Understanding the Nervous System

MEDICAL SURGICAL
OVERVIEW OF THE STRUCTURES & FUNCTIONS OF THE NERVOUS SYSTEM
3 PARTS OF THE NERVOUS SYSTEM
1. Central NS 2. Peripheral NS 3. Autonomic NS C-8

Brain & Spinal cord 31 Spinal & Cranial Sympathetic NS & Parasympathetic NS T - 12
L- 5
S–5
Somatic NS C-1
I. Autonomic Nervous System
A. Sympathetic NS (SNS)
1. Fight or Aggression Response
2. Release of Norepinephrine (adrenaline – cathecolamine)
= Adrenal Medulla (potent vasoconstrictor)
3. All body activities increased except GIT (GIT decreased motility)
Bodily Effects of SNS
a. Mydriasis = Dilated pupil , to be aware of surroundings
b. Dry mouth
VS = Increase c. BP & HR
c. RR
d. Constipation
e. Urinary Retention
f. Increased BF to heart, brain, skeletal muscles
4. Adrenergic or Parasympatholitic Response
Adrenergic Agents a. Epinephrine (Adrenaline) S/E : SNS Effects

b. Anti-Psychotics ex. Haldol (Haloperidol) S/E : SNS Effects
B. Parasympathetic NS
1. Flight or Withdrawal Response
2. Release of Acetylcholine (ACTH)
3. All bodily activities decreased except GIT
Bodily Effects of PNS
a. Meiosis = constriction of pupils

b. Increased salivation
VS:decreased c. BP & HR
d. RR =bronchoconstriction
e. Diarrhea =Increased Motility
f. Urinary Frequency
4. Cholinergic or Vagal or Sympatholitic Response
a. Beta-Adrenergic Blocking Agents (Beta-Blockers) (all end in –‘lol’)

Ex. Propanolol, Metopanolol
- Blocks release of norepinephrine, Decrease body activities except GIT (diarrhea)
S/E:
B – broncho spasm (bronchoconstriction)
E – elicits a decrease in myocardial contraction
T – treats HPN
A – AV conduction slows down
Given To/As: a. Angina Pectoris
b. MI – beta-blockers to rest heart
c. Anti HPN agents: -Beta blockers (-lol)
- Ace inhibitors (-pril) ex ENALAPRIL, CAPTOPRIL
- Calcium antagonist ex. CALCIBLOC or NEFEDIPINE
d. Anti-arrhythmic agents (arrhythmia= irregular contraction of the heart)
Created by Niňa E. Tubio 1
b. Cholinergic agents Ex. Mestinon (prostigmine) given to MG to increase ACTH
S/E = PNS
*Antidote – anti cholinergic agents Atropine Sulfate – S/E – SNS
II. CNS (Brain & Spinal Cord)

Part 1 : Parts:
A. Cells – neurons = Basic living units

Properties and Characteristics
a. Excitability – ability of neuron to be affected by changes in the external environment
b. Conductivity – ability of neuron to transmit a wave of excitation from one cell to another
c. Permanent cells – once destroyed, can not regenerate (ex. heart, retina, brain, osteocytes)
3 Types of Cells According To Its Regenerative Capacity:

1. Labile – once destroyed, can regenerate: Epidermal, GIT, lung cells, GUT cells
2. Stable – capable of regeneration BUT limited survival time: salivary gland, pancreas,
liver, kidney cells
3. Permanent – cannot regenerate: retina, brain, heart, osteocytes & myocardial cells
B. Neuroglia : can cause brain tumors

Functions & its 4 Types:
1. Astrocyte = maintain integrity of blood brain barrier (semi-permeable/selective)
2. Microglia = stationary cells
3. Ependymal Cells
4. Oligodendrocytes
1. Astrocytes:
 # 1 type of brain tumor= Astrocytoma ( 90 – 95%)
 Toxic substance that destroys astrocyte & passes the Blood Brain Barrier
a. Ammonia = a cerebral toxin , product of protein catabolism
Hepatic encephalopathy (liver cirrhosis) = death of liver d/t necrosis

Primary Cause : Malnutrition
Major Cause : Alcoholism
Early Sign : Asterixis (Flapping hand tremors)
Late Sign : Headache, Restlessness, Fetor Hepaticus (ammonia-like breath)
Hepatic Coma -----N.P. Airway
b. Bilirubin = yellow pigment -------- jaundice (Icteric Sclerae)
others: Bilivedrin = green pigment

Hemosiderin = golden-brown pigment Hepatitis
Hemoglobin = red cell pigment
* Carotenemia = yellowish discoloration of the skin

*Sign of Tumor in the Pituitary Gland
* Kernicterus (Hyperbilirubinemia)
- Increased bilirubin in the brain, irreversible brain damage
b. Carbon Monoxide :Tx for Carbon monoxide poisoning

= Hyperbaric Oxygenation (100%)
Parkinson’s Disease Seizure

Early Sign: Pill-Rolling Tremors
d. Lead = Antidote for lead poisoning ------ Calcium EDTA
e. Ketones - acids, CNS depressant

Ketones in Blood
DKA ---- Type 1 DM
d/t increase fat catabolism
free fatty acids
Cholesterol Ketones ----- DKA : Early Signs = Weakness/ Weight Loss

Leads to: Atherosclerosis Late Signs = Acetone Breath & Kussmaul’s Breathing
Leads to Coma
HPN ==MI or Stroke --Death
2. Microglia = Stationary Cells ------- Phagocytosis

Organ Macrophage
 Brain ---------- Microglia
 Blood ---------- Monocytes
 Kidney/Liver ---------- Kupffer Cells
 Lungs ---------- Alveolar Macrophages
 SC Tissues ---------- Histiocytes
3. Ependymal Cells = acts as a defense in the CNS along with microglia
secretes a glue ------ Chemoattractants
4. Oligodendrocytes = produces myelin sheath: acts as a cover for neurons

acts as an insulator w/c facilitates rapid nerve impulse transmission
No myelin sheath – degenerates neuron
Damage to myelin sheath causes demyelinating disorders
DEMYELINATING DISEASE
1. ALZHEIMER’S DISEASE – atrophy of brain tissue due to a deficiency of acetylcholine
- Degenerative disorder
- A type of Dementia
Predisposing Factors: 1. Aging 2. Aluminum Accumulation
S&Sx:
A – amnesia – loss of memory *Short-Term -- Anterograde Amnesia
*Long-Term Retrograde Amnesia
A – apraxia – unable to determine purpose of object thru movement
A – agnosia – unable to recognize familiar object
A – aphasia – 2 types:
1. Expressive – Brocca’s aphasia – inability to speak ex. (+) nodding
TX: use of picture-boards
- damage to frontal lobe
- Brocca’s ---- motor speech center in the frontal lobe
2. Receptive – Wernicke’s aphasia – unable to understand spoken words ex. (+) illogical thoughts
- damage to Temporal lobe
- Wernicke’s Area --- general interpretative area
- Common to Alzheimer – Receptive Aphasia
- Drug of choice – ARICEPT or COGNEX ----- best given : at bedtime
2. MULTIPLE SCLEROSIS (MS) -Chronic intermittent disorder of CNS

 Characterized by white patches of demyelenation in brain & spinal cord.
 Remission & exacerbation
 Common – women, 15 – 35 y/o
Predisposing factor:
1. Idiopathic
2. Slow growing virus
3. Autoimmune – (supportive & palliative treatment only) self-killing immunity
Normal Resident Antibodies: 5 types

IgG – can pass placenta – passive immunity, temporary
IgA – body secretions – saliva, tears, colostrum
IgM – acute inflammation
IgE – allergic reactions
IgD – chronic inflammation
S & Sx of MS:
1. Visual disturbances : a. *Blurring of vision = Initial sign
b. Diplopia/ double vision
c. Scotomas (blind spots)
2. Impaired sensation to touch, pain, pressure, heat, cold: a. Numbness
b. Tingling
c. Paresthesia
3. Mood swings – common : EUPHORIA (sense of elation )
4. Impaired motor function: a. Weakness
b. Spasticity –“ tigas”
c. Paralysis
5. Impaired cerebellar function
Triad Sx of MS (INA)
I – intentional tremors
N – nystagmus CHARCOT’S TRIAD (INA)
A – Ataxia - unsteady gait
6. Scanning of Speech
7. Urinary retention or incontinence
8. Constipation
9. Decrease sexual ability
Dx:
1. CSF analysis thru lumbar puncture : bet. L3 & L4 : Reveals CHON & IgG
2. MRI – reveals site & extent of demyelination
3. Lhermitte’s Sign : confirmatory Dx of MS
- continuous contraction & pain of the SC following laminectomy ( removal portion of lamina)
Nsg Mgt:
- Supportive mgt
1.) Administer Meds as ordered

a. ACTH ( adrenocorticotropic hormone) :
Acute exacerbation
– to reduce edema at the site of demyelination to prevent paralysis - compression of spinal nerves
b. Baclopen (Lioresol) or Dantrolene Na (Dantrene) : To muscle spasticity

c. Interferons – to alter immune response
d. Immunosuppressant
e. Diuretics
f. Bethanecol Chloride ( Urecholine) : N.M.
 Administer only SC
 Monitor S/E : wheezing, bronchospasm
 Monitor breath sounds 1 hr. after SC admin.
h. Anti-spasmodic (Prophanthelene Bromide) Pro-banthene & anti-cholinergic
2. Maintain side rails

