.
• Mortality benefit due to an early diagnosis of prostate cancer due to PSA
testing isn’t seen within less than 6-7 years of testing so PSA testing isn’t
recommended for men who are unlikely to live another 7 years (subject
to health status).
• A PSA testing decision aid for men and their doctors is under
• Plz see MCQS on prostate in recalls
▪ biopsy
• transurethral
• transrectal
Gleason score – 2 specimens, score of 1-5 -> combined score = 2-
10.
Gleason score Threat from cancer
2–4 Low
5–6 Moderate
7 Intermediate
- 8–10 High
- e.g. 5% undiff. cells – do nothing; decision is made on clinical
basis + Gleason score.
o Rx
▪ Do nothing – in elderly > 70 yrs (monitor, “watchful waiting”) Active surveillance
▪ Gleason based Rx
2- 4 …. Radical prostatectomy
5-7 ——- EBR
8-10 ——— Androgen ablation
▪
▪ Organ-confined dis. (early) T1 and T2
332

• Radical prostatectomy: (removal of entire prostate + Seminal vesicles ±

plevic lymphadenectomy)- Good cure rate
- indic. < 70 yrs, PSA < 20
- Cx
▪ ED – 70%
▪ Urinary incontinence – 10%
▪ Locally advanced dis. (organ involved + capsule invasion or seminal vesicles)
T3a Extra capsular extension, T3b Invasion of seminal vesicle , T4 external
sphincter involved.
OR old debilitated patient
• 2 mths of androgen (antiandrogens) deprivation to suppress gland, then
• External beam radiotherapy (EBR)
- Cx
▪ ED – after 2 yrs
▪ radiation proctitis – fecal urgency, diarrhea
▪ Metastatic disease: (Radical prostatectomy CI)
• androgen deprivation Rx (palliative) – 95% from testicle, 5% from
adrenal glands
- Bilat. orchidectomy – Gold standard in sp inal mets
▪ if spinal cord compression – Orchidectomy -> androgen
deprivation (ketoconazole) -> metastases stop growing
- Antiandrogenic tablets
▪ cyproterone acetate
▪ flutamide
- Exogenous estrogen: Block androgen metabolism at several
levels
▪ Stilboestrol
• SE – Cardiac failure
- LHRH and LHRH analogues (goserelin) SC – MC used now due to
decr. complic.
- Hormonal
▪ Ketoconazole -> “medical” orchidectomy and
adrenalectomy
▪ Glucocorticoid
- Benign prostate hypertrophy
o Sx
▪ acute on chronic urine retention
▪ bladder outlet obstruction:
• triad: poor urine flow + straining to void + frequency
▪ voiding flow rate < 10-15 mL/sec
o Cx
▪ retention
▪ UTI
▪ calculus formation
▪ uremia
o Rx
▪ acute retention
333

• 1. urethral catheter
• 2. suprapubic drainage if 1 fails
▪ drugs
• alpha blocking drugs (inh. contr. of muscle in bladder neck and urethra)
- phenoxybenzamine
- prazosin
- terazosin
• 5-alpha-reductase inhibitors (reduce prostatic volume)
- finasteride
▪ surgery
• indic.
- renal failure
- upper tract dil.
- retention
- bladder stones
• methods:
- TURP
▪ Cx
• retrograde ejaculation - MC
• ED – 5%
- laser ablation
- transurethral incision of prostate (TUIP) – for small glands
- open prostatectomy – less used these days (<1%)
- Prostatitis
o Sx:
▪ triad: dysuria + fever + perineal pain
▪ PR: very tender prostate, swollen, firm
o Rx:
▪ Amoxycillin + gentamicin
Electrolytes, ABG, dehydration, burns - OK
- Electrolyte disorders
o K
▪ Normal: 3.5-5 mmol/l
▪ usually intracellular
▪ hyperkalemia
• MC electrolyte disorder associated with cardiac arrest.
• CAUSES:
- ↑ K intake: banana, low fat milk, beans, sweat potato.
- Increased production – when cellular membranes are ruptured!
▪ e.g. Rhabdomyolisis, burns, ischemia, hemolysis.
- ↓ renal excretion: Acute and chronic renal failure, Addison’s
disease, hypoaldosteronism, drugs (K⁺ sparing diuretics –
Spironolactone, amiloride; ACE inhibitors and AIIRA, NSAIDs).
- Transcellular compartmental shift: acidosis, hyperglycemia, low
insulin, digoxin poisoning, β blockers
▪ Drugs:
• Digoxin
334

• Indomethacin
• IV Benzyl penicillin (contains K)!
• Sx
- Weakness, ascending paralysis, loss of deep tendon reflexes and
respiratory failure
• types:
- MILD: 5-6 mmol/L
- MODERATE: 6-7 mmol/L
- SEVERE: more than 7 mmol/L - ECG changes:
▪ (5.5-6.5mmol/L) Tall, peaked T waves.
▪ (6.5-7.5 mmol/l) Prolonged PR interval with flattened P
waves.
▪ ST segment depression.
▪ (7-8 mmol/L) - QRS widening, absent P waves and
sinusoidal wave pattern.
▪ VT, VF, PEA and (> 8 mmol/L) asystole
- MANAGEMENT:
▪ SEVERE:
• Immediate cardioprotection: 10% Ca gluconate
• Other therapies to shift K into cells, and
eliminate potassium from body (IV insluin &
loop diuretics)
▪ MODERATE:
• Shift K intracellularly with 10% dextrose 500 ml
IV/ glucose ē 25 units of insulin over 20 min
• 8.4% Sod bicarbonate 20 ml IV over 5 min
• Salbutamol 5-10 mg nebulized
• + cation exchanging enema while waiting for
dialysis
▪ MILD:
• Remove potassium from the body with:
o Furosemide 40-80 mg IV
o Potassium-exchange resin orally or
enema
▪ Hypokalemia
• ↑ incidence of cardiac arrhythmias esp. if pre-existing heart disease.
• CAUSES:
- Inadequate intake of K, e.g. Alcoholism, Starvation.
- Abnormal GIT losses: Vomiting, diarrhoea, laxative abuse
- Abnormal renal losses: Cushing syndrome, ectopic ACTH
production, hyperaldosteronism, diuretics and steroids.
- Compartmental shift: Metabolic alkalosis, insulin.
• types
- normal - Potassium levels less than 3.5 mmol/L
- SEVERE: L.
• CLINICAL FEATURES:
- muscle weakness, fatigue, leg cramps and constipation.
335

- Polydipsia, polyuria, rhabdomyolisis, ascending paralysis and

respiratory failure
• MCQ: Rx of digoxin (and thiazide) + acute abd. pain + tenderness +
irregular pulse = hypokalemia (with bowel sounds present: no bowel
sounds = acute mesenteric ischemia)
• ECG changes:
- Broad and flat P
- Mild – T waves merging with the the U-waves
- Flat or inverted T waves, prominent U waves.
- QT prolongation
- Prolonged PR interval.
- Ventricular arrhythmias, including Torsades de Pointes
(polymorphic VT) -> VF -> death
• MANAGEMENT:
- Immediate replacement: Serum K below 3.0 mmol/L or 3.0-3.5
mmol/L in patients with CHF, MI.
- Give K 10-20 mmol/h, DO NOT exceed 40 mmol/h.
- Change to oral supplements when K is above 3.5 mmol/L.
- Amit:
▪ > 2.5 or asympt.
• give oral K
▪ < 2.5 or sympt.
• give iv K
o Na+
▪ Normal: 130-145 mmol/l
▪ usually extracellular
▪ Hypernatraemia:
• Serum sodium level > 145mmol/L.
• CAUSES:
- Decreased fluid intake with normal fluid loss: Inability to
communicate water needs (CVA, infants, intubated pts).
- Hypotonic fluid loss with water loss in excess: Excessive sweating,
dermal burns, gastrointestinal loss, renal loss (diabetes
insipidus).
- Increased salt load: Hyperaldosteronism, ingestion of salt tablets,
administration of hypertonic saline.
• CLINICAL FEATURES: neurological
- Increased thirst, weakness, lethargy, irritability.
- Altered mental status, ataxia, tremor and focal neurological
signs.
- Seizures and coma.
• MANAGEMENT:
- High-flow oxygen.
- Fluid replacement
- Hypovolemic pts: IV normal saline without causing too rapid
reduction in serum sodium.
- Aim to reduce the sodium
336

▪ Hyponatraemia
• Serum sodium level < 130 mmol/L
• Clinical Features: The more rapid the fall the greater the symptoms:
- >125 mmol/L: usually asymptomatic.
- 115-125 mmol/L: lethargy, weakness, ataxia and vomiting.
- <115 mmol/L: confusion, headache, convulsions and coma.
- PSEUDOHYPONATREMIA - Associated with hyperglycaemia,
(hyper osmolar hyponatremia) hyperlipidemia, hyperproteinemia, azotemia.

- HYPOVOLAEMIC - Diuretics, Addison’s disease, vomiting,

HYPONATRAEMIA diarrhoea, pancreatitis.

- NORMOVOLEMIC - SIADH: due to head injury, lung cancer

HYPONATREMIA (paraneoplastic syndrome), meningoencephalitis,
CVA, pneumonia.
- Hypotonic fluids such 5% dextrose only, tea
and toast diet, psychogenic Polydipsia.
- HYPERVOLEMIC - CCF, cirrhosis, nephrotic syndrome, CRF.
HYPONATREMIA (Dilutional,
Hypo-osmolar hyponatremia)
• MANAGEMENT:
- Treat underlying medical condition.
- Aim to increase serum sodium gradually by 0.5 mmol/L /hr to a
maxim. rate of 12 mmol/L / 24 hours.
- Neurological symptoms (brain edema): 3% hypertonic saline,
20% hypertonic saline.
- if significant hyponatraemia: fluid restriction – 1.5 l (same as in
CHF)
- Osmolality (blood, urine) = 2Na + glucose + urea
o serum normal value: 275-300
o urine normal value: 500-800
o SIADH (incr. ADH) and diabetes insipidus (low ADH):
▪ Opposite effects, affect water only (not electrolyte)
▪ Hyponatraemia
▪ SIADH – common post-op.
• self-limited
• Rx – vasopressin (naso-spray)?
Serum Na Serum Urine Na Urine
osmolality osmolality
SIADH Decr. Decr. Very incr. Very incr.
Diabetes insipidus Incr. Incr. Very decr. Very decr.
Water intox. (psychotics – they Decr. Decr. Normal Normal
don’t do polyuria but intox.)
Renal failure: oliguria, incr. K Incr.

- Zinc deficiency
o after prolonged IV fluid admin.
337

o Zn = component of coenzymes involved in wound healing

o Sx
▪ exanthematous dermatitis
- Copper defic.
o anaemia, neutropenia
o bone demin.
- Cobalt defic.
o vit. B12 defic.
- Magnesium defic.
o vit. K-defic. syndrome
o => bleeding tendency
ABGs
- ABG – Oxford 684
o pH = 7.35-7.45
o PaCO2 = 35-45 mmHg
o HCO3 = 22-26 (24-28) mmol/L (~25)
o Anion gap: (Na+K) – (Cl- + HCO3-)
▪ Normal: 8-16 (7-14, 10-12)
▪ Na+ normal: 130-145 mmol/L
▪ K+ normal: 3.5-5 mmol/L
▪ Cl- normal: 95-107 mmol/L
▪ HCO3- 22-26 (24-28) mmol/L (~25)
pH CO2 (acidic) HCO3- (alkaline) Conditions
Resp. acidosis Decr. Incr. Incr. (chronic - to Hypoventil., muscle
(retention) compensate) or N relaxants, myasthenia
(acute) gravis, CNS causes (head
injury), lungs disease
(asthma, COPD - MC
Resp. alkalosis Incr. Decr. Decr. (chronic - to Hyperventil. (CO2
compensate) or N washout), aspirin intox.
(acute)
Metab. acidosis Decr. Decr. Decr a. with increased anion gap
(chronic - to (incr. acids):
compensate) lactic acid: shock, inf.,
or N (acute) lactic acidosis – tissue
ischemia
urate: chronic renal failure
ketone: DM, alcohol
- drugs: salicylates,
biguanides, ethylene glycol,
methanol
b. with normal anion gap
(hyperelim. of HCO3, Cl is
retained):
diarrhoea, pancr. fistula,
post-op in surgical
anastomoses, renal tubular
acidosis (acute renal
failure), Addison’s dis.
338

Metab. Incr. ↑(chronic to Incr. Vomiting (loss of HCl)

alkalosis compensate) Diuretics (hypokalemia)
or N (acute) Burns
Resp. acidosis Slightly Incr. Very incr.
with metabolic low or
compensation N
Chronic resp. COPD who develops
acidosis with diarrhoea due to viral
superimposed gastroenteritis
metabolic
acidosis (to
lower plasma
HCO3)
Acute resp. Vomiting due to theophyline
acidosis with toxicity, who then develops
superimposed acute asthmatic attact
metabolic
alkalosis
o Analysis methods
▪ oxford
• pH – acidosis/ alkalosis
• look at CO2 – CO2 keeps up with pH = resp.
▪ Ekatorina
• pH – acidosis/ alkalosis
• if all up or down = metabolic
o patterns
▪ pH 7.38, pC02 = 28, HCO3 = 14 – compensated metab. acidosis
▪ pH 7.28, pC02 = 28, HCO3 = 14 – decompensated metab. acidosis (lung couldn’t
compensate)
Dehydration and burns
- Fluid compartments
o intracel.
o extracel.
▪ intravasc. - blood
▪ interstitial
▪ third space: peritoneal cav., pleural cav.
- Rehydration:
o child with pyloric stenosis – 1/2 normal saline + 5% dextrose
o post-op – NS + dextrose
o burns, intestinal obstruction – Hartmann
o otherwise – normal saline
- physiopathol. classif.
o extracel. fluid deficit
▪ types:
• hyponatraemic type of dehydration
- electrolytes lost: salt depletion > water depletion
- e. (sun stroke, sweating), excessive diuretics usage
- BP is very decr.
339

• isonatraemic (relative Na+ remains the same) – water depletion is

proportional to the Na depletion
- vomiting, diarrhoea, DKA
- BP is decr.
o intracel. fluid deficit
▪ hypernatraemic type
▪ water depletion > salt depletion => relative increase of Na+
▪ e.g. fever (less sweating, rather perspiration), diabetes insipidus, insufic. water
intake
▪ BP is moderately decr.
Fluids & blood transfusion - Amit
o Crystalloids = water + solvents
▪ Ringer Lactate and Hartmann’s solution
• has Na, CL, K, Ca, lactate
• lactate metab. in liver -> releases bicarbonate -> alkaline
• slightly hypotonic
• for:
- burns
- intest. obstr.
- metabolic acidosis
- diarrhoea (causes met. acidosis, HCO3- lost; vomiting causes
met. alkalosis – HCl lost)
▪ Normal Saline (0.9% NaCL)
• 150 mmol Na + 150 mmol Cl
• isotonic
• for everything else
▪ 0.18% normal saline in 4% dextrose
• 30 mmol Na + 30 mmol Cl
• only in absence of 0.9% normal saline
- need 3 times the amount (at least 90 mmol needed)
▪ 5% dextrose
• isotonic
• defficit of water alone
- fever
- absence of water intake
- post-op
- DKA
▪ 50% dextrose – only in hypoglycemia
▪ Hypertonic saline
• for hyponatraemia, pulm. & cerebral oedema
o Colloids (plasma expanders) = polymers
▪ Dextrans
• not very good for blood
- interfere with blood grouping and cross matching
- can cause anaphylaxis
- interfere with platelet fc.
• used when you don’t have other options
340

▪ Gelatins (3.5%)
• no serious SE
• very common in use
• 2 hr of plasma expanding properties
▪ Hydroxyethyl starch – very good but also very expensive
• 6%, 10%
• no complic
• 4 hr of plasma expanding properties
• best solution in severe hypovolemia
▪ Albumin – 5%, 25%
• hypoalbuminemia: burns, malignancies, cirrosis, ascitis, etc.
o Blood components
▪ RBC (packed cells)
• indic. when volume replacement is not the issue
- e.g. Hb = 6.0
▪ FFP
• indic. in warfarin toxicity, advanced liver disease (causing
coagulopathy), antithrombin III deficiency
▪ Platelet concentrates
• the only ones that can be stored at room temp.
• can also be stored as powder
• but usually a solution
• indic. – thrombocytopenia
▪ Cryoprecipitate – contain fact. VIII , XIII, von Willebrand factor & fibrinogen
• indic. – Von Willebrand dis., hemophilia
- Blood transfusion
o 1 unit = 450 ml
o before – compatib. test
▪ ABO -> blood group
▪ Rh typing -> test with Anti-D AB, (RH + or -)
▪ cross matching – check other AB
▪ AB screening for other diseases (HBV, etc.)
o Cx
▪ Allergic reaction: itching, shivering, rigors, rash, anaphylactic shock
▪ hemolytic reaction:
• acute
- ABO incompat.
▪ MC cause – human error
▪ intravascular hemolysis: hemoglobinuria (acute RF)
• delayed
- Rh incompat.
▪ extravascular hemolysis
▪ Dx – Coombs test
▪ inf.
• HCV
• HIV
• CMV – MC inf. in organ transplant
341

• Epstein Barr v.
▪ metab.
• hyperkalemia (cellular destruction)
• hypocalcemia
• acid-base abnormalities
▪ coag. problems
• dilutional coagulopathy – dilutional thrombocytopenia
e.g. in massive blood transfusion: > 5 l in 24 hrs
- dilutional coagulopathy – dilutional thrombocytopenia
- DIC
▪ hypothermia
▪ immune suppression
▪ tissue hypoxia
- Blood loss
o 5-10% body can compensate
o > 20% - body can’t compensate anymore
o 30% = clinical shock (loss of 1.5-2l)
- Dehydration assessment – see printout from Afshan
o most specific indicator = lethargic and irritable (nervous system affected)
o water content by age group
▪ 12 wks fetus – 90 % water, 55% is extracel. fluid
▪ newborn – 80%, 40 % extracel.
▪ 12 mths – 60%, 25% extracel.
▪ adult – 60%, 20% extracel.
o clinical classif.
▪ mild
▪ moderate
▪ severe
% of body wt. loss Clinical
Mild 4 Dry mucosa
(70 kg man lost 3 L) (<5) Thirst
HTN, tachycardia
capil. refil > 2 sec (N < 2 sec)
Decr. skin turgor
Moderate 5-8 adults Dry mucosa, firm dry tongue, sunken eyes, decr.
(lost 4-6 L) 4-6% children skin turgor
Have to admit him! (5-10) capil. refil > 2 sec
Tachycardia
Oliguria (<0.5 ml / kg / hr)
(Normal 1 ml / kg / hr)
Orthostatic HTN
(keep the pt standing 5 min – systolic BP drops >
15-20 mm) Depreesed fontanelle in Child
Severe 8-10 Dry mucosa
(lost 7 L) > 7% children Thirst
(>10) capil. refil > 2 sec
Decr. skin turgor
342

Tachycardia
Oliguria (<0.5 ml/ kg/ hr)
(Normal 1 ml/ kg/ hr)
hT
Cardiovasc. collapse
- Dehydration - Afshan
o Mild < 5%
▪ no clinical signs, only thirst
▪ (deficit: 50 ml/ kg)
o Moderate 5-9%
▪ loss of skin turgor
▪ sunken eyes
▪ dry mucous membranes
▪ no tears
▪ depressed fontanelle in children
o Severe ≥ 10%
▪ circ. failure, shock
• hT
• tachycardia
• cold and clammy skin
• oliguria (< 0.5 ml/ kg/ hr)
• capil. refil > 2 sec (N < 2 sec)
▪ lethargy or irritability
▪ (deficit: 100ml/ kg)
- I. Hypovolemia
o e.g. 1: 1 yr old child, 10 kg,10% dehydration and shock
o e.g. 2: 20 yrs old man, 50 kg, 7% loss
o I. Maintenance/ongoing losses: (replacement of fluid)
▪ Infant, child < 5 yrs (Maria, Afshan)
• 0-3 mths: 120 ml/kg/24h
• 4-12 mths: 100 ml/kg/24h
• >12 mths: 80 ml/kg/24h
• e.g.1: 100 x 10 = 1000 ml / 24 hrs for the child
• (Amit- by body weight
- first 10 kg: 100 ml/ kg/ 24 hrs
- 11-20 kg: 75 ml/ kg/ 24 hrs
- > 20 kg: 50 ml/ kg/ 24 hrs
- e.g.1: 100 x 10 = 1000 ml/ 24 hrs) = Maintenance fluid
▪ Adult, child > 5 yrs (Amit, Maria)
- In eg, 2 of an adult of 50 kg.
- first 10 kg: 100 ml/ kg/ 24 hrs = 1000ml
- 10-20 kg: 50 ml/kg/24 hrs = 500ml
- > 20 kg: 20 ml/ kg/ 24 hrs = 600ml
- e.g. 2: 1000 + 500 + 600 = 2100 ml/ 24 hrs = Maintenance fluid
o II. Estimation of volume deficit (fluid loss due to dehydration)
▪ 5%
▪ 5-10%
343

▪ > 10%
o % Dehydration x body weight in kg x 10 in ml
▪ e.g. 1: 10 % x 10 kg x 10 = 1000 ml/ 24 hrs child
▪ e.g.2: deficit: 50 x 7 x 10 = 3500 ml/ 24 hrs man
o e.g. 1: total fluid to give: 1000 + 1000 = 2 L
o e.g.2: total fluid to give: 2100 + 3500 = 5600 ml
o steps:
▪ I. if severe dehydration with shock:
initial bolus – 20 ml/ kg of NS
• if still in shock, repeat with another 20 ml/ kg of NS
- e.g.1: 20 x 10 = 200 ml bolus, repeated one more time if needed
- e.g.2: 20 x 50 = 1000 ml bolus
▪ II. give half of the amount in the first 8 hrs (Amit)
• e.g.1: 2000/ 2 =1000 – 200 bolus = 800 ml
• e.g.2: 5600/ 2 = 2800 – 1000 bolus = 1800 ml
▪ III. Give the rest in remaining 16 hrs
• e.g.1: 1000 ml
• e.g.2: 2800 ml
▪ (II. Afshan - give more in the first 6 hrs
• 100 ml/kg in infants
- 100 x 10 = 1 L in the first 6 hrs – 200 ml bolus = 800 ml after the
initial bolus in the first 6 hrs
• 50 ml/kg in adults
▪ III. give the rest in the remaining 18 hrs
• 2L – 200 ml bolus – 800 ml = 1 L in the remaining 18 hrs of the first day )
- II. Intraop. fluid management - Amit
o 4-2-1 formula
▪ e.g. 50 kg patient
• up to 10 kg body wt. 4ml/kg/hr = 40
• 10-20 kg 2 ml/kg/hr = 20
• 20-50 kg 1 ml/kg/hr = 30
- total 90 ml/hr
- III. post-op rehydration (especially in abd. surgery)
o always 3 L daily requirements for adult
▪ 2 L NS + 1 L dextrose
o + losses, divided between normal saline and dextrose, based on the patient (he doesn’t
eat -> give more dextrose, etc.)
o + 70-90 ml of K
▪ e.g. blood loss of 2L + hypokalemia -> 3L normal saline + 2L 5% dextrose + 100
ml K
- IV. Burns
o rehydration: 2-4 ml / kg / % burned in the first 24 h + maintenance fluids
▪ 50% in the first 8 hrs
▪ 50 % in the other 16 hrs
▪ using ½ Hartman solution (with K+) and ½ NS
o minimum required urine output: 0.5-1 ml / kg /h
▪ min. 40-50 ml/h = 1000 ml/24hrs
344

o Rule of 9s
▪ head & neck 9%
▪ arm 9% (4.5% each)
▪ leg 18% (9% each leg)
▪ trunk
• front - 18%
• back - 18%
▪ perineum 1%
o MC common cause of death: renal failure – in first 2-3 days
▪ then death from inf. (after first 3-5 days)
▪ shock in major burn in first day (M 1381)
o indication for intubation
▪ horseness of voice
▪ stridor
▪ coughing black materials
▪ facial swelling
▪ nasal hair burned (singed)
▪ resp. distress
- Fluid replacement - Amit
o urgent – intravasc. fluid resuscitation (bolus) – only in severe cases
▪ hypovolemic shock or severe dehydr.
• 0.9% NS - 20 ml / kg IV ASAP stat run (bolus)
- e.g. 50 kg pacient = 1L
▪ vasodilatory shock: sepsis, anaphylaxis, spinal shock
• 0.9% NS - 20 ml / kg IV ASAP stat run (bolus)
▪ cardiogenic shock
• 0.9% NS - 10 ml / kg IV ASAP stat run (bolus)
▪ moderate dehydr., without shock
• 0.9% NS - 10 ml / kg IV ASAP stat run (bolus)
▪ minimum volume resusc.
• titrate perfusion in order to maintain a systolic BP of min. 90 /60)
• e.g. ectopic pregnancy, penetrating chest wounds, rupture of aortic
aneurysm
Respiratory/ lung pathology - OK
Lung volumes

- These values vary with the age and height of the person; the values that follow are for a 70 kg
(154 lb), average-sized adult male [2]:

Measurement Value Calculation Description

The volume of gas contained in the lung at the
Total lung end of maximal deep inspiration. The total
6.0L = IRV + TV + ERV + RV
capacity (TLC) volume of the lung (i.e., the volume of air in
the lungs after maximum inspiration).
Vital capacity The amount of air that can be forced out of the
4.6 L = IRV + TV + ERV
(VC) lungs after a maximal inspiration. Emphasis on
345

completeness of expiration. The maximum

volume of air that can be voluntarily moved in
and out of the respiratory system.[3][4]
The amount of air that can be maximally
Forced vital
4.8 L measured forced out of the lungs after a maximal
capacity (FVC)
inspiration. Emphasis on speed.[5][6][7]
The amount of air breathed in or out during
Tidal volume 500
measured normal respiration. The volume of air an
(TV) ml
individual is normally breathing in and out.
The amount of air left in the lungs after a
maximal exhalation. The amount of air that is
Residual
1.2 L measured always in the lungs and can never be expired
volume (RV)
(i.e., the amount of air that stays in the lungs
after maximum expiration).
The amount of additional air that can be
breathed out after the end expiratory level of
normal breathing. (At the end of a normal
Expiratory
breath, the lungs contain the residual volume
reserve volume = 1.2 l measured
plus the expiratory reserve volume, or around
(ERV)
2.4 litres. If one then goes on and exhales as
much as possible, only the residual volume of
1.2 litres remains).
The additional air that can be inhaled after a
Inspiratory
normal tidal breath in. The maximum volume
reserve volume 3.0 L measured
of air that can be inspired in addition to the
(IRV)
tidal volume.
Functional Volume of air left in the lungs after a tidal
residual 2.4 L = ERV + RV breath out. The amount of air that stays in the
capacity (FRC) lungs during normal breathing.
Inspiratory The volume that can be inhaled after a tidal
3.5 L = TV + IRV
capacity (IC) breathe-out.
Anatomical 150 The volume of conducting airways. Measured
measured
dead space ml with Fowler method.[8]

Physiologic = 155 The anatomic dead space plus the alveolar

dead volume ml dead space.
- The tidal volume, vital capacity, inspiratory capacity and expiratory reserve volume can be
measured directly with a spirometer. Determination of residual volume can be done by
radiographic planemetry, body plethysmography, closed circuit dilution and nitrogen washout.
- These are basic elements of a ventilatory pulmonary func. test. Results (in particular FEV1/FVC
and FRC) can be used to distinguish between restrictive & obstructive pulmonary diseases:

Type Examples Description FEV1/FVC

Restrictive Pulmonary fibrosis,
volumes are decreased often in a normal range (0.8 - 1.0)
diseases pneumothorax
 346

often low (Asthma can ↓ratio to

Obstructive volumes are essentially normal
Asthma or COPD 0.6, Emphysema can ↓ratio to 0.7
diseases but flow rates are impeded
- 0.4)
Lung Abscess
o MC - staph.
The most common pathogens include Bacteroides, Peptostreptococcus, and Fusobacterium(if aspiration)
o Sx
▪ Purulent sputum with foul odour
▪ pleuritic chest pain
▪ tachyc., tachypneic
▪ bronchial breath
▪ crepitations
▪ fever > 38.5o C

o RF-

▪ poor oral hygiene(dentition)

▪ impaired swallowing
▪ immunosuppression
▪ altered consciousness(includes seizures, dementia and alcoholism )

o Dx
▪ X Ray: small cavity with fluid level
▪ best investig: CT chest
▪ Bronchoscopy
o Rx
▪ O2, strong analgezic
▪ postural drainage, tapping
▪ IV A/B:
• Clindamycin (active on anaerobs; SE – Pseudomembranous colitis) +
Cephalosp. (ceftriaxone)
(Iv penicillin or clinda)
• Cephalosp. + flucloxacillin

Bronchitis
o Acute - sore throat, runny nose, persistent cough especially at night and in the morning,
small amount of yellow sputum
▪ Rx
• Symptomatic
• bronchodilators
• Amoxycillin or Doxycycline (if fever or sputum, usually not needed)
• A 23-year-old-male presents with a one week history of cough productive of whitish sputum. This was
preceded one week prior by an URI. He denies chills, night sweats, shortness of breath or wheeze. Temperature is
99.9°F (37.7°C)
Presentation
-patient with persistent cough > 5 days following an URTI with mild or no fever or constitutional symptoms
Management
o initial test:do a radiograph to exclude pneumonia if:
o fever >100.4°F(38°C)
o signs of consolidation on exam
o definite therapy:rehydration and antipyretics
 347

o Chronic - persistent cough especially at night and in the morning, large amount of yellow
sputum
o Dx
▪ X Ray
▪ pfts
▪ Biopsy (gold std)
A 46-year-old female presents to her primary care physician for follow-up for a severe,
unrelenting, productive cough that she had had on and off for more than two year
1) One of two major presentations of Chronic Obstructive Pulmonary Disease (COPD)
i) including chronic bronchitis and emphysema
2) Characterized by decreased lung function in the setting of airflow obstruction
3) Defined by productive cough for >3 months per year for two consecutive years
4) Patients identified as "blue bloaters"
i) color indicative of hypoxia observed in bluish tint of skin and mucous membranes
ii) barrel-chested secondary to hyperinflation of the lungs due to outflow obstruction

- Sputum types – Murtagh p. 467

- Fibrosing alveolytis – all pulmonary parameters
decreased
- Idiopathic pulmonary fibrosis-IPF
o Hx of shortness of breath and cough
o clubbing with coarse crackles in both lung bases
348

Sleep apnoea(do narcolepsy from 1604 and med)

o types
▪ Obstructive:
• decr. airway size
- Obesity
- Tonsillar hypertrophy
- Macroglossia
• upper airway muscle hypotonia
- Alcohol
• nasal obstruction
▪ Central:
• Neurological (sleep center affected)
• Needs bipap
o Dx
▪ Sleep study (somnography)
• bad when interferring with REM
sleep On polysomnography, less than 5 apneas and hypopneas per hour (the apnea-hypopnea
index) is considered normal. An AHI of 5-15 is mild OSA, 15-30 is moderate OSA, and >30 is
severe OSA
o Mx – Step ladder
▪ 1. lifestyle
• wt. loss
▪ 2. drugs
• stop
sedatives,smoking,alcohol
• use nasal decongestives
▪ 3. C-PAP mask(most efficacious)
▪ 4. Surgery
▪ 5. Mandibular implants (splint)
▪ 6. Amytriptilline(intolerant to cpap)
Cx- Complications
1) arrhythmias
a) may result in sudden death
i) most common in infants and elderly
2) pulmonary hypertension
a) due to chronic hypoxia stimulating pulmonary vasculature constriction
b) may result in cor pulmonale
chest findings – Murtagh 529
Dx Trachea Chest wall Percussion Breath Vocal Abnormal
movt. sounds fremitus sounds
(↑ in
consolid.
& fibrosis)
N Middle Equal Resonant Vesicular N None
expansion
Lung fibrosis Middle Decr. bilat. Resonant Vesicular Incr. Fine crackles
(generalised)
Pneumonia/ CA Middle Decr. Dull Bronchial Incr. Fine late
consolidation unilat. inspiratory
(CA: No fever, no crackles
crackles)
349

Lung collapse Towards Decr. Dull Absent or Absent or None

collapse unilat. decr. decr.
Pleural effusion opposite Decr. Stony dull Absent or Absent or None
side unilat. decr. decr.
Pneumothorax opposite Decr. Hyperresonant Absent or Absent or None
side unilat. decr. decr.
Emphysema Middle Decr. bilat. Resonant to Vesicular Decr. ± crackles &
hyperresonant wheezing
from chronic
bronchitis
Asthma Middle Decr. bilat. Resonant Vesicular ē N or decr. Expiratory
prolonged wheezes
expiration

Pneumonia (MCQ 2.082 p 72)

o types
▪ Staphylococcal Pneumonia: Round (cavitating, abscess) lesions with fluid level +
pleural effusion + flu-like sympt and dry cough
• Rx - Flucloxacilin
▪ Streptcoccal Pnmeumonia (Lobar pneumonia)+rust colour sputum MC community
acquired uncomplicated pnenumonia = lobar consolidation, empyema
• Rx – Benylpenicillin x IV
▪ Atypical pneumonia
• Paucity of chest signs (fever, headache, cough, white sputum) + significant X
Ray signs (patchy bilateral infilterates)= Multilobar pneumonia.
• Causes:
- MC = Mycoplasma
- Legionella(a.c also with diarrhoea), Chlamydia
• Rx - Erythromycin, doxycyclin, azythromycin (the best)-REDA
• Rx
- Azythromycin – the best
▪ covers Mycoplasma, Legionella, Chlamydia
- Erythromycin, roxythromycin,
▪ don’t cover Legionella
▪ SE – GIT sympt.
- Doxycycline, tetracycline
Streptococcal Staphylococcus Mycoplasma Pneumocystic carini
Popul./ All Indigenous All School going, Immunsuppressed
age (Lobar pneumona) young adults people (AIDS)
Sx Fever, rigor, cough, Fever, rigor, dry cough, Flu-like sympt., Dry cough, dyspnea,
purulent sputum, pleuritic pain followed by dry fever, look toxic/sick
pleuritic pain cough with few other signs
X Ray Lower lobar Bilat. Cavities with fluid Patchy bilaterl Can be normal, even
consolidation level, Pleural effusion Infiltrates (MCQ) though they look so
sick
Cx MC – empyema MC – abscess/ cavity Least likely to give
abscess
Rx Benzylpenicillin IV Flucloxacilin Azithromycin(reda) Cotrimoxazole
▪ Klebsiella Pneumonia
• Newborn, elderly, DM, alcoholics
• Cavitating pneumonia in upper lobe (diff. from staph.)
• Rx - Cefuroxime
350

Asthma
o Causes/ triggers
▪ Infections
▪ Allergies-house dust mites are the most common triggeR
▪ Cigarette smoke
▪ Sudden change in weather or temperature
▪ Drugs that can exacerbate asthma:
• β blockers
• Aspirin
• NSAIDs:
• Foods causing asthma
• Sulfites and metabisulfites preservatives
• MSG
• Sea food
• Nuts – peanuts
▪ stress
▪ exercise in a cold atmosphere
o Sx
▪ Triad: Dyspnoea, wheeze(exp) & cough
o Lab:
▪ FEV1/ FVC (FEV1%) – most accurate test (Forced expiratory volume at 1 sec/
Forced vital capacity)
• normal 75–80%.
• <75% = Obstruction
▪ PEFR - maximal flow or speed achieved during the maxim. forced expiration
initiated at full inspiration, measured in L/ min. It is measured with a peak flow
meter or mini peak flow meter.
• in children over 6 years and adults
• compared to graphs of predicted normal values based on a person's sex,
age and height
▪ Methacholine challenge
▪ used for definitive diagnosis
▪ tests for bronchial hyperactivity in a well patient

o types of attack
▪ mild
▪ moderate
▪ Severe – dangerous signs:
• SaO2 < 90%
- SaO2 <92% - give O2
• PEFR < 100 L/ min
• FEV1/FVC < 40%
• RR > 50 in children or > 25 adults
• HR > 120
• using access. resp. muscles = chest retractions = intercostal recession of
muscles
• sternal notch
351

• nasal flaring
• too breathless to talk or feed
• exhaustion, sleep deprivation, drowsiness, confusion
• silent chest
• cyanosis
o Drugs:
▪ Bronchodilators
• Beta receptor agonists:
- Short acting beta agonists (SABA) - effect starts after 1-2 min,
max. at 10-20 min.
▪ Salbutamol (albuterol USAN)
▪ Terbutaline
- Long acting beta agonists (LABA)
▪ Salmeterol
▪ eformoterol
- Adrenaline – sc, im or iv
• Anticholinergic medications:
- ipratropium bromide
• Methylxanthines: – limited use due to side effects and limited efficacy
- theophylline - Oral
- aminophylline – Injection(drip)
• Anti-IgE agents:
- Omalizumab
- Mauzumab
▪ Antiinflammatory - Long term control
• Glucocorticoids are the most effective treatment available for long
term control. (Best preventer)
- inhaled
▪ fluticasone (Best preventer)
▪ beclomethasone
▪ budesonide
▪ ciclesonide (single daily dose)
- Oral – for exacerbations
▪ prednisolone
• Mast cell stabilizers – inhaled; adverse effects are uncommon!
- sodium cromglycate
- nedocromil sodium
• Leukotriene antagonist – chewable tablets
- montelukast
- zafirlukast
o routes of delivery
▪ <3 yrs - metered dose inhalation (MDI) + small volume spacer + face mask
▪ 3-5 yrs - MDI + small volume spacer
▪ 5-8 yrs – MDI + large volume spacer
▪ > 8 yrs – MDI
o Sx - patterns in children – Murtagh 1280
352

▪ Mild - infrequent, episodic type

• not severe
• attacks > 6-8 wks apart
Mx-SABA: Salbutamol, Terbutaline – when required
▪ Moderate - frequent episodic
• attacks < 6 wks apart (4-6 wks)
• attacks more severe
• Mx:
- SABA during attack
- Montelukast or cromolyn or
- inhaled Corticosteroids = ICS
▪ beclomethasone
▪ fluticasone
▪ ciclesonide
▪ budesonide
▪ Severe - persistent asthma
• attacks on most of the days
• nocturnal attack > 1/ week
• multiple ED admissions
• Mx:
- SABA in attack
- ICS
- consider LABA (salmeterol, eformeterol)
- if needed:
▪ theophylline
▪ ipratropium bromide
▪ oral prednisolone
Status asthmaticus:
• Rx
- O2
- hydration
- salbutamol
- Corticosteroids oral or IV
▪ Mx of attack
• monitoring of attack:
- FEV1/ FVC
- PEFR
• hydration!
• O2
- when do you intubate:
▪ after other Rx have failed
▪ blood gases are affected
• Inhaled Salbutamol + Oral C/S
- wait 20 min and assess
▪ if 2nd attack or sympt. persist -> repeat inhaled
Salbutamol
353

• if 3rd attack or sympt. persist -> repeat inhaled

Salbutamol
o if sympt. persist other drugs:
▪ Theophylline
▪ Ipratropium bromide
▪ Oral prednisolone
▪ IV C/S
• Moderate/ severe asthma attack in children
- a. Salbutamol puffs with spacer + prednisolone
▪ 1 puff/ 4 breaths
▪ how many puffs
• 6 puffs < 6 yrs
o + 2 puffs ipratropium if severe attack
• 12 puffs > 6 yrs
o + 4 puffs ipratropium if severe attack
▪ then
• 20 min later – repeat(2nd)
• 20 min later – salbutamol (repeat)(3RD)
o if still not better -> ICU(4TH)
- or continuous nebulised salbutamol via mask
▪ Salbutamol with nebulizer + O2 (nebulizer better than
spacer)
• Salbutamol 2.5 mg < 6 yrs
• Salbutamol 5 mg > 6 yrs
- b. O2 through nebuliser
- c. IV infusion of salbutamol + hydrocortisonE
- d. Adrenaline IM
• Criteria for sending the child home
- off salbutamol > 4 hrs
- off the O2 for > 24 hrs
- eating/ drinking normally
- no sign of resp. distress
▪ exercise-induced asthma: (CROMOLYN PREFERRED)But Jm prefers Laba 929
• 1-2 puffs of Salbutamol before exercise (last for 1-2 hrs)
▪ antihistamine – not in children, except in severe asthma
▪ poor outcome if severe attacks requiring intubation
COPD
o Dx
▪ FEV1/ FEV
• <70% after bronchodilator
• < 80% predicted
o Rx
▪ stop smoking
▪ drugs
• SABA
• LABA
• Ipratroprium bromide
354

• Corticosterioids: COPD – only 10% respond to steroids

- Inhal.
- P.O.
• A/B – in infection
• Β blockers in associated CV problems
- decr. the need of home O2
- decr. the exacerbations
• Steroids and salmeterol (LABA) improve quality of life
▪ O2
• if SaO2 < 92%
• correct O2 admin in COPD:
- low flow 2-3 L
- prolonged > 15 hrs/ day
- low percent (conc.) 30-40%
• CO2 narcosis
- if Rx with too much O2 => CO2 retention => resp. depression
▪ -> anxiety
▪ -> progress to confusion: flapping tremors (asterixis)
• O2 – best factor for incr. long term prognosis
o sign of poorest prognosis in bronchospasm = high PaCO2
o MCQ: emphysema, V1-4 ST segm depression, normal axis, right bundle block: RV
Hypertrophy with right bundle block
o MCQ: COPD with incr. JVP, edema, decr. O2, incr. CO2, why advise for a home O2 therapy
system? because hypoxia is the cause of his heart failure
Pulmonary Embolism
- Acute pulmonary edema (APO)
o cause: MI, etc.
o Sx – dyspnea, etc.
o Rx
▪ O2
▪ CPAP, PEEP
▪ nitrates (GTN)
▪ morphine
▪ diuretics
- PE – my p.41
o predispoz. factors (same as for DVT):
▪ contraception – OCP
▪ obesity
▪ surgery or immobilisation or long flights
▪ thrombophilia
▪ trauma
▪ varicose veins
▪ malignancy
▪ pregnancy
▪ prev. episode of DVT or PE
▪ family Hx in first degree relative
o
355

o Sx
▪ Small PE: Sudden dyspnoea, pleuritic pain and pleural rub, and possibly
haemoptysis, with few physical signs
▪ Major PE: Dyspnoea, chest pain and light-headedness or collapse/ syncope,
followed by recovery.
▪ Look for cyanosis, tachycardia, hypotension, raised JVP and loud delayed
pulmonary 2nd sound (due to pulmonary HT)
o Dx
▪ FIRST: X-Ray: Mainly to exclude pneumonia, pneumothorax.
▪ SECOND & Best: CT Pulmonary angiogram (CTPA).
▪ THIRD - if CTPA unavailable or CI (e.g. renal failure – no contrast): Ventilation-
Perfusion isotope lung scan (V/Q scan)
• V/Q ratio (ventil/ perfusion)- isotope scanning ē Technetium Tc-99m

Result Interpretation Significance

Excludes pulmonary
Normal No perfusion deficit
thromboembolism

Low probability Perfusion deficit with matched ventilation deficit Non diagnostic

Intermediate Perfusion deficit that corresponds to

Non diagnostic
probability parenchymal abnormality on chest x-ray

Multiple segmental perfusion deficits with Diagnostic for pulmonary

High probability
normal ventilation thromboembolism

V/Q ratio measurement used to assess the efficiency and adequacy of matching of two variables:
"V" - ventilation - the air which reaches the lungs
"Q" - perfusion - the blood which reaches the lungs
- A lower V/Q ratio (with respect to expected value for a particular lung area in a defined position)
impairs pulmonary gas exchange and is a cause of low arterial partial pressure of O2 (paO2).
Excretion of CO2 is also impaired but a rise in paCO2 is very uncommon because this leads to
respiratory stimulation and the resultant increase in alveolar ventilation returns paCO2 to within
the normal range. These abnormal phenomena are usually seen in chronic bronchitis, asthma
and acute pulmonary edema.
- A high V/Q ratio increases paO2 and decreases paCO2. This finding is typically associated with
pulmonary embolism (where blood circulation is impaired by an embolus), but can also be
observed in COPD as a maladaptive ventilatory overwork of the undamaged lung parenchyma.