3. Assist passive ROM exercises – promote proper body alignment
4. Prevent complications of immobility (q 2 hr. elderly q 1 hr.)
5. Encourage fluid intake & increase fiber diet – to prevent constipation
6. Provide catheterization d/t urinary retention
7. Avoid heat application
8.. Give diuretics
9. Increase fiber & provide acid-ash diet – to acidify urine & prevent bacteria multiplication
Ex. Grape, Plums, Cranberry, Orange juice, Prune juice, pineapple juice,Vit C
*3 Causes of UTI In Women
 Shorter Urethra F= 1-2.5 inches (3-5 cm.) M= 5-6-8 inches (16-20 cm)
 Poor Perineal Care
 Moist Vaginal Area
PART II: Compositions of Cord & Spinal cord

80% - brain mass
10% - CSF
10% - blood
1st: Brain mass
A. CEREBRUM– Largest Part - Connects Right & Left cerebral hemisphere

- Corpus collusum
Function: 1. Sensory
2. Motor
3. Integrative
Compose of 6 Lobes:
1.) Frontal (garbled speech)
a. Controls motor activity
b. Controls personality development
c. Where primitive reflexes are inhibited
d. Site of development of sense of Humor
e. Control higher cortical thinking
f. Brocca’s area – speech center
Damage - expressive aphasia
2.) Temporal –
a. Hearing
b. Short term memory
c. Wernicke's area – gen. interpretative
Damage – receptive aphasia
3.) Parietal lobe – appreciation & discrimination of sensory impulses

- Pain, touch, pressure, heat & cold
4.) Occipital – vision
5.) Insula/island of reil/ Central lobe- controls visceral fx

Function: - activities of internal organ
6.) Rhinencephalon/ Limbic

- Smell, libido, long-term memory *Anosmia- absence of smell
Basal Ganglia – areas of gray matter located deep within a cerebral hemisphere
 Extra pyramidal tract
 Releases dopamine- a neurotransmitter
 Controls gross voluntary unit
Dopamine :Parkinson’s or Huntington’s Dopamine : Schizophrenia

Acetylcholine :Myasthenia Gravis & Alzheimer’s Acetylcholine : Bipolar Disorder
B. MID BRAIN/ MESENCEPHALON

 relay station for sight & hearing
 Controls size & reaction of pupil ( Normal: 2 – 3 mm)
 Controls hearing acuity ( Normal Hearing Acuity : 30-40 decibels)
*PERRLA= Pupil dilated round & reactive to light & accommodation :Normal
* Isocoria – normal size (equal) *Anisocoria – uneven size – damage to mid brain
C. DIENCEPHALON -------between brain

2 Parts:
1.Thalamus – acts as a relay station for sensation
2. Hypothalamus – Thermo-regulating center of temp, sleep & wakefulness,
thirst, appetite/ satiety center
Controls some emotional responses like fear, anxiety
Controls pituitary function.
D. BRAIN STEM
a. PONS – Pneumotaxic center – controls rate & depth of respiration

Cranial 5 – 8 CNS
b. MEDULLA OBLONGATA- lowest portion of the brain

-controls heart rate, respiratory rate, swallowing, vomiting, hiccups/ singutus
-Vasomotor center
- Site of Spinal Decuissation Termination, CN 9, 10, 11, 12
E. CEREBELLUM – smallest part of the brain

- Controls posture, gait, balance, equilibrium
Cerebellar Tests:
a.) R – Romberg’s test- needs 2 RNs to assist
- Pt. in Normal anatomical position 5 – 10 min
(+) Romberg’s test is (+) ataxia or unsteady gait/drunken movement w/ loss of balance --seen in MS.
b.) Finger to nose test –
(+) To FTNT – seen in Dymetria – inability to stop a movement at a desired point
c.) Alternate pronation & supination
Palm up & down . (+) To alternate pronation & supination or damage to cerebellum
– seen in Dymetria
2nd: CerebroSpinal Fluid (CSF)

10% Blood
10% Compose of lipids
 Normal amount produced: 125-250 ml /day
 Produced at the Choroid Plexus
 Composition: Clear, colorless, odorless: (+) glucose, protein,WBC but not RBC
 Fx: cushions the brain
 Alters if there is obstruction in the flow of CSF = Increase ICP
Enlargement of the skull posteriorly d/t early closure of the posterior fontanel----Hydrocephalus
3rd: Blood
Stroke: partial/total obstruction in brain blood supply : 2 Commonly Affected artery:
1. ICA or Internal Carotid Artery
2. MCA or Middle Cerebral Artery
*Composition of brain - based on Monroe Kellie Hypothesis
o Skull is a closed container. Any alteration in 1 of 3 intracranial components = increase in ICP
*Normal ICP – 0 – 15 mmHg
Foramen Magnum = the hole in the skull where spinal cord enters
C1 – atlas : carrying the entire skull
C2 – axis ------------After C1 is the location of the medulla oblongata
Brain Herniation = when the medulla forced thru in the foramen : Observe for signs of ICP
(+) Projectile vomiting , irregular respiration & HR
Observe for 24 hrs. before MRI
DISORDER:
1. INCREASED ICP – increase IC bulk is due to increase in 1 of the IC components

A. Predisposing factors: 1.) Head injury
2.) Tumor
3.) Localized abscess
4.) Hemorrhage (stroke)
5.) Cerebral edema
6.) Hydrocephalus
7.) Inflammatory conditions - Meningitis, encephalitis
B. S&Sx
Earliest Sx:
a.) Change or decrease LOC – Restlessness to confusion (conscious, lethargy, stupor, coma)
- Disorientation to lethargy *conscious = awake
- Stupor to coma
Late Sx: a. Change in V/S : always a late sx
1. BP (systolic increase, diastole- same) Normal adult BP 120/80 : 40 (normal PP)
2. Widening pulse pressure Ex. Increase ICP = BP 140/80 = 140 – 80= 60 PP (wide)
3. RR : Cheyne-Stokes =rapid respiration w/ periods of apnea
4. Temperature increase
DIFFERENCE BET. SHOCK : & INCREASE ICP:

Decrease BP Increase BP
Increase HR Decrease HR CUSHING’S EFFECT
Increase RR Decrease RR
Decrease Temp Increase temp
Narrowing PP Widening PP
b.) Headache
c.) Projectile vomiting
d.) Papilledima (edema of optic disk – outer surface of retina)
e.) Abnormal Posturing
1. Decorticate = abnormal flexion of arms
= damage to cortico spinal tract
2. Decerebrate = abnormal extension of arms
= damage to upper brainstem, cerebrum, midbrain & pons
Except: Flaccid = loss of muscle tone, damage to the lower brain, medulla
f. Uncal herniation – unilateral dilation of pupil

g. Possible seizure
Nursing Management:
1.) Maintain patent a/w & adequate ventilation
a. Prevention of hypoxia =decrease tissue oxygenation & hypercarbia =increase in CO2 retention
Hypoxia – cerebral edema - increase ICP
Early Sx: R – restlessness Late Sx: B – bradycardia
A- agitation “RAT” E – extreme restlessness “BEDC”
T- tachycardia D – dyspnea
C – cyanosis =late
* Powerful respiratory stimulant : CO2 ---an CO2 retention/ hypercarbia ---stimulate medulla O.
stimulate lungs to Hyperventilate

2. Before & after suctioning, hyperventilate 100% - decrease CO2 – excrete CO2
Suctioning – 10-15 seconds, max 15 seconds
Ambu bag – pump upon inspiration
3. Assist in mechanical ventilation
4. Monitor VS & I&O, neuro check
5. Positioning -- Elevate head of bed 30- 45 degrees angle neck in neutral position
unless C/I to promote venous drainage
4. Limit fluid intake 1,200 – 1,500 ml/day
(FORCE FLUID means: Increase fluid intake/day – 2,000 – 3,000 ml/day)- not for inc ICP.
5. Prevent complications of immobility
6. Prevent increase ICP by:
a. Maintain quiet & comfy environment
b. Avoid use of restraints – lead to fractures
c. Maintain side rails up
d. Instruct patient to avoid activities leading to:Valsalva maneuver or bearing down
-Avoid straining of stool(give laxatives/ stool softener Dulcolax/ Duphalac)
- Excessive cough – antitussive (Dextrometorpham)
-Excessive vomiting – anti emetic (plasil)
- Avoid Lifting of heavy objects, Bending & stooping
- Avoid clustering of nursing activities
7. Administer meds as ordered:
1.) Osmotic diuretic – Mannitol/Osmitrol: promotes cerebral diuresis by
decompressing brain tissue
Nursing considerations: Mannitol
1. Monitor BP – S/E: hypotension
2. Monitor I&O every hr. report if < 30cc out put
3. Administer via side drip
4. Regulate fast drip – to prevent formation of crystals/precipitate
5. Inform client, will feel flushing sensation as drug is introduced
2.) Loop diuretic - Lasix (Furosemide) in ampule