▪ D-dimer: Only on a patient with low pre-test probability

• if normal, excludes PE
▪ ECG: S1Q3T3 (deep S waves in I, deep Q waves in III, inverted T waves in III)
neither sensitive nor specific.
▪ Pregnancy: CTPA is inestigation of choice, 2nd is V/Q scan
o Rx
▪ MO (no NA)
• Morphine 5 mg IV if severe pain
356

• High-dose O2
▪ Heparin: LMW 1mg/ kg s.c 12 hourly or UH 5000 units IV bolus followed by 1000
units/ h infusion
▪ Massive PE in shock (acute heart failure, hypotension): Thrombolysis with rt-
PA
o Cx
▪ Consolidation -> bronchial breath sound
• Q62 p. 19/176 in purple book

Pneumothorax
Spontaneous Traumatic Iatrogenic
a. Normal thin tall male Tension pn. = emmergency
b. Lung disease, COPD, asthma,
a. CVP line in subclavian vein
cystic fibrosis, b. Pleural biopsy
Excessice coughing c. Rx for hyperhidrosis – blocking
stelate sympathetic ganglion
Rx Rx.
a. Needle aspiration -> observe -> didn’t Needle aspiration 2nd ICS
resolve, repeast aspiration -> still didn’t medioclavicular line.Then replace
resolve, chest tube with chest tube under water seal (5th
b. chest tube for drainage ICS mid-axillary or anterior axillary
line)
Sx: Hyperresonance, decreased vocal resonance on auscultation, shift of trachea to opposite site
Rx
Sympt – treat
Asympt < 2 cm – Observe
> 2 cm treat
> 15% loss of lung volume - Treat
- Needle aspiration
o Tension pneumothorax
o Spontaneous pneumothorax
- Chest tube
o Tension pneumothorax – after doing needle aspir.
o Sec. spontaneous pneumothorax
o Most traumatic pneumothoraxes
o Malignant pleural effusion
o Hemopneumothorax
o Empyema
Dx: Not done in emergency
Chest X Ray in expiration
357

- Pneumohemothorax
o If not urgent – do chest tube directly, without doing the needle first.

Pleural pathology
- Pleural effusion
o Sx
▪ Dullness on percution
o Dx
▪ Pleural fluid contains
• Mononuclear cells predominantly = TB
• Transudate vs. exudate
- Criteria for exudate:
▪ Ratio of pleural fluid protein to serum protein > 0.5
▪ Ratio of pleural fluid LDH and serum LDH > 0.6
▪ Pleural fluid LDH > 0.6 or 2/3 times the normal upper
limit for serum.
358
359

Lung CA
o 2nd MC CA in Australia after non-melanoma skin CA
o Most lethal CA in Aus.
o Prognosis at 5 yrs – 12-14%
o Risk factors
▪ Smoking
▪ Silicosis, working in a mine
▪ Asbestos
o Relationship with smoking:
▪ smoker
• squamous
• small cell
▪ non-smoker
• adenocarcinoma – MC in non-smokers
o Sx
▪ Triad: malaise + wt. loss + cough
▪ Hemoptisis
▪ Superior vena cava compression syndrome
• Jugular veins proeminent, subcut veins on upper chest dilated.
▪ Paraneoplastic phenomena
• Squamous cell carcinoma
- Parathyroid hormone-related peptide (PTHrP) - hypercalcemia
▪ Sx - fatigue,
• Small cell carcinoma
- SIADH – Hyponatremia (120mm/l or less) bc of ↑ total body water----Hypo-
osmolar hyponatremia.
- Ectopic ACTH secretion – Cushing syndrome: Moon face buffalo hump, central
obesity, striae and bruising ↑ secretion of melanocyte secreting horomone
(MSH) -> ↑ Pigmentation of mucosal membranes and skin. Hypokalemic
alkalosis bc of excess glucocorticoid and muscle weakness.
▪ Pancoast tumor/ Hornor syndrome:
• + compression on T1
- all small muscles of hand, including thenar and hypothenar eminences
- difficulty of precision grip and opposition of thumb to fingers, weakness
spreading and bringing together the fingers
- in time – claw hand
o types
▪ Small cell (SCLC) - 15-20%
• Rx
- Chemotherapy
- Radiotherapy - palliative
▪ Non-small cell (NSCLC)
• Squamous – 20-30%
• Adenocarcinoma – 20-30%
• Large cell carcinoma – 20-30%
• Rx
- surgery
- chemotherapy
- radiotherapy - palliative
o Dx
▪ sometimes incidental finding at chest X Ray
▪ Bronchoscopy and biopsy (if close to a bronchi)
360

Mesothelioma:
o Risk factors
▪ Asbestosis (boiler worker, electricity-generating plants) decades after(10 yr)
▪ Smoking
o Sx
▪ cough
▪ pleuritic pain
▪ massive recurrent hemorrhagic pleural effusion
▪ pleural plaques
o Dx
▪ Percutaneous biopsy(pleural)
361

o Rx
▪ surgery
▪ chemotherapy
▪ radiotherapy
o prognosis – very poor
Asbestosis:
o after a lag of 10-20 yrs or more from the exposure
o fibrosis/ scarring of the lungs
o assoc.
▪ mesothelioma
▪ TB more assoc. with silicosis (not asbestosis)
OCCUPATIONAL PULMONARY DISEASE-559

BRonchiectasis-475
362

TB
o Triad: Malaise + cough + wt. loss ± erythema nodosum
▪ Primary TB
• Sx – cough, hemoptysis, sweating , fever, malaise, anorexia
- Murtagh – in most cases asympt.
• X Ray: infiltrates in middle and lower zones + hilar lymph nodes
(unilat.) known as Ghon Complex
▪ Latent TB - MC
• Mantoux test – positive
• no clinical features
• usually no X Ray changes
• 10% (if weak immune system) will progress (progressive primary TB) to
reactivation =>
▪ Active secondary TB, within first 2 yrs of exposure
• clinical
- constit. – fatigue, night sweats, wt. loss
- site dependent sympt.
▪ Pulmonary TB – MC
• Sx
o chronic productive cough
o +/- hemoptysis
• X Ray
o infiltration and cavitations in upper
lobes (apical area)
o No hilar lymphadenopathy
o pleural effusion
o past. inf. - apical calcif. and scarring –
can still have surviving bact.
▪ Miliary TB
• X Ray: multiple small bilat. seed-like lesions
▪ Extrapulm TB
• Pericarditis, peritonitis, meningitis,
osteomyelitis, epididymitis or tubal TB
o MCQ: Constrictive pericarditis with
previous TB exposure (ventricular
failure, edema, JVP extremely high, abd.
distension)
▪ X Ray - infiltr. in apical lobes +
pleural effusion
o Dx
▪ Mantoux test:
• delayed hypersensitivity test
- evaluated after 72 hrs
• < 5 mm = negative
- do vaccination!
363

• 5-10 mm = past vaccination

• > 10 mm = positive
- evidence of inf.
▪ active
▪ inactive – latent TB
▪ chest X Ray
▪ if productive cough
• sputum – acid-fast bacili
- stain – Ziehl Nielson
- culture
▪ TB specific – interferon gama release assay
▪ bronchoscopy and biopsy can be considered
▪ pleural effusion – with monocytes
o Mx
▪ only by specialist! (not by GP)
▪ notifiable dis. -> Dept. of Human Services
▪ contact tracing by Dept. of Human Services
▪ bacterial confirmation and drug susceptibility testing first – only then will be
Rx
▪ no isolation!
o Rx
▪ Active TB (RIPE)
• 4 drugs (rifampicin, isoniazid, pyrazinamide, ethambutol) for 2 mths
• then 2 drugs (rifampicin and isoniazid) for 4 mths
- total 6 mths
▪ Latent TB (Mantoux positive, no sympt., no X Ray features)
• when active TB is excluded: isoniazid mono-therapy for 6-9 mths
• treat only specific groups:
- recent TB converters (Mantoux test neg., recently – within last 2
yrs - became pos.)
- children, adolescents
- close contact with patient smear-TB positive
- patient with HIV, DM uncontrolled, CRF, Ch liver Failure
- overseas trained people (immigrants)
▪ Pregnant (IRE)
• start Rx ASAP
- pyrazinamide not recommended
- isoniazid, rifampicin, ethambutol – 9months
▪ don’t cross placenta
▪ no teratogenic effect
▪ minimal conc. in milk – breast feeding is NOT CI
▪ Isoniazid resistant TB
• Streptomycin or Amikacin instead of isoniazide
364

Cardiac pathology - OK
- Infective endocarditis
o causes
▪ MC – Strepto. viridans > 50% (after dental work)
▪ in IV drug users – MC Candida and Staph. aureus
• MC affected valve = Tricuspid (blood goes to right side of heart first)
▪ Staph. aureus (50% of acute forms)
▪ Coxiella burnetti – Q fever
o Predisposing factors
▪ Valvular dis.
▪ Cardiac defects
▪ Prosthetic valves
▪ IV drug use
▪ after
• Dental work (dental extraction, etc.)
• Instrumentation (urethral dilatation, etc.)
• Minor or major surgical procedures (tonsillectomy, abortion)
• Central venous catheters
o mortality 6-30%
o 15% previously Dx with heart dis.
o Sx
▪ may be with no murmur
▪ Triad: fever of unknown origin + cardiac murmur + embolism
▪ presentations
365

• Acute endocarditis
• Subacute endocarditis
• Prosthetic endocarditis
o Mx
▪ take blood cultures, then
▪ start ASAP empiric Rx with:
• Benzyl penicillin + Flucloxacilin + Gentamicin x IV
- HOCM
o family Hx of father who died early – usually AD
o Sx
▪ exertional syncope
• collapse during physical effort (plays football) due to arrythmia
▪ ejection systolic murmur (same as aortic stenosis) non radiating
• non radiating & exacerbation with Valsalva manouver = HOCM
o Dx
▪ 1 – Echocardiography – every 5 yrs
• LVH
• Subaortic septal hypertrophy -> pushes valve -> similar to Aortic Stenos
o Rx
▪ No digoxin (can ↓ ejection fraction)
- JVP – internal jugular vein
o raised if > 4 cm
o Components:
▪ a wave – atrial systole
▪ c wave – closure of tricuspid valve (not normally visible)
▪ x descent – ventricular systole
▪ v wave – atrial filling against a closed tricuspid valve
▪ y descent – opening of the tricuspid valve
o Pathology:
▪ raised JVP with normal waveform: Right heart failure, fluid overload
▪ raised JVP with absent pulsation: SVC obstruction
▪ large a wave – Pulmonary hypertension, Pulmonary stenosis
▪ cannon a wave – right atrium contracts against a closed tricuspid valve -
complete heart block
▪ absent a wave – atrial fibrillation
▪ large v wave – tricuspid regurgitation
▪ high plateau of JVP with deep x and y descents – constrictive pericarditis
▪ absent JVP – reduced circulatory volume
o Positive abdomino-jugular reflux sign – rise in JVP presistent after 15-60 sec of abdominal
compression = right ventricular failure
- Cardiac tamponade
o Sx
▪ Beck triad
• hypotension
• muffled heart sounds
• increased JVP, distended neck veins
366

▪ Pulsus paradoxus: exaggeration of normal phyisiological resp. variation in BP

(fall in BP of > 10 mm Hg during inspiration)
o Dx
▪ X Ray
• loss of aortic knuckle
• widened mediastinum
o Mx - Pericardiocentesis
- Pericarditis
o types
▪ acute
▪ chronic – with hepatosplenomegaly and jaundice, incr. JVP, ascitis, edema
o Sx
▪ Pain improved when leaning forward MCQ
▪ Cardiac tamponade signs (see above)
o ECG
▪ ST elevation and PR depression (pathognomonic - Jay) in almost all leads
(except for aVR and V1)!!
▪ RX NSAIDS MCQ
Heart failure
o types
▪ Left
• tachypnoea, pleural effusion, crepitations/ bilat. basal crackles, gallop
rhythm (3rd heart sound)
▪Right
• ↑JVP, peripheral/ ankle edema, hepatomegaly, ascites
• Cor-pulmonale
- right heart failure
- secondary chronic pulmonar HTN
- Rx
▪ O2 – 3yr survival improved by 50%.
▪ Systolic
• LV ejection fraction < 40 %
▪ Diastolic
• impairment of LV filling
o Rx – Murtagh 1335
▪ Lifestyle
• Salt restriction < 2 g/ day
• Water restriction < 1.5 L/ day
▪ drugs
• 1. ACE inh (or AIIRA – losartan and other sartans, if cough is a problem)
- correct neuroendocrine problemes
- decr. the cardiac load
- decr. risk of death
• 2. add diuretic – if congestion
- furosemide
- hydrochlorothiazide
• 3. + selective β Blocker
367

- prolong survival!
- bisoprolol, carvedilol, metoprolol
• 4. + digoxin
- if indicated
▪ e.g. AF
- CI in bradycardia
• 5. + Spironolactone
- careful when combining with ACE inh. (risk of hyperkalemia)
• 6. + consider vasodil.
• 7. + consider transplant
o highest risk for non-cardiac operation: heart failure (> Hx of of DVT or MI)
o 50% will die in 5 yrs
Cardiac arrhythmias
- Arrhythmias
o causes:
▪ I - Medications: Side effect.
▪ II - Exclude myocardial ischemia from ACS as a priority.
▪ III - Electrolyte disturbances: Hyperkalemia.
▪ Hypoxia
▪ Hypovolemia
▪ Thyroid disease
▪ Septicemia
o types:
▪ Bradycardia < 60
• can be:
- SINUS
▪ Rx
• Bolus of atropine 0.5-0.6 mg IV
o Repeat if it persists (up to 3 mg IV)
• if pt conscious: Consider insertion of a
temporary transvenous pacemaker (2nd or
complete heart block)
- JUNCTIONAL
- AV BLOCK = Prolongation of PR interval to > 200 ms
▪ First degree: Benign
• PR > 0.2 s (5 small boxes)
• Rx
o none, unless sympt.
▪ Second degree:
• types:
o Mobitz I (Wenckebach Phenomon)
– Progressive prolongation of PR
interval then drop of a QRS complex
▪ AV node is blocked
▪ Rx - none
o Mobitz II
368

▪ intermittently nonconducted P
waves not preceded by PR
prolongation and not followed
by PR shortening.
▪ PR is constant (not progressively
prolonged) but 1:1, 1:2, 1:3, …
for every 1-3 P waves, a QRS is
dropped
▪ Rx – Pacemaker, especially
after myocardial infarction
▪ Third (complete) – no relationship between P waves
and QRS complexes, complete AV block, ventricles
contract at lower rate than atria.
• HR: 25-50
• Large volume pulse
• Increased JVP (CANNON WAVE)
• Systolic murmur
• Rx
o temporary pacemaker then arrange for
permanent pacemaker
o First check drugs, if no response give
treatment
o atropine?

- Atrioventricular blocks
o Grade I – PR extended > 0.20 sec - digitalis
o Grade II – PR extended and certain SA impulses are missed (do not make it to ventricles)
▪ Mobitz type I (Wenkebach) – digitalis
▪ Mobits type II – usually not from digitalis
o Grade III – complete AV block, ventricles contracting at lower rate than atria
- Atrioventricular dissociation
o Ventricles contracting at a higher rate than atria (unlike AV block Grade III)
▪ Tachycardia
• Broad-complex: (VT, VF, SVT with block)
▪ VT
• Broad QRS
• > 300/ min, regular, usually post MI
• Rx
o Pulseless VT or unconscious, unstable:
Give a synchronized DC shock 120-150 J
and repeat up to 3 times.
o with pulse, conscious, stable:
Amiodarone 300 mg IV over 20-60 min
followed by an infusion of amiodarone
900 mg over 24 hours.
▪ VF
• no QRS complex
369

• Rx
o cardioversion
▪ adrenalin
▪ CPR
o drugs: amiodarone, lidocaine
- WPW:
▪ Short PR interval on ECG
▪ Delta wave
▪ wide QRS
▪ Rx
• radiofrequency ablation of accessory pathway.
• Stable - IV procainamide (class Ia)/
Amiodarone
• Unstable – DC cardioversion
▪ CI
• Avoid adenosine, verapamil, digoxin and
diltiazem as they block the AV node and may
worsen a pre-excited AF leading to VT.
• Narrow-complex: SVT (presents with rapid palpitations in a young pt
after extercise).
- Sinus rhythm, narrow QRS complexes, 150-200/ min
- if unstable: Synchronized DC cardioversion 70-120 J.
- if stable:
▪ 1. Vagal stimulus such as:
• carotid sinus massage: Young, stable, with no
carotid bruit, no history of TIA or CVA.
• Valsalva manouver
▪ 2.a. Adenosine: 6 mg rapidly over 2-5 seconds IV
followed by 12 mg IV after 1-2 min, then further 12 mg
once more if still no response.
• SE – cardiac arrest
▪ 2.b. Alternatively Verapamil 2.5-5 mg as a bolus.
• pregnant woman: IV β blockers (verapamil is
teratogenic)
• Irregular narrow-complex tachycardia: AF
- Prevalence: 0.1% less than 55 years, 10% above the age of 80.
- risk factors
▪ HT – 20% cases of AF
- More prevalent in men.
- HR = 350-550/ min
- irregularly irregular rhythm + absent P waves
- Common underlying causes: IHD, thyrotoxycosis and HTN
(rheumatic fever in developing countries)
- Risk of stroke: 2.5-3% below age of 65, over 10 in older
population
- High risk of femoral artery embolism.
- Rx
370

▪ Alena
• acute onset (< 48 hrs) young age (<65 yrs), no
structural damage (no MI), stable -> rhythm
control: amiodarone + heparin
o Do first US to exclude thrombus in heart
o rate control – digoxin (Murtagh) or β
blocker (Oxford)
• unstable – cardioversion
• elderly pt, with risk factors, previous MI, etc.
o rate control: digoxin, beta blocker
o anticoag.
▪ (Maria) Unstable: Synchronized DC cardioversion 120-
150 J.
▪ Stable: more or less than 48 hours?
• Acute - less than 48 hours: Rate control, rhythm
control, anticoagulation.
o I - Rate control (Maria?):
▪ 1. digoxin – don’t give for low
BP (< 90/60) –(with heart
failure,exercise) Murtagh 779
▪ 2. Verapamil, diltiazem
▪ 3. Β blocker – metoprolol,
atenolol
o (Maria) II - Rhythm control (Amit = I =>
rate will be controlled as well):
▪ Murtagh: if symptomatic +
recent onset (< 6 mths)!!
▪ electrical cardioversion – if
unstable
▪ chemical – if stable: Flecainide
(don’t use in systolic heart
failure)(class Ic), Amiodarone
(class IIa), Sotalol (risk of acute
heart failure).
o Anticoagulation - heparin, then
▪ > 60 yrs, with risk factors –
warfarin (Jay)
▪ < 60 yrs, w/o risk factors –
aspirin
• 2. More than 48 hours
o main goal: rate control
▪ beta blocker
▪ digoxin –( AF and signs of
cardiac failure.)
o Anticoagulation: Enoxaparin 1 mg/kg or
UF heparin 5000 IV as a bolus followed
by an infusion.
o failure to revert chemically => DC shock
371

▪ first do transoesoph. U/S

- Paroxysmal AF
▪ spontaneously ends in less than 7 days (usually in 24
hrs)
• after heavy alcohol, drugs
▪ Rx
• if not rapid – don’t need to revert
• if rapid – convert(rhythm)
- Persistent AF – fails to revert within 7 days
▪ usually converts with DC cardioversion
- Permanent AF – elderly can’t be reverted (permanent damage of
conduction system in heart)
▪ just rate control
▪ anticoagulants
▪ AV node ablation + permanent pacemaker
• AV with rapid ventr. response over a long
period of time -> LV dysfc.
• Atrial Flutter:
- Usually asymptomatic.
- Common complication of HTN and hypertensive heart disease.
- Regular (or irregular) rhythm.
- flutter waves (saw-tooth)
- Rate 300
- Ventric. rate = 125-175 (150)
- with variable blocks -> is irregular
▪ Dx diff with AF
• if no P waves = AF
• if P waves = atrial flutter
- Rx
▪ similar with AF (Murtagh)
▪ permanent – radiofrequency ablation
▪ medical – amiodarone, sotalol
o Bundle branch blocks
▪ LBBB (William)
• wide QRS > 0.12---M pattern
• broad monomorphic R waves in I and V6
• broad monomorphic S waves in V1
• Rx
- newly diagnosed LBBB -> MI? -> thrombolise
▪ RBBB (Marrow)
• wide QRS ---- RSR pattern

MI
- Coronary ischemic syndr.
o stable angina
o acute coronary syndrome (ACS)
▪ STEMI
372

▪ NSTEACS
• NSTEMI
• unstable angina
- AMI
o STEMI
▪ if coronary block is not relieved, MI will progress over next 6-12 hrs (4 hrs =
window period)
▪ main goal of Rx is reperfusion
▪ causes of new systolic murmur post MI
• V septal rupture
• papillary muscle rupture
• papillary muscle dysfc. in ant. MI
• func. mitral regurgitation sec. to LV dil.
• pericardial friction rub, limited to systole
▪ Dx
• First step in management: ECG within 10 minutes of patient arrival.
- ECG: ST elevation in two or more contiguous leads:
▪ Inferior MI: II, III, aVF
▪ Anterior MI
• anteroseptal – V1-V3
• anterolateral – V3-V4
▪ Lateral: I, aVL, V5-V6
▪ Posterior: Mirror-image ST depression V1-V4
• Repeat ECG after 5-10 min if non-dx ECG.
- repeat ECG every 2-3 hours
• Send blood for laboratories: Cardiac biomarkers.
- Second step = Troponin I or T
▪ normal < 0.02
▪ rise after 4-6 hours after symptom onset.
▪ Repeat in 6-8 hours if normal.
▪ Indicate myonecrosis.
▪ Remains elevated for 5-14 days (not useful for re-
infarction).
▪ More sensitive for myocardium than CK-MB.
▪ can also be elevated in CRF – due to renal destruction
• Dx diff with CRF:
o do also CK – not elevated in CRF
o if troponin is gradually increasing – MI
▪ constantly increased = CRF
- + CK-MB, CK.
▪ If troponin is unavailable.
▪ rise after 4 hrs
▪ not specific for myocard infarction
• CK-MB is more specific than total CK
▪ Returns to normal within 72 hrs
• May be used to confirm re-infarction
373

-
▪ complic.
• LVF: pulm. congestion
- Rx: diuretics
- O2
- morphine
- digoxin is CI – ↑force of contr. -> risk of rupture
• cardiogenic shock – 90% mortality
- Rx – dopamine, dobutamine
• aseptic pericarditis (Dressler syndrome)
- Rx
▪ NSAIDS, paracetamol, aspirin
▪ C/S
▪ Mx
• I. MONA
374

- Morphine 2.5 mg IV with antiemetic. – up to 4 times every 10

min. (total 10 mg)
- O2 high dose: 40-60%
- GTN 150-300 µg sublingually.
- Aspirin 150-300 mg unless contraindicated.
• II. Reperfusion therapy:
- PCI if this is available within 90 minutes of patient arrival. (in
tertiary hospitals) and within 12 hrs of onset of sympt.
▪ angiography/ angioplasty (stents)
▪ Protocol:
• within 60 min of arrival if patient presents
within 1 hr. of sympt.
• within 90 min of arrival if patient presents
within 1-3 hrs. of sympt.
• within 90-120 min of arrival if patient presents
within 3-12 hrs. of sympt.
o otherwise - thrombolysis
- Thrombolysis: within 12 hours of onset of symptoms (preferrably
within 6 hrs and within 30 minutes of patient arrival) with rt-PA
▪ pain disappears + ST elevation disappears = MI was
resolved
▪ types:
• Streptokinase(don’t give in indegionous)
o 1.5 UI IV infusion over 30-60 min
o under strict control of BP
▪ if systolic < 70 => stop infusion
• Tenecteplase.(first)
• Reteplase(first)
• Alteplase.(first)
o 15 mg IV bolus, followed by infusion of
50 mg over 30 min, then 35 mg over
next 60 min
▪ SE
• severe hT
• bleeding
• allergic reaction – with streptokinase
o if allergic reaction, don’t use it for at
least 1 yr
• reperfusion arrhythmias
o thrombolysis done under strict ECG
control
o as bad as VF
o in necrotic zone there are all sort of
toxic substances: reperfusion causes
them to mobilize => they irritate
myocardium => arrhythmias
▪ CI
375

• absolute
o Intracerebral or subarachnoid hemrhg.
o Intracranial neoplasm ever.
o Stroke in previous 6 months.
o Active GI bleeding in last month.
o Major surgery or trauma in previous 3
wks
o Known bleeding diathesis.
o CRP > 10
o Aortic dissection
▪ first rule out aortic disection
before giving thrombolysis ->
can kill a patient with aortic
dissection
• relative
o Oral anticoagulant therapy
o Pregnancy within 1 week post-partum.
o Central line.
o Refractory hypertension.
o Infective endocarditis.
o Severe hepatic or renal disease.
▪ indic.
• ST elevation > 1 mm in limb leads
• ST elevation > 2 mm in chest leads
• new LBBB
• post MI-ST depression in V2-V3-> ask for V7-V9
▪ after 12 hrs, thrombolysis is still considered if:
• persistent pain
• preservation of R waves in infarct-related ECG
leads (not replaced by pathological Q wave)
• major complic. – cardiogenic shock
- Antiplatelets
▪ Aspirin 300 mg
▪ Clopidogrel 300 mg
-Heparin.
• III. After reperfusion
- Antiplatelet agents
- Cardioselective β blockers – increase the survival (MCQ)
▪ Atenolol
▪ Metoprolol
- ACE inh. – within 24-48 hrs after MI
- Statin therapy – regardless of cholesterol level
- + Warfarin
▪ drugs that ↓mortality in MI
• 1. β blockers
• 2. ACE inh. (if no renal failure)
• 3. aspirin
376

• 4. statins
- Neha:
o cardiac chest pain
▪ MONA -> hospital: ECG, Trop
No pain Hx of pain at rest or repetitive
pain or prolonged pain
No ECG/ enzyme changes Low risk Intermed. risk
ECG /enzyme changes High risk High risk
o Mx
▪ Low risk -> stress test
▪ Intermed -> reassess patient, repeat ECG and
troponins in 8 hrs -> if any risk factors
(↑cholesterol, fam. Hx, etc.) -> heparin SC
▪ High risk -> coronary angiography (PCI)
▪ if refractory pain – IV GTN (rare)
o NSTEMI
▪ Dx
• ECG: Within 10 min of patient arrival:
- ST depression
- T-wave inversion or flattening
- Non-specific or transient changes
- Normal
• Rise in troponin and CK-MB
▪ types – Afshan’s diagram for ACS
• high risk:
- > 10 min or elevation of troponins
• intermed. (>48 hrs)
• low risk – same as for stable angina (pain only on exertion)
▪ Mx
• MONA
• NO THROMBOLYSIS
• Heparin: LMW heparin such as enoxaparin 1mg/ kg or UF heparin 5000
units IV as a bolus followed by an infusion of 1000 units/ h.
- Angina
o types
▪ Stable (effort angina)
• ST depression
▪ Unstable – due to unstable plaque
• smaller rise in cardiac biomarkers, normal ECGs, normal stress test
• special types
- nocturnal a.
- decubitus a.
- variant a. or Prinzmetal a. (spasm a.)
▪ ST elevated
• don’t give β blockers!
o Rx
▪ acute
377

• GTN subling.
• isosorbide dinitrate subling.
• nifedipine capsules – suck or chew
▪ chronic
• Aspirin 150 mg daily
- or clopidogrel
• Nitrates
- GTN
- Isosorbide mononitrate
• β Blockers
- Atenolol
- Metoprolol
• Ca Channel blockers
- Nifedipine
- Amlodipine
- Felodipine
- Diltiazem
- Verapamil
- Recurrent pain in ACS
o consider IV nitrate infusion
o maximize dose of β blocker
o consider Amlodipine or Nifedipine
o if high risk pain (persistent)
▪ GP IIb/IIIa (strong antiplatelets): abciximab
▪ transfer patient for PCI
- Coronary artery bypass grafting indic. (otherwise – angioplasty)
o triple vessel disease: all 3 arteries > 50%
▪ left anterior descending (LAD)
▪ left circumflex a.
▪ right coronary artery
o 2 vessel disease + DM
o main one – left anterior descending > 50%

ECG
o Normal impulse conduction
▪ Sinoatrial node (right atrium) – 60-100 beats/ min
▪ AV junction – delay, so A can contract before V (including atrial kick at the end
of A contr.)
• AV node – 40-60 pacemaker
• Bundle of His
▪ Bundle branches (left and right)
▪ Purkinje fibers
▪ Ventricular cells – 20-45 beats/ min
o Small square=0.04sec, large square=0.2 sec
o ECG interpretation: RRAHIM
▪ Rate
▪ Rhythm
378

▪ Axis
▪ Hypertrophy
▪ Interval
▪ MI and miscellaneous
o 1. Calculate rate:
▪ Vertical bar every 15 large squares
▪ I. count 30 large squares (6 sec) – count the no. of R waves in those squares,
multiply by 10 -> in regular and irregular rhythms
▪ II. look for R wave falling on a line, then see where the next R wave falls – in
regular rhythms only
• 300 - next line in large square (300:1)
• 150 – next line … (300:2)
• 100 (300:3)
• 75 (300:4)
• 60 (300:5)
• 50 (300:6)
• …
▪ III. 300/ no. of large squares between 2 QRS complexes – in regular rhythms
o 2. determine Rhythm (RR intervals are regular?):
▪ Regular
▪ regularly irregular
▪ irregularly irregular – AF
o 3. Assess P waves – do they exist? are they followed by QRS? are they all same in size and
shape?
▪ MAT = Multifocal atrial tachycardia ≥ 3 P waves, each different, in same ECG
o 4. Determine PR interval – beginning of P to beginning of R
o 5. Determine QRS duration
o 6. QT interval – beginning of Q to end of T (T= terminal)
o Components
▪ P waves = Atrial depolarization (contraction) - best appreciated in lead II
• Present
• absent - AF
• relationship to QRS complexes (no rship. = AV block)
▪ PR interval: 0.12-0.2 (3-5 boxes)
▪ QRS complexes = Ventricular depolarization = 0.04-0.12 (1-3 boxes)
• narrow (supraventric)
• widened (> 0.12 s) (ventric.)
▪ ST segment
▪ T waves = Ventricular repolarization
• Elevated
• depressed
• inverted (ischemia)
▪ U wave = after repolarization
o Leads
▪ I, II, III – Limb leads
▪ aVR (right arm), aVL (left arm), aVF (feet) = Augmented limb leads
▪ V1-V6 = Chest leads (V1 = right -> V6 = left)
379

• V1-V2 = medial
• V2-V3 = septum
• V4-V6 = lateral
▪ Rhythm strip = longer strip of II
o Problems
▪ Sinus bradycardia
▪ Sinus tachycardia
▪ 1 extra atrial focus firing = Normal sinus rhythm with PAC-Premature atrial contc
▪ 1 extra ventricular focus = PVC
• wide and bizarre QRS (slower conduction of impulse from ectopic foci)
• can be
- Uniform. arises from single focus
▪ Bigeminism (normal QRS, ectpioc beat after 2 normal
QRS)
▪ trigeminism ectpioc beat after 3 normal QRS
▪ couplet: normal PVC PVC – 2 consecutive ectopic beats
▪ triplet: normal PVC PVC PVC- 3 consecutive ectopics
▪

-
- Polymorphic: arises from multiple foci
▪ Multiple extra atrial foci firing = A Fib
• 1. absent Ps
• 2. irregularly irregular rhythm
• 3. narrow (normal) QRS
▪ Multiple extra foci in V = V Fib
• 1. absent Ps
380

• 2. irregularly irregular rhythm

• 3. wide QRS
▪ Looping (re-entrant) circuit in A = Atrial flutter
• Picket fence, saw-tooth, seen in HTN pts
• regular
• flutter P waves
• type
- with regular AV block - every 2nd, 3rd or 4th P wave is transmitted
to the Ventricle generating a QRS (1:1, 1:2, 1:3)
- with variable AV block
▪ looping circuit in AV = Paroxysmal SVT = PSVT– with sudden start, captured
on ECG, triggered by a PAC (which can be seen); comes and goes - can only be
captured with Holter; no P waves
• SVT – has P waves,
• Presents as palpitations after exercise usually in young pts.
▪ Looping circuit in V = V Tach.
• regular
- Monomophic
- Polymorphic
▪ block impulses coming from SA node = AV junctional blocks. Seen Post MI
• 1st degree – Prolonged PR, no symptoms, so no treatment
• 2nd degree
- type I Mobitz = Wenkebach phenomena
▪ PR gets longer and longer, until a QRS complex is
dropped
▪ regularly irregular
- type II Mobitz
▪ not all P waves are transmitted to QRS
▪ tough to be differentiated from 3rd degree
• 3rd degree
- A contracts at 60-100
- V contracts at 20-45
▪ MI
• STEMI:
- ST elev. > 1mm in limb leads (farther from heart) and > 2mm in
chest leads (closer to heart) in 2 or more CONTIGUOUS leads
- or LBBB!
• location
- lateral - I, aVL, V5-V6
- inf – II, III, aVF
- ant – V1-V4
▪ septal – V2-V3
▪ or combinations
• antlat.
• antinf.
• nitrates are CI due to hT
- Posterior
381

▪ ST depression in ant. leads (V1-V4) (reciprocal change)

▪ tall R waves in V1-V2 (right side leads)
• normally - R wave progression: small in V1 –
gets taller – tallest in V5
▪ + ST elevation in V7-V9 = Post leads (on back)
- Right side MI: V1 + inf. leads (II, III,aVF)
▪ Cx – severe hT!
• Reciprocal changes
- inf. MI -> reciprocal in lat. leads
- post. MI -> reciprocal in ant. leads
• types of MI
- STEMI = Q wave MI = transmural MI (SQT)
▪ Stages:
• ischemia: ST depression, peaked T waves, then
T-wave inversion
• infarction – ST elevation
• ongoing infarction – Q waves and T-wave
inversion
• fibrosis – persistent Q waves but normal ST
segm. and T waves
- NSTEMI = non-Q wave MI = Subendocardial MI
▪ Stages:
• ischemia: ST depression, T-wave inversion
• infarction ST depression, T-wave inversion
• fibrosis ST returns to baseline, T wave
inversion persists
• Q waves in I, II, III = infarct
• Q waves
- Pathol. If > 1 mm
- can be normal in V1 and aVR
- appear in hrs – days later
▪ Ventricular hypertrophy
• RVH: tall R in V1-V2 taller than 7 mm
• LVH: even taller R in V5-V6 + deep S wave in V1-V2 ≥ 35 mm
- tallest R + deepest S ≥ 35 mm
▪ Atrial hypertrophy – P waves
• P > 2 ½ small squares in height = RAH (P pulmonale)
• P > 2 ½ small squares in length = LAH (P mitrale)
- simple – in II
- notched P (camel hump, bifid) in V1
- biphasic (+ and -) in V1
▪ ST depression in:
• Post. MI (+ tall R waves)
• Normal angina (troponins normal)
• NSTEMI (troponins incr.)
▪ BBB -> slow conduction through collaterals -> wide QRS
382

• any onset of new BBB = new MI

• William Marrow:
- WiLLiaM (W pattern in V1 and or M pattern in V6) = LBBB
▪ M pattern in V5/V6
- MaRRoW = RBBB – sign of RVH =
▪ (M) RSR’ in V1/V2
- W = QRS
- M = RSR’
▪ Axis deviation -> R wave predom + or – in I and II
I II
Normal + +
LAD = Leave (R in V1 & V2 are going in divergent directions) + -
In LVH
RAD = Romance (R in V1 & V2 are going towards each other = kissing) - +
In RVH
Indeterminate (superior or extreme RAD) - -
▪ Intervals
• PR
- ↑ in AV block: 1st degree & 2nd degree, type I
- decr. in
▪ WPW
▪ high catecholamines (fast rhythm)
• QRS
- incr.
▪
BBB
• incomplete BBB 0.10-0.12
▪ PVC
▪ Ventricular rhythm
• QT - QT length is influenced by heart rate
- adjust:
▪ corrected QT: QTc = QT/square root(RR) – Bazzet’s
formula
• Prolonged > 0.44
▪ QT > 1/2 RR = Prolonged
- Prolonged QT = Risk of Torsades de Pointes (polymorphic VT) ->
VF -> death
▪ causes:
• Hypokalemia
• TCAs
• Haloperidol, droperidol
• WPW syndrome
- mnemonic = wPWS
▪ PR is short
▪ Wide QRS
▪ Slurring (Delta wave)
• shortcut with faster conduction -> delta aspect
of first branch of R
383

• PE – S1Q3T3
- I – Deep S
- III – Deep Q and T wave inversion (positive)
• Hypokaleima:
ST depression, T wave inversion. Prol onged QT, Elevation of U wave
• Hyperkalemia
Tall tended T wave, Shortened QT interval, Wide QRS, Prolonged PR
interval, P flattens then disappears
Digoxin: ST depression, T wave inversion, Shortened QT interval,
Prolonged PR.
Vascular pathology - OK
- Surgery indication
o Carotid occlusion
▪ > 70% carotid occlusion
▪ 60-70% - grey area
• surgery in DM, elderly, hyperlip., recurrent TIP
▪ < 60%
• Rx – aspirin low dose
o > 50% coronary artery occlusion
- Angiodysplasia > 55 yrs
o AV malformation in intestine
o in ceceum + right colon
o Sx
▪ multiple episodes of profuse rectal bleeding
▪ assoc. with CREST syndrome
o Rx
▪ surgical resection

Arterial pathology
- Vasculary problems/ surgery
o Arterial
▪ Risk factors
• smoking
• DM
• HTN
• hypercholesterolemia
• family Hx
• AF
▪ Acute/ sudden onset = “cold white leg” – very painful
• causes:
- thrombosis
- embolism
- traumatic contusion
• MC site – common femoral artery
• Sx
384

- Pain, pallor, perishing cold, paralysis, paresthesia, pulselessness

(6Ps)
- most ominous signs – M 716
▪ 1. Paralysis or paresis (weakness)
▪ 2. Muscle compartment pain or tenderness
• Mx
- Reversible if Rx within 4 hrs
▪ IV Heparin 5000 U immediately
▪ emmergency embolectomy or stenting
▪ thrombolysis with Streptokinase or Urokinase
▪ then life time anticoagulant with warfarin!
- after 6 hrs can’t be reversed -> amputation
▪ Chronic
• Prevention
- stop smoking, wt. loss
• Types:
- Intermittent claudication:
▪ pain or tightness in muscles during daytime with
exercise/ walking
o agravating factors: walking, exercise
o relived by rest
• sites
o Superficial femoral a - MC
▪ pain in thighs and calfs after
200-500 m
o Profunda femoris a – pain after 100 m
o multiple segments involvment – pain
after 40-50 m
o External or common iliac a - pain in
buttocks and thighs
o Aortic bifurcation = Leriche syndr. –
with ED + bilat. ischemic buttock
claudication
▪ Dx
• FBE
• First test = ABI
o Normal: 0.9-1.1
▪ 0.9-0.7 Venous ulcer
o Intermittent claudic. 0.5-0.7
o Rest pain: 0.3-0.5
o Calcification >1.1
• Second test – color Doppler
• Gold standard = Angiography
o Reserved for proposed intervention
▪ Mx
• control DM and HT
• decr. wt.
385

• stop smoking
• keep legs warm and dry
• proper care of foot
• aspirin
• if ABI < 0.3 -> refer for urgent surgery
o endarterectomy or bypass grafting
- Resting pain: Constant severe burning pain in forefoot at rest
▪ During night time
▪ Pain in the forefoot, toes, heels
▪ Relieving factor: hanging the foot out of bed
▪ Emergency condition => refer to surgeon immediately
• indic. for vascular surgeon – Murtagh 719
o unstable claudic. of recent onset,
deteriorating
o severe claudic. – unable to maintain a
normal life
o rest pain
o tissue loss – ulcers, heel’s cracks, dry
gangrenous patches, inf.
Venous pathology
- Varicose veins
o predisposing factors
▪ family Hx.
▪ female
▪ pregnancy
▪ multiparity
▪ previous DVT
▪ extrinsic venous compression – intraabd. tumors, etc.
▪ occupation – dentist, etc.
▪ diet – low in fibre
o Rx
▪ High-fibre diet
▪ supportive stockings or tights
▪ Surgery
• Sclerotherapy
- for small, isolated veins
• Surgical ligation and stripping
- DVT
o risk factors
▪ Family Hx
▪ Hx of previous thrombo-embolism
▪ Thrombophilia
▪ Drugs: OCP, HRT, tamoxifen
▪ > 40 yrs
▪ Varicose veins
▪ significant illness: heart failure, CA
▪ Malignancy (in idiopathic DVT)
386