Nursing Mgt: Lasix
Same as Mannitol except
- Lasix is given via IV push (expect urine after 10-15mins) should be in the
morning. If given at 7am. Pt will urinate at 7:15
Action of Lasix within 15 minutes. Max effect – 6 hrs due (7am – 1pm)
S/E of LASIX
1. Hypokalemia (Normal K-3.5 – 5.5 meg/L)
S&Sx : Compared to Hyperkalemia:
1. Weakness & fatigue 1. Irritability & Agitation
2. Constipation 2. Diarrhea, abdominal cramps
3. (+) “U” wave in ECG tracing 3. Peaked T-wave
both will lead to arrhythmia
Nursing Mgt: 1. Administer K supplements – ex. Kalium Durule, Oral Kcl
Potassium Rich food: ABC’s of K
Vegetables Fruits
A - asparagus A – apple
B – broccoli (highest) B – banana – green (highest)
C – carrots C – cantaloupe/ melon
O – orange (increase)
Vit A – squash, carrots yellow vegetables & fruits, spinach, chesa
Iron – raisins,
*Food appropriate for toddler – spaghetti! Not milk – increase bronchial secretions, no grapes – may choke
S/E of Lasix:
2. Hypocalcemia or Tetany: life-threatening (Normal level Ca = 8.5 – 11mg/100ml)
S&Sx : Weakness
Paresthesia
(+) Trousseau sign or carpo-pedal spasm – pathognomonic
(+) Chvostek’s sign
Complications: Arrhythmia
Laryngospasm
N. M. - Administer – Ca gluconate – IV slowly
Ca gluconate toxicity: Sx : seizure – administer Mg SO4
Mg SO4 toxicity– administer Ca gluconate : “BURP” B – BP decrease

U – urine output decrease
R – RR decrease
P – patellar reflexes absent
3. Hyponatremia (Normal Na level = 135 – 145 meg/L)

S/Sx: Hypotension
Signs of Dehydration
Early signs – thirst and agitation for adults --------------children: tachycardia, dry mucous m.
Mgt: force fluid 2-3 L/day
Administer isotonic fluid sol
4. Hyperglycemia – Increase blood sugar level

P – polyuria
P – polyphagia 3 P’s of Hyperglycemia
P – polydipsia
Nsg Mgt:
a. Monitor FBS (Normal =80 – 120 mg/dl)
*Lasix can be given to DM but strict FBS monitoring
5. Hyperurecemia – increase serum uric acid = by product of purine metabolism
Gouty arthritis kidney stones- renal colic (pain)

Cool moist skin
Sx joint pain & swelling ----great toe affected ----gouty arthritis
Nsg Mgt of Gouty Arthritis

a.) Cheese (not sardines, anchovies, organ meat) (Not good if pt taking MAO)
b.) Force fluid
c.) Administer meds – Allopurinol/ Zyloprim – inhibits synthesis of uric acid – drug of choice for gout:
Colchicene – acute gout drug of choice ---promotes excretion of uric acid
Kidney stones – renal colic (pain). Cool moist skin
Mgt:
1.) Force fluid
2.) Meds – narcotic analgesic
Morphine SO4
3.) Strain all urine using gauze pads
S/E of Morphine SO4 toxicity

Respiratory depression (check RR 1st)
Antidote for morphine SO4 toxicity –Narcan (NALOXONE)
Naloxone toxicity – tremors
Cont. Increase ICP meds
3.) Corticosteroids - Dexamethsone – decrease cerebral edema (Decadrone)

*Steroids best given: 2/3 dose am &
1/3 dose pm - to mimic normal diurnal rhythm
4.) Mild analgesic – codeine SO
5.) Anti consultants – Dilantin (Phenytoin)
Increase ICP what is the immediate nsg action?
Administer Mannitol as ordered
Elevate head 30 – 75 degrees
Restrict fluid
Avoid use of restraints *Nsg Priority – ABC & safety
Pt. suffering from epiglotitis. What is nsg priority?
a. Administer steroids – least priority
b. Assist in ET – temp, a/w
c. Assist in tracheotomy – permanent (Answer)
d. Apply warm moist pack? Least priority
Rationale: Wont need to pass larynx due to larynx is inflamed. ET can’t pass. Need tracheostomy only-
Magic 2’s of Drug Monitoring Toxicity Level: “DLADA”
Drug Normal Range Toxicity Classification Indication
D – digoxin .5 – 1.5 meq/L 2 Cardiac glycosides CHF

L - lithium .6 – 1.2 meq/L 2 Antimanic Bipolar Disorder
A – aminophylline 10 – 19 mg/100ml 20 Bronchodilator COPD
D – Dilantin 10 -19 mg/100 ml 20 Anticonvulsant Seizures
A – acetaminophen 10 – 30 mg/100ml 200 Narcotic analgesic Osteoarthritis
D- Digitalis (Digoxin) – increase cardiac contraction = increase CO Cardiac Glycosides
Nursing Mgt:
1. Check PR, HR (if HR below 60bpm, don’t giveDigoxin) Increase force of cardiac contraction
Digitalis toxicity – antidote - Digibind
a. Anorexia increase cardiac output
b. n/v GIT
c. Diarrhea
d. Confusion
e. Photophobia
f. Changes in color perception – yellow spots-----Xantopsia
L – lithium (lithane) decrease levels of norepinephrine, serotonin, and acetylcholine

Anti-manic agent
Lithium toxicity
S/Sx - a. Anorexia *N.M. 1. Force Fluid
b. n/s 2. Increase intake in diet 4-10g/d
c. Diarrhea
d. Dehydration – force fluid, maintain Na intake 4 – 10g daily
e. Hypothyroidism
f. Fine Tremors
CRETINISM– the only endocrine disorder that can lead to mental retardation
A – aminophyline (Theophylline) ---dilates the bronchial tree *Seizure= 1st attack
*Febrile seizure= normal 5 y/o
S/Sx : Aminophylline toxicity: * Epilepsy = succeeding attacks
1. Tachycardia
2. Hyperactivity – restlessness, agitation, tremors (CNS excitability)
N.M. ---Avoid giving food with Aminophylline
a.Cheese/butter– food rich in tyramine, avoided only if pt is given MAOI
b. Beer/ wine –
c. Hot chocolate & tea – caffeine – CNS stimulant tachycardia
d. Organ meat/ box cereals – anti parkinsonian
MAOI – antidepressant

m AR plan
n AR dilcan lead to CVA or hypertension crisis
p AR nate
3 – 4 weeks - before will take effect
Anti Parkinsonian agents – Vit B6 Pyridoxine reverses effect of Levodopa
D – dilatin (Phenytoin) – anti convulsant/seizure

Nursing Mgt:
1. Mixed with plain NSS or .9 NaCl to prevent formation of crystals or precipitate
o Do sandwich method
o Give NSS then Dilantin, then NSS!
2. Instruct the pt to avoid alcohol – bec. alcohol + dilantin can lead to severe CNS depression
Dilantin toxicity: “GHAN” *Osteoarthritis: Sign –Heberdens nodes
S/Sx:
G – gingival hyperplasia – swollen gums
i. Oral hygiene – soft toothbrush ii. Massage gums
H – hairy tongue
A - ataxia
N – nystagmus – abnormal movement of eyeballs
A – acetaminophen/ Tylenol – non-opoid analgesic & antipyretic – febrile pts
a. Acetaminophen toxicity :
1. Hepato toxicity : Monitor liver enzyme
SGPT (ALT) – Serum Glutamic Pyruvate Transaminase
SGOT- Serum Glutamic Oxaloacetic Transaminase
2. Monitor BUN (10 – 20)
*Creatinine (.8-1)most reliable, indicative for kidney clearance
b. Acetaminophen toxicity can lead to hypoglycemia:”TIRED”
T – tremors / Tachycardia
I – irritability
R – restlessness
E – extreme fatigue
D – depression
Diaphoresis/Nightmares
*Antidote for acetaminophen toxicity – Acetylcesteine ---- Prepare suctioning apparatus
Exercise: The following are symptoms of hypoglycemia except:

a. Nightmares b. Extreme thirst – hyperglycemia symptoms c. Weakness d. Diaphoresis
PARKINSONS DISEASE (Parkinsonism)
- Chronic, progressive disease of CNS characterized by degeneration of dopamine producing cells in

substancia nigra at mid brain & basal ganglia (produces dopamine)

Mngt: Palliative & Supportive Only
Predisposing Factors:
1. Poisoning (lead & carbon monoxide)
2. Hypoxia
3. Arteriosclerosis
4. Encephalitis
5. Drug Overdose
High doses of the ff:
a. Reserpine (serpasil)-----than only anti-HPN with S/E of depression -----suicidal
----- only HPN known to be link to breast cancer
----- promote safety
b. Methyldopa (aldomet)---Anti-HPN
c. Haloperidol (Haldol) - anti psychotic
d. Phenothiazine - anti psychotic
S/E of anti-psychotic drugs – Extra Pyramidal Symptom