▪ Recent surgery
• Major/ orthopedic surgery
▪ Immobility
▪ Long flights
▪ Pregnancy/ puerperium
▪ Obesity
▪ Dehydration
o Recurrent DVT – pancr. CA
o Unilat. sudden onset of DVT – Ovarian CA
o Sx
▪ “Hot blue leg” = Acute venous obstruction
▪ painful, tender
▪ edema
o Dx
▪ Gold standard = Doppler U/S
▪ contrast venography – if U/S doubtful
▪ D-dimer – to exclude DVT when doubtful (if negative)
▪ don’t do Hoffman sign (plantar dorsiflexion causes pain) since it might
mobilise the thrombus
o Cx
▪ PE
• 20%
- of these 30% will be fatal
▪ varicose veins => venous ulcer
o Rx
▪ heparin, then
▪ warfarin
• 3-6 mths
• we need to treat at least for 3 mths (with warfarin)
• do not give aspirin
▪ mobilisation
▪ compression stockings
- Thrombophlebitis
o Red cord-like vein, tender on palpation
o Usually in superficial varicose veins
o Migratory superficial thrombophlebitis = Pancreatic CA
o Rx
▪ early mobilisation
▪ bed rest
▪ compression with uniform pressure over the vein
• prevent propagation of thrombus
▪ limb elevation
▪ NSAIDs
Aortic pathology
- Coarctation of aorta
o narrowing of distal ductus arteriosus and subclavian artery
o male 2:1
387

o Sx
▪ asympt. always
▪ headache, epistaxis, claudication, cold legs
▪ BP difference between upper and lower limbs
▪ weak delayed pulse in legs
▪ mid to late systolic murmur over aortic area
▪ infraclavicular murmur
o Rx
▪ surgical resection of the narrowed portion – if HTN
▪ angioplasty
- widened mediastinum + systolic murmur – can be:
o aortic aneurysm
▪ leaking aneurysm
• Sx
- severe abd. pain
- moderate abd. rigidity
- shock
- if leaked posteriorily -> pain radiates to back and down into
genitalia
- intense lower back pain
▪ ruptured aneurysm
• Sx
- lower abd. pain, generalised
o Aortic dissection – with shock, chest pain, etc.
- Aortic abdominal aneurysm
o risk factors
▪ Marfan syndrome
o Sx
▪ pulsating palpable mass in abd
▪ abd pain, back pain
o Cx
▪ Rupture
• Sudden abdominal pain.
• Radiating to back or groin.
• Syncope, collapse or unexplained shock.
• Feel for a tender mass with expansible pulsation on examination.
• Classic triad:
- Abdominal or back pain
- shock
- pulsatile or tender abdominal mass in men over 45 years.
• Dx
- Perform a rapid bedside USG to confirm presence of abdominal
aneurysm.
- X Ray – midline opacity with calcified border
▪ Dx diff. with chronic pancreatitis – calcifications like a
chain (2 parallel lines)
- CT scan
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• Rx
- High-flow O2 by face mask.
- Slow IV infusion: avoid giving massive fluid replacement, as this
leads to coagulopathy, hypothermia, ↑ bleeding.
- Refer urgently to vascular surgical team.
o Rx
▪ < 5 cm – observe, elective surgery
▪ > 5 cm – urgent surgery
▪ no matter what size + symptoms = urgent surgery
• method: stenting
- Aortic dissection
o PREDISPOSED BY:
▪ HTN
▪ pre-existing aortic aneurysm
▪ Marfan syndrome
▪ inflam. vasculitides (temporal arteritis, syphilitic aortitis, Takayasu arteritis)
▪ Bicuspid aortic valve.
▪ Coarctation
▪ Iatrogenic trauma.
o Sx
▪ Abrupt onset with sudden pain.
▪ Sharp or tearing pain, radiating to back
▪ Retrosternal, interscapular or lower in back, migratory, severe, resistant to
opiates
▪ Unequal radial artery pulses ± decr. or absent pulses at femoral arteries
▪ Difference of BP in arms.
▪ Diastolic murmur if Aortic Regurgitation occurred.
o Dx
▪ 1. investig. of choice = contrast CT
• 2. if renal fc. is abnormal -> transesophageal U/S
▪ X Ray – wide mediastinum
o Rx
▪ Morphine
▪ β blocker – relaxes muscles of aorta, decr. the extension of dissection
• or Ca channel blockers – if β blockers are CI
▪ + sod. nitroprusside – vasodil.
▪ Surgery – stent graft for type A (MCQ)
o Cx.
▪ MI – dissection before origin of coronary arteries will cause MI
• (inferior) MI with wide mediastinum
- Dx: transoesophageal U/S
▪ if aortic dissection, don’t give thrombolysis (can kill the
person) and don’t give aspirin (gets worse with aspirin)
▪ Aortic incompetence (regurgitation) – diastolic murmur
▪ Cardiac tamponade
▪ Pleural effusion
▪ Intestinal ischemia
389

▪ Oliguria and hematuria

- Steal syndromes
o from the other good leg
o Subclavian steal syndrome
▪ Retrograde (reversed) blood flow in vertebral a. or internal thoracic a, due to a
proximal stenosis or occlusion of subclavian a. Arm may be supplied by blood
flowing in a retrograde direction from the vertebral artery at the expense of
vertebrobasilar circulation.
HTN
- BP regulation
o Autonomous nervous system - baroreceptors are located in left and right carotid bulbs
and in aortic arch + under stress, etc
▪ Sympathetic system - ↑BP
• vasoconstriction
• ↑ force of heart's contractions
• ↑ speed of heart's contractions
▪ Parasympathetic system – ↓BP (opposite effect to sympathetic system)
o Renin-angiotensin(-aldosterone) system
▪ Angiotensinogen – under the action of renin (kidney) ->
• Angiontensin I – under the action of ACE (angiotensin-converting
enzyme, on the surface of pulmonary and renal endothelium) ->
- Angiotensin II ->
▪ Angiotensin III ->
• Angiotensin IV
▪ Renin: secreted by kidneys from specialized cells called granular cells of
juxtaglomerular apparatus in response to:
• A decrease in arterial BP (that could be related to a decrease in blood
volume) as detected by baroreceptors (pressure sensitive cells). It’s most
causal link between BP and renin secretion (other two methods operate
via longer pathways).
• A decrease in sod. chloride levels in ultra-filtrate of nephron. This flow is
measured by macula densa of juxtaglomerular apparatus.
• Sympathetic nervous system activity that also controls BP, acting through
β1 adrenergic receptors.
▪ Angiotensin II
• potent vasoconstrictor of arterioles.
• constricts glomerular arterioles, having a greater effect on efferent
arterioles than afferent. GFR is thus maintained and blood filtration can
continue despite lowered overall kidney blood flow.
• ↑Na and Cl reabsorption and K elimination, ↑water reabsorbtion
(directly and by increasing aldosterone)
• causes release of Aldosterone -> ↑ Na, Cl and water reabsorption and K
elimination.
• causes release of ADH -> ↑ water reabsorbtion
• stimulates sympathetic system
o Aldosterone – Mineralocorticoid hormone, released from adrenal cortex in response to
↑ serum angiotensin II, ↑ ACTH or ↑ serum K levels -> ↑BP.
390

▪ actions:
• increases water reabsorption
• increases Na and Cl reabsorption
• increases K elimination
• increases Ca elimination
▪ modified:
• increase in Hyperaldosteronism
- Sx
▪ weakness (hypokalemia)
▪ polyuria, polydypsia
▪ HTN
- Primary (hyporeninemic)hyperaldosteronism (MCQ 2022, P52)
▪ causes:
• Bilateral adrenal hyperplasia (90%)
• Adrenal adenoma – Conn’s syndrome
• Adrenal CA
▪ Diagnostic:
• low renin: If there is primary
hyperaldosteronism, decreased renin (and
subsequent decreased angiotensin II) will not
lead to a decrease in aldosterone levels (a very
helpful clinical tool in diagnosis of primary
hyperaldosteronism)
o Usually, renin levels are suppressed,
leading to a very low renin-aldosterone
ratio (< 0.0005)
• hypertension
• hypokalemia (normal Na and Cl)
▪ Rx
• Spironolactone
• resection of adrenal adenoma
• ACE inh. do not help (aldosterone works
outside the renin-angiotensinogen system)
- Secondary (hyper reninemic) hyperaldosteronism
▪ causes
• a juxtaglomerular cell tumor (renin producing
tumor) leads to increased aldosterone, as the
body's aldosterone production is normally
regulated by renin levels.
• renal artery stenosis in which the reduced
blood supply across the juxtaglomerular
apparatus stimulates the production of renin
▪ diagnostic
• high renin
• hypertension
• hypokalemia (normal Na and Cl)
• decreased in Addison’s disease.
391

▪ Antagonists:
• Spironolactone, eplerenone – competitive antagonist for aldosterone’s
receptors
o ADH (vasopressin) – synthesized by pituitary gland
▪ increases water reabsortion (main effect)
• ADH secretion is increased when body osmolality increases (more
concentrated blood; ADH reabsorbs more water, to dilute the blood) =>
more concentrated urine
• ADH defficiency leads to hypernatremia (more water than Na is lost)
▪ increases reabsorption of urea
▪ increases Na and Cl reabsorption
▪ ↑ peripheral vascular resistance and thus increases arterial BP
- High blood pressure
o Measurement
▪ Sphygmomanometer – use 3 sizes:
• types
o child
o adult
o large adult (obese)
• rules:
o cuff’s
▪ Width
• 40% of arm circumference (Murtagh)
• cover 2/3rd of arm (not more) – AMC
o children - cuff width should cover 75%
of arm (Murtagh)
• cuffs that are too wide underestimate BP, cuffs
that are too narrow overestimate it (AMC)
▪ Length
• at least double the arm circumference
(Murtagh)
▪ bladder length should not completely encircle the limb
(but only 80%) - AMC
• bladder width is half the length of bladder- AMC
o types of drugs used
▪ 1. Diuretics
• Thiazides
o actions:
▪ ↑Na and Cl excretion (inhibiting reabsorption of Na+
and Cl- ions from distal convoluted tubules in kidneys by
blocking the thiazide-sensitive Na+- Cl- symporter)
▪ ↑ K+ excretion
▪ ↑ serum uric acid
o side effects
▪ hypokalemia, hyponatraemia (SIADH), loss of Mg
▪ hyperuricemia
▪ hyperglycaemia
392

▪ dyslipidemia (↑ cholesterol and triglycerides)

▪ impotence
o contraindications
▪ type II diabetes
▪ hyperuricemia
▪ kidney failure
▪ dyslipidemia
▪ pregnancy
o indications
▪ Heart failure
▪ Older patients
o examples:
▪ Hydrochlorothiazide
▪ Chlorthalidone (thiazide-like)
▪ Indapamide (thiazide-like)
• Loop diuretics
o action: act on Na+- K+- 2Cl- symporter (cotransporter) in thick
ascending limb of loop of Henle to inhibit Na and Cl reabsorptin.
o side effects:
▪ loss of K, Na, Ca, Mg
o examples:
▪ furosemide - Lasix
• edema from heart failure, hepatic cirrhosis,
renal failure
• HTN – less potent than thiazides
▪ Bumetanide
▪ Ethacrynic acid
▪ Torsemide
• Potassium-sparing diuretics
o aldosterone antagonists
▪ spironolactone
o Epithelial sodium channel blockers
▪ amiloride
▪ triamterene
▪ 2. β-blockers
• types of β receptors
o β1-Adrenergic receptors are located mainly in heart and kidneys
o β2-Adrenergic receptors are located mainly in lungs,GIT, liver,
uterus, vascular smooth muscle and skeletal muscle.
o β3-receptors are located in fat cells.
• actions
o reduction in cardiac output (due to negative chronotropic and
inotropic effects)
o reduction in renin release from kidneys
o CNS effect to reduce sympathetic activity (for those ß-blockers
that cross BBB, e.g. Propranolol)
• indications:
393

o HTN - young patient, anxious patient

o angina, heart attack
o cardiac arrhythmia
• side effects
o fatigue, insomnia
o bronchospasm!
o dyslipidemia
o impotence
o stopping them can precipitate angina at rest!
o not to be used with verapamil/ diltiazem (bradycardia)
• contraindications
o Asthma, COPD
o Heart failure
o Bradycardia, heart block
o Dyslipidemia
o DM
o Peripheral vascular disease
• examples:
o Non-selective
▪ Propranolol
o Selective for β1-Adrenergic receptors
▪ Metoprolol, bisoprolol
▪ Atenolol
▪ Pindolol
▪ 3. Calcium-channel blockers
• actions
o Negative inotropic and chronotropic effects
o Vasodilation
o Relaxation of smooth muscle in bronchi
• indications:
o HTN
o angina, heart attack
o asthma
o cardiac arrhythmia
o peripheral vascular disease
• side effects
o edema
o CCF (with β-blockers and digoxin – verapamil, diltiazem)
o heart blocks
• contraindications
o heart failure
o flushing
o constipation (verapamil)
• examples:
o Dihydropyridine
▪ Nifedipine
▪ Amlodipine
394

▪ Felodipine
o Non dihydropyridine
▪ Verapamil
▪ Diltiazem
▪ 4. ACE inhibitors & AIIRA (Angiotensin II receptor antagonist, more selective
than ACE inhibitors, do not produce cough)
• actions
o vasodilation
o ↓ aldosterone (diuresis)
• indications:
o Hypertension
o Heart failure
o Peripheral vascular disease
o Diabetes
o Cardioprotective after a heart attack
• side effects
o dry cough
o disturbance in taste (dysgeusia)
o rash
o hyperkalemia
o first dose hypotension
o angioedema
• contraindications
o bilateral renal artery stenosis, precaution in CRF
o pregnancy
o hyperkalemia, avoid K sparing diuretics
o hypersensitivity to ACE inhibitors
• examples:
o ACE inhibitors
▪ captopril
▪ enalapril
▪ lisinopril
o AIIRA
▪ irbesartan
▪ losartan
▪ 5. Central-acting agents
• actions
o α 2 agonists - stimulate α 2 receptors in brain, which decreases
cardiac output and peripheral vascular resistance, lowering BP.
• indications:
o Hypertension – in asthma, pregnancy
• side effects
o sedation
o dry mouth
o constipation
o impotance
• contraindications
395

o Liver disease (methyldopa)

o Precaution in depression
• examples:
o Clonidine
o Methyldopa
▪ 6. α-Blockers
• Actions
o selective for α-1 receptors on vascular smooth muscle. These
receptors are responsible for vasoconstrictive action of
norepinephrine, which would normally raise BP. By blocking
these receptors, prazosin reduces blood pressure.
• Indications:
o HTN – Pt’s who can’t take Diuretics or β-blockers (diabetes,
asthma, dyslipidemia), peripheral vascular disease, heart failure,
prostatism (LUTS – lower urinary tract symptoms).
• Side effects
o first dose syncope
o orthostatic hypotension
o sedation, weakness
• Contraindications
o heart failure, orthostatic hypertension
o precaution in elderly pts
• examples:
o Prazosin
o Terazosin
▪ 7. α and β Blockers
• Labetalol
▪ 8. Vascular smooth muscle relaxants (other than Ca-channel blockers)
• indications:
o Refractory hypertensive states
o Hypertensive emergencies
• examples
- Hydralazine
- Minoxidil
- Diazoxide
- Sod. nitroprusside
- HTN – Murtagh 1296
o types
▪ Essential – 90-95%
▪ Secondary
• Kidney dis. – 3-4%
- GN
- Reflux nephropathy
- Renal aretry stenosis
- DM
• Endocrine
396

- Primary hyperaldosteronism (Conn’s syndrome)

- Cushing
- Phaeochromocytoma
- OCP
• Coarctation of aorta
• Drugs
• Pregnancy
• Immune disorders
- e.g. Polyarteritis nodosa
o approach in Rx
▪ 1. Lifestyle
• SNAP
- Smoking
- Nutrition
- Alcohol
- Physical exercise
• Wt. loss
• ↓ salt & stress
▪ 2. Drugs
• if lifestyle fails, treat if:
- Systolic 140 -180
- Diastolic 90 - 110
• targets
- < 140 - 90
▪ ≥ 65 yrs
▪ w/o
• DM
• Kidney dis.
• Proteinuria
- < 130/ 85
▪ < 65 yrs
▪ DM
▪ Kidney dis
▪ Proteinuria 0.25-1 g/ 24 hrs
- < 125/ 75
▪ Proteinuria > 1 g/ 24 hrs
• Strategy
- start with 1 drug
- not responding to Rx
▪ increase the antiHT drug to highest acceptable dose
▪ substitute with another drug from a compatible class
▪ add another drug from another class
- starting strategies – Murtagh 1307 + 1313
▪ thiazide
▪ diuretic +
• β blocker
• ACE inh.
397

▪ DM, dyslipidemia
• ACEI/ AIIRA
• Ca channel blockers
o Verapamil, diltiazem
o Nifedipine, felodipine
▪ coronary heart dis. (MI/ Ischemia)
• β blockers
• Nifedipine, felodipine
▪ congestive heart failure
• diuretic
• ACE inh./ AIIRA
- Cx in HTN
o HTN retinopathy – stages:
▪ I – Silver lining (silver wiring)-(Narrowing + ↑ reflectivity of vessels walls).
▪ II – Arterial & venous nipping (crossing over)
▪ III
• flame-shaped micro hemorrhages
• soft exudate (cotton wool)
▪ IV - Papilledema
o HTN ENCEPHALOPATHY
▪ Acute and malignant hypertensive crisis.
▪ Severe HTN (diastolic > 140 mmHg).
• very high BP (systolic > 200)
▪ Severe headache, confusion, vomiting and blurred vision.
▪ Focal neurological signs, seizures and coma may develop later.
▪ Fundoscopy: retinal hemorrhages, exudates and papilledema. (Grade IV
changes)
▪ DIAGNOSIS:
• ECG and CXR
• Examine a MSU for proteinuria and send it for microscopy to look for
evidence of renal disease, with casts or abnormal urinary RBC ( > 70%
dysmorphic)
▪ MANAGEMENT:
• Aim for O2 of 94%
• Aim to initially reduce main arterial pressure gradually by 25% or aim for
a diastolic BP of 100-110 within first 24 hours.
• Use Oral treatment with Labetalol 100 mg, Atenolol 100 mg or long
acting Nifedipine 20-30 mg.
Dyslipidemia
- Hyperlipidemia
o risk factors for
▪ Coronary artery dis.
• ↑ LDL and ↓HDL
• LDLC/ HDL > 4
▪ Pancreatitis
• TG > 10 mmol/L
o Goal:
398

▪ Cholesterol < 4 mmol/ L

▪ LDL < 2.5 mmol/ L
• < 2.0 in high risk pts
▪ HDL > 1 mmol/ L
▪ Triglyceride < 1.5 mmol/ L
o indic. to initiate the drug therapy: 1317 murtagh
▪ 1. Existing heart disease + cholesterol > 4mmol/ l
▪ 2. If one or more of these risk factrs + cholest. > 6.5 or cholest. > 5.5 & HDL < 1
• DM, HTN
• Familial hypercholesterolemia
• Family Hx of IHD: first degree relative < 60 yrs
• Peripheral vascular disease
▪ 3. HDL < 1 + cholest. > 6.5
▪ 4. Males 35-75 yrs and post menopausal women < 75 if cholest. > 7.5 or TG > 4
▪ 5. anyone if cholesterol > 9 or TG > 8
- Dyslipidemia drugs
o First line
▪ 1. HMG-CoA reductase inhibitors (Statins) - ↓ cholesterol synthesis + ↑
synthesis of LDL receptors, resulting in an ↑clearance of LDL from bloodstream
• Atorvastatin, Fluvastatin, Simvastatin.
- also combinations with Ezetimibe
• SE
- GIT side-effects
- myalgia, myositis
- liver dysfc. – uncommon
• monitor
- LFT
- CK
• 2. Ezetimibe – ↓ cholesterol absorption in GIT
• if statin-intolerant
▪ 3. Ezetimibe + statin
▪ 4. Bile acid sequestrants (resins) - they bind bile acids and sequester them from
enterohepatic circulation. Since bile acid sequesterants are large polymeric
structures, they are not well-absorbed from gut into bloodstream. Thus, bile
acid sequestrants, along with any bile acids bound to drug are excreted via feces
• Cholestyramine, colestipol
• SE
- constipation
- offensive wind
▪ 5. Fibrates: ↓ TG production in liver + ↑ HDL (less LDL reduction effect)
• Gemfibrozil, fenofibrate
• SE
- risk of myopathy
- Gallstones
- in combination with statins can cause rhabdomyolysis
• only used if other drugs are not tolerated
o Second line
399

▪ Nicotinic acid (Niacin, Vit. B3) – lowers cholesterol, increases HDL, lowers TG
▪ Probucol – lowers cholesterol absorption
▪ Estrogen – in postmenopausal women
▪ Omega-3 fatty acids in fish oil– lowers TG and cholesterol (VLDL)
o usage:
▪ Elevated LDL Cholesterol:
• statin + ezetimibe
• statin + resin
▪ Elevated TG:
• fibrates
• or nicotinic acid, n-3 fatty acids
• + decr. alcohol
▪ Mixed (CT and TG elevated):
• if TG < 4 – statin
• if TG > 4 – fibrate
- Familial hypercholesterolemia – Xanthoma (Yellowish plaque) on Achilles
- Familial combined hyperlidpidaemia – Xanthelasma ( yellowish plaque on superior & inferior
eyelid )
Rheumatology - OK
- Arthritis disorders:
o Simple analgezics – aspirin, paracetamol
o NSAID, Cyclo-oxygenase-2 (COX-2) specific inhibitors
o Disease-modifying agents
▪ Rheumatoid arthritis
• sulphasalazine
• hydroxychloroquine
• gold
• D-penicillamine
• methotrexate
• cyclosporin
• cyclophosphamide
• azathioprine
• leflunomide
• biological DMARDS
• fish oil – omega 3
▪ Systemic lupus erythematosus
• hydroxychloroquine
• azathioprine
▪ Spondylarthropathies
• sulphasalazine
• methotrexate
▪ Osteoarthritis
• glucosamine
• chondroitin
o Disease-suppresant agents
▪ corticosteroids
o Intra-articular injections
400

▪ corticosteroids
▪ hylan (hyaluronic acid)
o Surgery
▪ synovectomy
▪ joint replacement
▪ arthrodesis
- Gout
o men
o symptoms:
▪ arthritis
• monoarthritis 90%
- metatarso-phalangeal 75%
- other toes
- ankles
- knees
▪ tophi – in ears, elbow, big toes, fingers, Achilles tendon
▪ renal calculi
▪ high fever, fatigue
o risk factors:
▪ alcohol
▪ diuretic (thiazides)
▪ β blockers (?)
▪ niacin, aspirin, cyclosporin
▪ fructose sweetened drinks
▪ meat, seafood (purine-rich)
o precipitate an acute attack of gout in a susceptible individual
▪ alcohol
▪ surgery
▪ starvation
▪ drugs
• thiazides
• frusemide
• probenecid
• aspirin
• sulphonylpyrazone
o Dx
▪ monosodium urate crystals in synovial fluid or in tophus with strong negative
birefringence in polarized light microscopy
▪ hyperuricemia – 70%
▪ X Ray – punched out erosions at joints margins
o Rx of attacks
▪ 1. Indomethacin (or other NSAIDs) 50 mg until symptoms abate (3-5 days),
then taper to 25 mg until cessation of attack
▪ 2. Colchicine
• SE – diarrhoea
▪ 3. C/S intra-articular
▪ ACTH in difficult cases
401

▪ If gout + CRF = C/S

o Px of attacks
▪ Allopurinol
• indic.
- frequent acute attacks
- tophi or chronic gouty arthritis
- kidney stones or uric acid nephropathy
- hyperuricemia
▪ Probenecid – a bit less effective than allopurinol
- Pseudogout (Chondrocalcinosis)
o in elderly, on top of osteoarthritis
o Sx
▪ Knee
▪ Wrist
o Dx
▪ Ca pyrophosphate crystals -> polarized light microscopy of synovial fluid
shows weakly positive birefringent crystals
▪ X Ray: Calcification of articular cartilage
o Rx – Reverse compared to gout
▪ 1 - C/S intra-articular
▪ 2 - Colchicine
▪ 3 – Indomethacin
▪ Paracetamol
- Lordosis:
o 1st test – CT scan
o Most appropriate – densitometry
o MRI – best
Autoimmune diseases
- antibodies: Murtagh 284
o RF – RA, Sjogren
o Anti-CCP – RA Definite (MCQ)
o ANA – SLE, Scleroderma, autoimmune hepatitis
o Anti ds DNA (double stranded) --> SLE (more specific than ANA)
o Antiphospholipids - SLE
o AB to extractable nuclear antigen
▪ Anti Ro (SSA) – Sjogren, SLE
▪ Anti La (SSB) – Sjogren, SLE
▪ Anti Smith antibodies – highly specific for SLE (MCQ)
▪ Anti Jo-1, Anti MI-2 – Polymyositis, Dermatomyositis
▪ Anti-Scl 70 (anti-topoisomerase I) – Scleroderma (diffuse)
o Anticentromere AB – Limited sclerodema - CREST
o AMA (anti-mitochondrial AB) – Primary biliary cirrhosis, autoimmune hepatitis
o Anti gastric parietal cell antibodies – Pernicious anemia, atrophic gastritis
o Anti intrinsic factor AB: Pernicious anemia
o Celiac disease
▪ antigliadin AB (Screening only)
▪ antitransglutaminase AB
402

▪ antiendomysial AB
o Anti-thyroid microsomal AB - Hashimoto
o ANCA – antineutrophil cytoplasmic AB
▪ c-ANCA – Wegner granulomatosis
▪ p-ANCA – microscopic polyangitis, Churg-Strauss syndrome, Goodpasture?
o Anti-GBM – Goodpasture
o Anti acetycholine receptors AB – Myasthenia Gravis
o Anti smooth-muscle – Chronic active hepatitis
- Reiter vs. Behcet
Reiter (reactive arthritis) Behcet
Gender Men 10:1 Men 2:1
HLA HLA B27 HLA B51
Triad Triad: non-specific urethritis + conjunctivitis A rare immune mediated
(± iritis) + arthritis vasculitis (small arterioles) of
(similar, but w/o ocular and mucocutanous multiple organs
lesions = reactive arthrits)
Ulcers Painless ulcers Traid of oral, genital (scrotal,
labial ulcers) ulcers + Uveitis
Vision Conjunctivitis Uveitis, retinitis (severe pain
problems in eye,↓ eye vision)
Long term Rare Inevitable – prompt referral
ocular disability required!
Arthritis – long Frequent – 50% Rare (knees)
term Spondylitis, sacroilitis common + knees, ankle,
involvement toes polyarthritis
Cause After an acute inf. with specific venereal or Genetic, race
dysenteric organisms: Multiorgan dis. (vasculitis)
SARA (Shigella), CARA (Chlamydia)
Rx NSAIDs C/S, Immunosupressants
- Uveitis – always part of connective tissue/ autoimmune dis. (not inf. dis.)
o causes
▪ Behcet’s disease
▪ Reiter’s syndrome
▪ Ankylosing spondylitis
▪ IBS
▪ Psoriasis
▪ SLE
▪ (Sarcoidosis, Juvenile RA)
o Rx – treat underlying condition
- Connective tissue disorders
o WHEN TO SUSPECT?
▪ Middle aged person.
▪ Female: More common.
▪ Multisystemic involvement.
▪ Skin lesions + arthritis + other features
- SLE
o MC connective tissue disorder.
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o first investig. is always ANA

o Inflammation of muliple organs and production of autoantibodies that participate in
immunologically-mediated tissue injury.
o Incidence F:M = 10:1
o Age of onset: 15-40 years old.
o CLINICAL FEATURES:
▪ Arthritis: Peripheral polyarthritis with symmetric involvement of small and large
joints WITHOUT joint erosion.
▪ Skin lesions: Malar rash, discoid rash, rash on hands, photosensitivity.
• autoimmune thrombocytopenic rash ē Splenomegaly & menorrhagia
▪ Other features: Oral/ Nasal ulcers (painless), serositis (pleurisy, pericarditis,
peritonitis), renal, hematological and neurological involvement.
▪ alopecia
o DIAGNOSIS:
▪ For suspected SLE, the recommended approach is to perform an ANA test. If
positive then order dsDNA and ENA antibodies.
▪ ANA Test: highly sensitive 98%. – first test (Ket test)
▪ Anti-dsDNA Ab and anti-Sm Ab (ENA): highly specific 90%. – most specific
▪ ENA antibodies (anti-Sm).
▪ RF: Positive in 50%.
▪ ESR/CRP: Elevated in proportion to disease activity.
▪ we need at least 4 of these 11 criteria:
• 1. malar rash
• 2. discoid rash
• 3. photosensitivity
• 4. arthritis
- polyarthritis always – 2 or more joints
- symmetrical, non-erosive
• 5. serositis: pleuritis, pericarditis
• 6. nephritis
- MC cause of death in SLE! (MCQ)
- small proteinuria > 0.5 g/day
- 3 + casts
• 7. hematol. – anemia, neutropenia
• 8. neurol. – intractable headache, seizures, psychosis
• 9. oral ulcers – do not heal
• 10. immunol. – AntidsDNA, Anti-Sm, Anti-Ro, Antiphospholip., anti-
histone (drug induced: hydralazine, procainamide, propylthiouracil,
lithium, chlorpromazine)
• 11. ANA
o MANAGEMENT:
▪ MILD: NSAIDs for treatment of arthralgia.
▪ MODERATE: Low dose of antimalarials (hydroxychloroquine) specially with
dermatological lesions and constitutional symptoms.
▪ SEVERE: Steroids (oral, topical), Immunosuppressant (azathioprine,
methotrexate) drugs.
▪ UV sunscreen
404

- Scleroderma (Progressive systemic sclerosis)

o Generalized disorder characterized by fibrosis and degenerative changes in blood vessels,
visceral organs and skin.
o F:M = 3-4:1.
o Incidence peaks in fifth and sixth decade.
o No inflammation.
o CLINICAL FEATURES:
▪ I. Localized.
• Skin: Bilateral symmetrical swelling of fingers leading to skin tightening.
• Raynaud’s phenomenon (90%): Blanching and/or cyanosis of digits
followed by erythema, tingling and pain following cold exposure or
emotional stress.
- typical in scleroderma
▪ II. Generalised (limited or diffuse)
• limited cutaneous systemic sclerosis - involve areas distal to elbow and
knee but may involve face and neck
- CREST
▪ calcinosis of subcutaneous tissue in hands
▪ Raynaud syndrome
• present in:
o SLE
o RA
o dermatomyositis
o systemic sclerosis (scleroderma)
o worker with vibrating tools
o hematological
▪ thrombocytopenia?
▪ polycythemia
▪ cold aglutinin disease
o drugs - β blockers
o hypothyroidism
• not present in ankylosing spondylitis
▪ esophageal reflux
▪ sclerodactyly
▪ telangiectasia
• diffuse cutaneous systemic sclerosis - skin thickening on trunk and
proximal aspects of extremities in addition to involvement of face and
distal aspect of extremities
▪ Skin: hypo- or hyperpigmentation
▪ GI (90%): ↓motility with secondary dysphagia, GERD, diarrhoea, constipation.
▪ Joints: Polyarthralgias
▪ Kidneys (10-15%): Hypertension, oliguria.
▪ Lung: Interstitial fibrosis.
▪ Heart: Ventricular dysfunction.
o DIAGNOSIS:
▪ Anticentromere AB – limited sclerodema - CREST
▪ Anti-Scl 70 (anti-topoisomerase I) – scleroderma (diffuse)
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▪ ANA antibodies
▪ Skin biopsy
- Vasculitis
o Inflammation and necrosis of blood vessels resulting in ischemia and infarction.
o Any organ system can be involved.
o Keys to diagnosis: Clinical suspicion, laboratories are not specific, biopsy will confirm.
Small vessel Medium vessel Large vessel

Cutaneous vasculitis Polyarteritis nodosa Giant cell arteritis.

H-S purpura Kawasaki’s disease Takayasu’s disease.
Wegener’s vasculitis
- Henoch-Schonlein (anaphylactoid) purpura (HSP)-lasts 4 wks, autoimmune dis, IgA
mediated
o MC vasculitis in childhood.
o Peak incidence: 4-10 yrs.
o Recurrence: 1/3rd of pts.
o M > F.
o CLINICAL FEATURES:
▪ Often history of URTI 1-3 wks (Strep. group A) before onset of symptoms.
▪ Skin: Palpable, non-thrombocytopenic purpura (urticarial rash progressing to
purpura) in lower extremities, on extensor surfaces and buttocks.
▪ Joints: Arthritis involving large joints.
▪ GI: Colicky abdominal pain, Intussusception (2/3rd have mucosal hemorrhage
and edema and some of them will develop intuscs.)
▪ Renal: NEPHRITIS (Ig A nephropathy) hematuria, proteinuria -> can progress to
renal failure
▪ triad:
• Arthralgia
• Purpuric rash - palpable purpura - buttocks and down
• ± abd. pain
o DIAGNOSIS:
▪ Most appropriate – urine analysis: Up to 50% have microscopic hematuria
▪ FBE.
▪ Coagulation profile: Normal.
o complic:
▪ intussusception – very rare
▪ scrotal involvement (testicular torsion?)
o Rx.
▪ No treatment – self-limited in 90%
▪ C/S only for abd pain (if intussusception excluded - controversial)
▪ follow up on kidney function – renal disease may persist for a few yrs
- Polyarteritis nodosa = Vasculitis + mononeuritis (233- 428) MCQ.
o Inflammatory lesions of small and medium-sized arteries.
o Can present at any age: Average 35-50 yrs, men.
o MC organs involved are: Joints, peripheral nervous system, skin and kidneys.
o Sx
▪ Triad:
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• Arthralgia + weight loss + fever ± skin lesions + HTN

▪ migratory arthralgia and arthritis usually early in course.
▪ Peripheral neuropathy with sudden pain, paraesthesia, motor deficit and
mononeuritis multiplex, foot drop
▪ Skin: Digital infarcts, palpable purpura, skin nodules along arteries with
punched out ulcerations
▪ Kidney: Sec. HTN 25% of pts.
▪ fever, malaise, wt. loss
o Dx:
▪ p-ANCA AB – rarely pos.
▪ ANA AB – usually neg.
▪ Biopsy
• Muscle or skin biopsy – Necrotising vasculitis of small & medium arteries
• Renal biopsy: Important in diagnosis as this organ is commonly involved.
• Sural nerve biopsy – Best (Maria)
o Rx:
▪ C/S
▪ Immunsupressants
- Kawasaki – Vasculitis affecting medium size arteries
o < 5 yrs, boys
o Unknown aetiology. (Infectious?).
o Sx
▪ Acute stage = everything is red
• High fever > 39o C for at least 5 days + 4 out of these 5:
- Polymorphous rash (any kind) MCQ
- Dry, red, cracked lips + strawberry tongue + red pharynx
- Congested, red conjunctiva (non-exudated conjunctivitis) bilat.
- Red and edematous hand and feet,
- Cervical lymphadenopathy > 1.5 cm
▪ Later – peeling of skin
o Dx
▪ early – risk of myocarditis
▪ all the Ig are raised
▪ I – FBE:
• incr. leucocytes with premature forms in circulation
• incr. platelets (risk of thrombosis)
• incr. CSR, incr. CRP
▪ RF, ANA – exclude autoimmune diseases (Juvenile RA)
▪ rule out inf.
• Blood
• Urine
• CSF – sometimes
▪ II - then U/S
• repeated after 2 wks – monitor for aneurysms
o Cx
▪ Coronary artery disease.
▪ Aneurysm – risk 17-31%, mortality 0.5-2.8%
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o Rx
▪ Immunoglobulin IgG – 3-5 days + most imp to reduce aneurysms (MCQ)
▪ high doses of aspirin – risk of thrombosis
▪ If coronary artery disease: Anti-thrombotic therapy.
▪ NO C/S!!!
- Temporal arteritis
o Untreated can lead to blindness: 20-25%
o Commonly associated with Polymyalgia Rheumatica: 30% of pts.
o Peak onset: Over 50 yrs.
o MC in females.
o > 60% neurol. sequelae
o Sx
▪ Triad = fatigue + headache + jaw claudication
▪ Unilateral Temporal headaches and scalp tenderness.
▪ Sudden, painless loss of vision.
▪ Tongue and jaw claudication.
▪ Symptoms of polymyalgia rheumatica if present.
o DIAGNOSIS:
▪ Clinical Diagnosis.
▪ first test - Dramatically increased ESR.
▪ Increased CRP.
▪ Best test - Temporal artery biopsy: Confirms diagnosis.
o TREATMENT:
▪ High dose of prednisolone until symptoms resolve (1mg/ kg)
• IV – if visual symptoms present
• PO – if no visual sympt.
▪ Immunosuppressant drugs if refractory (?).
- Polymyalgia rheumatica (MCQ 2123 P 86)
o 30% association with temporal arteritis
o may be associated with carpal tunnel syndrome
o F:M=2:1, > 50yrs
o inflammatory condition of muscles: pain or stiffness usually in neck, shoulders and hips.
o Most PMR sufferers wake up in morning with pain in their muscles which are tender on
palpation.
o Sx
▪ triad: malaise + painful shoulder girdle + morning stiffness > 20 yrs
▪ pain and early morning stiffness (no weakness – but blue book MCQ 3.068
says: with proximal weakness) in proximal muscles or shoulder and pelvic
girdle, symmetrical
▪ Painful restriction of movement of shoulders and hips.
▪ O/E: Painful and tender muscles but no weakness or atrophy.
▪ weight loss, malaise, anorexia, fever, tiredness
▪ depression
o DIAGNOSIS: Requires:
▪ Age > 50 yrs.
▪ More than 2 affected muscle groups: Neck, hip and shoulder girdles, thighs.
▪ At least 2 wks duration
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▪ Increased ESR and CRP

▪ Normal CK!!!
▪ Muscle biopsy
o DIFFERENTIAL DIAGNOSIS:
▪ Chronic fatigue syndrome: Medically unexplained. Usually seen in younger pts,
associated with memory impairment, headaches, poor sleep, lymph node
tenderness. ESR, CRP and FBE are normal.
▪ Fibromyalgia: Medically unexplained, characterized by aching pains across
shoulders and upper back, skin tenderness, poor sleep pattern and
constitutional symptoms.
• ESR, CRP and FBE are normal
• Rx - Amytriptilline
▪ Polymyositis.
▪ Underlying malignancy: Prostate, breast in females, multiple myeloma, lung CA.
o Rx
▪ Start with Prednisolone 15-20 mg PO daily.
▪ If temporal arteritis is suspected, pt. should be given prednisolone
IMMEDIATELY (while arranging to confirm diagnosis with TA biopsy).
▪ Taper slowly over 2 year period monitoring ESR and symptoms closely.
▪ 50% relapse rate.
- Polymyositis/ dermatomyositis (233-427)
Polymyositis Dermatomyositis
CD8 cell mediated muscle necrosis. B cell & CD4 immune-complex mediated perifasicular vasculitis
Found only in adults Found in children and adults
No dermatological features. With dermatological features
F > M. F>M
o CLINICAL FEATURES:
▪ Proximal muscle weakness + Rash +↑CK
▪ Progressive symmetrical proximal muscle weakness: Shoulder and hip.
• The hip extensors are often severely affected, leading to particular
difficulty in going upstairs and rising from a seated position.
• Weakness is generally progressive, accompanied by lymphocytic
inflammation (mainly cytotoxic T lymphocytes).
▪ Atrophy of muscles
▪ muscle pain (50%)
▪ dermatomyositis
• Dermatological involvement:
- Gottron’s papules (70%) - erythematous, scaly eruptions over
knuckles of interphalangeal and metacarpophalangeal joints +
elbows
- heliotrope rash with edema
- shawl sign - diffuse, flat, erythematous lesion over back and
shoulders or in a "V" over posterior neck and back or neck and
upper chest, worsens with UV light
▪ Cardiac, GI, pulmonary involvement.
o DIAGNOSIS:
▪ 1 - Increased muscle enzyme levels: CK, LDH, ALT, AST.
409

▪ EMG
▪ Anti Jo-1, Anti MI-2 AB
▪ best - Muscle biopsy
o TREATMENT:
▪ Physical therapy
▪ Assessment of organ involvement
▪ High dose of C/S
▪ Immunosuppressive agents
▪ Immunoglobulin IV
▪ Malignancy surveillance (Ovarian, stomach, prostate, BCC, SCC increased)
- Sjogren’s syndrome:
o Chronic inflammatory disorder.
o CD4/ CD8 cell mediated infiltration and destruction of salivary and lacrimal glands.
o Pt’s with Sjogren’s syndrome are at higher risk of non-Hodgkin’s lymphoma.
o MC assoc. with RA
o CLINICAL FEATURES:
▪ Dry mouth: Difficulty swallowing food without drinking, carries, erythema of
oral mucosa.
▪ Bilateral swelling of salivary glands (parotids, submand.)
▪ Ocular: Burning, dry, painful eye relieved by tears, foreign body sensation,
blepharitis.
o DIAGNOSIS:
▪ Autoantibodies: Anti-Ro, Anti-La, RF
▪ Salivary flow measurements
▪ Salivary gland biopsy (MCQ)
▪ Schirmer test – shows ↓ lacrimal production
o TREATMENT:
▪ Good dental hygiene.
▪ Artificial tears
▪ Hydroxychloroquine, C/S, immunosuppressants for severe systemic
involvement
- Rheumatoid arthritis
o affects multiple joints, most commonly small joints of hands, feet and cervical spine,
symmetrically but larger joints like the shoulder and knee can also be involved.
o AB attack synovium – initially joint space is wider, then becomes narrow (not use it as an X
Ray criterion)
▪ then attack the bone (osteopenia, erosion)
o attacks synovium everywhere => symmetrical
o Sx
▪ Synovitis can lead to tethering of tissue with loss of movement and erosion of
joint surface causing deformity and loss of function
▪ Morning stiffness
▪ affects tendons and ligaments => Ulnar deviation of hands (Subluxation of
joints)
• Rx – fixation with metal rod in straight position (arthrodesis)
▪ Rheumatoid nodules – often subcut. usually found over bony prominences/
pressure points, such as olecranon, calcaneal tuberosity, metacarpophalangeal
joint or other areas that sustain repeated mechanical stress.
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• Nodules are associated with a +ive RF titer and severe erosive arthritis
▪ fatigue, malaise
▪ carpal tunnel syndrome
o lab:
▪ Rheumatoid factor – if negative, seronegative arthritis – 15% of patients
▪ anti-citrullinated protein antibodies (ACPAs). Like RF, these tests are positive in
only a proportion (67%) of all RA cases but are rarely positive if RA is not
present, giving it a specificity of around 95%.
• anti-CCP AB (cyclic citrullinated peptide) test and the Anti-MCV assay
(antibodies against mutated citrullinated Vimentin)
• RF and anti-CCP present = Worst prognosis
▪ ESR and CRP are elevated
o diagnostic - American College of Rheumatology has defined (1987) the following criteria
for classification of RA - at least 4 criteria have to be met for classification as RA
▪ Morning stiffness of >1 hr most mornings for at least 6 wks.
▪ Arthritis and soft-tissue swelling of > 3 of 14 joints/ joint groups, present for at
least 6 wks
▪ Arthritis of hand joints, present for at least 6 wks
▪ Symmetrical arthritis, present for at least 6 wks
▪ Subcutaneous nodules at specific places
▪ RF at a level above 95th percentile
▪ Radiological changes suggestive of joint erosion
o Murtagh 355 – DD of various arthritis types
o Rx
▪ Splintage
▪ Exercise
▪ Bed rest
▪ drugs
• Aspirin, paracetamol, fish oils
• C/S
• Methotrexate
• + sulfasalazine
• + hydrochloroquine
RA Osteoarthritis Gout
Primary joints MCP, PIP, wrist First MCP of thumb,DIP DIP
Symmetrical Cervical, lumbar spine, hips & knees joints
Heberden’s nodes on DIP Absent Frequently present
joint (osteophytes) +
Bouchard’s nodes (PIP
joint) less common
Joints Soft, warm, tender Hard and bony
Stiffness Worse after If present, worse after effort
resting (morning (evening stiffness)
stiffnes)
RF Positive Negative
anti-CCP AB Positive Negative
ESR and CRP ↑ Normal
411

X Ray 1. Erosion of joint 1. Loss of joint space 1.

margins 2. Periarticular bone sclerosis asymm
2. Osteopenia 3. Marginal osteophytes etl
3. Symmetrical + Cysts 2.
+ Cysts punche
+ Joint destruction d out
+ Subluxation erosio
ns
- Osteoarthritis
o wear and tear of cartilage (with poor blood supply) -> repair (poorer in elderly)
▪ body can’t give more cartilage, so it tries to compensate by producing more
bone
o earliest fc. lost in hip OA – internal rotation
o Rx
▪ NSAIDs, aspirin
▪ COX-2 inh.
▪ C/S intra-articular
▪ Glucosamine
- Juvenile chronic arthritis = Juvenile RA = Juvenile arthritis = Still’s disease
o Unknown etiolology
o < 16 yrs
▪ dis. frequently persists in adolescents
o types
▪ Pauciarticular ≤ 4 joints, M.C. - large joints: knee, wrist, ankle
• assoc with uveitis or sacroileitis
▪ Polyarticular > 4 joints
• large and small joints
• RF can be positive, rheumatoid nodules often present
• cervical spine is involved
▪ with systemic onset (with vasculitis) – with spiking fever, Salmon-pink rash on
trunks and extremities, arthritis, myalgia, hepatosplenomegaly, pericarditis
lymhpadenopathy, pleuritis.
o Dx:
▪ ESR incr., FBE (microcytic anemia, lymphopenia, platelet decr.)
▪ Pauciarticular – ANA +
▪ U/S – pericarditis?
o DD – rule out Septic arthritis -> perform arthrocentesis
o Rx
▪ Physiotherapy, occupational therapy
▪ NSAIDs
▪ IV IGs in systemic type with vasculitis
▪ C/S
▪ Methotrexate
▪ joint replacement
▪ Synovectomy may be required
- Rheumatic fever – see above
- Ankylosing spondylitis (HLA B27)
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o young men
o sacroiliac joints and spine – pain and stiffness
o also hips, shoulders, knees, ankles
o Morning stiffness
o Iridocyclitis, Uveitis
o Dx: XRAY of Sacro-iliac joint, investigation of choice.
o Rx
▪ Exercise
▪ NSAIDs
▪ Infliximab
- Psoriatic arthritis:
o Fingers and toes - DIP involvement
o Sacroilitis – like in Akylosing spondylitis
o RF neg.
- Goodpasture’s syndrome
o Hemoptysis + hematuria
o sore throat, cough, runny nose
o anti-GBM AB
o Dx
▪ Anti-glomerular basement membrane (anti-GBM) from lungs and kidneys
▪ p-ANCA?
o Rx
▪ C/S
▪ Immunosupressants
- Wegener granulomatosis
o Triads:
▪ Physiopathol: URT granuloma + fleeting pulmonary shadows (nodules) + GN
▪ Sympt: Malaise + URTs (rhinits, sinusitis), LRTs (wheeze, cough).
o 40-50 yrs
o Sx
▪ LRT + URT sympt.
▪ Polyarthritis
▪ Eye involv. – Orbital mass
▪ Oral ulcers
▪ GN 75%
o Dx
▪ C XRay: Multiple nodes (rubbery pulmonary masses) and cavitations
▪ c-ANCA (Antineutrophil cytoplasm AB)
▪ Dx confirmed by open lung biopsy
o Rx
▪ Cyclophosphamide
▪ Fatal w/o Rx!
- Takayasu’s arteritis – (Pulseless disease)
o Young Japanese females
o Large vessel vasculitis
▪ affects arch of aorta and other major arteries
o Sx
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▪ absence of peripheral pulse

▪ HTN
o Dx
▪ ESR, CRP
▪ Angiography of aorta
o Rx – C/S
Myopathies
- Proximal muscle weakness = can’t climb stairs & comb hair, no neurol. problems = Myopathy
- Polymyositis/ dermatomyositis – see above
- Duchenne’s muscular dystrophy – X linked recessive
o 2-5 yrs, Boys
o Progressive skeletal muscle degeneration, cardiac muscle involvement.
o Dystrophin, a missing muscle protein => muscle fibre fragility, breakdown and necrosis
o Sx
▪ Proximal muscle weakness by age 3
▪ Hypertrophy of calf muscles
▪ Wasting of thigh muscles
▪ Cardiomyopathy
▪ Can’t walk upstairs (14-22 mths should be able to do that)!
o Dx
▪ 1 - CK incr. 50-100 times
▪ 2 - Muscle biopsy – best for diagnosis
▪ EMG
o Prognosis
▪ wheelchair by 10-12 yrs
▪ die by age 20
o complic
▪ Scoliosis, flexion contractures, incr. risk of fractures
o Rx
▪ Supportive
▪ Oral prednisolone – slows progress of disease
- Post-viral myositis
o Rx – analgesia
▪ Paracetamol
▪ Ibuprofen
- Inclusion body myositis – Predominantly distal muscle weakness
- Myositis = SE of statins
o Statins + fibrates = Bad combination -> risk of myopathy (Simvastatin myopathy)
o even worst with Erythromycin – liver enzyme inhibitor
o causes Rhabdomyolysis
o Check serum CK and urine myoglobin
- Rhabdomyolysis
o Sx
▪ Muscle pain, swelling, red-brown urine
o causes
▪ burns
▪ trauma
414

o Dx
▪ CK
▪ urine
• Blood
• Myoglobin
o Rx – Supportive
- Myoglobinuria/ hemoglobinuria (not hematuria) – no RBCs on microscopy.
Endocrinology - OK
- Insulinoma
o incr. insulin, proinsulin and C-peptide levels
o hypoglycemia improved by eating
o U/S – pancr. tumor
- Paraneoplastic syndromes
o in CAs of lung, liver, stomach
o Sx
▪ hypercalcemia
▪ hypokalemia
▪ hypoglycemia
▪ etc.
o e.g.
▪ Squamous cell carcinoma
• Hypercalcemia – production of parathyroid hormone-related peptide
(PTHrP)
- Sx - fatigue, constipation, polyuria, confusion, coma
▪ Small cell carcinoma
• SIADH – hyponatremia (less than 120mmol/L) with hypervolemia.
• Ectopic ACTH secr. – (Cushing syndrome) Stimulates melanocytes -> ↑
skin and mucosal pigmentation.
o Dx diff. with carcinoid syndr. –> here Sx appear long before the local growth and metast.
▪ Carcinoid syndrome
• Symptoms sec to carcinoid tum. (which can occur anywhere in GIT +
lung).
- MC in appendix, ileum, rectum, caecum, lungs
• due to incr. production of serotonin metabolyte: 5-HIAA
• flushing of the skin, wheezing, bronhoconstr., diarrhoea, abd. pain, hT,
right side of heart affected (tricuspid valve dis. syndrome - prolif. of
myocytes on the valve)
• Dx
- urine 5HIAA
- chromograffin test
• Rx
- octretide
- tumor resection
• Bouts of flushed face
- w/ diarrhoea – Carcinoid syndr. – Dx. 5-HIAA
- w/o diarrhoea – Phaeochromocytoma
- Acromegaly
415

o Sx
▪ Triad: Nasal problems + fitting problems (rings, shoes, etc.) + incr. sweating
▪ excessive growth of hands, tissues (nose, lips, face), feet, jaw and tongue
▪ Weakness, sweating, headaches
▪ Amenorrhoea, loss of libido
▪ Sleep apnoea
▪ Glycosuria
o Dx
▪ Measurement of GH levels after glucose challenge test (OGTT)
• hyperglycemia inhibits release of growth hormone in normal people
▪ Insuline-like growth factor 1 (IGF-1) – Key test
Hyperprolactinemia
o causes
▪ Physiol. –Pregnancy, breast-feeding, intercourse, sleeping, stress
▪ tumors
• Prolactinoma = prolactin-producing tumor in anterior pituitary gland
- very high levels of prolactin (especially in macroadenomas)
• Pituitary adenoma - tum. that compress stock of pituitary gland (releases
dopamin which inhibits release of hormones from Anterior pituitary - FSH,
LH, ACTH, Prolactin - or Posterior - Vassopresin, Oxytocin)
▪ Hypothyroidism, PCOS, POF – through -ve feedback, stimulate pituitary gland
▪ sarcoidosis
▪ renal failure
▪ cirrhosis
▪ silicosis
▪ breast trauma
▪ breast herpes zoster
▪ drugs
• drugs that inhibit dopamine
- typical antipsychotics (haloperidol) and some atypical
antipsychotics (risperidone, amisulpride)
• fluoxetine (SSRI)
• metoclopramide
• ranitidine
• estrogen (HRT) – MC cause
• methyldopa
• Ca channel blockers
• estrogen
- (drugs causing gynecomastia:
- digoxin
- isoniazide
- spironolactone, steroids
- cimetidine
- omeprazole
- metyhldopa, marijuana
- estrogen
- + calcium antagonists, amiodarone, TCAs
416

- NOT: furosemide, labetalol)

▪
Purple book – causes in women:
• defic. in release of dopamine (70%)
• pituitary or suprapituitary tumor (25%)
• primary hypothyroidism (1%)
• other causes (4%)
o Sx
▪ Women
• Galactorhea – if very high levels of prolactin: in pituitary tumors
• Oligo – amenorhoea
• Infertility
• decreased libido
▪ Men
• decreased libido
• ED
• gynecomastia – rare (but not galactorrhoea)
▪ osteopenia
▪ headache
▪ bitemp. hemianopia
o Dx
▪ Prolactin – after fasting
▪ check cause: MRI, CT scan – pituitary tumor
• Microadenoma < 1 cm
- MRI every year – check growth
• Macroadenoma
- MRI every 6 mths
- test visual field
o Rx
▪ if primary – Dopamin agonists (inhibit release of prolactin from pituitary)
• Bromocriptine
- stop if woman gets pregnant
• Cabergoline – better but more expensive
▪ for Oligo – amenorhoea -> OCP
▪ drug induced – stop drug
▪ Pituitary tumor -> dopamin agonists:
• shrink tumor
• stop galactorhoea
- Adrenal glands:
o Medulla (MSR)
▪ Produces catecholamines: Epinephrine, Norepinephrine
▪ disease:
• Phaeochromocytoma
- encapsulated tumor
- incr. catecholamine
- Sx
▪ Sustained HTN with paroxyms of:
• throbbing headache
417

• sweating
• palpitations
• angina can occur
• Bouts of flushed face
o w/o diarrhea - Phaeocromocytoma
o w/diarrhea- carcinoid syndr. – Dx. 5-
HIAA
- Dx
▪ 24 hrs urinary free catecholamines – incr.
o Cortex (CSR)
▪ Produces:
• Glucocorticoids (Cortisone, Corticosterone)
• Mineralocorticoids - Aldosterone
• Androgens – Testosterone
▪ diseases
• Addison’s disease – deficit of glucocorticoids and mineralocorticoids
- causes
▪ TB in adrenal glands
▪ Amyloidosis
▪ Autoimmune destruction
▪ Adrenoleukodystrophy
- Symptoms:
▪ triad: fatigue + a/n/v + abd. pain + skin discoloration
▪ orthostatic hypotension– which doesn’t respond to NS
▪ fatigue, malaise
▪ hyperpigmentation on knuckles, creases of palms,
elbows and scars, oral mucosa, gums
▪ hyponatremia and hyperkalemia - deficit of
aldosterone
▪ hypoglycemia
▪ metabolic acidosis
▪ hypercalcemia
▪ Addisonian crisis:
• Symptoms aggravated after infection, sudden
steroid withdrawl or adrenal hemorrahge
• can be lethal if untreated
• Rx – Hydrocortisone IV
- Dx
▪ confirm:
• cortisol
• ACTH
- Rx - hydrocortison
• Cushing’s syndrome
- causes:
▪ taking glucocorticoid drugs
▪ Cushing’s disease – adenoma of pituitary gland that
produces too much ACTH (pituitary Cushing).
418

▪ Adrenal Cushing (adrenal gland tumor)

▪ Paraneoplasic syndrome – excess of ACTH - Small C CA
- symptoms
▪ Triad: Plethoric moon face + thin extremities + muscle
weakness.
▪ central obesity, buffalo hump, moon face, skin bruising
▪ thinning of skin, purple or red strie (due to wt. gain)
▪ Small cell CA -> ↑ACTH-> stimulates melanocytes -> ↑
skin and mucosal pigmentation.
▪ hypernatremia -> HTN
▪ DM --> Polyuria
▪ Hypokalemia
▪ Hyperhidrosis
▪ hirsutism, baldness, ↓ libido, impotence, infertility
- Dx
▪ Plasma cortisol
▪ Overnight Dexamethasone suppression test
▪ Abd. CT
- Adrenal tumor 1.5 cm + asympt
o Repeat CT scan in 6 mths
- Adrenogenital syndrome = Salt-losing congenital adrenal hyperplasia (↓Na & Cl, ↑K )= Baby
vomits soon after birth.
o Deficit of cortisol
o Leads to virilization

Thyroid pathology
- Murtagh – P 221 – table for Sx
Hypothyroidism Hyperthyroidism
Risk factors Autoimmune dis. (Hashimoto) Graves’
Down’s Excessive thyroxine
Turner’s Hot nodules
Rx: Radioiodine, Amiodarone, Lithium Amiodarone – less frequently
Thyroid surgery Inf. (De Quervain’s subacute
Postpartum (Sheehan’s syndrome) thyroiditis)
S/s General Tiredness, lethargy, cold intolerance Anxiety, agitation, restlessness,
heat intolerance
Psychiatric Depression, psychosis Psychosis
MSK Weakness, decr. reflexes, myalgia, carpal Weakness, incr. reflexes, clonus,
tunnel syndrome proximal myopathy, fine tremor
pain in shoulders due to calcific
tendinitis -> adhesive capsulitus
Skin Dry, cold, coarse Warm skin, moist or sweaty
Myxedema (non-gravity dependant)
Thin hair, brittle
Face Puffy Exophtalmos, lid lag
Cardiovasc. Bradycardia, AMI, cardiomyopathy, Tachycardia, heart failure, AF, HTN
cardiomegaly (Systolic) wide pulse pressure
419

Endocrine Goitre, infertility (PCOs) Goitre, gynecomastia

Hyperprolactinemia -> Galactorrhoea
O&G Menorrhagia, oligo- or amenorrhoea Oligo- or amenorrhoea
Neurol Ataxia Tremor
Other ↓ libido, constipation, wt. gain, anemia Wt. loss, fever (thyroid storm)

TSH T4 T3 Rx
Primary hypothyroid. Incr. Decr. Decr. Thyroxine:
Non-vasc. Pt: Start with 50 µg/day
Vasc. patient, > 65: do ECG (address any
vasc. problems first), then start 25
µg/day (thyroxine can cause an Acute
Cor. Synd.) Test TSH, T4 every 4-6 wks
until you reach desired level: if needed
↑ in increments of 25 µg. Then 1-2
times after 6 mths. Then yearly. In
pregnacy: check at least every trimester
Sec./ central hypothyr. N or Decr. N or ↓ Inx MRI
(hypothalamus) decr.
Hyperthyr. Decr. Incr. Incr. 1. β blockers (for tachycardia & palpit.)
2. First try Propylthiouracyl (PTU) or
Carbimazole (in pregnancy)
3. Radio iodine (before surgery)
4. Surgery
5. in subacute thyroiditis: symptomatic
Sick euthyroid N or a N or a N or a Only symptomatic (self-limited)
(post-op. – response to bit bit bit
stress: cortisol ↑ ≥ decr. decr. decr.
TSH, T3, T4 just a bit ↓
but with symptoms
- thyroid problems
o Sx
▪ dysphagia
• painful in inflamation – Hashimoto
• complete – anaplastic carcinoma
▪ stridor – requires urgent surgery
o Dx
▪ blood hormones: T1, T3, TSH, calcitonin, Ca
▪ U/S
▪ FNAC
• thyroiditis?
• nodules
▪ thyroid scintigraphy - scan
• diffusely increased activ.
- Graves dis.
• diffusely decreased activ.
- subacute thyroiditis
420

- silent thyroiditis
- post-partum thyroiditis
• diffusely heterogenous activity
- toxic multinodular goitre
• focally increased activity
- hyperfc. adenoma
o thyroglossal cyst
o thyroid cyst
▪ Dx – U/S
o nodules
▪ single – benign
▪ multinodular goitre – benign
• less likely to be malignant than a single nodule
• a multinodular goiter is with hyperthyr.?
▪ Toxic nodule
• Dx
- Localized increased uptake of radioiodine
▪ Cold nodule
• Dx
- Localized decreased uptake of radioiodine
- CA?
o Thyrotoxycosis
▪ types
• Primary = Grave’s disease
- autoimmune
- Sx
▪ Diffuse goitre
▪ Exopthalmia, lid lag
- Dx
▪ Diffusely increased uptake of radioiodine
• Secondary
- hot nodule
- De Quervain’s subacute thyroiditis
▪ post. inf. – Viral, URTI
▪ initially hyperthyr., then hypothyr.!
▪ Sx
• fever
• enlarged painful thyroid
• tender lump or swollen goitre
▪ Dx
• diffusely decr/ no uptake of radioiodine
• incr. T3 and T4, decr. TSH
• no AB
o Dx diff from Graves
▪ Rx
• Propranolol
• Paracetamol
421

▪ Self-resolving
▪ Sx
• triad: anxiety + wt. loss + weakness
• amenorrhoea (everything else incr.)
▪ Rx
• Antithyroid drugs (thyrostatics) - inhibit production of thyroid hormones:
carbimazole, methimazole, propylthiouracil
• β-blockers: propranolol, metroprolol
• Radioactive iodine therapy ( I131)
• Surgery
o Thyroid crisis (thyroid storm)
▪ An emergency life threatening condition caused by sudden rise in thyroid
hormones. Sx precip. by surgery or inf. in undiagnosed patient.
▪ Rx
• emmergency admission!
• antithyroid drugs
• C/S
• anti-heart failure and antiarrhythmic drugs
o Hyperthyroidism in pregnancy
▪ dangerous for baby
• Premature delivery
• IUGR
• Fetal death
• Malformations
▪ Rx
• medical
- Propylthiouracil
▪ passes less to baby
▪ risk of hypothyroidism in mother
• check level of T4 in mother regularly
- Carbimazole – if propylthyouracil doesn’t work
▪ long acting thyroid stimulator -> protector? detect
status of baby
• if not working -> surgery
• radioactive Rx is prohibited!
o Hypothyroidism
▪ Sx
• Triad: tiredness + husky voice + cold intoleration
• Menorrahagia (everything else decr.)
▪ Rx
• Thyroxin – monitor TSH levels:
- check every month, till stable
▪ check every 2-3 months, till stable
• check every 2-3 yrs
o Hashimoto’s thyroiditis
▪ autoimmune
422

▪ initially thyrotoxycosis, then myxedema

▪ MC cause of bilateral non-thyrotoxic goitre in Aus.
▪ Dx
• anti-thyroid microsomal AB MCQ
• aspiration cytology
o Non-toxic goitre
▪ Puberty – temporary
▪ Pregnancy – temporary
▪ Menopause
▪ Low iodine in water/ diet – in Tasmania
o Hypothyroidism in pregnancy
▪ Sx
• increased miscarriage
• still birth
• premature birth
▪ Rx
• thyroxine
• if woman already with hypothyr, ↑ dose by 25 µg during pregnancy
- return to normal dose after delivery
o Thyroid CA
▪ types
• Papillary – MC (75-85%)
- excellent prognosis
• Folicullar – 10-20%
- excellent prognosis
• Medullary – 5-8%
- part of MEN-2 syndrome (multiple endocryne neoplasia)
- poor prognosis
• Anaplastic < 5%
- can cause complete dysphagia
- poor prognosis - not responsive to Rx
• + lymphomas, SCC
▪ Sx
• Painless nodule
• Hoarseness of voice = spread to soft tissues in neck, affecting recurrent
laryngeal nerve = inoperable tumor
▪ Dx
• Scan - cold nodule
• FNAC – investigation of choice
▪ Rx
• very high cure rate with Rx!
• thyroid ablation
- thyroidectomy
- I131 ablation
• followed by thyroxine replacement Rx for rest of his life
- Causes of unilat. exophtlamia
o Grave’s dis. - MC
423

o contralateral Horner?
o cavernous sinus pathology
o intraorbital pathology
- Stridor post-thyroidectomy (due to haematoma) -> open wound/ all (superficial/ deep)
sutures in ward
Hyperparathyroidism
Ca PO4 ALP PTH
Multiple myeloma Incr. Incr. or N N N
Paget’s dis. N N Very very incr. N
Primary hyperparathyr. Incr. Decr. Slightly incr. or N Very very incr.
Osteoporosis N N N N
Osteomalacia (↓bone density) Decr. Decr. N N
Malignancy Incr. Incr. Incr. N
CRF Decr. Incr. Incr. or N N
o Types
▪ Primary
• Parathyroid adenoma →↑ PTH→ ↑ Ca
▪ Secondary
• ↓ Ca →↑ PTH
o MC cause of isolated (asymptomatic) hypercalcemia
o Sx
▪ Moans – muscle aching
▪ abd. groans – abd. pain, gastroesoph. reflux, constipation
▪ Stones - Renal
▪ Bones – pain, back pain
▪ Psychic overtones - fatigue, depression
o Dx
▪ PTH very incr.

DM
- Murtagh – 194 – Dx + 1320 Rx + Jay’s notes
- Sx
o Polyuria + polydipsia + Wt. loss
o Lethargy
o Neuropathy
▪ diabetic foot ulcer is MC cause of prolonged hospital stay in DM
▪ if DM is properly controlled, amputation can be reduced by 50%
▪ if untreated, 1/3 of DM patients will have amputation due to DM neuropathy
▪ with presence of normal pedal pulse, dev. of foot ulcer is unlikely
▪ types:
• MCQ: burning pains in feet, pins and needles in fingers and toes,
weakness and unsteadiness of legs, distal wasting and weakness in all
limbs, glove and stocking sensory loss of all modalities, areflexia.
• 1. Sensory polyneuropathy – Bilateral peripheral symmetrical (glove
& stocking distribution) ē numbness, tingling, pain often worse at night
- Rx
▪ Paracetamol/ aspirin
424

▪ Gabapentin
▪ TCA
• 2. Moneneuritis - cranial nerve neuropathy
- III, IV
- difficult to Rx – C/S
• 3. Amyotrophy – asymetrical motor neuropathy
- a. Painful wasting of quadriceps (lumbosacral radiculopathy)
▪ Dx – EMG
- b. focal neuritis – pain & tingling of anterior surface of thighs
▪ Rx - Immunglobulins
• 4. Autonomic neuropathy
- heart – Orthostatic hypotension, tahycardia
- GIT – Gastroparesis (bloating, early satiety)
▪ usually slower GIT movement => bacterial overwgrowth
=> diarrhoea
- Urine retention
- ED
▪ Rx
• Amytryptilline
o HbA1C < 6.5% normal
▪ control in last 3 months
o Childhood DM
▪ Polyuria, Polydypsia, wt. loss (despite polyphagia)
• Rx
- insulin: 2 divided doses
- 0.5 unit/kg/day - honeymoon period (first 2 weeks after Dx)
- 1 unit/kg/day – older child
- 1.5 unit/kg/day adolescent
▪ 2/3 in the morning + 1/3 in the evening
▪ 2/3 long / intermed. + 1/3 short acting
• Dx – blood sugar
o Rx
▪ types of drugs
o Insulin
o Oral hypoglycemic agents
▪ Insulin secretagogues
• sulfonylureas: glipizide, gliclazide, glibenclamide,
tolbutamide, chlorpropamide
• (me)glitinides: repaglinide
▪ Insulin sensitisers
• Biguanides: metformin
• Glitazones: pioglitazone, rosiglitazone
▪ alpha-glucosidase inhibitors - slow the digestion of starch in the
small intestine, so that glucose from the starch of a meal enters
the bloodstream more slowly, and can be matched more
effectively by an impaired insulin response or sensitivity
• acarbose
425

▪ Peptide analogs
• incretin mimetics
o GLP analogs: exenatide
• DPP-4 inhibitors
o vildagliptin
▪ Amylin analogs
▪ approach
• type II
- start with lifestyle changes – 2-3 month trial
- if not controlled, then start Metformin – incr. dose to max.
- then add Gliclazide – incr. dose
- then add Acarbose – incr. dose
- then insulin
• type I
- insulin
▪ ultra-short: Lispro
▪ short acting: neutral
▪ intermediate acting: Isophane, Protophane
- Cx
o 1. Hypoglycemia
▪ glucose < 3 mmol/L
▪ Sx - sweating, anxiety, hunger, palpitations, confusion, drowsiness, seizures,
coma
▪ types
• Mild-moderate = conscious patient
- Oral food containing glucose (20-25 g glucose)
• Severe = unconscious or delirious
- 20-30 ml of 50% glucose/ dextrose IV (hospital) in cubital fossa
(not in hand – high glucose concentration could cause
thrombosis of small veins) or
▪ 1 ml glucagon IM (at home, in ambulances)
- in kids – 10% glucose (50% could cause complic.?)
- neonatal hypoglycemia
▪ 5ml/ kg 10% dextrose IV over 5 min
▪ then 100 ml/kg/day IV infusion
- at home – apply instaglucose – rub gel on gums
o 2. DKA (Diabetic Ketoacidosis)
▪ Hyperglycemia + dehydration + ketonuria +hyperosmolality+ high anion gap
▪ Ketonuria = production of ketone bodies is a normal response to a shortage of
glucose, meant to provide an alternate source of fuel from fatty acids.
• causes
- in DM – especially type 1
- in significant dehydration and electrolyte loss (e.g. massive
vomiting)
- in starvation
▪ MCQ: K+ shifts to extracel space → K+ in blood is incr., but total body K+ (intra
+ extracel) is low (due to renal loss)
426

▪ child is very dehydrated (main problem), confused in the morning, with

urinary ketones
▪ Rx
• 10 U insulin IM
DKA 48hrs
Normal saline 30x85 + 30x10 – bolus (1hr) -> to be
1. Bolus: 10ml/kg given in the next 23 hrs
+ 2. Maintenance:
85ml/kg (or
First 10 kg – 100 ml/kg
Next 10 kg – 50ml/kg
> 20 kg - Left 25 ml/kg)
+ 3. Losses:
Maintenance: .45ml NaCl + 5% Dextrose -> till glucose
becomes 12-15 mmol/L -> then add insuline (1 unit/kg)
If hypokalemia:
40 mmol/L < 30 kg
60 mmol/L > 60 kg
o 3. Hyperosmolar hyperglycemia
▪ marked hyperglycemia + dehydration + high plasma osmolarity, but w/o
ketonuria
▪ in type 2 DM
▪ Rx
• fluids
• insulin
o 4. Lactic acidosis
▪ metabolic acidosis with large anion gap
▪ DM type 2 Rx with metformin, especially if RF is present
▪ Rx
• removal of cause
• fluids
• alkalinisation with IV sodium bicarbonate
Oral pathology - OK
- Submand. vs. Parotid gland pathology
o Angle of jaw
▪ Visible = Submandibular lesion
• Dx
- 1st - Bimanual palpation
- most appropriate - intraoral X Ray
- Best test = CT
- Orthopantomogram – Panoramic X Ray of all teeth
▪ can miss small stones
▪ Not clearly visible = Parotid
• Dx – 1st and best = U/S
- Parotid and prostate – U/S
• no FNAC for scrotum and parotid
o Submand. swelling and ear pain
427

▪ examine what? tongue CA (with retroauricular lymph nodes?)

o Pathology
▪ Parotid (Bening tumors no invasion of facial N but CA do)
• tumors
- Pleomorphic adenoma – Benign
▪ MC (benign) tumor of parotids
• admixture of polygonal epithelial and spindle-
shaped myoepithelial elements
▪ Displaces ear lobe
▪ dosn’t cause facial n. palsy
- Adenolymphoma (Warthin tum., monomorphic adenoma) –
benign tumour of salivary glands (e.g. parotids)
▪ 2nd MC benign parotid tumor.
- CA
▪ Salivary glands (parotid) cancers
• Mucoepidermoid CA – most popular
• Adenoid cystic cancer – 2nd most popular
▪ facial nerve palsy + palpable lymph nodes + later on
pain + lump of parotid
▪ Dx – initial test = U/S
▪ Cx - invasion of facial nerve -> facial palsy
▪ Rx: Total parotidectomy
• Stones
-
painful swelling precipitated by anticipation of food (before
meals)
▪ Swelling appears before eating and goes away a few
hrs after eating = Stone
▪ Submandibular
• tumors
- more common CA than parotid tumors
- lower and more anterior than parotid tumors
- don’t displace ear lobe

Head and neck masses - OK

MIDLINE ANTERIOR TRIANGLE POSTERIOR TRIANGLE
Thyroid nodule Branchial cleft cyst Developmental remnants
- Cystic hygroma
- Bronchial sinuses and cysts
Thyroglossal duct cyst Carotid body tumor Pancoast tumor (from apex)
Dermoid cyst Carotid aneurysm Cervical rib
Midline cervical lymph Lateral thyroid tumors (metastasis)
o locations
▪ Ant neck triangle
• Branchial cleft cyst – MC in ant. triangle
- MC cystic lesion of anterior triangle of neck in children
- Unilocular, cystic mass displacing submandibular gland anteriorly
and sternocleidomastoid muscle posteriorly. Overlapped by SCM.
428

- Dx diff with submandibular gland lesion

▪ when palpating cyst it will not produce any saliva or
puss etc in mouth
▪ closer to SCM (following its line) than mandible (lower)
- Rx
▪ Removal of cyst

•
• carotid body tumor
• carotid aneurysm
• lateral thyroid tumor (metastases)
▪ Post neck triangle
• developmental remnants
- Cystic hygroma

-
▪ can be huge
▪ soft, transilluminated
▪ May be macrocystic or microcystic
▪ MRI is gold standard for radiologic evaluation
- Bronchial sinuses and cysts
• Pancoast tumor (from lung apex)
• cervical rib
▪ Midline
• thyroid nodule
• Thyroglossal duct cyst:
- Midline lesion anywhere from foramen cecum and thyroid gland
- May contain ectopic thyroid tissue
- May contain all functioning thyroid
- Ultrasound, thyroid scans
- moves with protrusion of tongue + moves with swallowing
- Rx
▪ Surgical excision - Sistrunk procedure
429

o
• dermoid cyst – beneath the chin
• midline cervical lymph node swelling
▪ anywhere/ widespread
• sebaceous cyst
• lipoma
▪ submandibular
• salivary gland tumor
• cervical actinomycosis
• sternocleidomastoid tumor
ENT - OK
- uvula is shy (away from the lesion) and the tongue is bold (towards the lesion)
Laryngeal pathology
- Laryngitis
o acute
▪ hoarseness
▪ loss of voice
o chronic
▪ due to
• smoking
- active
- passive (in barmaids, etc.)
• voice abuse
- Laryngeal CA
o Hx of chronic laryngitis and smoking
o might be preceeded by leukoplakia
o hoarseness of voice + lump (cervical l. node) + sore throat + cough + stridor + earache
o Rx
▪ Radiotherapy, laser therapy
▪ Laryngectomy.
- Laryngomalacia
o MC cause of stridor in infants
▪ Usually presents as inspiratory stridor within first 6 months of life.
o 90% of pts will have spontaneous resolution of symptoms usually by 12 mths of age (18
mths – 2 years).
▪ 10% require surgery.
430

o Main congenital abnormality of larynx.

o Immature aryepiglottic folds and glottis.
o Increased tendency of larynx to collapse in inspiration.
o Sx
▪ Stridor is intermittent and variable in intensity
▪ Symptoms worsen during sleep and positional variations occur (worse when
supine, improve when prone)
o Diagnosis
▪ Confirmed upon flexible laryngoscopy with findings of supraglottic tissue into
laryngeal inlet during inspiration.
• tongue and epiglotis falls back causing stridor
▪ Laryngotracheobronchoscopy to rule out any synchronous airway pathology
▪ Polysomnography to detect episodes of hypoxia or hypercapnia
o Management
▪ Most don’t require intervention due to a high rate of spontaneous
improvement
▪ 10-20% of synchronous airway lesions (patients with more severe symptoms
should undergo direct laryngoscopy & bronchoscopy to assess entire
tracheobronchial tree)
▪ GER (reflux) can exacerbate laryngomalacia & should be treated medically
▪ Surgical intervention is indicated for appx. 10% of pts – indications are severe
stridor, apnea, failure to thrive, pulmonary HTN and cor pulmonale.

Ear and hearing problems

- Screening for hearing loss
o 8-9 mths
o school entry
- Audiologic Testing
o 0-3 months
▪ ABR
▪ Auditory Steady State Response (ASSR)
o 2-12 months
▪ BOA (behavioural observation audiometry)
o 7-30 months
▪ VRA (visual reinforcement audiometry)
o 24 months – 6 years
431

▪ Play audiometry
o 6 years +
▪ Modified play audiometry
o 8 years +
▪ Standard adult audiometry

1. Rinne test - Place a vibrating tuning fork (512 or 256 Hz) initially on mastoid process until sound
is no longer heard, tuning fork is then immediately placed just outside ear. Normally, sound is
audible at ear. It’s a test of outer and middle ear.
2. Weber test - A vibrating tuning fork (either 256 or 512 Hz) is placed in middle of forehead, chin,
head equidistant from patient's ears. Pt. is asked to report in which ear sound is heard louder.
a. A patient with a unilateral conductive hearing loss would hear tuning fork loudest in
affected ear (because conduction problem masks ambient noise of room, whilst well-
functioning inner ear picks up sound)
b. A patient with a unilateral sensorineural hearing loss would hear sound louder in normal
ear (because affected ear is less effective at picking up sound even if it is transmitted
directly by conduction into inner ear.)
Normal ear, air conduction (AC) is better than bone conduction (BC) AC > BC = + Rinne
In conductive hearing loss, bone conduction is better than air AC < BC = - Rinne
In sensorineural hearing loss, BC and AC are both equally depreciated,
AC > BC = + Rinne
maintaining relative difference of bone and air conductions
MCQ 2012, P 49
Conductive hearing loss
Criteria Sensorineural hearing loss
(weird behavior!)

Anatomical Inner ear, cranial nerve VIII or central processing Middle ear (ossicular chain), tympanic
Site centers membrane or outer ear

Sound localizes to affected ear (ear

Weber Test Sound localizes to normal ear
with conductive loss)

+ Rinne; AC > BC (both air and bone conduction

Rinne Test are decreased equally but difference between them - Rinne; BC > AC (Bone/Air Gap)
is unchanged)

Hear better in noisy conditions

Environment Difficult hearing in noisy conditions (paracusis) – because we raise our
voices when there is noise

Hearing Loss
o Degrees
▪ normal: 0-20 dB (20 = soft speaking voice)
▪ mild: loss of 20-40 dB (40 = normal speaking voice)
▪ moderate: 40-70 (70 = shout)
▪ severe: 70-90 dB
▪ profound: > 90 dB
432

o MC causes
▪ Impacted cerumen (wax)
▪ Serious otitis media
▪ Otitis externa
▪ Children – congenital deafness
▪ Elderly - presbyacusis
o Types
▪ Conductive Hearing Loss
• acquired or congenital, caused by blockage or damage in outer or middle
ear. Bone conduction is normal.
• A conductive hearing loss leads to a loss of loudness and can often be
helped by medical or surgical treatment.
• Causes:
- Blockage of ear canal by impacted wax or foreign objects
- Otitis externa
- Middle ear infection (glue ear)
- Perforated eardrum (due to infection or trauma)
- Otosclerosis
- Partial or complete closure of ear canal.
▪ Sensorineural Hearing Loss
• acquired or congenital and is caused by damage to or malfunction of
cochlea (sensory part) or hearing nerve (neural part).
• leads to a loss of loudness as well as a lack of clarity. Quantity & quality
of sound are affected and sometimes may limit benefit of a hearing aid.
• Causes:
- Presbyacusis - Ageing process (MCQ 2064 P66)
▪ bilat. high frequency (s, f, th) progressive hearing loss
- excessive noise exposure (occupational and traffic noise)
- meningitis and Meniere's disease
- viruses, such as mumps and measles
- Ototoxic drugs
- head injuries
▪ Mixed Hearing Loss
• Mixed hearing loss results when there is a problem in both conductive
pathway (in outer or middle ear) and in nerve pathway (inner ear).
• An example of a mixed hearing loss is a conductive loss due to a middle-
ear infection combined with a sensorineural loss due to damage
associated with ageing.
o Rx
▪ Hearing aid – in conductive hearing loss
▪ Cochlear implant - effective if implanted early
• children > 2 yrs
• adults
- Otosclerosis (MCQ 2099 P78) 3022 P 214
o Disease of bone surrounding middle ear and is MC cause of CHL in adults with a normal
tympanic membrane.
o Normal middle ear bone is replaced by vascular, spongy bone that becomes sclerotic
433

o Progressive disease, bilateral.

o Develops in 20s and 30s
o Family history (AD)
o Unilateral or bilateral
o Female preponderance
o Stapes footplate is affected
o May progress rapidly during pregnancy
o Treatment
▪ Referral to an ENT consultant
▪ Stapedectomy (approximately 90% effective)
▪ Hearing aid fitting (less effective alternative)
• while waiting for surgery
- loudness recruitement
- Hearing loss causes
o Sensorineural – damage to cochlea
▪ Presbyacusis (ageing)
▪ Noise exposure
• when exposed to noise > 8 hrs/ day for 10 yrs
▪ Meningitis, Meniere
▪ Viruses – mumps, measles
▪ Ototoxic drugs
o Conductive – Blockage in outer or middle
▪ Wax
▪ Otitis externa
▪ Middle ear infection
• Chronic - cholesteatoma
▪ Perforated eardrum (inf., trauma)
▪ Otosclerosis: (AD in females esp during pregnancy MC involves Stapes)
- Tinnitus
o Assumption of ringing in ears or assoc. symptoms in deafness
o types
▪ non-pulsatile, constant – the cause is in ear
▪ pulsatile
o Rx
▪ treat cause
▪ Betahistine
▪ Clonazepam
▪ Carbamazepine
▪ Acute tinnitus – Lignocaine IV
- Normal otoscopy:

-
434

- Acute otitis media:

o
o 2/3rd of children have at least one episode by age of 3 yrs, 90% by school entry
o 2 cardinal features
▪ Inflammation & effusion
o Clinical Features:
▪ Earache, pulling of ear, reduced hearing, irritability, anorexia, lethargy
▪ Fever, vomiting – bacterial -> A/B
o EXAMINATION:
▪ Usual middle ear landmarks are not well seen.
▪ Tymp membrane is dull and opaque with loss of light reflex and may be
bulging, yellow-grey colour
▪ Fluid level might be seen
▪ On pneumatic otoscopy TM mobility is reduced
▪ May have associated signs of URTI
o CAUSES:
▪ Streptococcus pneumonie 35-40%
▪ H. Influenzae 25-30%
▪ Viral: 25%
▪ Moraxella catarrhalis 15-20%
▪ least common – Staph.
▪ Do not accept otitis media as sole diagnosis in a sick febrile young child
without elimination of a more serious cause
• Meningitis – frequently assoc. with otitis media
o Rx
▪ try to avoid using A/B
• never use A/B in children, except for this!
▪ > 1 yr old, mildly unwell, immuncompetent
• just observation for 12-24 h, analgezia, no A/B
• if symptoms not resolving or severely ill (Vomiting, fever---Bacterial)
- First line = Amoxycillin
- still not resolving after 48 hrs
▪ 2. Cefaclor or
▪ Amoxycillin + clavulanic acid – if resistance is
suspected
▪ < 1 yr, moderate/ severe, immuncompromised
- amoxycillin
- still not resolving after 48 hrs
▪ amoxycillin + clavulanic acid
o Complications:
▪ Effusion – 70%
435

▪ Perforation of TM results in purulent otorrhoea and usually relief of pain.