Over medication of anti psychotic drugs
– neuroleptic malignant syndrome characterized by tremors (severe)
S/Sx: Parkinsonism:
1. Pill-rolling tremors of extremities – 1st Sign
2. Bradykinesia – slow movement-----2nd Sign
3. Over fatigue
4. Rigidity (cogwheel type) ------- a. Stooped posture
b. *Shuffling
c.Propulsive gait
5. Mask like facial expression with decrease blinking of the eyelids
6. Monotone speech
7. Difficulty rising from sitting position
8. Mood labilety – Depression– suicide Nsg priority: Promote safety
9. Increase salivation – drooling type
10. Autonomic signs:
 Increase sweating
 Increase lacrimation
 Seborrhea (increase sebaceous gland)
 Constipation
 Decrease sexual activity
Nsg. Mgt.
1.) Administer Meds:Anti-parkinsonian agents
- Levodopa (L-Dopa)-------short-acting
- Carbidopa (Sinemet), Amantadine Hcl (Symmetrel)----long-acting
Mechanism of action: Increase levels of dopa – relieving tremors & bradykinesia
S/E of anti-parkinsonian
 Anorexia
 n/v
 Confusion
 *Orthostatic hypotension
 Hallucination
 Arrhythmia, GIT irritation ( administer with meals)
Contraindication:
1. Pt. with glaucoma----because L-dopa intra-ocular pressure (N: 12-21 mmHg)

2. Pt. taking MAOI (Parnate, Marplan, Nardil)
MAOI = Monoamine Oxydase Inhibitor ( anti-depressant)
= Takes effect : 2-6 wks.
=If on MAOI avoid: Tyramine, tryptophan rich foods
ex. aged cheese, liver, beer, alcohol----leads to hypertensive crisis—stroke
Nsg. Mgt. when giving anti-parkinsonian
a. Take with meals – to decrease GIT irritation

b. Inform pt – urine/ stool may be darkened
c. *Instruct pt. not to take food Vit B6 (Pyridoxine) cereals, organ meats, green leafy veg
 Because Vit. B6 reverses therapeutic effects of levodopa
 Only increase intake of Vit. B6 in taking INH (isoniazid, anti-TB)
 Isonicotinic Acid Hydrazide-----effect-----peripheral neuritis
2.) Anti- cholinergic agents – relieves tremors

*Artane mechanism – inhibits acetylcholine
*Cogentin action ---S/E - SNS
3.) Antihistamine – Diphenhydramine Hcl (Benadryl) – take at bedtime---relieves tremors

S/E: adult– drowsiness – avoid driving & operating heavy equipment.
Child – Hyperactivity (CNS excitability)
4.) Dopamine agonist:

Bromocriptine Hcl (Parlodel)---relieves rigidity, bradykinesia
S/E: CNS depression, Check RR
Nsg. Mgt.
1.) Maintain siderails to prevent falls

2.) Prevent complications of immobility
- Turn pt every 2h
- Turn pt every 1 h – elderly
-Turn affected extremity every 30 minutes
3.) Assist in passive ROM exercises to prevent contractures
4.) Maintain good nutrition: Protein

CHON – in am
CHON – in pm – to induce sleep – d/t Tryptopan ex. milk
5.) Increase fluid in take, high fiber diet to prevent constipation
6.) Assist in surgery – Stereotaxic Thalamotomy

Common complications: a. Subarachnoid hemorrhage
b. Encephalitis
c. Aneurysm
7.) Assist in ambulation
MYASTHENIA GRAVIS (MG)

–A neuromuscular disorder characterized by a disturbance in transmission of impulses from
nerve to muscle cell at neuro muscular junction leading to descending muscle weakness.
 Common in Women, 20 – 40 y/o, Unknown cause or idiopathic
 Autoimmune – release of cholenesterase (enzyme that destroys acetylcholine)
Pathophysiology: Cholinesterase destroys ACTH
ACTH Descending muscle weakness M.G.
S/ Sx:
1.) Ptosis – drooping of upper lid ( initial sign)
Palpebral fissure – normal opening of upper & lower lids
2.) Diplopia (double vision)
3.) Mask-like facial expression
4.) Dysphagia
5.) Weakening of laryngeal muscles – hoarseness of voice
6.) *Respiratory muscle weakness – lead respiratory arrest. Prepare at bedside tracheostomy set
7.) Extreme muscle weakness during activity especially in the morning.
Priority: to watch out for: a. A/W
b. Aspiration
c. Physical immobility
Dx. Test:
1. Tensilon test (Edrophonium Hcl) – an anti-cholinesterase/cholinergic agent----short-acting only)
Administer to pt. for temporary relief for 5 – 10 mins. (+) for M.G.
2. CSF analysis- reveals cholinesterase
Nsg Mgt.
1. Maintain patent a/w & adequate ventilator by:
a.) Assist in mechanical ventilator – attach to ventilator
b.) Monitor pulmonary function test using spirometer
2. Monitor VS, I&O neuro check, muscle strength or motor grading scale (4/5, O/S, etc)
3. Siderails up
5. NGT feeding to prevent complications
6. Administer medication as ordered
a. Cholinergics or anticholinesterase agents
Mestinon (Pyridostinine) Action: Increases ACTH
Neostignine (prostigmin) S/E : PNS
b. Steroids, Corticosteroids – to suppress immune response
Decadron (dexamethasone)
Monitor for 2 types of Crisis:
Myastinic crisis Cholinergic crisis

Cause: 1. Under medication Cause: Over medication
2. Stress 3. Infection S/Sx - PNS
S&Sx: 1. Unable to see – Ptosis & diplopia Mgt.
2. Dysphagia Administer anti-cholinergic
3. Unable to breath 1. Atropine SO4
Mgt.: Administer cholinergic agents: Mestinon S/E: SNS – dry mouth
7. Assist in surgical procedure – Thymectomy (removal of thymus)
8. Assist in plasmapheresis – filtering of blood
9. Prevent complication – Respiratory arrest----prepare tracheostomy set at bedside
GBS – GUILLIAN BARRER SYNDROME
 A disorder of the CNS characterized by bilateral symmetrical polyneuritis leading to ascending

paralysis
 Polyneuritis ----- inflammation of the peripheral nerves
 Can leadto slow but complete recovery

1. Cause – unknown, idiopathic
2. Auto immune
3. *R/t antecedent viral infection (from LRTI)
4. Immunizations
S&Sx
1. Clumsiness -------- Initial sign of GBS

2. Ascending muscle weakness – lead to paralysis
3. Dysphagia
4. Decrease or diminished DTR (deep tendon reflexes) -----Paralysis
5. *Alternate HPN to hypotension – complication: Can lead to arrhythmia
6. Autonomic changes:
a. Increase sweating
b. Increase lacrimation
c. Increase salivation
d. Constipation
Dx:
Most important: CSF analysis thru lumbar puncture reveals increase in : IgG & CHON---same with MS
Nsg Mgt.
1. Maintain patent a/w & adequate vent

a. Assist in mechanical vent
b. Monitor pulmonary function test
2. Monitor vs., I&O neuro check, ECG tracing due to arrhythmia
3. Siderails
4. Prevent complicarions – immobility
5. Assist in passive ROM exercises
6. Institute NGT feeding
7. Administer medications as ordered:
1. Anti-cholinergic – Atropine SO4
2. Corticosteroids – to suppress immune response
3. Anti arrhythmic agents:
a.) Lidocaine /Xylocaine—S/E: confusion & agitation

b.) Bretyllium------blocks release of norepinephrine
c.) Quinidines/Quinitine – anti malarial agent & anti-arrythmic
> Toxic effect – Cinchonism
Quinidine toxicity: S/E – anorexia, n/v, headache, vertigo, visual disturbances
*Malaria ---king of tropical disease----antidote----Queen (Quinidine)

8. Assist in plasmapheresis
9. Prevent complications – a. Arrhythmias b. Respiratory arrest
INFLAMMATORY CONDITIONS OF THE BRAIN
Anatomy:
Meninges –a 3-fold membrane that covers the brain & spinal cord
Fx:
1. Protection & support
2. Nourishment
3. Blood supply
3 layers:
1. Duramater (outermost in bet. is sub dural space
2. Arachmoid matter (middle)
3. Pia matter (outermost) sub arachnoid space where CSF flows L3 & L4
1. MENINGITIS
– An inflammation of the meninges of the brain & spinal cord
Etiology: a. Meningococcus---most dangerous type

b. Pneumococcus
c. Hemophilous influenza – common to children
d. Streptococcus –a type of adult meningitis
MOT: Direct transmission via droplet nuclei (airborne)
S&Sx
 Stiff neck or Nuchal Rigidity ------Initial Sign of meningeal irritation
 Headache
 Projectile vomiting
 Photophobia
 Fever chills, anorexia
 General body malaise
 Weight loss
 Decorticate/decerebration – abnormal posture
 Possible seizure
 Opisthotonus (arching of the back)-----2nd intital sign
*Pathognomonic Sign: (+) Kernig’s & Brudzinski sign
Leg pain Neck pain
Dx:
1. Lumbar Puncture: lumbar/ spinal tap – use of hallow spinal needle
Aspiration in the sub arachnoid space between L3 & L4 or L4 & L5.
Nsg Mgt . For Lumbar Puncture------- invasive
1. Consent / explain procedure to pt