▪ Febrile convulsions are commonly related to AOM < 1yr
▪ Repeated suppurative inf. can cause hearing loss
▪ Mastoiditis
• swelling, tenderness behind ear
• deterioration
• Mx – referral!
▪ Serous otitis media (Glue ear –middle ear fluid has become thick and glue-
like) = incomplete resolution of acute otitis media
• hearing loss, loss of drum mobility
▪ rarely
• suppurative labyrinthitis or intracranial infection (meningitis – child
unwell, extradural or subdural abscess, brain abscess): uncommon.
• Facial nerve palsy, lateral sinus thrombosis, and benign intracranial
hypertension.
o Aboriginals – frequent chronic otitis media – don’t use A/B
- Chronic otitis media:
o infected otorrhea through a tympanic membrane perforation or tympanostomy tube
o pain in chronic otitis media – relieved after spontaneous rupture of TM
o cause
▪ pseudomonas
▪ staph. aureus
▪ proteus
o Treatment:
▪ Antipseudomonal penicillin or cephalosporins (children)
▪ Ear drops & quinolones (adults)
o Safe vs. unsafe perforation
▪ Safe Perforation:
• Affects mucosa of lower front part of ME cleft (tubotympanic portion)
▪
• Central perforation
– always a rim of
drum or annulus
around edge.
• Involves vibrating
part of TM – pars
tensa, below
malleolar folds at
level of lateral process of malleus.
▪ Unsafe Perforation:
• hazard of spreading infection intracranially.
• Associated with erosion of surrounding bone.
• Cholesteatoma or chronic osteitis involves upper back part of ME cleft
(atticoantral portion)
- types:
▪ Congenital (embryonic rest of epithelium in anterior-
superior space)
436

▪ Acquired (usually develops from retraction of pars

flaccida into Prussack space, internal desquamation,
enzymatic erosion, osteitis)

•
- Cholesteatomas are expanding lesions of the temporal bone
composed of a stratified squamous outer epithelial lining and a
desquamated keratin centre
- Clinically defined as an abnormal extension of skin into middle
ear and mastoid air cell spaces
- The point of entrance of skin into middle ear is reliably
identifiable on otoscopic examination
- Otoscopy is the most reliable and sensitive means of diagnosing
a cholesteatoma
▪ Signs of an unsafe perforation on otoscopy:
• Superior and or posterior edge of tympanic
membrane perforation
• Perforation involving fibrous edge or annulus
of tympanic membrane
• Associated granulation tissue
• White mass within middle ear seen through
perforation
• Bone erosion
Dizziness (a condition of faint, wekness and unsteady gait)
o can be with
▪ Central cause – brain, cerebellum
• acoustic neuroma
• MS
• head injury
• vertebrobasilary insuf.
▪ Peripheral cause – inner ear
• Meniere
• Benign Paroxysmal Positional Vertigo
• Vestibular neuritis/ labyrinthitis
o causes:
▪ COMMON
• Benign Paroxysmal Positional Vertigo
• Vestibular neuritis/ labyrinthitis (unilateral peripheral vestibulopathy)
• Meniere’s syndrome
• Vestibular migraine
• Psychogenic
• Idiopathic
▪ LESS COMMON
437

• Acoustic neuroma
• Vertebro-basilar transient ischaemic attack/stroke
• Multiple sclerosis
• Posterior fossa tumours
• Arnold-Chiari malformations
• Autoimmune inner ear disease
• Perilymph fistula/semicircular canal dehiscence
• Invasive middle/inner ear disease (e.g. otomastoiditis, tumours,
cholesteatoma)
• Bilateral peripheral vestibulopathy (if asymmetric)
o Diagnostic Triads (J.Murtagh)
▪ only vertigo caused by movement = BPPV
▪ Acute vertigo + nausea + vomiting = Vestibular neuronitis
▪ (acute vertigo + nausea + vomiting) + hearing loss ± tinnitus = Acute
labyrinthitis (similar symptoms to Meniere). Symptoms upto days.
▪ Vertigo + vomiting + tinnitus + SNHL = Meniere’s syndrome
▪ (unilateral) Tinnitus + SNHL + unsteady gait = Acoustic neuroma
- duration of common causes of vertigo
Seconds Benign positional vertigo
Minutes Vertibrobasillar insuf., migraine
Hours Meniere’s disease
Days Vestibular neuritis, labyrinthine infarcts
o 4 common causes
▪ 1. Benign paroxysmal positional vertigo (BPPV)
• MC of vertigo seen by otolaryngologists (20-40% of pts with peripheral
vestibular disease)
• Affects all ages.
• Approximately 50% of people > 70y have experienced at least 1 episode
• Symptoms & signs are brought about by changes in head position, in
relation to gravity, 5-10 sec later, lasts 10-60 sec.
• May be associated with closed head injury, infections, surgery and
prolonged bed rest.
• Pathophysiology:
- Otoconia become dislodged and pass through endolymphatic
space of vestibule into one of the semicircular canals.
• Pathognomonic sign:
- nystagmus towards affected ear on doing a Dix-Hallpike test
• Treatment:
- Epley repositioning maneuver
- Brandt-Darrof exercises
▪ 2. Vestibular neuronitis – M 508
• 20-40 yrs
• only vestibular portion of VIII N is affected, unilateral & no hearing loss
- if both vestibular and auditory portions (hearing loss) are
affected = labyrinthitis
• 2nd MC disorder affecting labyrinth
438

• Slef limiting viral infection of Vestibular N and is unilateral.

• Signs/symptoms:
- previously absolutely healthy, sudden onset of severe rotatory
vertigo + nausea and vomiting
▪ vertigo relieved by lying down
- Spontaneous nystagmus and diminished VOR
- Usually subsides over a course of several days or wks
• DD: Cerebellar hemorrhage and infarction
• Treatment:
- Bed rest – mild case
- More severe -Vestibular sedatives & anti-emetics in 1st 24-72 hrs
▪ Dimenhydrinate - Dramamine
▪ Prochlorperazine – Stemetil x IM
▪ Diazepam
- Severe
▪ + short course of C/S
- Vestibular adaptation exercises/ rehabilitation in recovery phase
▪ Meniere’s disease (MCQ 3034 P 219) 3038 P 220)
• Meniere’s syndrome is an inner ear disorder marked by attacks of
vertigo, fluctuating SNHL, aural fullness and tinnitus
• When syndrome is idiopathic and not attributable to other causes (i.e.
syphilis) it is referred to as Meniere’s disease.
• Dilatation of endolymphatic -> sensation of fullness or pressure in ear +
damage to both vestibular and cochlear sense organs-> hearing better
in noisy environment (bc of blockage)-> SNHL
• Duration of vertigo during attacks may last from 20-30 min up to few
hrs
• Commonest in 30-50 age group
• Characterised by paroxysmal attacks of:
439

-
- Vertigo, fullness in ear (due to distension labyrinthitis)
- Tinnitus
- Nausea and vomiting
- hearing better in noisy environment MCQ
- Deafness (progressive) – sensorineural hearing loss
- + nystagmus during attack
• Treatment:
- Vestibular sedative, antiemetic for acute episodes
▪ Prochlorperazine
▪ urea crystals in orange juice
▪ Diazepam
▪ Betahistine
- Low salt diet ± diuretic for maintenance treatment
- Meniett device
- Intra-tympanic gentamycin or surgery for refractive cases
▪ 4. Acoustic neuroma = Vestibular schwannoma
• tumor of Schwann cells on 8th cranial n.
• slow growing –> brain has time to adjust => less vertigo
• 78% of all cerebellopontine angle tumors
• 0.8% to 2.7% of population: 0.7 to 1 per 100,000
440

• Pathology: vestibular division of VIII cranial N; Schwann cells

• Type 2 Neurofibromatosis
- Bilateral tumors
- Chromosome 22 abnormality, AD

•
• Symptoms:
- Unilateral progressive SNHL 85% (handbook 401 )
- Sudden hearing loss 15%
- Tinnitus 56%
- Vertigo 19%
- absence of corneal reflex
- Facial paresthesia from 5th cranial N irritation.
- (7th 9th 10th and 11th N involvement) - Diplopia, facial weakness
and hypoaesthesia, Cerebellar ataxia (Unsteadiness of gait) MCQ.
• Treatment:
- Observation
▪ 50-55% show little or no growth in 1-3 years
▪ less than 0.2mm/ year
▪ Repeat MRI to monitor growth
- Surgical resection
▪ Translabyrinthine, middle fossa or suboccipital
retrosigmoid approaches
▪ Stereotactic radiosurgery (gamma knife)
- Vertigo + Nystagmus + Horner Syndrome = Cerebellar lesi on = PICA (MCQ)
- Nystagmus: (Dancing eyes) involuntary rapid eye moevemts, can be horizontal, vertical or
rotatory.
o VOR: Head movement (vestibular stimulation) in one direction stimulates eye movement
in opposite direction. Important in reading as head constantly moves a little.
o Physiological = Part of vestibulo-oculo reflex (VOR)
▪ tested with caloric reflex test (VIII N nucleaus)
• Syringing of ears with warm water: eyes will turn towards the
contralat. ear + horizontal nystagmus towards the ipsilateral ear
• with cold water – opposite effect
o Pathological
▪ caused by lesions of
• Inner ear
• VIII nerve
• Brainstem
• Cerebellum
• Cortex
441

Ophtalmology - OK

-
o normal left eye fundus
- Dx
o vision
▪
6/4
▪
6/5
▪
6/6
▪
6/60
▪
…
▪
count fingers at 6 m
▪
count fingers at 1 m
▪
see fingers?
▪
perception of light
o Optic disc - nasal
▪ clear contour
o Retinal vessels
▪
narrower arteries
▪
wider veins
o Macula – temporal
▪ no blood vessels in the middle
▪ darker in color
- Cranial nerves for eye muscles
o III
▪ MR
▪ SR
▪ IR
▪ IO
▪ levator palpebral superioris
▪ palsy:
• Ptosis + fixed (non reactive) dilated pupil + down & out eye
- DM or any ischemic problem – pupil normal (peripheral fibres
will still get supplied, here are ones for the pupil)
• causes
- DM (diplopia with normal pupil) or other ischemic problems
- cavernous sinus lesions
- sup. orbital fissure
442

o IV
▪ SO
▪ Palsy: diplopia on downward (vertical) and lateral gaze
▪ Diabetic ocular neuropathy: Vertical binocular diplopia with normal pupil (MCQ
3023 P 214)
o VI
▪ L.R
▪ Palsy: divergent squint on lateral gaze
- Diplopia
o Monocular – persists after occluding 1 eye
▪ causes: in same eye!
• early cataract
• dislocated lens
• severe astigmatism
• psychogenic/ functional
▪ Rx – not urgent
o Binocular – (doesn’t persist when ocluding 1 eye)
▪ REFER URGENTLY!!
▪ causes: in higher nerve centres
• ocular nerve palsy – III, IV, VI
- CVA or TIA
- tumor
- aneurysm
- DM ocular neuropathy
- arthritis
- head injury
- migraine (ophtalmic) - transient
• blow out fractures (MCQ)
• concussion
• MS – recurrent diplopia
• myasthenia gravis
• hyperthyroidism
- Blocked naso-lacrimal duct
o repeated inf.
o usually self-corrected between 6-12 mths
o Rx
▪ repeated bathing with normal saline
▪ massage over lacrimal sac
▪ local A/B for inf.
▪ refer – probing of lacrimal sac, if
• severe blockage or
• if not self-corrected by 12 mths
o Cx
▪ Dacryocystitis – inf. of lacrimal sac sec. to obstruction
▪ Rx
• Systemic A/B – Flucloxacillin
• Drainage
443

- Orbital vs. periorbital cellulitis

Orbital – Big emmergency! Periorbital - also urgent
Unilat. swollen red eyelids
Post-septal Pre-septal
Pain on eye movement No pain and restriction
Restriction of eye movement of eye movement. No
Proptosis proptosis. No loss of
Loss of vision vision
Causes: Cause:
Sinusitis – MC After an abrasion
Infection of nearby structures
Trauma
Previous surgery
> 2yrs
Cx: blindness – may develop in hrs
Dx - scan of head: possibility of abscess within brain (from
ethmoidal sinus) -> needs to be drained, otherwise child
will never recover
Refer to opthalmologist (tertiary hospital) IV cefotaxime until
IV antibiotics: IV cefotaxime + di(flu)cloxacilin until afebrile, then amoxiclav
afebrile, then amoxiclav for 10 days for 7-10 dys
Surgical decompression of affected eye
- Red eye – Murtagh 554 + Alena’s notes:
Pain Photophobia Vision Pupil Discharge
Conjunctivitis No No N N Yes
Keratitis Yes Yes Blurred N Yes
Iritis Yes Yes Blurred Irregular/ constricted No
Glaucoma Yes Yes Blurred Dilated No
- Acute conjunctivitis
o School exclusion till there is discharge MCQ
o lasting < 3 wks
o causes
▪ infectious - usually bilat., with discharge and a gritty or sandy sensation
• Bacterial
- purulent discharge ē sticking together of eyelashes in morning
- hyperemia of conjunctiva
- causes
▪ Strep. pneumoniae
▪ Strep. pyogenes
▪ Haem. inflammation
▪ Staph. aureus
▪ Pseudomonas
• Rx – Gentamycin, Tobramycin
▪ Gonococcal (hyperacute onset) Neonatal JM 55
• very rare and dangerous – immediate referral
o can give severe corneal inf. with
▪ perforation
444

▪ septicemia
• neonatal conj. (+ chlamydia)
• Rx
o IV cephalosporins or penicillin
o topical sulfacetamide
▪ Chlamydia
• brick red follicular conj. with stringy mucus
discharge
• types
o neonatal
o young patient with venereal inf.
o isolated Aboriginal people with
trachoma
▪ MC cause of blindness in world
▪ recurrent & untreated => lid
scarring & inturned lashes
(endtropion) ē corneal
ulceration & visual loss
• Dx
o swabs for culture and PCR
• Rx
o local sulfacetamide eye drops
o systemic
▪ neonates – Erythromycin
▪ children > 6 kg: Azithromycin
- Dx
▪ clinical
▪ swab
- Rx
▪ severe cases - cloramphenicol eye drops
▪ milder cases
• saline irrigation
• antiseptic – propamidine isothionate
• Viral
- MC assoc. with an URTI
- highly contagious –> good hygiene
- Hx of infected contacts
- resolves in 3 wks
- caused by adenovirus
- Cx – sec. bact. inf.
- preauric. Lymph node
- Rx —cool compress and topical lubricants (artificial tear
preparations), naphazoline (e.g. Albalon), vasoconstrictors (e.g.
phenylephrine) or saline bathing.
▪ C/S are CI
▪ Non-infectious
• from welding (actinic)
445

▪ Allergic
• types
- assoc. with hay fever
▪ Rx
• topical antihistam.
• topical sodium cromoglycate
• topical C/S
- contact hypersensitivity
▪ assoc. with topical opthalmic drugs (A/B) contact lens
sol., cosmetics, etc.
▪ Rx
• remove cause
• naphazoline
• topical C/S
- Episcleritis
o no discharge
o no watering
o N vision
o self-limiting
o Rx
▪ topicl and oral C/S
- Scleritis – assoc. with autoimmune dis. FIGURE 51.1 JM P 577
o painful loss of vision
o urgent referral
- Uveitis
o acute
▪ anterior uveitis = iritis and iridocyclitis
• Sx
- photophobia
- iris is sticky and sticks to lens => adhesion => constricted/
irregular pupils
- blurred vision, floaters in field of vision
• causes
- 80% isolated
- 20% Reiter, ankylosing sponditlytis, Crohn, IBS, psoriasis
(seronegative arthropaties), SLE – HLA B27
• Rx
- referral
- pupil dil. with atropine
- topical C/S
- systemic C/S
• frequently recurrs after Rx
▪ post. uveitis = choroiditis
o chronic
▪ Sx
• pupil is bound to the lens by synechiae and distorted
▪ Cx – loss of vision due to:
446

• glaucoma
• cataract
- Refractive errors
o Presbyopia
▪ > 45 yrs
o Myopia
▪ image formed IN FRONT of the retina (long eye or steep cornea)
▪ Rx – concave lenses
▪ Cx in high myopia
• retinal detach.
• macular degen.
• glaucoma

o Hypermetropia
▪ image formed BEHIND retina (long eye or steep cornea)
▪ Rx – convex lenses
▪ Cx – closed angle glaucoma
o astigmatism
▪ causes – conical cornea (keratoconus – e.g. Down)
o pinhole test – 1 mm hole
▪ corrects any refractive error
▪ if not => not just a refraction error!

▪
▪ Cx – Closed angle glaucoma.
- Acute visual loss
o flashers and floaters
▪ causes
• constant – less of a concern
- age
447

- myopia
- eye surgery
• fresh onset = concern
- retinal detachment
o Retinal detachment
▪ types
• Posterior vitrous degen. and detachment – in everybody
- sudden onset of floaters
- flashing lights = Traction on retina
- Rx – Urgent referral

▪
• some people – pathol. detachment
- causes
▪ trauma
▪ high myopia (thin retina)
▪ previous surgery (e.g. cataract)
▪ DM retinopathy
- Sx
▪ no pain
▪ more dangerous if affecting macula
▪ sudden onset of: (the 4 Fs)
• flashes
• floaters (spots, dots, cobwebs)
• field loss
• fall in visual acuity
o Partial
o Total – if macula detached
▪ then suddenly irreversible blindness.
• “a curtain came down over the eye”
• if revers. = carotid stenosis and embolism
- Dx
▪ Opththalmoscopy: detached retinal fold as a large grey
shadow in the vitreous cav.
- Mx
▪ transport to the hospital ASAP!
• can’t transport by air
▪ tilt head back and cover eye
• keep pressure on the detached retina
o Upper curtain (MC) – lower
detachment – keep head up.
448

o bottom curtain – upper detachment –

lie down.
▪ specialist Rx
• surgery – sealing of retinal tears
o macular degen. (see below)
o Amaurosis fugax (MCQ 3020 P 213)
▪ Unilat. transient painless loss of vision or blurring of vision due to transient
occlusion of retinal a. Lasts usually less than a minute.
▪ causes
• Emboli from
- carotid stenosis - MC
- carotid aneurysm
- heart
- temporal arteritis
▪ Risk of stroke after an episode of amaurosis fugax = 2%/ year
o Central retinal artery occlusion (CRAO)
▪ Elderly people – smokers, etc.
▪ Obstruction by emboli, thrombi, AS
▪ Hx of TIAs or amaurosis fugax
▪ Exclude temporal arteritis

▪
▪ Sx
• Acute painless loss of vision (usually profound) with sudden onset.
- “curtain descending over one eye.”
- Irreversible.
• Waxy, swollen, pale retina, thin arteries.
• chilly red spot in macula – init. still vascularization but then same color
as the rest of retina.
▪ Rx
• lower intraocular pressure (glaucoma medication)
• inhale CO2 (paper bag).
▪ poor prognostic, unless treated within 30 min.
o Central retinal vein occlusion (CRVO)

▪
449

▪ in HTN, dyslipidemia, DM, anemia, glaucoma.

▪ Sx
• Similar to CRAO, but milder vision loss.
• usually more gradual loss of central vision.
▪ Dx
• hemorrhage in all the 4 quarters, including borders of optical disc
• “tomato ketchup and cheese” or “stormy sunset” appearance.
▪ Rx
• find and treat cause
▪ poor prognostic
• better if the initial presentation was better
CRAO CRVO

Embolic occlusion of central retinal artery Due to blood clot in central retinal vein
Sudden Gradual (hours/ days)
Painless loss of vision Painless loss of vision
Unilateral Unilateral Often hypertensive
Mx: Mx:
Exclude GCA & TIA Elective referral to ophthalmologist within
Refer ophthalmologist 1 wk
Ocular massage Screen for HTN, DM &
Acetazolamide oral – reduce IOP Hypercholesterolemia
o Ischemic optic neuropathy – irrevers.
▪ Temporal arteritis:
• sudden and often bilat. occlusion of the short ciliary aa. supplying the
optic nerve.
• Sx
- revers. loss of vision, then can lead to irreversible
- sudden loss of central vision
▪ unilat., can rapidly become bilat.
- assoc. temporal headache, temporal aa. tender, thickened and
nonpulsatile.
• Dx
- ESR (> 40), CRP (sometimes ESR can be normal, then we do CRP)
- FBE (Hb – anemia; gives you higher ESR)
- temporal a. biopsy – confirm Dx
• Rx – Predisolone for 18-24 mths
- IV if patient has transitory loss of vision
- after 10 days of Rx – changes biopsy result (modif. have
disappeared)
o Optic (retrobulbar) neuritis Most Common Dif Dx = MS (MCQ)
• neurosyphilis
• toxins
▪ woman, 20-40 yrs
450

▪ Sx
• retrooc. discomfort with eye movement
• central field loss (central scotoma)
- or peripheral circumferential blindness
▪ Dx: Visual evoked potentials (VEPs) are an important means of evaluating
patients with suspected optic neuritis. They may be abnormal even when MRI of
the optic nerve is normal
• optic disk swollen, then atrophic, then disc pallor
▪ Rx
• IV C/S
• most pts recover spontaneously but are left with diminished acuity
o Migraine:
▪ zigzag lines and lights
▪ multicolored flashing lights
▪ unilat. or bilat. field deficit
• self-resolution within a few hrs
o Hysteria
▪ bilat. loss of vision, with tunnel vision
o Vitreous haemorrhage

▪
▪ assoc. with
• trauma
• DM retinopathy
• tumor
• retinal detachment
▪ Sx
• sudden onset of floaters
• loss of vision
▪ Dx
• clots of blood that move with the vitreous (black swirling cloud)
▪ Mx
• urgent referral – exclude retinal detach.
• may resolve spontaneously
• surgical vitrectomy for persistent haemorr.
o Closed angle glaucoma (see below)
- Chronic loss of vision
o in children = Amblyopia = ↓visual acuity due to abnormal visual experience in early
childhood
▪ strabismus
451

▪
cataracts
▪
refractive errors
▪
retinoblastoma
o Glaucoma (Optic n is slowly damaged bc of ↑ IOP)
▪ Dx for incr. intraoc. pressure
• Cup: Disc
- N ≤ 30%
- if > 30% = raised intraocular pressure
• Tonometry
- Normal 10-22 mm Hg
▪ incr. – can go up to 55-60
▪ Acute angle closure glaucoma: (Acute painful Red eye) 3024,P 215
• acute -> acute loss of vision
- ciliary flush (hyperemia)
- Common in middle aged or elderly hypermetropes.
- Narrowed anterior chamber.
- Precipitated by pupillary dilation – in the evening, (peripheral iris
blocks aqueduct outflow and an abrupt rise in intraocuolar pressure)
- Sx – similar with migraine without aura, but with visual Sx –
diagn diff.!
▪ Severe throbbing pain.
▪ Headache.
▪ Nausea and vomiting.
▪ Weakness.
▪ Visual changes:
• Vision is ↓ with HALOES around lights/ objects.
• The cornea is HAZY/edematous.
• Fixed and DILATED oval pupil.
• corneal or scleral injection
• On palpation: eye feels firm/ stony hard.
- MANAGEMENT:
▪ Ocular emergency.
• Urgent referral to the Ophthalmology team.
▪ 1. Miotic drops (Pilocarpine every 5 min for up to 1 hr).
▪ 2. Acetazolamide (carbonic anhydrase inhibitor) 500
mg slowly IV then 250 mg orally t.d.s. – diuretic
▪ 3. Peripheral iridotomy – perforation in the iris to
evacuate the liquid
▪ Antiemetic such as metoclopramide 10 mg IV and
▪ analgesia such as morphine 2.5 mg.

▪ Primary open angle glaucoma (painless) = “Glaucoma”chronic and insidious

• MC cause of irreversible painless blindness in middle age
• risk factors:
- Age (after 40 yrs – check for glaucoma, especially with fam. Hx)
- Family Hx
- High myopia
452

- DM
- HTN
• Screening
- > 40 yrs – every 2-5 yrs
- if family Hx – start from 30 yrs, every 2 yrs
• Sx
- Progressive painless loss of vision (tunnel vision) + cupping of
optic disc + raised intracranial pressure.
▪ also in
• retinitis pigmentosa
• hysteria
▪ central vision is N
• Rx – for life!
- drugs
▪ β blockers: timolol, betaxolol
▪ acetazolamide (diuretic)
▪ pilocarpine - parasympathomimetic alkaloid
▪ latanoprost - PG analogue
▪ dipivefrine – prodrug of epinephrine, converted to
epinephrine in the eye
- surgery or laser therapy – if drugs failed
o Cataract
▪ cause
• age – everybody > 80 yrs have opacities
• DM
• trauma
• C/S
• UV light
• uveitis
▪ Sx
• blurring of vision in bright light
▪ Dx
• diminished red reflex
• change in appearance of lens
▪ Rx
• lens extraction + intraoc. lens implant
- CI:
▪ Intraoc. inflammation
▪ Severe DM retinopathy
▪ Px – UV sunglasses
▪ Cx
• Hypopyon (puss in ant. chamber of eye)
453

-
- causes
▪ in case of endophtalmitis after
• penetrating injuries
• surgery
▪ cataract
- urgent referral!
- Rx
▪ avoid movt.
▪ avoid smoking/ alcohol
▪ don’t give heparin
▪ bed rest 5 days
▪ sedative
▪ check daily
• if floaters / flashes -> emmergency!
• bleeding 2nd, 3rd, 4th day?
o Retinitis pigmentosa
▪ displacement of melanin-containing cells from pigment epithelium into more
superficial parts of retina
▪ Sx
• night blindness in childhood
• tunnel vision
• blind by adolescence/ middle age
▪ Dx
• patches of dark pigment especially at the periphery

•
o Macular degeneration
454

▪
▪ causes/ risk factors
• age related
• high myopia
▪ types
• acute – exudative
• chronic – pigmentary (slow onset)
▪ drusen (neovasc. membranes which develop under the retina of the macular
area and leek fluid or bleed ) + visual loss
▪ Sx
• central visual loss
- acute – sudden fading of central vision
- eventually central vision is completely lost
• distorted images = macular degen.!
- lines of the words bend / seem wavy while reading
▪ Dx
• screening: using a grid pattern (Amsler chart)
- shows distorted lines
- cannot see the central dot

-
• ophthalmoscopy – white exudates, haemorrhage in the retina
• fluorescein angiography
▪ can be
• wet – acute?
- hemorrh., fluid leaks in macula
- Rx
▪ laser photocoagulation
▪ inj. inside the eye – vascular growth factor inhibitor =
new Rx
• stabiliz.
• 1/3 improve
• dry – chronic?
- “worn-out jumper”
- Rx
455

▪ nutritional supplements
• antiox. – Vit. A, C, E + Zn
- corneal disorders
o Keratoconjunctivitis sicca - “dry eyes”
▪ causes
• ageing, menopause
• systemic dis.
- RA
- SLE
- Sjogren
• drugs
- Beta blockers
▪ Rx
• artificial tears – hypromellose, polyvinyl alcohol
o Keratitis
▪ causes
• UV light (“arc eye”)
• herpes simplex
• herpes zoster ophthalmicus
• superficial punctate keratitis
- in various conditions:
▪ e.g. UV light exposure = flash burns
• microbiol keratitis
- risk factors
▪ contact lenses – MC with pseudomonas
▪ corneal trauma or surgery
▪ post-herpetic corneal lesion
▪ etc.
▪ Cx
• perforation and blindness
▪ Rx
• urgent referral!
• topical A/B – ciprofloxacin oint.
o Abrasion/ ulceration
▪ causes
• trauma
• contact lenses
• fingernails
• UV burns
• dendritic ulcer
- primary herpes simplex I inf.
▪ can also cause follicular conjunctivitis
- Dx
▪ stain with fluorescein
- Rx
▪ Acyclovir
▪ atropine – prevent reflex spasm of the pupil
456

▪ Dx
• slit lamp and fluorescein staining
▪ Rx
• chloramphenicol oint.
• eye pad
- Pterygium

o
o fleshy overgrowh of the conjunctiva onto the nasal side of the cornea
o in dry, dusty, windy areas
o Rx
▪ surgical excision
- Pinguecula

-
o yellowish elevated nodular growth of the cornea
o Rx
▪ surgery – if uncomfortable
- corneal ulcer with hypopyon - emmergency
o rheumatoid arthritis
o contact lenses abuse
- Blepharitis
o inflam. of lid margins
o freq. assoc. with seborrhoeic and atopic dermatitis and rosacea
o types
▪ seborrhoeic
▪ staphylococcus
▪ assoc. with rosacea
o Rx
▪ eyelid hygiene – mainstay of Rx
▪ topical C/S
▪ topical A/B
• tetracycline
• chloramphenicol
- Stye (hordeolum ext.) – inflam. external glands (2026, P 54)
457

o
o Acute abscess of eye lash follicle
o Staph. aureus
o Red tender swelling of lid margin, usually on medial side
o Rx
▪ Hot compress
▪ Lash epilation
▪ Chloramphenicol oint.
- Chalazion (Internal hordeolum, Meibomian cyst)

o
o Granuloma of the Meibomian glands (embedded in tarsal plates)
o Inflammed tender irritant lump in the eyelid
o Chronic – Chalazion
o Rx
▪ Hot compress
▪ Chloramphenicol oint.
▪ If large and uncomfortable -> surgery – incision and curretage under LA
- Herpes zoster ophtalmicus (Shingles)
o Ophtalmic distribution of V nerve (trigeminal)
o Respects the midline!
o Ocular problems: conjunctivitis, uveitis, keratitis, glaucoma
o Rx
▪ Topical acyclovir
▪ Systemic acyclovir – Oral, IV
- Penetrating eye injury
o not a lot of pain
o do not give pain killers – Morphine, etc. – can cause vomiting, making things worse
▪ small dose + antiemetic (metoclopramide)
o no local anestetic eye drops – can be retinotoxic
o don’t put bandage (pressure), just a shield or cone
o urgent referral!
▪ if delay – give systemic A/B
- Ectropion – rolling outward of the eye lid
458

o cause
▪ age – involution
▪ facial nerve palsy
o Rx – lubricant Rx
- Entropion – rolled inward
o irritation of the cornea
o Rx – attach eyelid to the cheek
- Lid tumor
o BCC 90 %, SCC 9 %, other 1%
o with loss of eye lashes (madarosis) – serious!
- Subluxated lens

o
o Marfan syndrome
o trauma
- MRI – don’t do if metalic foreign body in the eye (magnetic)
- burn
o acid – injury just on the spot
o alkaline – injury keeps evolving
▪ wash with excess water for 30 min
- Leukoria- White eye reflex

-
- Retinoblastoma!, Toxocariasis, Retrolental fibroplasias, Coat’s diease
- Retinopathy
o typical
▪ Cotton wool (intra-retinal infarcts) - DM
▪ Flame shaped haemor., AV nicking - HTN
o DM
▪ Non-proliferative

•
• Related to ischaemia of blood vessels and include:
459

- Hemorrhages: Dot and blot.

- Microaneurysms.
- Exudates: Soft and hard.
- hemor., hard exudates (lipids – yellow, clear margins), around
macula
- cotton wool spots – ischemia of nerve fiber layers, indistinct
margins
• Venous beeding – severe
▪ Proliferative

▪
• Proliferative: Changes in blood vessels in response to ischaemia to retina.
- New vessel formation.
- Vitreal hemorrhage.
- Retinal detachment.
• can leak, rupture with hemorrhge in vitreous, healing with fibrosis,
retractional retinal detachment
- Rx - Panretinal argon laser photocoagulation
o HTN
▪ Grade 1: ‘Silver wiring’ of arteries only.
▪ Grade 2: Grade 1 plus arteriovenous nipping or nicking.
▪ Grade 3: Grade 2 plus flame shaped hemorrhages and cotton wool exudates
(soft or hard).
▪ Grade 4: Grade 3 plus papilledema.
▪ deposits around macula – cartwheel
- Papiloedema – bilat. disc edema due to ↑intracranian pressure
o vs. disc edema
- Lymph drainage
o Preauricular -> submandibular nodes
- Hyperemia
o Ciliary – close to the centre – central (eye) origin
o Conjunctival – peripheral
460

▪
- Visual field problems – M 837 + Jay’s notes
o Retrobulbar neuritis -> circumferential blindness
o Optic nerve affected -> complete loss of vision in that eye
o Partial lesion of chiasma (perichiasmal area) -> unilat. nasal hemianopia
o Optic chiasma lesion -> Bitemp. Hemianopia (or bitemporal upper field blindness)
▪ cause - pituitary adenoma (MCQ)
• macroadenoma of pituitary gland
- init. upper bitemp. hemianopia
- then complete bitemp. hemianopia
o Homonymous hemianopia (e.g. left temporal and right nasal hemianopia)
▪ Optic tract
▪ Optic radiation
▪ Visual cortex (occital lobe)
o Quadrantanopia (same side quarter in both eyes – e.g. left in both eyes)
▪ Sup. quadrants – temporal lobe
▪ Inf. quadrants – parietal lobe
Emergency medicine - OK
- Emmergency situations >- Rapid primary survey = assess ABCD (disability) E (exposure)
o 1. Airway
• Secure airway
461

• consider cervical spine injury (in trauma) – neck collar

• airway management
- identify the cause of airway obstruction
- Assessment of airway
▪ Look for clinical signs of hypoxia
• Cyanosis, agitation, confusion
▪ Look for signs of obstruction
• 1. Stridor
o laryngeal
▪ upper airway
▪ inspiratory
o tracheal
▪ lower airway
▪ expiratory
• 2. Hoarseness of voice - laryngeal
• 3. Aphonia – can’t speak at all (suffocating)
o most dangerous – may lead to circulatory collapse
▪ Breathing patterns
• tachypnea, bradypnea, use of accessory muscles
- Establishment of airway
▪ Basic Mx
• caution with cervical spine injury
• anatomical positioning of pt
• suction of mouth content, etc.
• use of nasopharyngeal or oropharyngeal tubes
• laryngeal mask
• transtracheal jet ventilation – cricothyrotomy
▪ Definitive Mx
• Endotracheal intubation:
o indic.
▪ Unable to protect airways (risk of
aspiration) – unconscious pt
▪ Inadequate spontaneous response
▪ SaO2 < 90% with 100% O2 admin.
▪ GCS ≤ 8 (MCQ)
o Oro- or nasotracheal
o Preferred = rapid sequence intubation (RSI)
▪ During surgery we give 4 drugs: Anesthetic,
Muscle relaxant of choice (= Succinyl
choline = Suxamethonium), Narcotic
analgesic, Benzodiazepine (midazolam).
▪ but here we use only 2: Succinyl choline +
Midazolam.
▪ first pre O2: 100% O2 with mask for 3 min (-
> then intubate)
462

▪ w/o doing bimanual valve ventilation (BVM)

– don’t push air in stomach -> to prevent
aspiration.
▪ w/cricoid pressure = Sellick manouver
o best method to confirm successful intubation:
ventilation (can also be confirmed with
auscultation and chest X Ray) and Oxygenation:
end tidal CO2 (ET-CO2) – Checks both ventilation
and oxygenation.
▪ ET tube size:
• in children: uncuffed ET tubes used (cuffed ET
tubes can damage the trachea)
• endotracheal tubes
• Length: age/ 2 + 12 cm
• Width
o >1 yr: age/4 + 4mm
o < 1 yr:
▪ < 1kg: 2.5 mm
▪ 1-2 kg: 3 mm
▪ 2-3 kg: 3-3.5 mm
▪ > 3 kg: 3.5 mm
▪ 1 month-1 year: 4 mm
• O2 delivery systems
o Nasal prongs (canula) – recommended today
▪ flow rate: up to 3 L/min
▪ max. received 40 % O2 (in emmergency we
always give 100% O2; in other situations –
with smaller conc.)
o Simple face mask – used to be the preferred one
▪ flow rate: 10-12 L/min
▪ max. 60 % O2
o Face mask with O2 reservoir
▪ flow rate: 15 L/min
▪ max. 90% O2
o ET tube
▪ Flow rate: 15-20 L/min
▪ 100% O2
o 2. Breathing
▪ look, feel, listen
▪ pulse oxymetry
▪ ABG
o 3. Circulation - BP
▪ adm. fluids
▪ cardiopulm. resuscitation
• Basic life support (BLS)
- DRABC
▪ danger
463

▪ response
▪ A
▪ B
▪ C
• CPR
o how:
▪ 30 compress. : 2 breaths
▪ chest depression: 4-5 cm
▪ rate of compressions: 100/min
o most important sign of successful
resuscitation: Pupillary light reflex OK
o how long to continue CPR: as long as
you can, till specialized team has
arrived (usually max. 45-50 min)
o if cardioversion is not available, IV
adrenalin should be given every 3 min.
▪ Disability
• neurological signs
• Defibrillation
o use it right away if available
o for a witnessed cardiac arrest, using a
manual defibrillator:
▪ give 3 consecutive shocks in
first defibrillation attempt
▪ further shocks –> single shock
o 1st shock: 200 J Biphasic (before 360 J
monophasic – no longer used)
o continue CPR for 2 min
o 2nd shock:200 J Biphasic-> max. 3shocks
o Shockable rhythms:
▪ Unstable VT
▪ VF
o Non-shockable rhythms:
▪ Asystole (no pulse)
▪ Pulseless electricl activity (PEA)
• Advanced life support (specialized team has arrived)
- continue CPR
- in shockable rhythms (VT/ VF) - defibrillate again
- non-shockable rhythms – drugs only
- drugs
▪ Adrenalin 1 mg IV or intracardiac repeat every 3 min
during defibrillation
▪ Atropine 1-3 mg
• in asystole or severe bradycardia
▪ Amiodarone – 300 mg bolus
• in VT or VF
▪ Mg – muscle relaxation, etc.
464

• in any critical patient

▪ Bicarbonate – controversial
• 1 mmol/ kg
- think of and address reversible causes of cardiac arrest: 4Hs, 4Ts
▪ hypoxemia
▪ hypovolemia
▪ hypo/ hyperthermia
▪ hypo/ hyperkalemia
▪ tamponade
▪ tension pneumothorax
▪ toxins
▪ thrombosis (pulm., coronary)
- Cardiac arrest
o Basic life support -> ECG, monitor BP ->
▪ VF
• -> Defibrilation -> Adrenaline (1:10,000) 10 ml IV -> Defibrilation
- + consider lignocaine.
▪ Asystole:
• Adrenaline dilute 1 mg 1:10,000 give 10 ml IV from it -> continue CPR,
consider more adrenaline every 10 min -> Atropine 1.2 mg x IV
▪ Electromechanical dissociation.
• causes:
- 4 Ts
▪ cardiac tamponade
▪ PE/ thrombembolism
▪ tension pneumothorax
▪ toxic/ drug abuse
- 4 Hs
▪ hypoxia
▪ hypovolemia
▪ hypothermia
▪ hypoglycemia
▪ hypokalemia + other electrolyte imbalance
• after ruling these out -> treat as asystole
▪ VT
•Stable – Amiodarone, Lignocaine
•Unstable – treat as VF (Defib -> Adren-> Defib))
▪ Bradycardia – Atropine 0.5 mg IV.
• consider external pacemaker.
- CPR
o External cardiac massage –
best indication that massage is effective: size and reaction of pupils
o most important factor that will result in a successful resuscitation = Early cardioversion
- Anesthesics
o Ketamine
▪ one of the few analgezics which dosn’t cause hypotension
▪ incr. everything: BP, ICP, bronhodilation
465

▪ very good analgezic effect

▪ dissociative anesthetic
▪ SE – unpleasant hallucinations (in high dose), nausea, vomiting
▪ indic.
• for small pediatric procedures
• anesthetic of choice in patients with low BP
• in asthma
▪ CI – head trauma (incr. ICP)
o Thiopentol sodium
▪ decr. BP, decr. ICP
▪ cerebroprotective effect (↓ O2 consumption of brain)
▪ indic.
• neurosurgery
▪ SE
• resp. depression, hT
• endogenous histamine release -> careful in asthma
o Propofol – very popular and efficient
▪ stable anesthesia
▪ no hallucination
▪ SE – resp. depression, hT
• can be contam. very easy (made with eggs) -> careful with antiseptic
procedures
- Muscle relaxants
o depolarizing
▪ Succinyl choline – MC used in emmergency
• cholinergic drug
• short acting (3-5 min)
• SE
- incr. ICP
▪ CI – head injury
- hyperkalemia
▪ CI in burn injury, crash injury
- bradycardia (Rx – atropine)
- malignant hyperthermia – very rare
▪ non-dose dependant
▪ very high mortality
o non-polarizing
▪ types
• intermed.
• long acting
▪ curaniums
• pancuronium, etc.
- Anaphylaxis
o causes:
▪ MC of food allergy:
• 1. Peanuts
• 2. Seafood
466

▪ in health professionals – latex

o Rx
▪ ABC
▪ Seize the suspected allergic trigger
▪ O2 - 6-8 L
▪ Adrenalin IM or IV (not S C for anaphylaxis – too slow) + on endotracheal tube
• ampules contain 1 mg Adrenaline (1000 µgrams)
- 1: 1,000 conc. = 1 mg Adrenalin in 1 ml sol. (1 to 1)
- 1: 10,000 = 1 mg in 10 ml (10 times diluted)
• admin.
- adults
▪ 0.5 mg IM. 1:1000 (0.5 ml)
▪ 0.5 mg IV 1:10,000 (5 ml)
- children under 15 kg
▪ 10 µgms/ kg
• IM 1:1000
• IV 1:10,000
- Laryngeal edema
▪ 5 mg (5 ml) 1: 1000 through endotracheal tube
- repeat after 3-5 min – 1-2 times
▪ if persistent do adrenalin infusion: 0.25 µgms/ kg/ min
▪ + antihistamins
▪ + hydrocortisone
▪ if nothing else worked, especially in kids with asthma taking β 2 agonists (can
develop adrenaline resistance): Glucagon 2 mg IV + Noradrenaline infusion
o Indic for intub. post-severe allergic reaction
▪ Wheezing or persistent cough
▪ Loss of consciousness or collapse
▪ Difficult or noisy breathing
▪ Swelling of tongue (MCQ)
▪ Swelling of throat
▪ Difficulty in talking or hoarseness of voice
- Bee sting:
o Local
▪ Promethazine (antihistam.) Oral
▪ Hydrocortisone cream – local
o General sympt. (facial edema, swollen tongue)
▪ IM adrenaline (vasoconstriction -> reduce edema)
o if anaphylactic shock – venom immunotherapy
- Snake bite – M 1345
o tiger snake – MC
o Sx
▪ Nausea and vomiting – reliable sympt.
▪ abd. pain, excessive perspiration, severe headache
▪ Blurred vision
▪ Difficulty speaking or swallowing
▪ Coagulation defect (e.g. hematuria)
467