 RN – will explain if laboratory exams
 MD – will explain if operation procedure
2. Empty bladder, bowel – promote comfort
3. Arch back – to clearly visualize L3, L4
Nsg Mgt. Post Lumbar:
1. *Flat on bed – 12 – 24 h to prevent spinal headache & leak of CSF

2. Force fluid
3. Check punctured site for drainage, discoloration & leakage to tissue, discomfort
4. Assess for movement & sensation of extremities
Result:
1. CSF analysis: a. Increase CHON & WBC

b. Decrease glucose
Confirms Meningitis c. Increase CSF opening pressure (Normal: 50 – 160 mmHg)
d. (+) Culture microorganism
2. Complete blood count CBC – reveals increase WBC (Leukocytosis)

Mgt:
1. Adm meds
a.) Broad-spectrum antibiotic: Penicillin
S/E :
1. GIT irritation – take with food
2. Hepatotoxicity, nephrotoxcicity
3. Allergic reaction
4.* Super infection – alteration in normal bacterial flora
 Normal flora: throat – streptococcus

 Normal flora : intestine –E. Coli
Sx: of superinfection of penicillin Diarrhea
b.) Antipyretic
c.) Mild analgesic for headache
2. Strict respiratory isolation 24 hrs. after start of antibiotic therapy

3. Comfy & dark room – due to photophobia & seizure
5. Maintain F & E balance
6. Monitor VS, I&O , neuro check
7. Provide client health teaching & discharge plan
a. Nutrition – Increase CHON & CHO but Small freq feeding

b. *Prevent complication of Hydrocephalus & Nerve Deafness
8. Institute measures to prevent Increase ICP & seizures

9. Rehabilitation for residual deficit ( mental retardation & delayed psychomotor development)
Exercise: Where to bring 2 y/o post meningitis ?

 Audiologist due to damage to post repair myelomeningocele
 Urologist -Damage to sacral area – controls urination
REVIEW:
3 Types of ISOLATION: 1. Strict Isolation

2. Reverse Isolation
3. Enteric
Ex. Pt. with -Cushing’s syndrome – reverse isolation
-Aplastic anemia – reverse isolation------ bone marrow depletion----pancytopenia
-Cancer any type – reverse isolation
-Post-Liver transplant – reverse isolation
-Prolonged use steroids – reverse isolation
-Meningitis – strict isolation
-Asthma – not to be isolated
- Hepatitis A - Enteric
- Measles – Strict
- Mumps – Strict
- Pneumonia – Strict
- PTB -Strict
REVIEW:
*Thrombosis & Stroke leads to atherosclerosis
Initial sign: Headache

Late sign: Pruritus ------
* Anemia : Initial sign: Weakness & Fatifue
Blood:
Leukopenia WBC Leukocytosis
Anemia RBC Polycythemia
Thrombocytopenia Platelets Thrombocytosis
CEREBRO VASCULAR ACCIDENT :
Or Stroke, Brain Attack or Cerebral Thrombosis, Apoplexy
 A partial or complete disruption in the brains blood supply

 2 largest & common artery in stroke :
a. Middle cerebral artery
b. Internal carotid artery
 Common to male – 2 – 3x high risk, increases as you grow older
1. Thrombosis – clot (attached)-----------No. 1 cause of Stroke
2. Hemorrhage
3. Embolism – dislodged clot – pulmo embolism---2nd cause
S/Sx: Pulmonary Embolism

1. Sudden sharp chest pain
2. Unexplained dyspnea, SOB
3. Tachycardia, palpitations, diaphoresis & mild restlessness
S/Sx: Cerebral Embolism

1. Headache, disorientation, confusion & decrease in LOC----lead to coma
4. *Compartment Syndrome – compression of nerves/ arteries
Test Analysis:
*Femur Fracture
Fx. Complications:> Fat embolism – most feared complication w/in 24hrs
>Hemorrhage
*Yellow bone marrow – produces fat cells at medullary cavity of long bone
*Red bone marrow – provides WBC, platelets, RBC found at epiphysis
Risk factors of CVA:

a. HPN
b. DM
c. MI
d. Artherosclerosis
e. Valvular heart disease
f. Post cardiac surgery-----*Mitral valve replacement
g. Lifestyle:
1. Smoking – nicotine – potent vasoconstrictor

2. Sedentary lifestyle
3. Hyperlipidemia –genetic-genes that easily binds to cholesterol
h. Obesity ------20% of BW
Overweight -----10% of BW
i. Prolonged use of oral contraceptives
2 types: - Macro pill – has large amount of estrogen

- Mini pill – has large amount of progestin
Mini-pill---- Promote lipolysis – artherosclerosis – HPN – stroke
j. Type A personality
a. Deadline driven person

b. 2 – 5 things at the same time
c. Guilty when not dong anything
k. Diet – increase saturated fats -----ex. whole milk

l. Emotional & physical stress
S & Sx:
1. Transient Ischemic Attack ( TIA)- 1st sign of Impending stroke attacks

-
o Headache – initial sing of TIA
o Dizziness/ vertigo, numbness, tinnitus, visual & speech disturbances, paresis or phlegia (monoplegia – 1
extreme) (Paraplegia—lower extremeties)
o Increase ICP, *Temporary memory loss
2. Stroke in evolution – progression of S & Sx of stroke

3. Complete stroke – resolution of stroke
a.) Headache
b.) *Cheyne-Stokes Resp
c.) Anorexia, n/v
d.) Dysphagia
e.) Increase BP
f.) (+) Kernig’s & Brudzinski – Sx of Hemorrhage Stroke
g.) Focal & neurological deficit
1. Phlegia
2. Dysarthria – inability to vocalize
3. Aphasia
4. Agraphia – difficulty in writing
5. Alexia – difficulty in reading
6. Homonymous Hemianopsia – loss of half of field of vision
Left sided hemianopsia – approach Right side of pt – the unaffected side
Nsng. Dx. = Unilateral Neglect
Dx.
1. Computerized Tomography Scan – reveals brain lesion
2. Cerebral Arteriography – rveals site & extent of mal-occlusion
 Invasive procedure due to inject dye
 Allergy test
*All Dx ending in graphy/gram are invasive: injection of a dye, ask if allergic to seafoods
Post-CT Scan
1.) Force fluid – to excrete dye because it is nephrotoxic---check BUN & Creatinine
2.) Check peripheral pulse
3.) Check Fluid imbalance----dye is an osmotic diuretic
Nsg. Mgt.
1. Maintain patent a/w & adequate vent
- Assist mechanical ventilation
- Administer O2 inhalation
2. Restrict fluids – prevent cerebral edema
3. Instruct client to avoid valsalva maneuver
4. Monitor vs., I&O, neuro check
5. Prevent compl of immobility by:
a. Turn client q2h
Elderly q1h
- To prevent decubitus ulcer/ bed sores
- To prevent Hypostatic pneumonia –type of pneumonia r/t long immobility
b. Egg crate mattress or H2O bed
c. Sand bag or foot board- prevent foot drop
6. NGT feeding – if pt can’t swallow
7. *Passive ROM exercise q4h to prevent contractures & to promote proper body alignment
8. Alternative means of communication

- Use Non-verbal cues
- Magic slate
- (+) To hemianopsia – approach on unaffected side
9. Position pt.: elevate heat 30 degrees angle/ semi-fowlers

10. Maintain siderails
11.Meds
a. Osmotic diuretics – Mannitol ( Osmitrol) ---Side-drip—fast drip ----S/E: decrease BP
b. Loop diuretics – Lasix/ Furosemide-----IV push
3. Corticosteroids – Dextamethazone (ends in one)
4. Mild analgesic------codeine Sulfate-------S/E: Respiratory Depression
5. Thrombolytic/ fibrolitic agents – tunaw clot
Ex. Streptokinase-----S/E: Allergic Reaction

Urokinase---------S/E: Hypertension
Tissue Plasminogen Activating Factor ( TPAF)----S/E: Chest Pain
*Monitor bleeding time

6. Anti-coagulants – Heparin & Coumadin----” sabay”
Why : Coumadin will take effect after 3 days---long-acting
Anti-Coagulants
Heparin Coumadin or Warfarin

(Short-Acting) (Long-Acting)
Monitor: PTT (Partial Thromboplastin Time) PT (Prothrombin Time)
If prolonged, indicates bleeding if prolonged, indicates bleeding
Antidote: Protamine Sulfate Vitamin K (Aquamephyton)
7. Anti-platelet (PASA) – aspirin paraanemo aspirin

-the only NSAID that has anti-platelet property
- Do not give to pts. With Dengue, Ulcer & Headache
- Aspirin----- No. 1 ulceronegenic agent
S/E: Tinnitus, Anemia, Heartburn & Dyspepsia
*EPISTAXIS/ nose bleeding--- parameter that indicates effectiveness of thrombolytic therapy
Health Teachings:
1. Avoidance of modifiable lifestyle

- Diet, smoking
2. Dietary modification
- Avoid caffeine, decrease Na & decrease saturated fats
3. Prevent Complications:
*Subarachnoid hemorrhage
4. Rehab for focal neurological deficit
1. Mental retardation
2. Delay in psychomotor development
CONVULSIVE Disorder (CONVULSIONS)
o A disorder of the CNS characterized by paroxysmal seizures with or w/o loss of consciousness,
abnormal motor activity, alteration in sensation & perception & changes in behavior.
Exercise: Can you outgrow febrile seizure?