▪ tender lymphadenopathy
o Cx
▪ greatest danger: Resp. obstruction and failure
▪ neurological – Ptosis
▪ hematological (anticoag.) – affects clotting
▪ +don’t rely on abdominal sympt.!
▪ + cardiology
▪ + nephrology
o Mx
▪ 1st aid: firm bandage, starting from distal to proximal + splint 2 limbs together
• if on buttocks – no bandage but do not move
• not too tight, no turniquet, no ice.
• make window in bandage to do the swab (don’t displace the bandage)
▪ No sympt. – no treat.
• observe patient for 12 hrs, then release
• no helicopter/ air transportation
▪ Sympt. – Antivenom + antihistamine + C/S (to avoid Serum sickness – if it
happens, use adrenaline)
• Venom detection kit: Take swab (if scratch marks) or use fresh urine and
detect type of snake.
- Monovalent antivenom preferred (e.g. specific for tiger snake)
over polyvalent (since it can cause anaphylaxia).
- if we can’t detect the type of snake -> polyvalent.
- Dilute antivenom 1: 10 in NS, prolonged 30 min. infusion
- Air transportation
o CI in:
▪ Snake bite
▪ Retinal detachment
- Spider bite
o Only one spider is life-threatening – Sydney funnel-web spider (Murtagh 1346)
▪ Sx
• Muscle fasiculation, salivation and lacrimation, piloerection, dyspnea,
neurological symptoms.
▪ Mx – like for snake bites
• Resuscitation
• Specific antivenom
o Red-back spider and black widow spider can also cause envenomation
▪ rarely fatal, more serious in the young, frail, elderly
▪ Mx
• Antihistamine
• Antivenom x IM
o Rest – life support
▪ Mx
• Apply ice pack
• No bandage
CA metastases - OK
- Murtagh p. 242-243
468

- 1. Lymph Nodes
o Supraclav. nodes
▪ Right – 1. Breast (women), lung (men)
• also lung (Pancoast tumor)
▪ Left – Gastric (small percentage of gastric – to right as well) – Troisier’s sign
• also lung (Pancoast tumor)
- by location/ destination
o Metastases in brain (same as lungs)
▪ Breast
▪ Lung
▪ colon
▪ lymphoma
▪ kidney
▪ melanoma
▪ prostate
•

o
o Metastases in the lungs (same as brain)
▪ 1. breast – MC - Murtagh
▪ 2. lung
▪ 3. colon
▪ 4. (MC at MCQ course) kidney – cannon ball
▪ 5. testis
▪ melanoma
▪ + thyroid – cannon ball
o Metastases in bone – all are osteolytics, except for prostate CA (osteosclerotic)
▪ from
• Breast – MC (Murtagh) mixed
469

• Prostate CA (+ transitional cell CA of bladder) = Osteosclerotic -> have

to be excluded (do PSA)
• lung
• Hodgkin’s
• (MC at MCQ course) kidney CA – rarefying bone lesions
▪ Dx - Bone scan – with Technetium 99
▪ Rx
• 1 - Paracetamol
• 2 – NSAIDs + codeine
• 3 – Morphine ± paracetamol/ NSAIDS
▪ (Paget’s dis. of bone
• X Ray features
▪ larger bone/ bony extension
▪ thickened cortex
▪ coarse/ thicker trabeculation
o Metastasize in liver:
▪ 1. colon
▪ 2. pancreas
▪ 3. liver
▪ 4. stomach
▪ 5. breast
▪ 6. lung
▪ 7. melanoma
▪ least likely to metastasize to liver: Kidney
o Metastases in ovaries (blue book p. 531) – only 5% of CA in the ovaries
▪ in Aus. MC from colon CA
▪ in underdeveloped countries – MC from Breast CA
▪ in Japan (with a very high incidence of stomach CA) – MC from stomach CA
(Krukenberg tumor in both ovaries)
- By origin
o Kidney CA, metastasizes to
▪ lungs
▪ brain
▪ bones
▪ Liver, least common
o Thyr. CA what makes it inoperable
▪ X Ray - cannon balls metastases in lung
▪ hoarseness of voice – maybe?
o Breast CA metastasizes to
▪ 1 – other breast
▪ 2 – bones and brain
▪ lung
▪ liver
o Stomach CA metastasizes to
▪ liver
▪ ovary (Krukenberg)
o Malignant melanoma metastasizes to
470

▪ lungs
▪ liver
▪ brain
▪ small bowel
o Testicular CA metastasizes to
▪ lungs
▪ liver
o Prostate CA metastasizes to
▪ bones: pelvis, spine
▪ brain
- Malignant ascitis
o source
▪ Ovary - MC
▪ Uterus
▪ Colorectal
▪ Stomach
▪ Liver
o can be associated with:
▪ nodules on PR
▪ hepatic bruit
▪ supraclavicular lymph nodes
▪ absent ankle edema
Genetic diseases - OK
- inheritance patterns – Murtagh 167
o AD – Anatomical/ morphol. defects = 50% of all MCQ (male or female) inherit the dis.
▪ Familial adenomatous polyposis (FAP)
▪ Huntington’s disease
▪ Von Willebrand
▪ Neurofibromatosis
▪ Marfan’s syndrome
• Triad: tall stature + dislocated lens and myopia + coarctation of aorta
• tall and thin
• long fingers
• mitral v. prolapse
▪ Gilbert’s disease
▪ Tuberous sclerosis
▪ Hereditary spherocytosis
▪ Achondroplasia
▪ Noonan’s syndrome
▪ Acute intermittent porphyria
o AR – enzymes = 25% Cystic Fibrosis, 50% unaffected, 25% carrier, if both mother and
father are carrying the dis.
▪ Cystic fibrosis
▪ β thalassemia
▪ Hemochromatosis
▪ Wilson’s disease
▪ Phenylketonuria
471

• if untreated causes intellectual disability, seizures, musty urine color

• neonatal screening: Guthrie test
▪ Galactosemia
▪ Sickle cell anemia
▪ α-1 antitrypsin defic.
o X-linked recessive = 50% of males affected, 50% of female carriers; 50% of males and
females are normal (if just mother is carrying the gene)
▪ Hemophilia A
▪ G6PD deficiency
▪ Duchenne muscular dystrophy
o X-linked dominant
▪ Vit. D resistant rickets, fragile X Syndrome
o Y-linked
▪ hairy pinna
- Fragile X syndrome
o triad: Faces (long narrow face, low large ears) + large testes + low IQ
o MC inherited cause of intelectual disability (low IQ)
- 47xxy = Klinefelter syndrome
o Tall stature, long limbs. One of the MC causes of hypogonadism in males.
o Presents with testicular atrophy, tall stature, long extremities, gynecomastia and female hair
distribution.
o Small testes (< 2 cm), infertile, gynecomastia.
o Rx: testosterone (prevents gynecomastia, improves 2° sexual characteristics)
Pain – OK
- chronic pain management
o pharm.
▪ step-wise approach:
• 1. Panadol on when required basis
• 2. Panadol on a regular basis – 4 x 1 g / day
• NSAIDs? – depending on condition
• 3. Opioids on a self-management approach – PO or self-injected
• adjuvant therapy: TCA - Amitryptiline
o non-pharm. Rx
▪ e.g. swimming is good in Ankylosing spondylitis
- Analgesics
o Simple analgesics (actually NSAIDs too):
▪ Paracetamol
• effects:
- moderate analgezic (same as aspirin)
- moderate antipyretic
- minimal anti-inflammatory
• Excellent safety: doesn’t affect stomach (in ulcer) + doesn’t affect
platelet function -> first line analgezic in mild to moderate pain
• dosage: 1 g 4 hourly (max. 4 g / day)
▪ Aspirin
• short half-life
• effects:
472

- moderate analgezic
- moderate antipyretic
- anti-inflammatory
• side effects:
- affects stomach (ulcers, stomach bleeding)
- has an antiplatelet effect (by inhibiting production of
thromboxane, which under normal circumstances binds platelet
molecules together)
• Dosage:
- 600 mg 4 hourly (max. 4 g / day)
o NSAIDs – it takes 10 days for them to achieve maximal effectiveness (recommend
intermitent 14 day courses). Most NSAIDs act as nonselective inhibitors of enzyme
cyclooxygenase (COX), inhibiting both (COX-1) & (COX-2) isoenzymes. COX catalyzes
formation of prostaglandins and thromboxane from arachidonic acid. Prostaglandins act
as messenger molecules in process of inflammation.
▪ types by chemical structure
• Propionic acid derivatives
- Ibuprofen – short half-life
- Naproxen
▪ long half-life – in bony metastases in cancer
- Fenoprofen
- Ketoprofen
- Flurbiprofen
- Oxaprozin
• Acetic acid derivatives
- Indomethacin – short half-life
- Sulindac
▪ long half-life – in bony metastases in cancer
- Etodolac
- Diclofenac – short half-life
• Enolic acid (Oxicam) derivatives
- Piroxicam - non-selective cox inhibitor - analgesic antipyretic
▪ long half-life – in bony metastases in cancer
- Meloxicam - preferential inhibitor of COX-2 over COX-1
- Tenoxicam
▪ long half-life – in bony metastases in cancer
- Droxicam
- Lornoxicam
- Isoxicam
• Fenamic acid derivatives
- Mefenamic acid
- Meclofenamic acid
- Flufenamic acid
- Tolfenamic acid
• Selective COX-2 inhibitors = coxibs – don’t have G. intestinal side effects
of COX-1 inhibitors, but they can cause CV problems (high BP,
thrombosis – fatal MI & stroke), kidney problems
473

- Celecoxib (FDA alert)

- Rofecoxib (Vioxx - withdrawn from market)
- Valdecoxib (withdrawn from market)
- Parecoxib (FDA withdrawn)
▪ postoperative pain – IV, IM
- Lumiracoxib (TGA cancelled registration)
- Etoricoxib (FDA withdrawn)
• Phenylbutazone
▪ types by mechanism
• non-selective inhibitors of COX-1 & COX-2, mainly in CNS – paracetamol
• non-selective inhibitors of COX-1 and COX-2, in CNS and periphery –
aspirin, other NSAIDs
• Selective COX-2 inhibitors (see above)
• Preferential inhibitors of COX-2 over COX-1 – Meloxicam
▪ prevent side-effects:
• combine NSAID (e.g. diclofenac) with misoprostol (synthetic
prostaglandine E1 (PGE1) analogue)
• to be avoided in significant renal failure or CCF
o Opiods – reserved for severe pain
▪ types
• popular weaker opioids
- Codeine – strength simililar to aspirin (stronger when combined
with paracetamol)
- Oxycodone
▪ synthetic
▪ very effective orally and rectally
▪ in moderate pain (between NSAIDs and strong opioids)
- Dextropropoxyphene – controversial
• popular strong opioids
- Morphine
▪ most effective in cancer pain
▪ dosage:
• Orally: 10 mg 4 x / day
• IM or SC: 7.5-15 mg
• IV: bolus, slow or infusion
- Pethidine – synthetic
▪ risk of accumulation of its toxic metabolite
(norpethidine) causing myoclonic and general seizures
▪ not very used these days
- Methadone – oral
▪ in chronic pain – now replaced by long-acting morphine
▪ used in opiod dependency
• other opioids
- fentanyl – synthetic opioid
▪ administration:
• IV
• SC, IM
474

• transdermal
• epidural
▪ efficacy similar to morphine but with fewer side effects
(10 mg morphine SC = 150 micrograms fentanyl SC)
- hydromorphone – 5 - 7 times more potent than morphine
▪ high risk of dependence
- tramadol – atypical, with opiod and non-opiod features
▪ more and more popular
• analgesia without sedation or respiratory
depression
• low abuse/ dependence
- buprenorphine
▪ limited use, in opioid dependence
- pentazocine – not recommended
- diamorphine = heroin
▪ side effects:
• nausea, vomiting
• constipation
• respiratory depression
• dysphoria
• tolerance/ physical dependence/ psychological dependence
o Combined analgesics: Paracetamol/ aspirine + opioid (codeine)
▪ not recommended – rather prescribed separately
o Methoxyflurane – inhalatory – in emergencies, roadside accidents (ambulance)
o in neuropathic pain:
▪ Tricyclic antidepressant (TCA) – Amitryptilin – 1st choice in diabetic neuropathy
▪ Antiepileptics:
• Carbamazepine - trigeminal neuralgia
• Gabapentin – newer - diabetic neuropathy (2nd choice after TCAs), post-
herpetic neuralgia)
o by age:
▪ Children
• Paracetamol
• Aspirin – not used < 18 years – risk of Reye’s syndrome (fatty liver,
encephalopathy)
• Opioids
- Oral
- Parenteral
▪ bolus – IM, IV, SC
▪ continuous infusion – IV, SC
▪ Elderly – more sensitive, lower doses
- Psychogenic pain
o Periumbilical
o during the day
o not referred
o exclude from Hx: constipation, UTI, dairy product allergy
o Hx – emotional changes in family
475

o Rx
▪ enough dietary fibre and fluids to have normal transit
▪ family meeting to support the child (do not punish the child)
Radiology - OK
- X Ray
o Abdomen
▪ Erect/ supine
▪ Chest – pneumonia in lower lung lobes, can cause abd. pain
▪ Bowel obstruction
• location
- Small bowel – center
- Large bowel – periphery
• folds
- Small – continuous from side to side---valvulae coniventi
- Large – can’t see whole fold--Haustration
• size
- Small – 3 cm
- Large – 6 cm
▪ Cecum – 9 cm
▪ Sigmoid volvulus
• inverted U, pointing up and right (distended sigmoid loop)
- bed-ridden elderly people, chronic constipation -> stretching ->
twisting
- young paralyzed people, bed-ridden
▪ Cecal volvulus – small bowel obstruction
▪ Emphysematous cholecystitis – air in the wall of gall bladder
▪ Gas in the liver
• Biliary tracts
• Portal vein
▪ Hydatic cyst – multilocular, with multiple daugther cysts inside a big cyst
▪ Cyst vs. abscess – abscess might have air inside
▪ U/S can’t see through air – e.g. Retrocecal apendix
o Fractures
▪ cortical disruption
▪ Colles - post. dislocation of distal fragm. compared to the proximal fragment
▪ Pathological fracture (malignancy) = Fracture through lucency
- CT Brain
o Bleeding
▪ Intra-axial bleeding – inside brain
▪ Extra-axial bleeding – outside brain
• SAH
- cause
▪ Aneurysm, trauma, anticoagulation
▪ AV malformation
• Surgery – immediate effect
• Radiotherapy - after 12 months they scar;
during these 12 months they can still bleed
476

- Dx
▪ CT scan
• 75% show up on CT scan
• 25% - small amount of bleeding not seen on CT
o do a lumbar puncture
▪ to locate aneurysm or AV malformation
• contrast angiogram
• U/S through fontanelle – till 12 (max. 18) mths
• CT angiogram
• MRI angiogram
• Subdural hematoma
- elderly
- Multiple minor trauma
- Sx – confused
- Venous
- Sickle-shape (crescent) concavo-convex
- With dark areas inside (chronic, acute on chronic hemorrhage)
- can cause midline shift (if large)
• Extradural
- young
- major trauma
- Sx – headache
- arterial (middle meningeal)
- biconvex
- can cause midline shift (if large)
• Scalp hematoma after head injury
- Rx – with no loss of consciousness -> observe them for 4hrs., then
discharge them
▪ Blood = white
• would be at the botton of the pic/ bottom of the ventricles as the
patient is in supine position (heavier than CSF)
o Stroke
▪ cause
• Emboli
- if multiple vessels obstructed, MC with emboli (2 emboli coming
from a proximal source)
▪ e.g.
• Elderly – AF
o Dx U/S – clot in a heart chamber
• Young
o HOCM
o Mitral valve dis.
o DVT + patent foramen ovale -> could
cause an emboli to brain
• Thrombus
▪ types
• Ischemic
477

- loss of grey (cortex, on the outside) - white matter

differentiation + swelling of the brain
▪ Arteries
• anterior cerebral a.
• middle cerebral a. – from carotid a.
• posterior cerebral a. – from vertebral a.
• Hemorrhagic
o tumors
▪ Intra-axial – completely surrounded by brain on 3 axial images (in all planes)
• MRI better – volume/ 3D image
▪ Extra-axial – meningioma usually
o calcif.
▪
Choroid plexus
• produce CSF
• can calcify ( 2 lower branches of ventricle H)
▪ Pineal gland – on mid-line (shifted to one side > 5mm = sign of midline shift =
↑ ICP)
o Older patient – larger ventricles, deeper gyri due to CNS atrophy
- Brain MRI
o 1. you can see skin/ scalp - is white
▪ skin can’t be seen on CT (white bone, then brain)
o 2. bone is black
o 3. brain
o method - 2 basic sequences:
▪ T1 – CSF is black
• Contrast images in T1 Seq: contrast will be white on black background
(CSF)
▪ T2 – for Pathology (for extra fluid in brain)
• CSF + any fluid is white – high signal
o Dx for MS – White spots = demyelination plaques around ventricles (Dawson fingers)
Other stuff - OK
- treatment options
o conservative - symptomatic
o medical
o surgical
o others
- Planes
o median (midsagittal) plane – divides left/right
o transversal plane - horizontal
o coronal (frontal) plane – divides ventral (ant.) / dorsal (post.)
- Postural hypotension= drop of > 10 mm Hg when standing
- Intestinal absorbtion
o Terminal ileum
▪ Bile salts
▪ Vit. B12
o Proximal jejunum
▪ Iron
478

▪ Folic acid
▪ Vit. C and Ca
- Edema
o Pitting – pressing with finger leaves an indentation that persists for some time
▪ cardiac
▪ hepatic
▪ renal
▪ DVT/ varicose veins/ thrombophlebitis
o Non-pitting oedema
▪ Lymphoedema
• lymphatic obstruction – do abdmino-pelvic CT to look for tumors
• check for DVT - Doppler U/S??
▪ Myxedema
- Hereditary angioedema – bouts of abd. pain and facial edema
o Dx – C1 esterase inhibitor
- Autonomic nervous system
o Sympathetic
▪ originate from thoracolumbar region of spinal cord (levels T1 - L2, specifically) -
"thoracolumbar outflow"
o Parasympathetic
▪ arise from CNS with the:
• III, VII, IX and X cranial nerves
• S2, S3, and S4 spinal nerves
• "craniosacral outflow"
- CNS membranes and spaces
o Epidural (or peridural) space – just in spine
o Dura mater
o Subdural space – virtual, becomes real in cases of haemorrage (subdural hematoma)
o Arachnoid
o Subarachnoid space – contains CSF
▪ hemorrhage from aneurysms
o Pia mater

- Types of tissues
o epithelium is classified as a primary body tissue - cells which line the cavities and surfaces
of structures throughout the body. It is also the type of tissue of which many glands are
formed. Epithelium lines both the outside (skin) and the inside cavities and lumen of
bodies.
o connective tissue
o muscle tissue
o nervous tissue.
- Marital disruption – single most powerful sociodemographic predictor of stress-related dis.
- greatest predictor of cardiovasc. dis. and DM = low educational level
- prevention
o primary – prevent the disease from occurring
o secondary – stop or delay the progression of dis.
▪ screening and early detection of dis.
479

o tertiary – minimise disability in case of irreversible damage from the dis.

▪ rehabilitation
- Organ transplant
o storage times
▪ 24 hrs – kidney, pancreas, liver
▪ 12-24 hrs – lung
▪ max. 6 hrs – heart
o Cx
▪ malignancies
• 40% will develop a CA within 10 yrs
- Universal
o Donor - O Rh-
o Recipient – AB Rh-
- Sexual abuse
o risk factor for:
▪ mood disorders (depression)
▪ anxiety disorders
▪ eating disorders
▪ substance abuse
- MC causes of death in Aus.
o 1 – Circulatory disease: cardiovasc. disease
o 2 – CA
o 3 – Accidents, poisoning, violence
o 4 – Resp. disease
o 5 - Suicide
- MC causes of suddent death in Aus.
o 1 – MI
o 2 – Accidents
o 3 – CVA
o 4 – PE
o 5 – Suicide
LEADING CAUSES OF DEATH(a), Males - 2008(b)(c)

Underlying Cause of Death Rank Males Total

Ischaemic heart diseases (I20-I25) 1 12 444 23 665
Trachea and lung cancer (C33-C34) 2 5 025 7 946
Strokes (I60-I69) 3 4 727 11 973
Chronic lower respiratory diseases (J40- 4 3 387 6 255
J47)
Prostate cancer (C61) 5 3 031 3 031
Dementia and Alzheimer disease (F01-F03, 6 2 707 8 171
G30)
Colon and rectum cancer (C18-C21) 7 2 230 4 120
Blood and lymph cancer (including 8 2 220 3 889
leukaemia) (C81-C96)
480

Diabetes (E10-E14) 9 2 141 4 191

Suicide (X60-X84)(d) 10 1 709 2 190

LEADING CAUSES OF DEATH(a), Females - 2008(b)(c)

Underlying Cause of Death Rank Females Total
Ischaemic heart diseases (I20-I25) 1 11 221 23 665
Strokes (I60-I69) 2 7 246 11 973
Dementia and Alzheimer disease (F01-F03, 3 5 464 8 171
G30)
Trachea and lung cancer (C33-C34) 4 2 921 7 946
Chronic lower respiratory diseases (J40-J47) 5 2 868 6 255
Breast cancer (C50) 6 2 774 2 788
Diabetes (E10-E14) 7 2 050 4 191
Heart failure (I50-I51) 8 2 034 3 360
Colon and rectum cancer (C18-C21) 9 1 890 4 120
Diseases of the kidney and urinary system 10 1 756 3 224
(N00-N39)

- MC cause of exposure to ionizing radiation in normal population = Background radiation

- Fall in elderly – MC cause = multi-pharmacy (≥ 3 drugs, causing postural hypotension)
- Kappa = (Observed agreement – change of agreement) / (1 – change of agreement)
- Sarcoidosis
o young woman
o multisystem dis.
o non-caseating (not-cavitatory) granulomatous inflam.
o Sx
▪ 20-40% asympt
▪ Dry cough, fever, malaise, bilat. hilar lymphadenopathy, arthralgia
▪ erythema nodosum ( = Sarcoidosis for AMC)
▪ Uveitis
▪ State of cutaneous alergy – no allergic reaction, TB test negative (like in
immunsupressed people) – decr. in T cells
o Dx
▪ X Ray: bilat. symmetrical hilar lymphadenopathy
▪ lung biopsy
▪ if erythema nodosum – skin biopsy
▪ ↑serum ACE levels
▪ hypercalcemia – due to incr. absorbtion of Ca from intestine
o Rx
▪ may resolve spontaneously
▪ C/S – Prednisolon – Oral 6-8 wks, then taper
- BMI
o < 18.5 = underweight
481

o 18.5-24.9 = normal
o 25-29.9 = overweight
▪ Rx – lifestyle changes
o 30-34.9 = Grade 1 obesity
▪ Rx - Supervised lifestyle changes
o 35-39.9 = Grade 2 obesity
▪ Rx
• Supervised lifestyle changes
• Medical Rx:
- local
▪ bulking agents – methycellulose
▪ lipase inh. - xenical
- central
▪ decr. hunger – amphetamines derivates: Phentermine,
diethylpropion
▪ incr. satiety – SSRI
o ≥ 40 = Grade 3 (morbid) obesity
▪ Rx – as above +
• consider Gastric banding
- SaO2 < 92% - give O2
o in COPD – cut off value = 88%
- Adrenergic receptors
Receptor Agonist
Location / Action Mechanism Agonists Antagonists
type potency order
Smooth muscle. In blood
vessels the principal effect is
vasoconstriction. Blood (Alpha
vessels with α1 receptors are blockers)
Gq:
present in the skin and GI phenoxyben
α1: phospholipa noradrenaline
noradrenaline≥ system, and during the fight- zamine
ADRA1A, se C (PLC) phenylephrine
adrenaline >> or-flight response phentolami
ADRA1B, activated, methoxamine
isoprenaline vasoconstriction results in ↓ ne
ADRA1D IP3 and Cirazoline
blood flow to these organs. prazosin
calcium up
This accounts for an tamsulosin
individual's skin appearing terazosin
pale when frightened. In GI
tract, effect is relaxation.
Gi:
clonidine (Alpha
α2: adrenaline > adenylate
Pre- and postsynaptic nerve lofexidine blockers)
ADRA2A, noradrenaline cyclase
terminals. Mediates synaptic xylazine yohimbine
ADRA2B, >> inactivated,
transmission. Tizanidine rauwolscine
ADRA2C isoprenaline cAMP
Guanfacine idazoxan
down
isoprenaline > Heart and cerebral cortex. In Gs: noradrenaline (Beta
β1:
noradrenaline heart, agonists enhance adenylate isoprenaline blockers)
ADRB1
> adrenaline myocardial contractility and cyclase dobutamine metoprolol
482

increase heart rate. Also found activated, atenolol

on juxtaglomerular cells, cAMP up
activation results in renin
release.
(Short/long)
salbutamol
Lung, smooth muscle,
(albuterol in
cerebellum, skeletal muscle.
USA)
In lung, agonists cause Gs: (Beta
bitolterol
isoprenaline > bronchiole dilation. Agonists adenylate blockers)
β2: mesylate
adrenaline > can be useful in treating cyclase butoxamine
ADRB2 formoterol
noradrenaline asthma. In smooth muscle, activated, propranolol
isoproterenol
relaxes walls. Relaxes uterine cAMP up ritodrine
levalbuterol
muscle and promotes release
metaproterenol
of insulin.
salmeterol
terbutaline
Gs:
L-796568
isoprenaline > adenylate (Beta
β3: Adipose tissue. Agonists CL 316,243
noradrenaline cyclase blockers)
ADRB3 enhance lipolysis. LY 368842
= adrenaline activated, SR 59230A
Ro 40-2148
cAMP up
- Average height in Aus.
o Man - 1.62m
o Woman - 1.52m
- Post-op complications
o 1st day – Atelectasis
o 3-6 days -> Wound inf.
o 3rd (48-72 hrs) day -> Fat embolism
▪ MC after fracture of long bones
▪ Sx
• Fever, tachycardia, hypoxia
• CNS - paranoid delusions, agitation, seizures, confusion, coma
• Skin - rash in upper part of body (face, neck, upper limbs)
- oil stays on upper aorta -> sent to upper body
• Retina – fat emboli on fundoscopy
• Fat in sputum or urine
▪ Dx
• Chest X Ray: multiple bilateral infiltrates in lungs
• CT/ MRI brain – edema, multiple small infarcts in brain after 1 week,
cerebral atrophy later
• hypoxemia – PaO2 < 60 mm Hg
• thrombocytopenia
▪ Rx
• Symptomatic/ supportive Rx only:
- unconscious - intub., monitoring
- in agitation – sedation
483

- in delusions - Haloperidol
- hypoxia - O2 40%
- C/S?
o 10 days + fever + mucous diarrhea = Pelvic abscess
▪ without fever: resolved paralytic ileus
o Serosanguinous discharge = Wound dehiscence (rupture)
▪ Surgical emergency: Rx – return to OT: wound toilet and resuturing
▪ in first 10 days after op.
▪ Wound dehiscence = Paralytic ileus (MC cause)
▪ MC with Vertical incisions
o Pulmonary emb. with pulmonary infarction – Chest pain, hemoptysis, pleural friction
rub on 10th day Post-op
o Postop. confusion and disorientation = Acute delirium
▪ causes
• Hypoxia – MC, due to:
- Atelectasis
- Analgesics
- Anesthetic from surgery
- Lifestyle changes
o SNAP
▪ Smoking
▪ Nutrition
▪ Alcohol
▪ Physical exercise
Psychiatry - OK
Main pathology
Defense mechanisms (MCQ 2071 p146)
- types: http://en.wikipedia.org/wiki/Defence_mechanism
o I. Pathological
▪ 2. Denial = Avoid to become aware of some painful aspect of reality, you’re
not ready to accept it
• e.g. patient doesn’t accept that he has cancer (“no, you are lying”)
• Rx – don’t confront him, just give him time to accept it (unless he’s
dealing with a life-threatening situation)
▪ 3. Splitting = external objects are divided into “all good” or “all bad”
• e.g. patient doesn’t talk to any nurse because doctors are better than
nurses; morning stuff is better than evening stuff
• mainly in borderline personalities.
• Resistance refers to the conscious and informed decision of a patient not
to change behaviour or comply with treatment. e.g, refuses for ECT
o II. Immature – MC in adolescents, often also in adults
o Blocking, regression, somatisation, introjections, projections are examples of immature
defense mechanism (MCQ)
o
▪ 1. Projection=projecting your own vicious thoughts/ feelings onto someone else
484

• e.g. husband is cheating on wife -> tells her “I think you are cheating on
me”
▪ 5. Somatisation = Phsychic derivatives are converted into bodily symptoms
• e.g. you think of an exam and you develop symptoms (e.g. diarrhoea)
o III. Neurotic – in adults
▪ 6. Displacement = An emotion or drive is shifted to another that resembles
original in some aspect.
▪ e.g. stressed from work/ boss, get home, take it on your partner/ family/ pet.
7. Intellectualization = excessive use of intelectual processes to avoid affective
expression (mood) but emotions are missing in the talks/ arguments.
• e.g. patient finds out he has cancer, he researches it, he talks about it like
in a speech, with no emotion
▪ 8. Rationalization = rational explanations are used to justify unacceptable
attitudes or behaviour (blame game)
• e.g. blaming something else for your mistakes
▪ 9. Isolation = Separation of an idea from the emotional effect that
accompanies it
• e.g. when seeing body of her dead son, mother is very cold and detached
▪ 11. Repression: Ideas or emotions which the person finds painful or
unacceptable are forced out of consciousness and are forgotten.
▪ 10 Suppresion: Suppression refers to conscious or 'semi-conscious' decision of
an emotionally mature, healthy adult to postpone dealing with conflict ideas.
e.g., in interview a pt avoids discussion of certain topics
▪ 12. Reaction formation: Unacceptable impulse is transformed to its opposite
• e.g. we are afraid of an exam, but when asked we tend to say “I’m fine”
• Choosing medicine as a career solely to treat other’s illness as a defence
against ones own death or illness anxieties.
• Pyromanic becomes firefighter
▪ 13. Regression = you don’t behave according to your age (but like a younger
person) MC in males
• e.g. after sister born a boy (6yrs) start sucking his thumb & wetting
bed. MCQ 2071 p146
• after his parents’ divorce, a 7 yrs old boy starts to wet his bed again
14. Jealousy: A normal human emotion.
• 15. Compensation or counter dependancy: a form of denial where
individuals respond to limits being recommended by taking more work,
responsibilities or becoming more energetic.
Example, CHF patient who has been told by doctors to remain in home
and not to do exercise recently attends aerobic classes and do 2 km
jogging every day
• Acting out: a dramtic or sometimes aggressive behaviour that occurs under
stress/ anxiety eg. throwing tantrums, shouting and yelling.
o IV. Normal, healthy, mature
▪ 14. Sublimation = impulse gratification has been achieved but the aim or
object has been changed from unacceptable to acceptable.
• the most mature one
485

• e.g. you like pornography, but you achieve satisfaction by focusing on

something else (e.g. you become part of the censorship board – you
watch it, but in an acceptable way)
▪ 10. Suppresion = conscious forgetting
• the only conscious defense mec.
• e.g. lost a beloved dog, denies he ever had one (to avoid suffering)
▪ 13. Humour = something is wrong with you and you are making fun of yourself
before anybody else has chance to do it
▪ 16. Introjection (Samir) = Identifying some idea or object so deeply that it
becomes a part of that person.
▪ 17. Identification (Samir) = Unconscious modeling of one's self upon another
person's character and behaviour.
o + 4. Blocking (Shipra) = temporary block in thinking (in stressful situation)
▪ e.g. at exam, you know the answer but it just doesn’t come to our mind
▪ Rx – relax, it will pass
o + Transference (Samir)
▪ patient becomes emotionally involved/ has negative feelings for her
psychiatrist, based on the patient’s childhood rships (with parents, teachers,
siblings) – transferring to the psychiatrist the feelings originally developed in
her childhood.
• can be
- positive (with positive feelings)
- negative (with negative feelings)
▪ counter transference – the other way around
• therapist develops pos. or neg. feelings bc a particular pt reminded them
consciously or unconsciously of another patient or close person

Personality disorders (Read examples in MTB 3 page 483)

o they were like this from the beginning, but can change/ control it if they want
o = Maladaptive behav.
o Men: MC - Antisocial PD (Aggressive, criminal acts, many violent offences, abusive, lack of
respet for others).
o Women: MC – Borderline (Slef harm and unstable relations, splitting DM)
o Key Sx
▪ interpersonal relationships are affected
▪ failure to achieve goals at work
▪ chronic unhappiness
o these are not diseases:
▪ they are functioning
▪ no trigger point/ beginning for it
▪ no psychotic sympt. (delusions, illusions, hallucinations, etc.)
o types:
▪ Cluster A – Isolated, detached, aloof + OK with that (but surroundings are not
OK)
• 1. Paranoid: Suspicious, secretive and mistrustful, e.g., everybody
around is plotting against them or neighbours are stealing my mail.
- Main defence mechanis is projection.
486

• 2. Schizoid: Shy, loner (happy to be alone), doesn’t talk to you e.g., a

man living alone in a remote village, has no friends or family members,
seen once or twice a yr in town.
• 3. Schizotypal: Like Schizoid (Shy, alone) +
- Magical thinking
▪ e.g. plants talk to him
- superstitious
- on the verge of getting psychotic
▪ they might get psychotic for a short time under stress
▪ Cluster B
• 4. Borderline: “Unstable mood + marked impulsivity unstable/ difficult
relationships, recurrent suicidal behaviors or self harm, chronic feelings
of emptiness, identity disturbance and inappropriate anger. Become
intensely angered if they feel abandoned. Main defense mechanism is
splitting.
Exmp. 30-yr old woman presents to the clinic. She has seen many
doctors, she said they were all wonderful until they started ignoring her.
She starts visit saying that assistant at the front desk is "worst she's ever
seen" because she didn't smile at her. The other assistant was just
wonderful according to her.
Rx- Dialectical behavior therapy (MCQ).
5. Antisocial- Aggressive, criminal acts, many violent offences, abusive,
lack of respet for others). HO going to jail many times.
• 6. Histrionic = “look at me” (center of attention), Paris Hilton
- uses seduction to attract attention.
- in celebrities, dramatic, theatrical and dress in attractive way
- sexually frigid.
• 7. Narcissisitic – “I am the best, unique or VIP”.They believe they are
special. Try to attract special attention.(like VIP wards/ rooms)
- Don’t take criticism or care about others. Seen in celebrities,
politicians, actors, fashion models and sport stars.
▪ Cluster C
• 8. Anxious avoidant – “loner” but not happy about it (difference from
schizoid). Avoid social gatherings or parties.
- because they are scared of criticism/ rejection or getting
embarrased (forced to be alone but don’t wanna be alone)
- obsessed to do everything right.
- prone to depression.
• 9. Dependant – can’t take decisions, want somebody else to decide for
them
- won’t leave their partner even if abused
- very prone to depression
• 10. Obsessive compulsive personality disroder (ankastic?) –
“Perfectionist”
- likes things in a certain way or order
- very thrifty (not wasting things or money), inflexible
- not prone to OCD, but prone to depression
- Rx: Psychodynamic psychotherapy MCQ
487

▪
+ Passive-aggressive personality? (purple book) – negativistic attitudes and
passive resistance to demands for adequate performance at work or in other
social contexts, always complaining about these demands.
Thought broadcasting: A belief of pt that his ideas and thoughts are known by people in the
surroundings.
Types of disorders
o I. Anxiety disorder
▪ components
• Psychological comp. – always worried, hypervigilance, restlessness,
difficulty concentrating, sleep disturbance
• Physiological comp. – hyperactivity: tahic., hands shaking, dry mouth,
tension headache, constip. or diarhhoea, etc. (adrenal release –
syndrome)
▪ types:
• 1. Panic disorder = unexpected and recurrent panic attacks + avoidance
behaviour (avoiding what could trigger the panic attack)
Example: 19-year-old ballet dancer presents because of extreme anxiety on stage. She repots that she fell 3
months ago at a national ballet competition and since then suffers extreme anxiety, trembling, diaphoresis, a
breathlessness when she has to go on stage. She denies any problems with ballet practice and has no other medical
problems.
- MC people coming to the ED
- panicogens: lactate, CO2, caffeine
- young women (mid twenties)
- reach peak within ½ min
- +/- agoraphobia = afraid of public spaces (scared of having panic
attacks in public)
- they fear they will lose their mind / go crazy
- ABG: pH incr., PaCO2 decr., SaO2 normal
- Sx
▪ panic attacks:
• Lasts minutes to hours: 20 minutes.
• Self-limited.
• Occurs in pts with or without chronic anxiety.
• Spontaneous – no significant trigger
• Age of presentation: Mid 20s
• Variety of somatic symptoms (not faked).
o Sympathetic discharge: Release of
noradrenaline which produces
cardiovascular and other autonomic
symptoms.
o Palpitations, chest pain and tightness,
sweating, dizziness, trembling,
chocking, abdominal pain.
o Hyperventilation: Exhaling carbon
dioxide, increasing pH which affects
neuromuscular transmission (chest
tightness).
488

• DIFFERENTIAL DIAGNOSIS:
o Panic attack secondary to a medical
condition.
o Panic attack secondary to medications.
o Caffeine intox. – no chest tightness
o Other anxiety disorders: Panic attack
are unexpected. The fear is of having an
attack, not of a specific situation.
• TREATMENT:
o CBT/ Relaxation, training or
desensitization.
o SSRI, Benzodiazepines or TCAs.
▪ long term – between attacks
• 1. Breathe in paper bags or relaxation
techniques
• 2. SSRIs
• 3. TCAs
• 2. Phobic disorders
- irrational fear focused on certain things (not generalized like in
the generalized anxiety) disorder
- with insight – the person recognizes that the fear is irrational and
out of proportion with the real danger
- resistance is usually minimal and unsuccessful
- types:
▪ Agora phobia – fear of the market, public, busses or
confined places, far from home, you cannot run away
from there
• untreated may culminate in a panic attack
▪ Social phobia – talking / eating / socializing with
people; ok 1 on 1, but not with a larger group of people
(public speaking, "stage fright," urinating in public
restrooms)
• may be a predisposing factor for alcoholism
(alcohol is anxiolytic)
▪ Specific phobias
• Fear of spiders, snakes, illness, contamination,
etc.
- Rx
▪ 1. CBT:
• systematic desensitization
• assertive thinking
▪ 2. SSRI
▪ in social phobia (stage fear):
• Beta blockers (control the physiological comp.)
• 3. OCD
- Recurrent and obtrusive false thoughts (Obsession) with insight,
they know it’s wrong but can’t help it + repeated action
489

(compulsion) required to calm the thoughts just like a person

thinks his hands are dirty followed by repeated washing of hands.
• Stuck song syndrome/ ear worms/ musical obsessions are MC in
OCD (MCQ)
• A 40-year-old man with OCD mentions annoying songs during a period of
stress. These disruptive songs are present day and night, and cause
severe insomnia. The more he tries to suppress them, the worse it gets,
and his fear of losing control reinforces this. Short tunes continue for
hours, usually songs he hates. The patient is exhausted and his life is
negatively affected by the earworms.
- What will wad to diagnosis here answer is insight (MCQ)
- Hoarding disorder: a subtype with pt unable to discord used
items. MCQ Patient brought by wife. wife complains that she is
tired of his habit of collecting rubbish.he denies any problem by
saying I have lots of property and bank balance and 3
residence..wife says bitterly that they r all filled with rubbish.what
is the most appropriate pharmacological approach?
A.Venlafaxine.
- No option for SSRI.
- Rx
▪ 1. CBT
• exposure and response prevention therapy
▪ 2. SSRI, Clomipramine.
• 4. Post-traumatic stress disorder (PTSD)
severe anxiety symptoms that follow a life threatening event (death,
winess a vilonet crime or combat). Acute SD = symptoms last < 1
month. PTSD = symptoms last > 1 month.
• Following are 3 key symptom groups:
1. Re-experiencing of the traumatic event: Dreams, flashbacks, or
intrusive recollections.
2. Avoidance of stimuli associated with the trauma.
3. Increased arousal: Anxiety, sleep disturbances, hypervigilance,
emotional lability or impulsiveness.
Treatment:
Give benzodiazepines acutely for anxiety symptoms. SSRis and other
antidepressants can be helpful for long-term therapy.
▪
- 3 Clusters of symptoms:
▪ 1. intrusive phenomenon: recollections, nightmares,
flashbacks
▪ 2. hyperarousal phenom. = exagerated startle response
(e.g. when you call their name a little loudly)
▪ 3. avoidance or reminders and emotional numbning
(they avoid the topic)
- Rx
▪ 1. CBT
• crisis intervention therapy - goal: bring the
patient back to pre-crisis status
490

▪ 2. group therapy
▪ 3. SSRI
▪ for nightmares: zopiclone, zolpidem (non-benzos
anxiolytics)
• 5. Generalized anxiety disorder – anxious about everything
- mild, > 6 mths
- charact. = anticipatory feelings, especially in the morning (things
will go wrong today) + physical sympt.
- difficulty falling asleep (thinking about what happened during
the day) and then walking up during the night.
- women
- Rx
▪ 1. CBT
▪ 2. SSRI
• 6. Adjustment (reactive) disorder
an acute reaction to overwhelming stress (minor stress like accident) at
any age, who have no underlying mental disorder.
▪ Rx
• all antidepressents: SSRI, SNRI, TCA
• Benzodiapines – with a clear time limit (otherwise – addicted)
• CBT
- Relaxtion + gradual exposure to trigger
o II. Somatoform disorder (MTB3 477)
▪ Physical sympt. with no medical explanation
• transform psychological emotions to physical problems, without being
able to connect the 2.
▪ types:
• 1. Somatisation disorder – Classical form - never seen
- Young women (starts < 30 yrs)
- 8 or more complaints:
▪ 4 of pain
▪ 2 GI
▪ 1 Neurol.
▪ 1 Sexual
- + atypical forms – with less complaints
- Rx
▪ CBT
▪ keep rescheduling their appts., don’t confront
• 2. Conversion disorder
- MC in women
- Psychological symoptoms (stress) convert into physical symptoms
(paralysis or blindess).
- e.g. husband had MI => woman can’t move her legs, but on
physical examination reflexes are normal and she can sit up.
- Woman fell from horse and complains of paralysis of leg.
- Rx
▪ CBT – comforting
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• 3. Hypochondriasis (overvalued idea)