Febrile seizure Normal if < 5 y/o
Pathologic if > 5 y/o
Predisposing Factor:
a. Head injury d/t birth trauma------ No .1 cause of convulsions
b. Toxicity of carbon monoxide

c. Brain tumor
d. Genetics
e. Nutritional & metabolic deficit
f. Physical stress
g. Sudden withdrawal to anticonvulsants-----No .1 of status epilepticus
Status epilepticus – Drug of Choice: Diazepam & glucos
S & Sx. Of Epilepsy dependent upon stages:
I. Generalized Seizure –
1.) Grand mal / tonic clonic seizures-----most common type of seizure

- With or w/o Aura – warning symptoms of impending seizure attack
Epigastric pain ---1st sign of aura
This is associated with olfactory, tactile, visual, auditory sensory experience

 Epileptic cry – fall
 *Loss of consciousness 3 – 5 minutes
 Tonic-clonic contractions
Tonic - Direct symmetrical extension of extremities
Clonic - contractions
 Post ictal (state of lethargy or drowsiness) sleep- unresponding sleep after tonic clonic
2.) Petit mal seizure – (same as daydreaming!)

- Blank stare
- Decrease blinking eye
- Twitching of mouth
- *Loss of consciousness – 5 – 10 seconds (quick & short)
- *Common to children
II. Localized/partial seizure
1. Jacksonian seizure or Focal seizure

– tingling/jerky movement of index finger/thumb &
spreads to shoulder & 1 side of the body with janksonian march
2. Psychomotor/ Focal-motorseizure
-*Automatism – stereotype repetitive & non-purposive behavior

- Clouding of consciousness – not in contact with environment
- Mild hallucinatory sensory experience
3 Types of HALLUCINATION:
1. Auditory – schitzophrenia – paranoid type

2. Visual – Korsakoffs psychosis – chronic alcoholism
3. Tactile – addict – substance abuse
III. Status Epilecticus
– Continuous, uninterrupted seizure activity leading to hyperpyrexia – coma – death

Drug of Choice : Diazepam & Glucose
Pathophysiology: Status Epilepticus
Increase electrical firing in the brain: if left untreated
Increase Heat production -------hyperpyrexia
Increase metabolism using glucose & O2 ------need for glucose therapy

Coma------Death
Dx: For All Types:
1. CT scan – revealsbrain lesion

2. EEG electroencephalography --revealsHyperactivity brain waves
3. ECT therapy
Nsg. Mgt.
Priority – Airway & Safety *If with seizure: S/E is PNS
1. Maintain patent a/w & promote safety Before seizure:

1. Remove blunt/sharp objects
2. Loosen clothing of pt.
3. Avoid restraints----can lead to fracture
5. Turn head to side to prevent aspiration
6. Tongue guard or mouth piece to prevent biting of tongue (emergency—clean piece of cloth)
7. Avoid precipitating stimulus – bright glaring lights & noises, drafts
8. Administer meds
a. Dilantin (Phenytoin) –( toxicity level – 20 )
S/E: Gingival hyperplasia
H-hairy tongue
A-ataxia
N-nystagmus
b. Acetaminophen- febrile pt
Mix only with NSS, sandwich method
- Don’t give alcohol – lead to CNS depression
c. (Tegretol) Carbamazepine
d. Phenobarbital (Luminal) -------common S/E: hallucination & mild arrythmia
e. Diazepam
2. Institute seizure & safety precaution

By Post seizure: Administer O2 inhalation. Suction apparatus ready at bedside
3. Monitor onset & duration of

- Type of seizure
- Duration of post ictal sleep----the longer the duration, the danger of status epilepticus
4. Assist in surgical procedure

- Cortical resection
Exercise: 1 y/o grand mal – immediate nursing action = a/w & safety
a. Mouthpiece – 1 yr old – little teeth only
b. Adm o2 inhalation – post!
c. Give pillow – safety
d. Prepare suction
Neurological Assessment:
4 Objectives of Neurological Assessment:

1. To know the exact neurological deficit
2. To localized lesion
3. For rehabilitation
4. Guidance in nursing care
2 Types of N.A.
1. Glasgow Coma Scale (GCS)– objective measurement of LOC or quick neuro check
3 components of ECS (“MVE”)
M – motor 6
V – verbal response 5
E – eye opening 4
15---- highest score
Scaling:
15 – 14 – Conscious
13 – 11 – Lethargy
10 – 8 – Stupor
7 – Coma
3 – Deep coma – lowest score ( no 0 score on any response, lowest is only 1)
2. Comprehensive Neuro Exam
A. Survey of Mental status & speech (Comprehensice Neuro Exam)

1.) LOC & Test of memory
2.) Levels of orientation
3.) Cranial Nerve assessment
4.) Motor assessment
5.) Sensory assessment
6.) Cerebral test – Romhberg, finger to nose
7.) DTR
8.) Autonomics
1. a. Levels of consciousness (LOC)

1. Conscious (conscious) – awake – levels of wakefulness
2. Lethargy (lethargic) – drowsy, sleepy, obtunded
3. Stupor (stuporous) – awakened by vigorous stimulation
Pt. has general body weakness, decrease bodily reflex
4. Coma (Comatose) Light – (+) all forms of painful stimulations
Deep – (-) to painful stimulation
*Watch out for the rise & fall of the chest
b. Different types of pain stimulation

o Don’t prick
1. Deep sternal pressure/stimulation: 3x– fist knuckle
With response – light coma
Without response – deep coma
2. Pressure on great toe – 3x
3. Orbital pressure – pressure on orbits only – below eye
4. Corneal reflex/ blinking reflex
*Wisp of cotton – used to illicit blinking reflex among conscious patients
*Instill 1-drop saline solution – unconscious pt if (-) response pt is in deep coma
c. Test of memory – consider educational background
a. Short term memory –
 What did you eat for breakfast?
Damage to temporal lobe – (+) antero grade amnesia
b. Long term memory
(+) Retrograde amnesia – damage to limbic system (rhinencephalon)
2. Levels of orientation:
1st: Time 2nd:: Person 3rd: Place
Exercise: Describe a conscious pt ?

a. Alert – not all pt are alert & oriented to time & place
b. Coherent
c. Awake
d. Aware
3. Cranial Nerve Assessment: 12 pairs of cranial nerves
I– Olfactory Old s Some

II – Optic Opie s Say
III – Oculomotor Occasionaly m Marry
IV – Trocheal Tries m smallest CN Money
V– Trigeminal Trigonometry b largest CN But

VI – Abducens And m My
VII – Facial Feels b Brother
VIII – Acoustic/auditory (V) Very s Says
IX – Glossopharyngeal Gloomy b Bad
X– Vagus Vague b longest CN Business
XI– Spinal accessory And m Marry
XII – Hypoglossal Hypoactive m Money
I. Olfactory – don’t use ammonia, alcohol, cologne irritating to mucosa – use coffee granules, vinegar
* Hyposmia – decrease sensitivity to smell
*Diposmia – distorted sense of smell
*Anosmia – absence of sense of smell
*Either of 3 might indicate head injury – damage to cribriform plate of ethmoid bone where olfactory cells are
located or indicate inflammation condition – sinusitis
II Optic (Sensory or Vision)
1. Test of visual acuity or central or distance vision (test of near vision)

Use Snellens Chart:
a. Snellen’s Alphabet -----used for literate client

b. Snellen’s E chart --------used for illiterate
c. Animal Chart -----used for children
Normal: 20/20 vision

20 numerator is constant: 20 ft (6-7 m) distance from the chart
20 denomenator ---vision distance the person can see the letters
OD – Rt eye 20/20 =20/200 – blindness – can’t read E – biggest
OS – left eye 20/20
OU – both eye 20/20
2. Test of Peripheral Vision/ visual field: facing the client
a. Superiorily
b. Bitemporally
c. Inferiorly
d. Nasally
Common Disorders
1. Glaucoma – (Normal 12 – 21 mmHg intra-ocular pressure)

- Increase IOP - Loss of peripheral vision – “tunnel vision”
2. Cataract – opacity of lens - Loss of central vision, “Blurring or hazy vision”
3. Retinal detachment – curtain veil – like vision & floaters
4. Macular degeneration – black spots
III Oculomotor, IV (Throclear), VI (Abducens)
– Tested simultaneously because it controls or innervates the movement of extrinsic ocular muscle
*6 Cardinal Gaze Extrinsic Ocular Movement
Rt eye N left eye

IO SO O
S
LR MR E
SR
Throclear – controls superior oblique (1)

Abducens - lateral rectus (1)
9. Oculomotor- controls the size & response of pupil (Pupil size 2 -3 cm or 1.5 – 2 mm)
- controls opening of the eyelids
- controls the 4 gaze
V – Trigeminal
– Largest nerve – consists of - ophthalmic, maxillary & mandibular branch

1. Sensory – controls sensation of the face, mucus membrane; teeth & corneal reflex
Unconscious – instill drop of saline solution
2. Motor – controls muscles of chewing/ muscles of mastication
*Trigeminal neuralgia – difficulty in chewing & swallowing

- damage to the trigeminal nerve
- Drug of Choice: Tegritol
-Extreme food temperatire is not recommended
-Avoid hot or cold preparation
Exercise: Trigeminal neuralgia, RN should give

a. Hot milk, butter, raisins
b. Cereals
c. Gelatin, toast, potato – all correct but
d. Potato, salad, gelatin – salad easier to chew
VI Facial:
a. Sensory – controls taste – anterior 2/3 of tongue: Test cotton applicator with sugar.
-Put applicator with sugar to tip to tongue.
-Start of taste insensitivity: Age group – 40 yrs old
b. Motor- controls muscles of facial expression, smile frown, raise eyebrow

if Damage causes --------Bells palsy or facial paralysis
Cause of Bells palsy in children---No 1 cause : R/T forcep delivery
Temporary only, resolve w/in 4-6 months
*Most evident clinical sign of facial symmetry: Nasolabial folds
VIII Acoustic/ Vestibulocochlear
a. Cochlear ----controls hearing
b. Vestibule-----controls balance (kinesthesia /position sense)

-----Movement & orientation of body in space
------located in the inner ear—if it moves—the head moves too--kinesthesia
*Meniere’s Disease----only disease of the inner ear----loss of balance---Nsg. Priority: Safety
Parts of Ears:
Outer – tympanic membrane, pinna, oricle (impacted cerumen), cerumen
Middle – hammer, anvil, stirrup or melleus, incus, staples. Mid otitis media
 Eustachean ear
Inner ear- meniere ear, sensory hearing loss
Remove vestibule – meniere’s dse – disease inner ear
*Archimedes law --Bouyancy
*Daltons law – Partial pressure of gases (Diffusion)
*Inertia – law of motion (dizziness, vertigo)
Exercise:
1.) Pt. with multiple stab wound in the chest
- Movement of air in & out of lungs is carried by what principle?
- Diffusion – Dalton’s law
2.) Pregnant – check up – ultrasound reveals fetus is carried by amniotic fluid
- Archimedes
3.) Severe vertigo d/t Inertia
Test for acoustic nerve: ---------Repeat words uttered
IX – Glossopharyngeal – controls taste – the posterior portion 1/3 of the tongue
X – Vagus – controls gag reflex
Test 9 – 10
Pt say ah – check uvula (in the middle tonsils) – should be midline
If there is deviation from L to R ----Damage to cerebral hemisphere
Gag reflex – place tongue depression post part of tongue
 Don’t touch uvula
 Gag reflex----vagal stimulation -----PNS Effect
XI – Spinal Accessory - controls sternocleidomastoid (neck) & trapezius

 Shrug shoulders, put pressure. Pt should resist pressure. Paresis or phlegia
XII – Hypoglossal - movement of tongue – say “ah”

If L or R deviation-----damage to the cerebral hemisphere
- Push tongue against cheek. Normal= tongue in midline,
if (-) disorder called ------- Short frenulum lingue –or tongue tied – “bulol”
EYES
A. External Parts:
1. Orbital cavity – made up of connective tissue, protects eye from trauma.
2. EOM (Extrinsic Ocular Muscles ) – involuntary muscles of eye, needed for gazing movement.
3. Eyelashes/ eyebrows – aesthetic purposes
4. Eyelids – palpebral fissure – opening upper & lower lid. Protects eye from direct sunlight
Meibomean gland – secrets a lubricating fluid inside eyelid

a.) Stye/ sty or Hordeolum- inflamed Meibomean gland
5. Conjunctiva
6. Lacrimal apparatus – tears
B. Intrinsic Coat
I. Sclerotic coat – outer most

a.) Sclera – white. Occupies ¾ posterior of eye. Refracts light rays
b.) Canal of sclera – site of aqueous humor drainage
c.) Cornea – transparent structure of eye
II. Uveal Tract – provides nutritive care

Uveitis – inflammation of the uveal tract
Consist of:
a.) Iris – colored muscular ring of the eye
2 Muscles of Iris:
1. Circular smooth muscle fiber - Constricts the pupil
2.radial smooth muscle fiber - Dilates the pupil
2 Chambers of the Eye:
1. Anterior
a.) Vitereous Humor – maintains spherical shape of the eye
b.) Aqueous Humor – maintains intrinsic ocular pressure
(Normal IOP= 12-21 mmHg)
II. Retina (innermost layer)

a. Optic discs or blind spot – nerve fibers only
No auto receptors
Cones (daylight/ colored vision) Rods – night, twilight vision
Phototopic vision “Scotopic vision” = Vit. A deficiency – rods insufficient
b. Maculla lutea – yellow spot center of retina

c. Fovea centralis – area with highest visual acuity oracute vision
Physiology of Vision:
4 Physiological Processes for Vision to occur:
1. Refraction of light rays – bending of light rays
2. Accommodation of lens
3. Constriction & dilation of pupils
4. Convergence of eyes
*Unit of measurements of refraction – Diopters

*Normal eye refraction – Emmetropia
*PERRLA ---Normal Reaction
ERROR of Refraction:
1. Myopia - near sightedness – Tx: biconcave lens

2. Hyperopia - farsightedness – Tx: biconvex lens
3. Astigmatisim -distorted vision – Tx: cylindrical
4. Presbyopia - “old slight” – inelasticity of lens d/t aging – Tx: bifocal lens or double vista
*Accommodation of lenses – based on Thelmholtz Theory of accommodation
Near vision: Far vision:

-Ciliary muscle contracts - Ciliary muscle dilates / relaxes
-Lens bulges -Lens is flat
Convergence of the Eye:
Error:
1. Exotropia – 1 eye normal
2. Esophoria – corrected by corrective eye surgery
3. Strabismus- squint eye
4. Amblyopia – prolong squinting

1. GLAUCOMA
–An increase Intra Ocular Pressure – if untreated, atrophy of optic nerve disc – blindness
- Preventable but not curable
1. High risk group – 40 y/o & above
2. HPN
3. Hereditary
4. Obesity
5. Recent eye surgery, trauma, inflammation
Type:
1. Chronic -------- (open angle G.) – *most common type
Obstruct in flow of aqueous humor at trabecular meshwork of canal of schlema
2. Acute --------- (close angle G.) – *Most dangerous type
Forward displacement of iris to cornea leading to blindness.
3. Chronic--------- (closed – angle) - Precipitated by acute attack
S/Sx:
1. *Loss of Peripheral Vision – a Tunnel-like vision
2. *Halos/Rainbows around lights
3. Headache & Dizziness
4. n/v
5. Steamy cornea
6. Eye discomfort
7. *Ocular Pain
7. If untreated – gradual loss of central vision – blindness
Diagnosis:
1. *Tonometry –reveals increase IOP >12- 21 mmHg
2. Perimetry – reveals decrease peripheral visual field
3. *Gonioscopy – reveals abstruction in anterior chamber
Nursing mgt:
1. Enforce CBR
3. Administer meds
a.) *Miotics – lifetime ------ contracts ciliary muscles & constricts pupil.
Ex. Pilocarpine Na (Carbachol)
b.) Epinephrine eye drops ------decrease formation & production of aqaueous humor
c.) Carbonic anhydrase inhibitors. ----- Promotes increase out flow of aquaeous humor(drainage)
Ex. Acetazolamide (Diamox)
d.) Timoptics (Timolol maleate)- Increase outflow of aquaous humor (drainage)

2. Surgery:
Invasive:
a.) Trabeculectomy --- eye-trephining
– removal of trabelar meshwork of canal or schlera to drain aqueous humor
b.) *Peripheral Iridectomy – portion of iris is excised to drain aqueous humor
Non-invasive:
a. Trabeculotomy (eye laser surgery)
Nursing Mgt.: Pre –operative for all types of surgery:

1. Apply eye patch on unaffected eye to force weaker eye to become stronger.
Nursing Mgt. Post-operative – all types of surgery

1. Position unaffected/ unoperated side - to prevent tension on suture line.
2. Avoid valsalva maneuver
3. Monitor symptoms of IOP
a.) Headache
b.) n/v
c.) Eye discomfort
d.) Tachycardia
2. Eye patch – for both eyes – post-operatively
2. CATARACT
–A partial/ complete opacity of lens, can lead to blindness
1. Aging : 90-95% (degenerative/ senile cataract)---60 y/o & above
2. Congenital (very rare)
3. Prolonged exposure to UV rays
4. DM
S/Sx:
1. *Loss of Central Vision - “Hazy or blurring of vision”
2. Painless
3. Milky white appearance at center of pupil
4. *Decrease perception of colors *Elderly can only see Red & Green
Dx:
1. Opthalmoscopic exam – reveals (+) opacity of lens
Nsg Mgt:
1. Reorient pt. to environment – due opacity
2. Siderails
3. Medications a.) *Mydriatics – dilate pupil – not lifetime Ex. Mydriacyl
b. ) Cycloplegics – paralyzes ciliary muscle. Ex. Cyclogyl
c.) Atrophine
4. Surgery
a. E – extra
C - capsular
C – cataract Partial removal of lens
L - lens
E – extraction
b. I - intra
C - capsular
C – cataract Total removal of lens & surrounding capsules
L - lens
E – extraction
Complications of Lens Extraction: Hemorrhage