- convinced they have 1 disease + tell you the diagnosis, despite
examinations and investigations denying his diagnosis
- Rx
▪ Psychotherapy
▪ Keep rescheduling their appts., don’t confront
• 4. Body dysmorphic disorder (overvalued idea)
- one part of their body (usually face) is not correct/ sick
- MCQ: keeps looking in the mirror, changing clothes
- diff. from body image disturbance = eating disturbance (the whole
body is not correct).
- High doses of SSRIs are first-line therapy.
- If the only concern is body shape and weight, anorexia nervosa is
the more accurate diagnosis.
- If the only concern is sex characteristics, gender identity disorder
is the more accurate diagnosis.
• 5. Psychological pain – Persistent pain even though the etiology
doesn’t match.
- e.g. torn ligament –After Rx – should go away – but they still have
pain (they have no motivation to get well – others, well motivate,
like sportsmen, get well in 1 wk)
▪ Rx
• Drugs + Psychotherapy
- conversion – good prognosis
- the others – bad prognosis
o III. Factitious disorder (Munchausen disease)
▪ they simulate symptoms in order to get admitted in the hospital.
▪ variant: Munchausen by proxy - they simulate sympt. in a relative (their kids) in
order to get admitted in the hospital.
▪ diff. from Malingering = they simulate sympt. in order to achieve obvious gain
or to avoid punishment or responsibility or court proceedings.
o IV. Impulse control disorders – can’t control their impulses + are anxious about it (they
have to do it)
▪ 1. Intermittent explosive disorder
• uncontrolled reaction of anger/ violence at small triggers. MCQ: Fights
with friends
• followed by remorse
• can’t control their anger
▪ 2. Cleptomania
• Can’t control their impulse to steal unnecessary objects they don’t even
require or need -> relived after they do it.
• ¼ of bulimics are also cleptomaniacs (MCQ)
• Rx
- CBT: Systematic desensitization
▪ 3. Pyromania
• love to put things on fire + get sexual gratification/ satisfaction from
doing it
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• usually low IQ. Pyromania is not the diagnosis if the motive is personal
gain (i.e., insurance money) or to show anger, which differentiates
• this from conduct disorder.
▪ 4. Trichotillomania
• pull their hair out when stressed
• Life change (parents separated, new father, etc.)
• Some also eat their hair => Bezoars of hair causing intestinal obstruction
• with unequal areas of balding and hair shafts of different lengths.
• Dx diff – KOH preparation to exclude a fungal infection
o V. Adjustment disorder
▪ an acute reaction to overwhelming stress (minor stress like accident) at any
age, who have no underlying mental disorder.
▪ inability or maladaptive reaction to an identifiable stressful life event like:
divorce, family crisis, failing exams, etc.
▪ Sx must occur within 3 mths of event and shouldn’t persist longer than 6 mths
▪ females
▪ genetic comp.
▪ Sx = Variety of disturbances at home or work, like: rage, shame, guilt, anxiety,
depression
o VI. Delusionals disorder (A fixed false belief)
▪ just delusions – non-bizarre, initially seem reasonable, but upon investig. no
foundation is found for them
▪ no insight
▪ personality doesn’t desintegrate, well inserted in society
▪ types
• Paranoid disorder (MC)
- subtype – pathological jealousy
- can occur as a psychological reaction to deafness
▪ tinnitus may produce or aggravate auditory
hallucinations
• Erotomanic – they believe a celebrity is in love with them
▪ can be dangerous – if their delusion refers to another person
• e.g. pathological jealousy, Othello`s syndrome, attracted to a celebrity
• could kill the person they fantasize about
▪ Rx very difficult, don’t usually respond to antypsychotics
• early detection is very important
o VII. Eating disorders –
o Anorexia nervosa – feeling fat (MTB 480) feeling fat, overvalued idea of body image –
even tough they are skin on bone
▪
• 90% women- a young female who is underweight.
• 11-21 yrs -MC
• Risk factor Athlete (MCQ)
• Sx
- stop eating
▪ subtype/ some patients – binge eating (like in bulimia)
- Heavy exercise – this keeps them healthy for a long time!
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- Amenorrhea bc of↓ FSH & LH. (more than Bulimia) ≥ 3 cycles

- purging: laxatives, vomiting
- motivation:
▪ tired of family control, broke up with her boyfriend
(who were telling her to eat more)
▪ don’t like food
- lanugo hair – due to emaciation - Pale fine and downy hair over
dorsal aspects of limbs
- hT, hypothermia, bradycardia
- parotid gland hypertrophy
- dental enamel erosion of the post. surface of the teeth
- lost shivering response to cold
- loss of breast development (MCQ).
- Normocytic normochromic anemia
• Associated psychopathology:
- depression
▪ suicidal ideation leading cause of death in An. nervosa
- anxiety sympt. focused on eating
- social withdrawal
- obsessional behav. concerning food, diet, wt. and exercise
- perfectionistic and preoccupied with external appearance
• Cx
- Liver, thyroid function abnormalities
- Normocytic anemia, iron defficiency
• BMI < 17.5 (or body wt. with 15% less than expected for the person’s
height, sex and age)
• DSM criteria
- 1.Failure to maintain 85% of wt. according to age/ height/ physical
activity.
- 2. Intense fear of putting on wt.
- 3. Body image disturbance = unrealistic self-evaluation (they are
really thin but believe they are overweight
- 4. Amenorrhoea (No hirsutism)
- Ankle swelling- Sign of hypothyroidism. Presents later with
increased BMI (MCQ)
• risk of hypokalemia
▪ Bulimia : associated with OCD (MCQ)
• young female with normal weight, HO binge eating, then induce vomiting
• ¼ of bulimics are also cleptomaniacs. (MCQ)
• motivation:
- love food but feel bad because of their weight (they used to be
fat at one point in the past)
• Risk factor: Family obsity (MCQ)
• BMI - normal
• Sx
- Anemia
- Parotid enlargement
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- Teeth marks on dorsum of hand (Calloused knuckles on the back

of 2nd and 3rd fingers)
- Dental decay
- Irregular cycles, oligo - rarely amenorrhoea (No hirsutism)
• DSM criteria
- I. recurrent episodes of binge eating, consuming abnormal
amounts of food compared to normal persons + lack of control
during the binge
- II. recurrent inapropriate compensatory behav. to prevent wt.
gain
▪ self induced vomiting, laxatives, fasting, excessive
exercise
- III. self-eval. is influenced by their body size and shape
- IV. disturbance doesn’t occur only during an episode of anorexia
nervosa (one of the 2 types of anorexia is the bulimic type)
• complic
- lose HCl – electrolytes imbalances -> Metabloc alkalosis (MCQ)
- oesophageal lacerations
▪ Investigation (for both)
• electrolytes – decr. K+, ↓ Cl- and Met. alkalosis
• excessive laxatives cause metabolic acidosis
▪ Rx
• electrolyte correction – give K, Ca, Mg, Vit. D
• Olanzapine in anorexia nervosa to help weight gain
• parenteral nutrition
• family support
• refer to eating disorder clinic: CBT
• drugs:
- SSRI (Fluoxetine)
- never prescribe TCAs!!! (they can decr. K)
▪ Cx
• can be life-threatening: they take lots of multivit. which can cause
hypophosphatemia!
o Overvalued idea: an abnormal belief (not obsession or delusion) which dominates
sufferer’s life. It causes disturbed functioning and pt’s whole life is hostage to
belief which is held with intense passion. Examples: Extensive litigation, morbid
jealousy, body dysmortphic disorders, transexualism, hypochondriasis and
anorexia nervosa. No specific Rx (MCQ 2122 P 182).
o VIII. Brief psychotic disorder
▪ 1-30 days
▪ a stressor is always present
o IX. Schizophreniform disorder
▪ sympt. 1-6 mths
• > 6 mths = Schizophrenia
▪ much better prognosis than schizophrenia
o X. Schizo-affective disorder
▪ Psychosis (predom). + mania or depression
495

▪ diff. from psychogenic depression = depression (predom.) with psychotic

elements
• Rx – ECT
▪ Rx
• antipsychotics first, then treat depression
o XI. Cyclothimic disorder = Minor form of bipolar going on for > 2 yrs
o XII. Dysthimic disorder = Minor form of depression going on for > 2 yrs
▪ no suicidal ideation
Abuse: Neglect MC in elderly and physical in children and adults (esp women). Must report all cases
(including suspected) of child and elderly abusing but not in case of adult. Separate child and elder and
consider admission and inform child protection services.
Schizophrenia (1st aid 404) + MTB3 459 MCQ 2080 p 71
o When there are +ve psychotis symptoms (hallucination, delusion, thought disorder and
behaviour disturbances) that affect social and occupational function for > 6 months.
o Tought disorder: is an abnormality of expressed language (written or spoken) that occurs
in psychotic mental disorders. It occurs in a no of different forms including thought
blocking, derailment, flight of ideas and word salad. Interviewing a pt. with thought
disorder it may be difficult to grasp logical meaning of statements that are made (MCQ).
o Thought insertion: A belief that one’s thoughts have been placed inside head by some
mysterious external source.
o very complicated, difficult to diagnose, takes a long time (4-5 long sessions)
o point prevalence = 1% in general population, 40% risk in children if both parents have
schizo. 10% risk if only 1 of parents is affected.
o good prognosis in schizophrenia
▪ late age of onset
▪ female
▪ shizoid – poor prognosis
• extroverted personality – better
▪ abrupt onset = good
• insidious = bad
▪ positive without negative sympt. = good
▪ good response to Rx early on = good
o MC causes of death: (MCQ 2105 p 81)
▪ I – Cardiovasc. disease
▪ II – Suicide – 10%
o Genetic factors
o Male
o Late teen, early 20s
▪ later in women (estr. protection)
o Occupational functioning
- School going – drop in grades at school (MCQ)
-Adults – Poor job performance
o more you delay the Rx, poorer the prognosis
o Late onset schizophrenia shows persecutory delusions (MCQ)
o they can live a normal life with Rx!
▪ not bad news these days anymore!
o tend to drift down the social scale due to their disease
496

o stigma for life – don’t diagnose: refer to specialist

o Dx – sympt. > 6 mths
o Sx
▪ Positive
• lack of insight – MC sympt. in acute schizophrenia (97%). Poor prognosis
if present. Insight means, self awareness of a situation and
acknowledgement of symptoms, illness and need for treatment.
• Delusions
- paranoid
- grandiose: false sense of self superiority
- passivity phenomena – thought insertion/ extraction/
broadcasting
▪ thought insertion – believe some outside is inserting
ideas in their heads
▪ thought extraction – believe someout outside is
extracting ideas from their heads
▪ thought broadcasting – his thoughts are not private but
shared with everyone (people are reading their minds)
- idea of reference – believe that irrelevant unrelated things in the
world are referring to them directly or indirectly
▪ TV, radio is telling you to do something
▪ they are special and the radio/ TV/ newspapers are
talking about them + they are followed around.
• Hallucinations : A false perception of ineternal stimuls which is
interpreted as being from outside. Its a sensory experience.
- auditory – characteristic types:
▪ 1. audible thoughts (hearing his thoughts spoken out)
▪ 2. hearing voices - hear 2 people talking about pt or
quarrelling, hearing voice of GOD.
▪ 3. hearing voices speaking about pt
▪ + hearing commands – in depression as well
• (illusions are not characteristic in shizophrenia)
• disorganized speech
- “word salad” = incoherent sequence of words
- derailment – they keep changing the subject
- “loose association” – with some connection between the ideas
(diff. from “flight of ideas”no connection between ideas – Mania)
▪ formal thought disorder – disturbance in the way
thoughts are linked together
• types:
o flight of ideas – in mania
o perseveration – persistent repetition of
the same responses to a series of
different Qs – in dementia
o loose association – in schizophrenia
• difficult communication: as though a “pane of glass” is between the
doctor and the patient
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• disorganized behaviour
• psychomotor disturbance
- agitation
- retardation – catatonic
• saccidic eye movement – when asked to follow an object with their eyes,
they do it in steps
▪ Negative sympt.
• Lack of motivation
• Blunted affect/ emotional blunting
• Poverty of speech (Alogia ---- Inability to speak)
• Anhedonia- lack of interest in pleasureable activities.
• Social withdrawal
o types:
▪ Paranoid
▪ Disorganized – bizarre
▪ Catatonic
• psychomotor disturbance (agitation or retardation)
• catalepsy - keep their body in weird positions for a long time, e.g. with
the head above the pillow
- diff. from cataplexy – sudden loss of muscle tone + temporary
episodes of paralysis
▪ part of the narcolepsy syndrome
o Rx
▪ Typical (conventional) antipsychotics – not used very much; very few used
these days (5-6 out of 25-30) due to SE
• Dopamine receptor antagonists, most effective for +ve features of
Schizo.
- dopamine hypothesis in schizophrenia: positive features in Sch.
are due to overactivity of dopaminergic pathways
• e.g.
- Haloperidol – tablet, inj long or short acting
- Droperidol – PO only
- Chlorpromazine , Thioridizine, fluphenazine
- trifluperazine
- flupenentixole – inj long acting
- zuclupentixol – inj long acting
• SE (MTB 3 463 table)
- Extrapyramidal
▪ 1. Acute dystonia – within hrs to days of Rx
• young males at higher risk
• severe sustained painful agonizing spastic
contr. of axial muscles: around the eyes
(oculogyric crisis – eyes rolled up and open –
“the look-ups”), tongue (protrudes to 1 side),
spasm of the masticatory muscles (trismus),
neck (torticolis), dysarthria, dysphonia,
dysphagia.
498

• MC after haloperidol and fluphenazine +

chlorpromazine.
• caused by effect on the nigrostriatal tract
(dopamine decr. => incr. acetylcholine)
• prophylaxis + Rx – inj. of anticholinergic:
benzatropine (cogentin) 2 mg IM or IV bolus –
quick response to it (5 min)
o if no response, repeat in 30 min
o then continued for a week or longer
▪ 2. Parkinsonism – rigidity and tremor
• within 1-4 wks
• Parkinsonism – extrapyr. – Murtagh 296
o rest tremor
o cogwheel ridigity
o bradykinesia
o shuffling gait
• Rx – inj. of anticholinergic: atropine or
benzatropine
▪ 3. Akathesia – Motor restlessness (extra energy in my
legs), generalized restlessness, always moving
(confused with anxiety)
• also caused by antiemetics and SSRI
• Rx
o β blockers
o Benzodiazepines
o + lower the dose
o + indic. to change the drug!
▪ 4. Tardive dyskinesia - Choreoathetosis = Involuntary
movements: grimaces, protruding the mouth, lip
smacking, winking, etc. + stiffness
• After mths to yrs of use
• irreversible
• involuntary movements disappear when
sleeping
• lots of dopamine supression => supersensitive
dopamine
• 3:1 = female:male, in 40s-50s
• no Rx
o even if stopping Rx
o change to newer atypical antipsychotic
-- Clozapine
o tetrabenazine – cau cause Parkinson
- Photosensitivity – discol. of exposed skin
- Retinal deposits
- Jaundice
- Leucopenia
- ECG changes
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- Neuroleptic malignant syndrome – acute medical condition:

degen. of the muscle (CK very much incr.), fever, rigor, shivering,
disturbed consciousness, seizure and death.
▪ Atypical
• work on dopamine and serotonin (serotonergic)
• e.g.
- Clozapine – 1976 (2nd line choice of drug)
▪ can cause death due to agranulocytosis
• Sx – inf. (URTI)
• Dx - FBE
▪ Reintroduced in 1992 US/ 1994 Aus.
▪ Aus. very good system- Pt/ doctor/ pathology/ lab – All
registered.
▪ Blood test for WCC every wk for 16 wks, then every 4
wks
• drugs dispensed based on the blood results
▪ Only used as the third option (1 and 2 failed or bad SE)
▪ Very potent, very strong SE (“very dirty”)
• blocks every receptor in brain (shuts it down)
- Olanzapine (1st line choice of drug)
▪ SE - wt. gain
• not dose related
• as GP we can’t change the dose – psychiatrist
only can decide this
• Rx
o lifestyle modif. advice
- Quetiapine
- Risperidone & amisulpride – causes hyperprolactinemia
▪ add quetiapine or olanzapine (MCQ) and taper 1st
antipsychotic after 2 weeks
- aripiprazol
- ziprasidone
- sertindol – just listed
• Similar SE – but much less often
- Extrapyramidal
- Bone marrow problems
- Liver problem
- MC = Metabolic syndr.– ↑ Wt., hyperlip., hyperglyc. – especially
Olanzapine
- sedation
- cardiac SE – Prolonged QT interval – Thioridazone/ ziprasidone
- Antipsychotic medication
o effects:
▪ Dopamine antagonits => ↓dopamine => hypreprolactinemia = Gynecomastia,
galactorrhea, amenorrhea.
▪ Block the muscarinic cholinergic receptors (M blockers) => Anticholinergic
effects: Dry mouth, constipation, urinary retention, confusion
500

• avoided in elderly
▪ Block histamine => sedation, Wt. gain
▪ Block α receptors => hypotension
▪ Atypical antipsychotics good for both positive and negative symptoms of
schizophrenia. Typical only for positive symptoms.
o act on 3 tracts in the brain:
▪ 1. tuberoinfundibular tract -> decr. dopamin -> incr. prolactin
▪ 2. nigrostriatal tract
• important in Parkinson: dopamine goes down, acethycholine goes up
• cause extrapyramidal effects.
▪ 3. meso-limbic tract -> Clozapine works only here => no endocr. effects (1), no
extrapyr. effects (3)
• but not a first line drug (but as the 3rd line of attack, after 2 drug failure),
due to the life-threatening risk of agranulocytosis
- I choice in psychosis = Risperidone (causes least sedation)
- II – e.g. Olanzapine
- III – Clozapine = indic. no. 1
▪ also indicated in tardive dyskinesia = indic no. 2
▪ SE:
• Hypersalivation, drooling of saliva
• Wt. gain
• Diabetogenic
• leucopenia or agranulocytosis – 1% of pts.
o 85% in the first 9 months
o FBC once a week
o Check FBC for neutropenia in any pt
presenting with fever, sore throat or
other infection.
▪ CI
• myeloprolif. disorders
• severe CNS depression
• previous Hx of leucopenia or agranulocytosis
o types:
▪ Typical = pure D2-antagonists
• Butyrophenones
- Haloperidol – the only one available IV
▪ e.g. ED – pacient with agitation
• 1 – lorazepam (other benzodiapines)
• 2 – haloperidol – available IV
- Droperidol – p.o. only
• Phenothiazine
- chlorpromazine
▪ Atypical
• D2-5HT2 (serotonin)
- Risperidone
• D2-D4-5HT2
- Clozapine
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- Olanzapine – drug of choice in newly Dx schizophrenia

- Quetiapine
o SE
▪ Risperidone and amisulpride – Hyperprolactinemia, replace with Quetiapine
▪ Risperidone – postural hT
▪ Olanzapine, clozapine, quetiapine
• Dramatic wt. gain, abnormal lipid profile and DM type 2
- must be monitored for Weight, BP, BMI, fasting lipid profile and
glycosylated HB.
- Rx
▪ lifestyle changes
▪ prophylactic metformin
- indic. to change antypsychotic – ↑ HbA1C (MCQ)
▪ Quetiapine – used if insomnia is a major problem in psychoses
• causes sedation but also wt. gain
▪ Use Resperidone when sedation is problem after use of antipsychotics
▪ Exprapyr. – see above
- Neuroleptic malignant syndrome:
o uncommon but most dangerous
o due to low dopamine caused by dopamine receptor blockage
o caused by:
▪ Antipsychotics: Haloperidol, trifluoperazine (cause dopamine blockade)
▪ Dopaminergic drugs (as in Parkinsonism) if abruptly stopped.
o Sx
▪ gradual onset with:
• 1st - Muscle rigidity (tardive dyskinesia), then
• fever
• HTN and tachycardia
• Encephalopathy, delirium - then
• Hyporeflexia
• Confusion, tremors, coma
• Normal pupils, normal or decreased bowel sounds, hyporeflexia
o Life-threatening situation, mortality = 50%
o Esp. with antidopaminergic antipsychotics – Haloperidol: pt with fever and rigidity ->
send to ICU
▪ Dx: Order CK - incr. (thousands)
▪ Rx:
• Stop abruptly antipsychotics
• resp. and circ. support
• Dantrolene (muscle relaxant)
• Bromocriptine (dopamine agonist).
- first psychotic episode
o ASSESSMENT: make sure there is no organic cause
▪ A thorough psychiatric history.
▪ Mental status examination.
▪ Physical examination, with particular attention to neurological assessment.
▪ It is critical to assess the patient's risk of self-harm or danger to others.
502

▪ Rule out drug-induced or drug-withdrawal states.

o Rx
▪ Clinical practice is generally to start treatment in first episode psychosis with an
oral form of a second-generation antipsychotic.
• Amisulpride.
• Aripiprazole.
• Olanzapine.
• Quetiapine.
• Risperidone.
▪ Parenteral treatment:
• Should be avoided if at all possible in the acute care of patients with
schizophrenia.
• If necessary:
- Olanzapine.
- Haloperidol.
▪ Once a pt has responded to a drug it is usually possible to use once-daily dosing.
▪ It is essential to monitor closely for adverse effects of antipsychotic drugs.
Mood disorders
o ± psychotic symp. = reality check problems
▪ delusions of sin, etc.
o with risk of self harm, suicide
▪ we need to do a risk assessment!
o a relationship breakup would cause depression, not a psychosis
o Classification
▪ Major mood disorders.
• Major depressive disorder.
• Bipolar disorder.
▪ Other specific mood disorders.
• Dysthymic disorder: Depression alone – no other sympt.
• Cyclothymic disorder: depressive and hypomanic disorders (consistently
over the past 2 yrs).
▪ Mood disorder due to a general medical condition.
▪ Adjustment disorder with depressed mood.
o Major depression = Pseudodementia
▪ Mental symptoms (memory loss, etc.) + mood instability, but normal MMSE =>
Pseudodementia (depression)
▪ Min. 2 wks
▪ as a mood = very common, not necessarily pathological
▪ Lifetime prevalence: 13-20%.
▪ can be present in other diseases
• strokes – especially in the left anterior hemisphere
• Aphasia – types:
- Broca aphasia in ant. speech area (middle and inf. frontal gyri) –
MC in middle cerebral a. infarcts
▪ with dysarthria, other motor deficits
▪ many of them are depressed or agitated
503

- Wernicke aphasia in post. speech area (sup. temporal gyrus and

post. temporo-parietal areas)
▪ rumbling, incomprehensible speech, full of neologisms
▪ with euphoria or paranoid combativeness
• Parkinson’s dis. – in 40% of cases
• Alzheimer – in 25-33% of cases
▪ Mood disorders are familial but exact mode of transmission is not understood.
▪ May begin at any age with an average age at onset in the mid-teens to late 20s.
▪ good prognosis in bipolar depression
• female
• late onset
• not extroverted
• acute onset
• not biological (bad appetite, bad sleep, etc.)
• not melancholic (anhedonia)
• not psychotic
• good response to treatment
▪ Sx
• 1. depressed mood most of the day
• 2. anhedonia – lack of pleasure for activities that were pleasureable
before
• 3. significant wt. gain or wt. loss
• 4. incr. or decr. appetite
• 5. insomnia or hypersomnia
- sleep problems
▪ wakes up early in the morning (middle insomnia) and
can’t fall back asleep = depression
▪ can’t go to sleep, keeps thinking about what happened
during the day (initial insomnia) = Anxiety
- typical D. – 3,4,5 all decr.
- atypical D. – 3,4,5 all incr.
• 6. feelings of guilt and worthlessness
• 7. suicidal ideation
• children, teens
- tearful child, poor performance at school = depression
- irritability (rather than depressed mood)
- insomnia
- lack of concentration
- psychomotor agitation
▪ Dx - disease:
• Cardinal feature is depressed mood that predominates for at least 2
WkS and causes significant impairment in individual’s areas of
functioning
• + Must also exhibit at least 4 of the following: (SIGE CAPS)
- Anhedonia
- Change in appetite
- Change in sleep
504

- Change in body activity

- Loss of energy
- Feelings of worthlessness and excessive or inappropriate guilt
- Decreased concentration.
- Suicidal ideation.
• total: 5 sympt. out of 9 (not just 1 = feeling depressed)
• exclude dis. causing Depresseion.
- hypothyr. Alcohol and drugs
- thiamine defficiency (Wernicke – Korsakoff)
▪ DIFFERENTIAL DIAGNOSIS:
• Medical conditions: They present to the GP often with a somatic
complaint ‘I can’t sleep’ or ‘I have no energy’.
• Bipolar disorder.
• Schizoaffective disorder.
• Grief reaction
- normal
▪ Stage 1 –few hrs – few days
• denial generally
• disbelief and emotional numbness
▪ Stage 2 – few wks – 6 mths
• sadness, restlessness, poor sleep, guilt or
blame, anxiety, somatic sympt., auditory and
visual hallucinations
▪ Stage 3 – from 6 mths
• all sympt. resolved
• only memory of good time left
-
abnormal
▪ stage 2 > 6 mths
▪ stage 3 with anniversary reactions
- anniversary grief reaction vs. hypochondriasis
▪ Hypochondriasis = multiple admissions, multiple
doctors, all negative
▪ anniversary reaction, it only started on the anniversary
Grief (Bereavment) Depression
Sx Wax and wane (audit & visual hallucin) Constant
Shame and guilt Less More
Suicidal ideation Less More
Return to normal < 2 wks only.Rx supportive therapy Only under Rx (Antidepressants)
Other Anniversary reaction
There is a cause/ reason
Sadness, tearfulness, wt. loss, decr. appetite

Post-partum blues Post-partum depression Post-partum psychosis

Right after Starts 2-3 wks post-partum, during Starts 2-3 wks post-partum,
delivery -> goes the puerperium (until wk 6) – when during the puerperium (until wk
away in max. 1 wk high level of hormones during 6) – when high level of horm.
505

(3-5 days) pregnancy have fallen abruptly during preg. have fallen abruptly
Due to hormonal Mother doesn’t want the baby to be Mother has psychotic sympt.:
changes. Mother a sad/ unhappy like her – she thinks life believes or hears voices telling
bit sad/ depressed is not worth living her that the baby is evil/ devil
and she must kill him. They may
also harm themselves.
Baby is at risk!
(Purple book)
- 1 in 500 births
- MC in primiparous women, Hx of major psychiatric illness or family Hx of
major psychiatric history.
- clinical pictures: organic, affective (MC – predom. with manic disorders)
and schizophrenic
- abrupt onset with insomnia, followed by confusion, fluctuating agitation
and labile mood.
Recurrence in future pregnancies – as high as 20%
Also risk of relapse of mood disorder independant of future pregnancies.
Rx – just family Rx: Rx:
support - antidpressants in milder forms - antipsychotics (Olanzapine)
- ECT in severe depression - if not responding early -> ECT
▪ type - Psychogenic depression = Depression (predom.) with psychotic elements
• Rx – ECT
▪ Rx
• Antidepressants
- 1. TCA – not used so much anymore
▪ e.g.
• Amitriptyline
• Nortriptyline
• Imipramine
Clomipramine
• dophiepin

▪ SE – not used anymore due to their SE (risk of overdose

– pts might use them to comit suicide)
• Anticholinergic SE: dry mouth, constipation,
flatulance, urinar ret.
• Tachycardia, HT then postural HTN, blurred
vison, wt. gain
• Hypokalemia, prolongation of QT interval,
arrhythmias
- 2. SSRI
▪ e.g.
• Fluoxetine
o first indic. in adolescents with major
depression
▪ monitor for suicidal ideation,
violence
506

• Paroxetine
• Citalopram
• Escitalopram, Sertraline
• Fluvoxamine
- 3. SNRI (serotonin-norepinephrine reuptake inhibitor)
▪ e.g.
• Venlafaxine
• duloxetine
• Mirtazapine – not commonly used (Samir
Ibrahim = part of a SSRI subgroup - serotonin
agonists)
o heavy sedation, crazy stimulation of
appetite -> wt. gain
o takes effect very fast compared with
the other drugs
• Venlavaxan
• Desvenlavaxan
▪ SE for SSRI and SNRI
• headache, nausea (serotonin surge)
• drowsiness, sedation, lack of sleep
• impotence (10-35%) – become depressed over
this
• SNRI – more cholinergic side effects
- 4. MAOI – not used today
▪ SE - food with tyramine (cheese reaction) – surge in
catecolamines – HTN emmergency -> crisis (can cause
death).
▪ pts had to avoid 50% of the the food items
▪ subtype: RIMA (reversable inhibitor of MAO)
• just 1 drug – moclobemide
• weak antidepressant, but used when SSRIs
cause ED
• SE – same as SSRI
o but no ED!!
- 5. Lithium – mood stabilizer
▪ SE
• fibrosis of thyroid -> hypothyroidism (check
every 3 mths)
• renal failure (check every 3 mths)
- 6. Dopaminergic
▪ wilberton (Zyben) – used only for cessation of smoking
• very expensive
• not used in Aus. for depression
- if stopping antidepressive medication, do it gradually over 2 wks
• ECT (MCQ 2146 P 94)
- treatment of choice if pt has suicidal ideation
- consent from pt. is required
507

- done under GA + muscle relaxants (Succinyl choline)

▪ usually with the electrods on the right lobes
- 6-8 sessions total over 2-3 wks, may be daily or alternate days.
- Indications
▪ Primary indic. = major depression, in these types:
(Murtagh 189)
• Melancholic depression unresponsive to
antidepressants
• Psychotic depression
• Substantial suicide risk
• Depression or severe psychomotor agitation
causing life-threatening refusals (refusing to
eat)
• ineffective antidepressant medication
• + (purple book) post-partum depression, when
mother should return quickly to care of baby
▪ recent onset (not chronic) of schizophrenia
▪ catatonic stupor and lethal catatonia
▪ mania and especially lithium-resistant manic episodes
- SE
▪ muscle aches from relaxant
▪ headaches and transient confusion
▪ short-term amnesia – for the period of time when
doing the ECT
▪ loss of memory – forget some good things in their lives
- drug interaction
▪ e.g.
• benzos should be tapered and seized – they
↑seizure threshold and impair efficacy of ECT
o if sedation is required before ECT (can’t
go to sleep), use Zopiclone, Zolpidem
(non-benzos anxiolytics) MCQ
• taper and discontinue all the antidepressants
before ECT
• Lith. doesn’t affect the efficacity but causes
severe post-ictal confusion
▪ all drugs are resumed after ECT
• + counseling
- supportive counselling
- CBT (Indications)
▪ Chronic insomnia (> 4wks)
▪ Psychosis
▪ Depression
▪ Phobias
▪ Eating disorders
▪ Change
• Thinking – change -ve into +ve thinking
508

o identify the negative thoughts - written

at the top of the page
o discuss the evidence for that thought
o try to reverse that thought
• Behaviour psychotherapy: OCD, anxiety, phobia
- psychoanalytic
o Mania (Overactivity/ Overexcitement state) + euphoria
▪ Min. 7 days of symptoms (4 days for hypomania)
▪ More often requires involuntary admission (at least overnight) – brought by
relatives bc of boundless energy.
▪ Sx
• Pathological elevation of mood combined with:
- Overactivity. Overexcitement state/ euphoria.
- Irrationality.
- Poor judgement.
- Lack of insight.
• Severe disruption of relationships, employement or finances
• everything increased
• ONSET:
- Acute or insidious.
- Can arise spontaneously or follow:
▪ Depressive illness
▪ Severe stress
▪ Surgery.
▪ Infection
▪ Childbirth
• Precipitants:
- Antidepressant medication
- ECT
- Steroids
- Amphetamines
Lithium withdrawal
• Primary features
- High mood = euphoria
- Over talkativeness – but there is logic in what they say
▪ Pressured speech – not smooth
- Overactivity
▪ too many activities -> less need to sleep – (not insomnia
= wants to sleep but can’t)
• Other features
- Flirting due to Sexual promiscuity (↑ sexual interest)
- Irritability
- Pressured speech: rate at which pt. speaks is much faster making
it difficult to follow what is being said
- Flight of ideas. (Shift from one topic to other quickly)
- Elevated mood (euphoria)
- Reduced Sleep
509

- Grandiosity (false thinking of self superiority or importance).

- Delusions (mood-congruent) – but not bizarre like in
Schizophrenia
- Hallucinations
- Poor business judgement (over spending) - e.g. buys 5 cars, goes
bankcorrupt
- Gambling
▪ DIFFERENTIAL DIAGNOSIS:
• Schizophrenia: Can present with disorganised behaviour, violent
excitement, delusions and incomprehensible speech.
- The content of delusions (bizarre rather than mood-congruent),
will help to distinguish this from mania.
▪ Rx (MTB 3 470)
• Best managed in hospital to avoid self-harm and to others
• with mood stabilizers
- 1. Benzodiazepines: First & oral if possible
- 2. Antipsychotics
▪ Haloperidol
▪ atypical
- 3. Lithium - mainly for prophylaxis
- 4. Anticonvulsants/ antiepileptics
▪ all of them
▪ SE
• liver
• bone marrow
• skin rash (Steven – Johnson)
• ECT: Severe cases.
• no psychotherapy – they are too agitated
▪ Bipolar: = Mania + depression (If > 2yrs = Cyclothimc)
▪ very strong genetics and linkage with substance abus
- Antidepressant medication:
o indic.
▪ for mood disorders: depression
▪ adjustment disorders
▪ anxiety disorders
▪ eating disorders
▪ impulse control disorders
▪ chronic pain (amytryptilline – ↑endogenous opioids)
o take 2-6 wks to kick in
▪ used for min. 4-6 wks (unless SE) before changing it, increasing the dose
• if they still didn’t work after 6 wks of usage, change the drug
o Up to date recommendations for for depression
Venlafaxine + Risperidone (1st choice) MCQ, Venlafaxine + Quetiapine,
Olanzapine + Sertraline, Olanzapine + Fluoxetine, Amytryptiline + Haloperidol
(VR, VQ, OS, OF, AH).
o categories
▪ 1. TCA
510

• work on
- norepinephrine, serotonin, dopamine receptors (block their
reuptake) -> increase in the brain
- alpha receptors
- muscarinic rec.
- histamine
• e.g.
- Imipramine
- Clomipramine – OCD, premature ejaculation (MCQ)
- Amitryptiline – Diabetic neuropathy, chronic back pain, post
herpetic neuralgia.
▪ 2. MAOI – MAO breaks down norepinephrine, serotonin, dopamine; MAOI
causes incr. in norepinephrine, serotonin, dopamine
• e.g. Tranycypromine, selegiline, phenelzine.
• Can’t have cheese, red wine, chocolate, sausages – (all foods containing
high tyramine) => HTN crisis: headaches, nose bleeds, palpitations
▪ 3. SSRI – only work on serotonin (hence the name SSRI)
• 1,2,3 have the same efficiency, but SSRI preferred due to less SE
- Fluoxetine (Prozac) 1st indic. in adolescents ē major depression
- paroxetine (Aropax)
- sertraline (Zoloft)
- citalopram
- escitalopram
▪ 4. Newer antidepressants (Atypicals)
• Trazodone - used if insomnia is a major problem (highly sedating)
• Buproprion - least sexual dysfc.
- also used in quiting smoking
▪ acts on dopamine, which is responsible for causing
craving and hunger, (CI in pts with eating disorder)
o General SE
▪ Sedation (antihistaminic effect) – less with SSRIs
▪ HTN and tachycardia – more with TCAs
▪ anticholinergic – more with TCAs
▪ cardiac problems – only with TCAs (hypokalemia, prolongation of QT interval -
> risk for torsade de pointes)
▪ decreases the seizure threshold--> should be stopped before ECT
• ↑depending on the washout period: 2-3 days in SSRI, 2-3 weeks TCA
• if anxious, non-benzodiazepine anxiolitic = zolpidem (because BD also
decr. the seizure threshold)
▪ Sexual dysfc. (ED, ejaculatory dysfc.) – more with SSRIs, less with escitalopram
▪ MCQ: nausea, vomiting, diarrhea, abdominal pain – SSRIs (especially
sertraline) switch to another SSRI
o TCA intoxication:
▪ SE
• Anticholinergic (dry mouth, constipation, urinary retention & sedation)
• Cardiotoxic: Cardiac arrythmias, prolongation of QT interval
▪ Overdose Rx:
511

• observation and supportive measures in ICU for 3-4 days

• activated charcoal
• convulsions –> diazepam
• cardiotoxic effect -> IV sodium bicarbonate
- if no improvement of arrythmia, use lidocaine
- Serotonin Syndrome: emmergency condition caused by excessive serotonin in CNS when
combining antidepressants (SSRI ē MAOI)
o Sx
▪ rapid onset with:
• fever
• agitation
• Hyper reflexia (MCQ) (hypo in NMS)
• tremor
• tachycardia, HTN
• dilated pupils
▪ then confusion, coma
o Dx - clinically
o Most dangerous combinations:
▪ I. SSRI (sertraline, fluoxetine, paroxetine) + MAOI (phenelzine, moclobemide,
selegiline)
▪ II. SSRI + TCA (amitriptyline, imipramine, clomipramine)
▪ III. SSRI + Opiates or Lithium
▪ IV. SSRI + Anticonvulsants
▪ also SSRI + OTC drugs (e.g. NSAIDs)
▪ AL SSRI + aspirin = CI= Risk of Upper GI bleed icreased
▪ Amitryptyline + aspirin = is safe MCQ
o Rx
▪ don’t stop the SSRI, but the other drug
▪ stabilize pt --> urgent referal to ICU
▪ Serotonin antagonist:
• Methylsergide
• Cyproheptadine, Chlorpromazine
o Changing drugs
▪ Antipsychotics taper gradually drug one, while gradually increasing drug two,
no break.
▪ Antidepressants stop first one abruptly – or even better taper, allow for break
and washout time, then start the second one.

-
- washout periods
From To Washout period
Short acting SSRI Short acting SSRI Nil
512

Fluoxetine Short acting SSRI 1 week

TCA 2 weeks
MAOI 5 weeks
TCAs Short acting SSRI 2-4 days
Fluoxetine 2-4 days
MAOIs 1 week
MAOIs Anything 2 weeks
- Switching antidepressants (Amit):
o SSRI to MAOI
▪ wait 4-5 wks (break/ washout time)
o MAOI to SSRI
▪ wait 2-3 wks (break/ washout time)
- Suicide & self-harm:
o Self harm
▪ 80% using drugs
▪ 5% using self-cutting
• MC – wrists
o Suicide
▪ Seasons
• MC in spring
• 2 – summer
• 3 – fall
• 4 – winter
▪ Week days
• Men – Mon
• Women - Fri
- Mood stabilizers = Antiepileptics (Lithium, Na Valproate, Carbamazepine)
o used in:
▪ Bipolar – in mania
▪ Seizures
▪ Impluse control disorder
▪ Violence
o types:
▪ 1. Lithium – drug of choice
• discovered in 1949 in Melbourne – John Caid (Nobel prize – 1962)
• neither habit forming, nor addictive
• Indications
- Bipolar
▪ Rx of choice in acute mania
▪ Prophylaxis of bipolar disorder (depression & mania)
• less effective in pts with rapid cycling mood
disorders (women)
• if discontinued, pts responding to it in the past
might not respond anymore
▪ in treatment refractory depression: Lithium + TCAs
▪ in aggressiveness associated with developmental
disability (mental handicap)
513

- Schizoaffective disorder
- Adjustment disorder
• admin.
- 750-1000 mg P O in 2-3 divided doses
▪ incr. by max. 250-500 mg/ day
- plasma level
▪ maintain at start 0.8-1.4 mmol/L
▪ chronic users 0.6-0.8 mmol/ L
▪ very narrow therapeutic range – keep blood level at
0.6-1 (< 0.6 not effective, > 1.2 toxic, > 1.6 fatal)
- monitor every 1-3 months!
- Pregnancy: Stop in 1st trimester (Ebstein’s anomaly in babies) Use
ECT for 1st trimester manic episodes, Use lamotrigene in 2nd and
3rd trimester.
• CI - in kidney disease
• SE
- Acne and wt gain MC problems (MCQ)
- nausea, vomiting, diarrhoea
- metallic taste
- headache
- afects the cardiac conduction
- hypothyroidism (used in hyperthyr.)
- Polyuria – nephrogenic diabetes insipidus
- kidney failure (very small risk)
▪ test thyroid and kidney evey 2-3 months
• toxicity
- sympt. – indic. to decr. the dose
▪ fine tremor
▪ apathy, lethargy, slurred speech
▪ muscle weakness
▪ ataxia, anorexia, nausea
▪ muscle fasciculations
▪ choreoathetosis, convulsions, coma, death
- for pt - important not to get:
▪ Dehydrated
▪ Hyponatraemic
• -> both incr. lithium toxicity (by ↑ renal
reabsorbtion)
- Rx
▪ stop drug
▪ dialysis
• indic.
o Convulsions, coma
o Lithium > 4 mmol/L
o in renal failure
▪ 2. Valproic acid (sodium valproate)
• Indic.
514

- kidney disease (where we can’t give Li)

- pregnancy as mood stabilizer!
• SE
- sedation
- cognitive impairment
- GI distrub.
- hepatotoxic
- teratogenic --> causes spina bifida
▪ 3. Carbamazepine
• in pregnancy as antiepileptic!
• Trigeminal neuralgia
• SE
- hepatotoxic
- rashes
- agranulocytosis
- teratogenic
- Benzodiazepines:
o enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA - the chief
inhibitory neurotransmitter in the mammalian central nervous system), which results in:
▪ sedative
▪ hypnotic (sleep-inducing)
▪ anxiolytic (anti-anxiety)
▪ anticonvulsant
▪ muscle relaxant
▪ amnesic action.
o These properties make benzodiazepines useful in treating:
▪ anxiety, agitation
▪ insomnia
▪ seizures
▪ muscle spasms
▪ alcohol withdrawal
▪ premedication for medical or dental procedures
o not metab. in the liver -> safe to use in liver diseases
▪ e.g. lorazepam, temazepam, oxazepam
o types
▪ Short acting (1/2 life = 1-12 hrs)– alprazolam, midazolam,
▪ Intermediate acting (1/2 life = 12-40 hrs) – clonazepam, lorazepam
• short & intermed. – Rx for insomnia, seizures
▪ Long acting (1/2 life = 40-250 hrs) – diazepam (NOT i.m.)
• Rx. for anxiety
o SE
▪ Resp. depression, paradoxical disinhibition, chronic dependence on oral benzos
o Antidote = flumazenil
Dementia and mental retardation
o A group of medical conditions caused by degeneration or vascular insult leading to
symptoms affecting daily life routine like amnesia, orientation, planning & visuospatial
skills.
515

o MMSE < 24
o 1 in 10 over 65 years.
o 1 in 5 over 80 years.
o CAUSES:
▪ Degenerative cerebral diseases:
• Alzheimer’s disease: 60%
• Dementia of frontal type: (up to 10%)
• Dementia with Lewy bodies: (up to 10%)
▪ Vascular: 15% (after stroke) – is reversible
▪ Alcohol excess: (5%)
o Forgetfullness and loss of cognitive functio.
o Dx of exclusion – after excluding organic causes
o Types
▪ 1. ALZHEIMER’S DISEASE:
• Insidious onset (Prgressive dementia of degenerative cause).
• Initial forgetfulness.
- Forgets: I time, then II place, then III person (faces)
• Progresses to severe memory loss.
• Dx at autopsy – post mortem
▪ 2. FRONTAL LOBE DEMENTIAS:
• Young age
• Personality changes (rudeness).
• Alteration of behaviour including social dysfunction (running naked,
cursing, masturbatingh in front of nursing station (MCQ) hypersexual –
inhibitions from frontal lobe are erased).
• Progressive aphasia.
▪ 3. LEWY BODIES:
• Visual hallucinations and fluctuating confusion.
• Spontaneous motor parkinsonism.
• Fluctuation in the mental state.
▪ 4. VASCULAR (Multi infarct, stroke):
• Sudden onset.
• Focal neurological signs
• Hx of HTN or stroke
o Differential diagnosis: Depression which is termed pseudodementia.
DEMENTIA PSEUDO
DEMENTIA

Onset Insidious Clear-cut

Insight Nil Present

Orientation Poor Reasonable
Memory loss Recent > remote Recent = remote

Responses to mistakes Agitated Gives up easily

516

Response to cognitive Near miss! ‘Don’t know’

testing
Course Worse at night Worse at morning

oDelirium vs. Dementia

▪ no language impairment in delirium (only confusion)
▪ level of consciousness
o Dementia vs. old age
▪ Dementia – brought by their relatives
▪ Old age – the patients are concerned and come to you
- MMSE
o Done at bed side to asses the cognitive function of pt
o assesses cognitive impairment due to delirium, dementia, head injury & focal left
hemisphere lesion.

- Mini-mental state examination:

o Normal ≥ 25
o Mild dementia 18-24
o Moderate impairment 10-17
o Severe impairment <10
o + a decline of > 2 points/ yr is significant
o assess
▪ 1. Orientation – name, date, month, location
▪ 2. Registration – a test of antegrade memory i.e. new information
▪ tell 3 objects/ a short story/ address/ names to pt --> ask pt to repeat them. The
no. of trials required to repeat the objects/ story/ address correctly immediately
after testing should be recorded. Normal pt is able to recite and register
correctly within 3 attempts.
• short term memory
▪ 3. Attention & concentration (calculation)
• “Serial 7s” (or “serial 3s”)
- keep substracting 7 from 100 – for 5 times
• “Digit span” – how many of the digits he was told, he can remember
(beginning from 3 and increase upto 7 digits)
▪ 4. Recall – recall the 3 items during registration (after some interval/ task)
▪ 5. Language
▪ 6. Visuo-spatial – draw the overlapping pentagons
▪ 7. Abstract thinking –high order cognitive or intellectual functioning, eg.
Crossword puzzles or explaning similarities and differences bw familiar objects.
Frontal lobe lesions impair abstract thinking.
• verbal fluency test (say 15 words with the letter “f” within 1 min) or
semantic categories (list 10 animals, 10 countries, etc.)
• Interpretation of proverbs
• similarities and differences (e.g. between a table and a chair)
• motor sequencing test: fist-edge-palm
- Mental retardation
517

o incidence – 3%
- Creutzfeld-Jacobs disease
o Mad-cow disease
o spongiform disease of brain
o rapidly progressive mental deterioration + myoclonus
o Death within 1 year of symptom onset
Behavioral emmergencies
o Situations where pts show behaviour that potentially “put them or other people at risk of
physical harm”.
o Requires immediate intervention.
o The criteria for defining behavioural emergencies are vague.
o WORKING DEFINITION:
▪ Refusal to cooperate
▪ Intense staring
▪ Motor restlessness
▪ Purposeless movements
▪ Affective lability
▪ Loud speech
▪ Irritability
▪ Intimidating behaviour
▪ Aggression to property
▪ Signs of imminent intentional or unintentional self-harm
▪ Demeaning or hostile verbal behaviour
o DIAGNOSIS: May be unknown or provisional:
▪ 1. Medical disorders: Usually associated with delirium
▪ 2. Substance intoxication or withdrawal with or without delirium
▪ 3. Psychiatric disorders – after ruling out 1 and 2
• Schizophrenia
• Mania
• Psychotic depression
• Personality disorder
• Post-traumatic stress disorder
o LEGAL AND PROFESIONAL OBLIGATIONS:
▪ Treatment without consent is conducted under relevant mental health act.
▪ Those treating an acutely disturbed person in such an emergency will need to be
aware of the provisions of relevant legislation and be satisfied that the person
meets criteria for involuntary treatment.
▪ When situation is too dangerous for medical personnel to intervene (weapons
are involved or there is a high likelihood of extreme violence) emergency
personnel such as security staff or police will be required to disarm and restrain
pt.
o Rx
▪ INITIAL STEPS IN MANAGEMENT:
• In approaching the patient, care should be taken to ensure the safety of
yourself, other patients and staff, and of the patient.
• Measures that can reduce the risk of harm include:
- Room with two exits.
518

- Furniture that can’t be thrown.

- Adequate backup from staff
- Alarm
- Placing yourself at a safe distance between patient and an exit
▪ PHARMACOLOGICAL TREATMENT:
• acutely disturbed patient = Murtagh 488
- 1. Diazepam (PO)
- 2. Midazolam (IM)
- 3. Diazepam IV (never IM)
- 4. Haloperidol IM or Droperidol IM – (Blue book) no longer
available as cause cardiac arrhythmias.
• In acute medical settings, usual problem is violence in context of acute
delirium, often secondary to substance intoxication or withdrawal.
Immediate objective is to achieve SEDATION (put to sleep).
- IV route is preferred for achieving acute sedation as it allows
titration of dose and provide a more immediate effect of drug.
▪ IV medication:
• First choice - Diazepam: 2.5-5 mg increments
repeated every 3-5 minutes.
• Second choice - Droperidol: 5-10 mg IV. (less SE
than haloperidol)? – blue book says it’s no
longer available parenterally
- If pt can’t be physically restrained IM route is appropriate (higher
incidence of over and undersedation).
▪ IM medication:
• Midazolam 05-10 mg (MCQ)
• Droperidol 5 mg. - blue book: no longer
available
• In contrast, behavioural emergencies in acute psychiatric settings vary
widely in their nature and severity and encompass a broad spectrum of
psychiatric diagnoses, typically psychotic illnesses. In these settings
immediate objective is to achieve TRANQUILLISATION (do not put to
sleep).
- Oral route is preferred for medication as it encourages
engagement between pt and staff, allows pt to feel more in
control, aids future medication adherence and reduces risk of
adverse effects.
- If not possible IM or IV medication.
- Drugs:
▪ Benzodiazepines are generally the drugs of first choice
in tranquillisation, as they have fewer adverse effects
than antipsychotic drugs.
• Diazepam P.O
▪ Antipsychotics if:
• Pt already taking antipsychotics.
• Adequate tranquillisation is not achievable
with a benzodiazepine alone.
519

- Delirium:
o Confusion + hypo or hyperactive behaviour
o Usually affects elderly people admitted to hospital.
o 10% to 15% are delirious on arrival.
o 5% to 40% will develop delirium while inpatients.
o Pts with dementia are at particular risk.
o Children and the seriously ill are also more likely to develop delirium.
o Impaired cognitive function (especially in orientation and memory) and reduced ability to
focus, sustain or shift attention.
o Psychomotor changes:
▪ Agitation or withdrawal.
▪ Drowsiness.
▪ Illusions, hallucinations, delusions.
o Symptoms develop over hrs to days.
o CAUSES:
▪ Infection: especially systemic but also pulmonary, urinary or ear infections.
▪ Toxicity due to drugs: especially anticholinergic drugs or narcotic analgesics.
▪ Withdrawal from sedative drugs or alcohol: This should be suspected when
tremors, sweating and visual hallucinations are present.
o DD
▪ Mania.
▪ Schizophrenia.
▪ Dementia: especially dementia with Lewy-bodies.
o PREVENTION is most important
▪ Adequate hydration and nutrition.
▪ Adequate pain relief.
▪ Promotion of sleep.
▪ Correction of visual and hearing impairments.
▪ Avoidance of restraints.
▪ Provision of lighting appropriate to the time of day.
▪ Close involvement of family members.
o MANAGEMENT:
▪ Identification.
▪ Treatment of its underlying cause.
▪ The delirious pt must be nursed in a setting where they can be observed at all
times, because behaviour may be unpredictable.
▪ UTI (MC cause of confusion in elderly)
▪ FBE – U & E, Blood sugar
▪ X Ray
o Rx
▪ Frequently no medication will be needed.
▪ If delusions or hallucinations are causing distress or if behavioural disturbance
threatens pt's treatment or care or is causing significant threat to others, then
use Haloperidol 1-5 mg orally.
• If oral administration is impossible: Haloperidol 2.5-5 mg IM.
• If significant extrapyramidal adverse effects:
- Benztropine 1 to 2 mg orally.
- Benzhexol 2 mg orally.
520

- Avoid chlorpromazine.
Child psychiatry
- ADHD
o Boys 6:1
o 5 % of school age children
o in 60% no complete recovery
o can’t be Dx < 4 yrs
o Age: 7 yrs, going to school
o Dx. of exclusion
o Dx diff. with autism
o Family Hx
o Very common
o Sx
▪ very easily distracted – can only focus for 1 min to the TV
▪ usually only picked up in school (not noticed by parents)
▪ attention + behavior: attention deffict +
• with hyperkinesis ADHD
- non-goal directed behav. (he doesn’t want to achieve something
specific)
- can’t help it
• without hyperkinesis ADD
▪ impulsiveness and hyperactivity
• inattention
• hyperactivity, impulsiveness
o Dx
▪ first exclude other causes
• Always need to check vision, hearing, lead level first
• Exclude outside causes for the child’s behavior: e.g. if his parents
divorced, etc. – talk to both parents (MCQ)
• Psychometric assessment– exclude intellectual impairment & learning
disorders
▪ 2 situations – home and school
• obtain behavioral rating scales from both
▪ sympt. present for at least 6 mths, causing significant functional impairement
o Dx diff. with conduct disorder – were antisocial during childood
▪ Angry child
▪ Abused by parents – friends
▪ is goal directed + full of anger
o Mx
▪ Refer to child phychiatryst
▪ Confirm from family/ home or school
• exclude social causes, social disruption
▪ Speech therapist
▪ Involve teacher
▪ Audiometry
▪ Drugs:
• Dexamphetamine
521

• Methylphenidaze (ritalin)
Autism ADHD
Before 36 mths < 7 yrs, (5 % of school going children)
No family Hx. Family Hx – Boy inherited from father
Criteria: 2 situations – home and school
Autistic spectrum 3 specific issues: Impulsiveness + overactivity + loss of
1. Verbal problems concentration
2. Non-verbal communication and
no social interaction (hugging, etc.)
3. Fixation/ specific focus on
something (e.g. he likes dinosaurs) &
doesn’t like when his life is changing
Asperger – only 2 and 3
Any sex Boys
Rx - Refer to child psychiatrist Ask for school report
Dexamphetamine –> ↓hyperactivity
o Autism
▪ Autistic spectrum disorder – many subtypes
• e.g. Asperger syndrome – very mild form of autism
- many will have an almost normal life
- sedentary, isolated life
- avoid eye contact
- normal speech
- some are very good in mathematics
- communication through language is preserved
Autism Asperger
Boys 4:1 Boys 8:1
Onset before 3 yrs (30 mths) after a period of normal development
Low IQ Normal or high IQ
No social interaction, use of 2 word phrases only Can speak, normal speech, likes friends
Lack joint attention: Fascination with things
No eye contact. No pointing No eye contact
Lack of pretend play (feeding doll)
Lack of social interest (no peekaboo)
Lack of social play (plays alone)
Lack of communication (verbal, non-verbal) communication is preserved
Lack of peer-rship
Lack of spontaneous seeking
Stereotype repetitive behav.
Don’t like change in routine Rigid to routine
Assoc. with: tuberous sclerosis, epilepsy,
rubella, tourette syndr.
No Rx. Need regular check-ups (don’t complain Rx: behav. therapy, individual assessment,
even when sick or in pain) speech therapists
▪ used to be called childhood schizophrenia
▪ 25% develop epilepsy during adolescence
522

▪ can be sec. to rubella, phenylketonuria, tuberous sclerosis, neurolipoidoses

▪ main problem: no communication, no normal rship with the ones around + like
to be on their own
• no eye contact, no seeking behav. (looking for a hug), not playing with
other children
• doesn’t want to be kissed, embrassed
• plays with toys in an unusual ways
• odd in many ways
▪ onset
• early – 6 mths
- doesn’t start the language
• late
- started talking, then loses the talk
▪ Doesn’t enjoy peekaboo
▪ Stereotypical repeatitive movts. – bulding tower of blocks repeatedly etc.
▪ restricted repetitive interest:
• have fixations for certain things - likes dinosaurs and Bob the builder
• doesn’t like changes to his routine – throws tantrums and explosive
outbursts if change is attempted
Other conditions
- CBT
o Package of treatments, useful in many/ most psychiatric disorders
o indic.
▪ Chronic pain – due to associated anxiety, depression and avoidance behav.
▪ Phobias
▪ Depression
▪ Eating disorders etc.
- Depersonalization
o Sx
▪ Pt feels unreal, detached from his own experience and unable to feel emotion
▪ time distortion
▪ changes in body image
▪ out of body experience (autoscopy)
▪ reality testing is intact (knows the border between inner experience and the
outer world)
▪ often + derealisation = the external world is strange and unreal
o occurs in:
▪ healthy people – when tired or sleep-deprived (lasting only a few min.)
▪ anxiety disorders
• panic disorder
• post-traumatic stress disorder (PTSD)
• agoraphobia
▪ schizophrenia
▪ depression
▪ acute intox. or withdrawal from alcohol, hallucinogens, etc.
▪ ecstatic and trance practices – e.g. religioius
▪ epilepsy – especially temporal epilepsy
523

- Seasonal affective disorder

o young women
o in areas with decr. sunlight
o mediated by melatonin
o onset and remission of major depressive episodes at certain time during the year
▪ MC onset in winter, recovery in spring
o Sx
▪ irritability, hypersomnia, hyperphagia with carbohydrate craving, wt. gain,
energy loss
- Capgras syndrome – person believes that a relative or close friend has been replaced by a
double or impostor pretending to be that person
o in schizophrenia, etc.
- Fregoli syndrome – person misidentifies or recognizes familiar people in other people
(strangers)
o in schizophrenia
- De Clerambault syndrome (erotomania)
o women
o they believe an important or famous person is in love with them and comunicaticates
their love in obscure, indirect ways
o in schizophrenia
- Querulant paranoia – person keeps having litigations with the civil authorities, lawyers and
judges involved in the earlier trials (suspects conspiration)
- Migrant psychosis – in people who have just immigrated in a another country
- Irritable bowel syndrome (IBS)
o very frequent in Aus.
o women
o triggered by a gastroenteritis or a major stress
o at least 2 of the following:
▪ abd. pain relieved by defecation
▪ onset of abd. pain is assoc. with change in bowel frequency (diarrhoea or
constip.)
▪ onset of abd. pain is assoc. with change in consistency of stools (loose , watery,
pellet)
o MCQ: pain in the left iliac fossa (fluctuating diarrhea and constipation)
o urgency, straining, tenesmus, bloating, passage of mucus
o almost always assoc. with depression or anxiety (disturbance of gut-brain axis).
o Rx
▪ Dietary modif. – identify the specific food that triggers IBS and remove it
▪ CBT
▪ SSRI
• Fluoxetine (blue book) MCQ
• Mebeverine – controls spastic peristalsis e.g. in diarrhea before exam
(SSRI)
- Limbic encephalitis
o autoimmune dis. – AB to nerve cell antigens
▪ a large proportion are paraneoplastic (small cell lung CA, non-Hodgkin
lymphoma, etc.)
524

o Sx
▪ recent onsef of irritability, angry outbursts, anxiety symptoms or depression
then memory problems and confusional episodes.
▪ memory disturbance
• short term memory only is affected
• long term/ autobiographic memory is preserved
▪ episodic confusion
▪ hallucinations
▪ paranoid ideation
▪ insomnia
▪ psychomotor seizures
▪ history: recent onset of irritability, anger outbursts, anxiety or depression ->
then memory and confusional problems (MCQ).
o Rx
▪ C/S
▪ plasma exchange
▪ immunomodulation
▪ cyclophosphamide
- hypnagogic hallucinations – vivid dreamlike hallucinations occuring at the onset of sleep
- REM sleep disorder – acting out (yelling, punching, etc.) of dreams that are vivid and intense
Ekbom syndrome
o types
▪ 1 - they believe they have an insect/ worm on their body
▪ 2 - restless legs syndrome
• middle-aged, elderly
• up to 10% of population
• familial Hx – AD with variable penetrance
• precip. factors
- anemia
- hypothyroidism
- renal failure
- DM
• Sx
- irresistible urge to move legs, “tingling, burning and crawling” of
the skin, from thighs to feet
- occurs when sitting down or lying in bed
- worse during the evening and at night before sleep
- relieved by walking
- typically pt complaints of limb discomfort at rest and then urge to
move the affected part, relieved by walking.
• Rx
- mild
▪ lifestyle changes – good sleep hygiene (bed just for
sleeping: no reading, TV, etc.)
▪ Levodopa
▪ Benserazide
▪ Dopamine agonists – amantadine, selegilin
525

- Illusion - there is something there, but incorrectly interpreted (interpreting string as a snake)
o diff. from hallucination (there’s nothing there)
- types of thoughts
o Overvalued idea – quantitatively different from reality
▪ in anorexia nervosa, morbid jealousy, hypochondriasis, querulous paranoia,
body image disturbance
o Delusion – qualitatively different from reality (fixed false belief)
o Phobia – with excessive arousal or anxiety in presence of the trigger, with minimal
resistance to it
o obsession – recognized by the patient as senseless and irrational and is resisted by him
▪ rumination – more complex obsessional thoughts, which are repetitive,
intrusive, unwanted and upsetting
- reassurance should only be offerred when the pt’s concerns have been fully understood and
investigated
- Vaginismus
o Spasm of perineal musculature of the lower 1/3 of vagina
o Young women of high socioeconomic standard
o can be caused by:
▪ a sexual trauma (rape, childhood sexual abuse) or very strict upbringing (sex =
sin)
▪ scarring following episiotomy
o can be assoc. with a phobic anxiety of anticipating vaginal intercourse, e.g. in the
presence of an inexperienced partner
- Diogenes – people who like to collect garbage or have a dirty life style.
- Charles Bonnet - Visual hallucinations due to organic reasons in blind or partilly sighted elders
o if organic reason (occipital or ocular disease) is resolved, the hallucinations will go away
- Cotard syndrome – they believe they have lost body parts, blood, their soul, they are dead or
never born.
- Folie-a-deux
o rare
o one psychotic sympt. is transm. from one person to another (sympt. manifest only when
they are together)
- amygdala – in the temporal lobe, regulates affects
o regulates limbic system
- corpus calossum – responsible for sexual dimorphysm
- cingulate gyrus – part of limbic system, involved in emotion formation, processing, learning and
memory
- Transient global amnesia < 8 hrs
o loss of both recent and biographical memory
o in vertebro-basilar insufficiency
- which psychiatric dis. is increasing in incidence = Dementia (incr. ageing population)
- Paraphilias
o unusual sexual preferences, “perverts”
o types:
▪ 1. Exhibitionism – Recurrent urge to expose oneself to strangers
▪ 2. Fetishism – use/ collection of non-living objects (e.g. bras, etc.) usually assoc.
with the human body
▪ 3. Pedophilia – Recurrent urge or arousal towards pre-pubescents (children)
526

▪ 4. Frotteurism - Recurrent urge or arousal involving touching or rubbing against

a non-consenting partner
▪ 5. Voyeurism (peeping tom) - Recurrent urge or arousal involving the act of
observing an unsuspecting person who is engaging in sexual activity
▪ 6. Masochism - recurrent urge or arousal involving the act of humiliation (the
love to receive pain)
▪ 7. Sadism - recurrent urge or arousal involving the act of giving pain
▪ 8. Transvestic fetishism - recurrent urge or arousal involving cross dressing
(but don’t feel they belong to the opposite sex)
- Gender identity disorders – persistent discomfort and sense of inappropriateness regarding
their assigned sex
o + preoccupied with wearing opposite gender’s clothes
o feel trapped in their body – they feel they are girls in boys’ body or vice versa (born with
wrong body)
▪ + experience anxiety, depression and suicidal thoughts because of this =
Gender dysphoria
o from birth
o will have preferences for friends of the opposite sex.
o request surgery to change their sex.
o adopt the opposite gender’s behaviour.
Ethics - OK
- Mental health act (1986) + Mental health regulations (2008)
o only for mentally ill persons
o consent is not required – treatment will be involuntary
o criteria for involuntary treatment
▪ a. person appears to be mentally ill
▪ b. person’s mental illness requires immediate treatment
▪ c. treatment is necessary for safety or protection of member of the public
▪ d. person has refused or is unable to consent to treatment
▪ e. person can’t receive treatment in less restrictive manner
o involuntary treatment order (ITO)
▪ involuntary vs. voluntary patient
- sexual rships between doctors and patients
o are usually initiated by the doctors
- rape
o presents right after rape – call police
o presents a while after rape – call child protection agency
- domestic violence
o step 1 – take photos
o step 2 – refer to safe shelter
- patient refuses to pay for the consultation
o select “free of charge” or
o send the bill to her home
- parents can give consent until 18
o as long as it’s in the best interest in the child
- consent in minors
o legal age of consent in Aus. = 18 yrs
527

▪ Legal age for sex, including abortion and OCP – 16 yrs (South Aus. and
Tasmania – 17)
• > 16 yrs – OK to prescribe OCPs or perform abortion at her request/ with
only her consent.
• 14-16 Gillick test (or the stem will tell me that she lives alone, she is
mature, etc.) – asses whether:
- Mature minor – treat as a 16 yrs old
▪ lives independently of her parents + is mature and
understands the potential risks and complications of
the required medical procedure.
▪ e.g. pregnant girl, 14 yrs, asking for abortion – blue
book 573
• if she is mature (Gillick test)
• and if it was by consent
o OK
▪ even if > 2 yrs between her and
her boyfriend
▪ even though it’s illegal, she is
under 16 yrs
- Immature minor – treat as a kid and request her parents’
consent.
• < 14 yrs - request her parent’s consent.
- mom wants her mentally retarded girl to have an hysterectomy
o we can’t do that (we refuse) – the girl is entitled to have her uterus (human rights)
o mom can make a request to the child health court (?)
▪ she will probably be refused
- mentally retarded girl - contraception
o under institutional care – OCP
o alone – contact guardianship court
- consent form checked by
o HMO
o nurse
o anesthetist
o surgeon – he is the only one legally responsible
- adopted children have the right to be informed they were adopted
o but this remains the decision of their parents at least until the child is 18 yrs old
- consent in incompetent patients (e.g. elderly demented people)
o 1. advance directive from the patient
▪ The first source of guidance for doctors on the treatment to be offered to an
incompetent patient is the patient’s own advance directive given BEFORE he or
she became incompetent.
▪ This may state whether pt wishes to have particular treatment or to refuse it.
o 2. Surrogate decision maker appointed by the patient (Health attorney, medical agent or
enduring guardian).
▪ If a patient is incompetent and has not previously consented to treatment or
refuse it, a person appointed in advance by the patient may have authority to
decide on the patient’s behalf.
528

▪ Most Australian jurisdictions now have legislation enabling patients who are
over the age of 18, while competent, to appoint someone else to make
medical decisions for them if they later become incompetent.
o 3. Guardian appointed by a board, tribunal or court.
▪ If a patient is not competent (and, in jurisdictions that have legislation allowing
people to make advance directive or to appoint their own substitute decision
maker, has not done so), it may be necessary for a substitute decision maker to
be appointed by a guardianship body.
▪ A guardianship body will not intervene by appointing a guardian unless that is
NECESSARY.
• IF THE PERSON’S RELATIVES ARE CARING FOR THE PERSON
SATISFACTORILY, IT IS GENERALLY CONSIDERED THAT THERE IS NO
NEED FOR A GUARDIAN.
• If, however, there is a dispute between family members about the
person’s care, a formally appointed guardian may be needed to make or
review decision about the person.
o 4. The bottom line: Relatives and carers.
▪ If there is no person who has been formally appointed as a surrogate decision
maker, either by the patient or by a guardianship body, a relative or carer may
be able to consent.
▪ This Acts set out a hierarchy of people to decide the ‘person responsible’
including relatives and carers, for consenting to treatment (different
depending on state).
• e.g. Victoria:
1. A person appointed by the patient under the Medical
Treatment Act.
2. A person appointed by the Victorian Civil and Administrative
Tribunal to male decisions in relation to the proposed
treatment.
3. A person appointed under a guardianship order with power to
make such decisions.
4. An enduring guardian appointed by the patient while
competent.
5. A person appointed by the patient with power to make such
decisions.
6. The patient’s spouse of domestic partner.
7. The patient’s primary carer.
8. The patient’s nearest relative.

Statistics – OK (+ 1st AID page 99)

- MCQ 3196 (P299-520)
- Prevalence = total number of old and new cases (no of diseased) at a specific time
o Point Prevalence = measure of proportion of population having a condition at a particular
time.
o Period Prevalence = measure of proportion of population having a condition over a period
of time
- Incidence = No. of new cases
529

Prevalence Incidence
New vaccine introduced Decr. Decr.
Disease that kills patients Decr. Constant
Drug that cures a disease Decr. Constant
Drug that doesn’t cure the dis. but extends life Incr. Constant
- Sensitivity & Specificity
Disease present Disease absent
Test pos. A = true positive B = false positive
Test neg. C = false negative D = true negative
o Prevalence: A+C/ (A+B+C+D) = Incidence x Duration
o Accuracy: A+D/A+B+C+D
o Sensitivity – Ability to detect true positives
▪ Sensitivity = A/(A + C) = (true pos./total pos.) = TP/ TP + FN
▪ not related to prevalence
o Specificity – Ability to detect true negatives
▪ Specificity = D/(B + D)= (true neg./ total neg.) = TN/ TN + FP
▪ not related to prevalence
o Positive predictive value – Proportion of true +ves identified in a defined population.
▪ PPV = A/(A + B) = (true pos./ total population)
▪ PPV = TP/TP+FP or (sensitivity x prevalence)/(sensitivity x prevalence) + (1 –
specificity) x (1 – prevalence)
▪ computation of sensitivity, specificity and prevalence
▪ When prevalence is low = PPV ↓ and NPV increases. (MCQ 3339 P 352) test
loses PPV when prevalence is low.
▪ Sensitivity and specificity are inversely related.
o An ideal test would be 100% sensitive and 100% specific. No test can attain this ideal. In
screening population one needs a highly sensitive test for screening.
o Negative predictive value – Proportion of true -ves identified in a defined population =
TN/TN+FN
▪ NPV = D/(C + D) = (true neg./ total p opulation)
▪ Computation of sensitivity, specificity and prevalence.
- All these above 4 formulas have A& D always up
- Odd Ratio: AD/ BC
- Number need to teat: is the no of pts required to be treated to prevent bad oucome. NNT =
1/incidence = 1/Absolute risk reduction.
- Absolute risk reduction: Incidene in unexposed – Incidence in exposed.
- Reliability how well a test performs when repeated 2nd time and or by 2nd tester (test-retest
reliability) and how well test items correlate with each other. It is not affected by prevalence
- Likelihood ratio: an explnation for Likelihd ratio what it means. e.g If LR + = 9 for a test say
ELISA, then it means that likelihood of ELISA test to be positive in HIV pts is 9 times more than
not having HIV.
- LR + = Sensitivity/ 1-Specificity
- LR - = 1- Sensitivity/ Specificity
- Case fatality rate: total no of deaths/ total no of diseased.
- Standard Deviation.
o Mean BP + 2 std. deviation = Systolic (CI)
o Mean BP – 2 std. deviation = Diastolic
530

o 66% 1SD, 95% 2SD, 99% 3SD.

- types of studies: (MCQ 2084 P 72)
o Case report – Least important in evidence
o Case-control studies -- Retrospective
▪ In a case-control study, people with a disease (often, a specific diagnosis,
perhaps lung cancer) are matched with people who do not have the disease
'controls'. Further data is then collected on those individuals and the groups are
compared to find out if other characteristics (perhaps a history of smoking) are
also different between the two groups.
▪ non-randomised
▪ retrospective
▪ provide circumstantial evidence and Odds ratio.
o Cross-sectional studies = Prevalance (use Chi Square)
▪ type of one-dimensional data set. Cross-sectional data refers to data collected
by observing many subjects (such as individuals, firms or countries/regions) at
the same specific point of time that is corss, or without regard to differences in
time. Analysis of cross-sectional data usually consists of comparing the
differences among the subjects.
▪ For example, we want to measure current obesity levels in a population. We
could draw a sample of 1,000 people randomly from that population (also
known as a cross section of that population), measure their weight & height,
and calculate what percentage of that sample is categorized as obese. For
example, 30% of our sample was categorized as obese. This cross-sectional
sample provides us with a snapshot of that population, at that one point in
time. Note that we do not know based on one cross-sectional sample if
obesity is increasing or decreasing; we can only describe current proportion.
▪ Cross-sectional data differs from time series data also known as longitudinal
data, which follows one subject's changes over the course of time.
Both case control and cohort are suspect bc non randomized group of people
are studied which intoduce bias.
o Longitudinal case series – follows a population group over a prolonged period:
▪ Cohort studies (Relative risk, Incidence, non randomized) = CI
• form of longitudinal study (a type of observational study) used in
medicine, econometrics, actuarial science and ecology. It is an analysis of
risk factors and follows a group of people who do not have the disease,
and uses correlations to determine the absolute risk of subject
contraction. It is one type of clinical study design and should be
compared with a cross-sectional study.
• A cohort is a group of people who share a common characteristic or
experience within a defined period (e.g., are born, are exposed to a
drug or a vaccine, etc.). Thus a group of people who were born on a day
or in a particular period, say 1948, form a birth cohort. The comparison
group may be the general population from which the cohort is drawn, or
it may be another cohort of persons thought to have had little or no
exposure to the substance under investigation, but otherwise similar.
Alternatively, subgroups within the cohort may be compared with each
other.
531

• In medicine, a cohort study is often undertaken to obtain evidence to try

to refute the existence of a suspected association between cause and
effect; failure to refute a hypothesis strengthens confidence in it.
Crucially, the cohort is identified before the appearance of the disease
under investigation. The study groups follow a group of people who do
not have the disease for a period of time and see who develops the
disease (new incidence).
▪ panel study - sample a cross-section, and survey it at regular intervals.
o Randomised controlled trials: Gold standard
▪ some authors distinguish between:
• "RCTs" which compare treatment groups with control groups not
receiving treatment (as in a placebo-controlled study), and
• "randomized trials" which can compare multiple treatment groups with
each other.
Absolute Risk = Incidence
Attributable risk: Incidene in exposed – Incidence in unexposed
Relative risk: Incidenc in exposed/ Incidence in unexoosed.
Relative risk reduction: Incidenc in exposed-incidence in unexposed/ Incidence in unexposed
RR < 1: Protective/ beneficial
=1: No association
>1: + association (i.e association of disease with Risk factor)
Absolute risk reduction: Absolute rik in control (normal) group – absolute risk in treatment group
Þ – Value: an estimate of probability that difference in treatment effects in a study have happened by
chance. Standard P value is 0.05 which means there is 5% chance of difference to occur. If p value
exceeds 0.05 in a research, test hypothesis is nullified. P value less than 0.01 means something is highly
specific, i.e there's only 1% chance of an observed difference.
- all studies have to be approved by the Human Research Ethics Committee.
- A good screening test: High sensitivity, high PPV, inexpensive, safe and easy to administer.

Normal values
Australia: (Murtagh – p. 148)

Erythrocyte sedimentation rate (ESR):

Normal < 20 mm/h (with OCP normal up to 20-25 mm/h)
↑ in inflamation and cancer

Child: 2-15 mm/h

Adult Male:
17-50 years 1-10 mm/h
> 50 years 2-15 mm/h

Adult Woman:
17-50 years 3-12 mm/h
> 50 years 5-20 mm/h

Troponin I or T: Normal < 0.1 µg/L

532

C-Reactive Protein (CRP)

Normal < 10 mg/L

4-10 ml/L mild inflammation

10-20 mg/L moderate inflammation
> 40 mg/L marked inflammation

> 100 mg/L 80% sensitivity and 88% specificity for bacterial infection
10-40 mg/L 69% & sensitivity and 54% specificity for viral infection

Urinary Tract Infection

WBC count > (5 -) 10 x 106/L
Counts > 108 organisms/L

Iron metabolism + anemia testing

Iron normal: 14-30 µmol/L
TIBC, evaluates the transferrin in blood: 45-80 µg/L
Transferrin saturation: normal 20-55%
Serum ferritin (deposits): normal 20-250 µg/L males, 10-150 µg/L females
Hb – 11.5-16.5 g/dL (men) or 13-18 g/dL (women)
or 115-165 g/L (men) or 130-180 g/dL (women)
Haematocrit or packed cell volume (PCV) 40-53 male, 35-47 female
" (MCV) 80-95 – 100 fL (81-98)
Vit. B12 >220 pmol/L (< 148 = defficiency)

Renal fuction
Creatinine: 0.04 – 0.1 mmol/L
Urea: 3-8 mmol/L
eGFR > 60 ml/min/1.72 m2
Normal urinary output = Normal 1 ml/ kg/ hr.

Hematology
Red cells 4.5-6 x 1012/ L male, 4-5.5 female
Reticulocytes 0.5 – 2 % (1%) (immature cells in circulation)
Leucocytes 4.5-11 x 109/ L
Platelets 150-400 x 109/ L
Neutrophils 2-7.5 x 109 / L
Eosinophils 0.2-0.4 x 109 / L (<0.44)
Lymphocytes 1-4 x 109 / L (<4.5)
Monocytes 0.2-0.8 x 109 / L (<0.8)
Basophils ?

Coagulation Profile:
Bleeding time 2-8 min
Fibriongen
Prothrombin time – (12-15) seconds
Prothorombin international normalized ratio (INR) 1-1.2
533

- The prothrombin time is the time it takes plasma to clot after addition of tissue factor
(obtained from animals). It measures quality of extrinsic pathway (as well as the common
pathway) of coagulation.
- The speed of extrinsic pathway is greatly affected by levels of factor VII in body. Factor VII
has a short half-life & its synthesis requires Vit. K.
- The prothrombin time can be prolonged as a result of deficiencies in vit. K, which can be
caused by warfarin, malabsorption, or lack of intestinal colonization by bacteria (such as in
newborns). In addition, poor factor VII synthesis (due to liver disease) or increased
consumption (in disseminated intravascular coagulation) may prolong the PT.
- A high INR such as INR = 5 there is a high chance of bleeding, if INR = 0.5 there is a high
chance of having a clot. Normal range for a healthy person is 0.9–1.3 and for people on
warfarin therapy, 2.0–3.0, although target INR may be higher in particular situations, such
as for those with a mechanical heart valve, or bridging warfarin with a LMW heparin (such as
enoxaparin) perioperatively.

Liver Function Tests:

Plasma biliubin:
Unconjugated (indirect after RBCs breakdown) &
Conjugated (direct, after metabolism in liver, < 3 µmol/L)
Total bilirubin < 20 µ mol/L
Total protein - 60-80 g/L
Liver disease - 38 to 50 g/L
Globulin
Alanine aminotransferase (ALT) ???, Aspartate aminotransferase (AST normal < 40 U/L) –
Hepatocellular damage (over 10x = 10-100 times the normal value)
Gamma-glutamyl transferase (GGT) – indicator of cholestasis + liver disease, drug and alcohol intake, F
<45, M <65 U/L
Alkaline phosphatase (ALP) – indicator of cholestasis (> 3 times the normal value), <120 U/L

Thyroid function tests

Serum TSH
Tri-iodothyronine T3
Thyroxine T4
Anti-thyroid antibody tests
thyroxine-binding globulin
Thyroglobulin

Serum Electrolytes (Normnal Values)

Na+ 130-145 mmol/L
K+ 3.5-5 mmol/L
Cl- 95-105 mmol/L
HCO3- 22-26 (24-28) mmol/L (~25)
Anion gap (Na+) - (CL- + HCO3-) normal: 8-16
PH 7.35-7.45
PaCO2 35-45 mmHg
PaO2 85-100 mmHg
can be > 100 since this is partial pressure
534

SaO2 98%

Lipids:
Total Plasma cholesterol: < 4 mmol/L
Triglycerides: < 1.5 mmol/L (Use mono or PUFA, marine Omega 3 (fish oil) and fibrates as Rx)
HDL cholesterol > 1mmol/L (Gemfibrozil and nicotinic acid increases HDL)
LDL cholesterol < 2.5 mmol/L (Simvastatin and Ezetimibe as Rx to lower). Ezetimbe decreases
cholesterol absorption.

BMI: (Measure of adiposity) = Mass (kg)/ height (m)2

Normal 20-25
Young Women Normal 19-24
Mean BMI in Aus. 25
o < 18.5 = underweight
o 18.5-24.9 = normal
o 25-29.9 = overweight
▪ Rx – lifestyle changes
o 30-34.9 = Grade 1 obesity
▪ Rx - Supervised lifestyle changes
o 35-39.9 = Grade 2 obesity
▪ Rx
• Supervised lifestyle changes
• Medical Rx:
- Local
▪ Bulking agents – methycellulose
▪ Lipase inh. - Xenical
- Central
▪ decr. hunger – amphetamines derivates: Phentermine,
diethylpropion
▪ incr. satiety – SSRI
o ≥ 40 = Grade 3 (morbid) obesity
▪ Rx – as above +
• consider Gastric banding
> 16 definitely abnormal, > 14 seriously emaciated.
It may incorrectly identify people esp. men as overweight when they are fit and have high BMI because
of high muscle bulk through excercise. Combination of BMI with waist circumference is useful in such
cases.
BMI in children 2-18yrs:
Overweight = BMI 85th to 95th %.
Obese is ≥ 96th %.
For children below 2yrs
Overweight is > 97% on WHO growth chart and gaining wt rapidly.
(Royal children hospital of Melbourn guide lines)

Predictors of effects of obesity on health: Waist to Hip ratio (MCQ) and Waist circumference and these
are less accurate than BMI alone
535

Obesity indicator in children: Weight/ Standard weight and BMI

Bioimpedance analysis: Measure of blood flow and body composition. It is a more accurate measure of
fat mass in children than BMI.
Glucose:
Fasting (after 12 hrs of fasting) 3.5-6 mmol/L ( > 7 diabetes)
Random (no fast, at least 2 hours after a meal) 3.5-9 mmol/L (>11.1 diabetes)
Oral glucose tolerance test (OGTT) – after a 12 hrs fast; measures glucose at 0 hrs (before glucose
administration) and at 2 hrs after glucose administration (75 g)
Glycosylated Hb 4-6% of total Hb (> 7 diabetes).

Eye tonometry: up to 22 mmHg (above – Glaucoma)

Optic disc cupping: > 30% of the total optical disc area = Glaucoma

Trachoma prophylaxis:
a. Contacts of cases identified through community screening:

Active trachoma community prevalence in 5-9 year old Aboriginal and Torres Strait Islander children:
i. ≥ 20%: Treat all people > 3kg living in households with children <15 years of age.
ii. ≥ 5 to < 20% and there is no obvious clustering of cases: Treat all people > 3kg living in households
with children <15 years of age.
iii. ≥ 5 to < 20% and cases are obviously clustered within several households and health staff can easily
identify all household contacts of cases: Single-dose azithromycin to all people > 3kg living in households
with an active trachoma case.
iv. < 5%: Treat all people > 3kg living in households with an active trachoma case.

c. Contacts of cases identified outside of screening programs

Treat people > 3kg who living in the same household (s) as the case

3. Subclincal hypothyroidism is TSH high, T4 normal

4. Secondary hypothyroidism due to pit dysfunction = TSH normal T4 dec Inx MRI
Brain
Early dumping consists of abdominal and vasomotor symptoms, which are found in about 5–10% of
patients following gastrectomy or vagotomy and drainage. It also affects a small percentage of patients
following highly selective vagotomy because of the loss of receptive relaxation of the stomach. The small
bowel is filled with foodstuffs from the stomach, which have a high osmotic load, and this leads to the
sequestration of fluid from the circulation into the gastrointestinal tract. This can be observed by the
rise in the packed cell volume while the symptoms are present.. The principal treatment is dietary
manipulation. Small, dry meals are best, and avoiding fluids with a high carbohydrate
content also helps. Fortunately, following operation, the syndrome tends to improve with time. For
some reason, however, there is a group of patients who suffer intractable dumping
536

regardless of any of these measures. The somatostatin analogue octreotide, given before meals, has
been shown to be useful in some individuals and the long-acting preparation may also be
useful. However, this treatment can lead to the development of gallstones and it does not help the
diarrhoea from which many patients with dumping also suffer. Revisional surgery may be occasionally
required. In patients with a gastroenterostomy, the drainage may be taken down or, in
the case of a pyloroplasty, repaired. Alternatively, antrectomy with Roux-en-Y reconstruction is often
effective, although the procedure is of greater magnitude; following gastrectomy, it is the
revisional procedure of choice.
#Late dumping syndrome :
This is reactive hypoglycaemia. The carbohydrate load in the
small bowel causes a rise in the plasma glucose level, which, in
turn, causes insulin levels to rise, causing a secondary hypoglycaemia.
This can be easily demonstrated by serial measurements
of blood glucose in a patient following a test meal. The treatment
is essentially the same as for early dumping. Octreotide is very
effective in dealing with this problem.