Retinal Detachment
Endopthalmitis
Nursing Mgt:
1.Position unaffected/ unoperated side - to prevent tension on suture line.
2.Avoid valsalva maneuver
3.Monitor symptoms of IOP
a.) Headache
b.) n/v
c.) Eye discomfort
d.) Tachycardia
4.Eye patch – both eyes - post op
3. RETINAL DETACHMENT
- The separation of 2 layers of retina, can lead to blindness
Predisposing factors:
1. *Severe myopia – near sightedness
2. Diabetic Retinopathy
3. Trauma
4. *Following lens extraction
5. HPN
S/Sx:
1. *“Curtain –veil” like vision
2. Flashes of lights
3. *Floaters d/t seepage of blood (Photopsia)
4. Gradual decrease in central vision

Dx: Opthaloscopic exam
Drug of Choice: Cycloplegics
Nursing Mgt:
1. Siderails (all visual disease)
2. Surgery:
a.) Cryosurgery (cold application)
b.) *Scleral buckling
c.) Diathermy ------heat application
4. MACULAR DEGENERATION
-----the appearance of black spots in the eyes

PATHOGNOMONIC SIGNS
Addison’s Disease Bronze-Like Skin
Angina Pectoris Levine’s Sign
Appendicitis Rebound Tenderness
Asthma Wheezing On Expiration

Bulimia Nervosa Chipmunk Face
Cataract (loss of central vision) Hazy Vision
Cholecyctitis (+) Murphy’s Sign
Cholera Rice-Watery Stool
Cushing’s Disease Moon Face Appearance
Dengue Petechiae
Diptheria Pseudomembrane
Down Syndrome Protrusion Of Tongue
Down Syndrome Simean Creases on Palms
Emphysema Barrel Chest
Glaucoma (peripheral vision) Tunnel-like Vision
Grave’s Disease (Hyperthyroidism) Exopthalmus
Hepatitis Jaundice
Hyperpituitarism ( Acromegaly) Carotenemia ( yellowish skin)
Kawasaki Disease Strawberry Tongue
Leprosy Leioning Face
Liver Cirrhosis Spider Angioma
Malaria Chills
Measles Koplik’s spot
Meningitis (+) Kernig’s & Brudzinski’s Sign
Myasthenia Gravis Ptosis
Pancreatitis( Ectopic Pregnancy) (+) Cullen’s Sign (ecchymosis of umbilicus)

(+) Grey-Turner’s (ecchymosis of flank)
Parkinson’s Disease Pill-Rolling Tremors
Patent ductus Arteriosus Machine-like Murmur
Pernicious Anemia Beefy Red Tongue
Pneumonia Rusty Sputum

PTB Low-Grade Fever
Pyloric Stenosis Olive Shape Mass
Retinal Detachment Curtain Veil-Like Vision

Systemic Lupus Erythematosus Butterfly rash
Tetanus Risus Sardonicus
Tetany (+) Trousseau & (+) Chvostek Sign
Tetralogy Of Fallot Clubbing of Fingers
Thombophlebitis (+) Homan’s Sign
Typhoid Fever Rose Spots in Abdomen
RELATED DISORDERS:
1. COPD = # 1 cause: Smoking ----- 4 Types: ---- all needs bronchodilators

BRONCHITIS ASTHMA BRONCHOIECTASIS EMPHYSEMA
Blue bloaters Wheezing on Expiration Hemoptysis Barrel Chest
Dyspnea on Exertion Cause by allergens Undergo Pneumonectomy Pink Puffers
Lead to cor pulmonale Hereditary Bronchoscopy Dyspnea at Rest
Reversible Lead to Cor Pulmonale
Cause by Allergens
Hereditary
CO2 narcosis
Purse Lip Breathing
Irreversible
Terminal Stage
To Prevent STD Local – practice monogamous relationship

CGFNS/NCLEX – condom
ENDOCRINE SYSTEM

The endocrine system integrates body functions by the synthesis & release of hormones.
Hypothalamus: link between the nervous system & the endocrine system.
ENDOCRINE GLANDS:
– Secrete their products directly into the bloodstream

– Different from exocrine glands
– Exocrine glands: secrete through ducts unto epithelial surfaces or into the GIT
Parts:
• Pituitary Gland
• Adrenal Glands
• Pancreas
• Thyroid Glands
• Parathyroid Glands
• Gonads
HORMONES:
- Are chemical substances that are secreted by the endocrine glands.

- Can travel moderate to long distances or very short distances.
- Acts only on cells or tissues that have receptors for the specific hormone.
- Target Organ: The cell or tissue that responds to a particular hormone
- Regulation of Hormones: Negative Feedback Mechanism
• When the hormone concentration rises, further production of that hormone is inhibited.
• When the hormone concentration falls, the rate of production of that hormone increases.
2 BASIC PATHOPHYSIOLOGICAL DISORDER OF THE ENDOCRINE
A. Hyposecretion/ Hypoactivity B. Hypersecretion / Hyperactivity
D/T D/T
1. Congenital absence of glands 1. Tumor w/n or outside the gland
Ex. No pancreas Ex. Tumor in adrenal gland
2. Surgical removal of glands

Ex. Total Thyroidectomy
Primary” Disease  Problem in target gland; autonomous “Secondary” disease  problem outside the target gland;
Most often d/t a problem in pituitary gland
Parts:
I. PINEAL GLAND
Function: Secretes Melatonin

– Inhibits leutenizing hormone (LH) secretion
– Regulates body clock, sleeping pattern or circadian rhythm
II. PITUITARY GLAND (Hypophysis Cerebri)

The main gland located at base of the brain at Sella Turcica

Fx: Master gland of body/ Master clock of body---it controls all the metabolic activity of the body
2 Divisions:
Anterior Pituitary Gland – Adenohypophysis Posterior Pituitary Gland – Neurohypophysis
A. ANTERIOR PITUITARY GLAND
Function:
1. Responsible for Growth Hormone (GH) (Somatotropic Hormone)

Function: For elongation of long bones
*Puberty age: 9 y/o – 21 y/o & the Epiphysial plate closes at 21 y/o
GHh
DISORDER: Hypopituitarism Hyperpituitarism
*Dwarfism -- Children Acromegaly -- Adult
1. Frohlick’s Syndrome 1. Gigantism

-Dwarf w/ obesity - If s/s appear before closure of epiphyseal plate
- Mentally retarded - rapid growth of long bones
- Loss of reproductive ability d/t genital atrophy
2. Simmond’s Disorder/ Pituitary Cachexia 2. Acromegaly

- Appearance of a “wizened old man” - If s/s appear after closure of epiphyseal plate
- Premature senility, Skin dry & wrinkled - Hyperthrophy of soft tissue & bone thickness
- Mental retardation - Disproportional growth
- Male: Absence of spermatogenesis
- Female: Amenorrhea Enlargement of cartilage ( nose & ears)
Enlargement of larynx (deep voice)
Progmatism: Protrusion of jaw
Dx: Square face & jaw
- X-ray, MRI or CT scan: pituitary tumor Macroglossia  Obstructive Sleep Apnea
- Plasma hormone levels: decreased
Tx:
Drug of Choice in acromegaly:
Octreotide (Sandostatin) --S/E: Seizure & GIT irritation
Somatostatin Hormone - antagonizes the release of GH
2. Melanocytes Stimulating Hormone (MSH)

Function: For skin pigmentation
DISORDER:
*Albinism ---hyposecretion of MSH *Vitiligo -----hypersecretion of MSH

----prone to develop skin cancer & blindness
3. Prolactin/ Lactogenic Hormone

 Initiates milk let-down reflex with help of oxytocin
 Promotes development of mammary gland/breast tissue
Disorder: Prolactin Deficiency : Failure to lactate
4. Adrenocorticotropic Hormone – ACTH

 Development & maturation of adrenal cortex
S & Sx in Deficiency:
- Results in diminished cortisol secretion.
- Weakness, fatigue, weight loss, and hypotension.
5. LH -----Progesterone
6. FSH----Estrogen
B. POSTERIOR PITUITARY GLAND: secretes----
1.) Oxytocin
a. Promotes uterine contractions-----preventing bleeding/ hemorrhage.
- Best time to administer Oxytocin: after placental delivery to prevent uterine atony.
b. Initiates the Milk let-down reflex with help of prolactin.
2.) Anti-Diuretic Hormones (ADH) /ADH-replacement ---Vasopressin or Pitressin

Function: Prevents urination – conserve H2O
Regulates water metabolism
Released during stress or in response to an increase in plasma osmolality to stimulate
reabsorption of water & decreased urine output
DISORDERS OF THE POSTERIOR PITUARY GLAND
1. DIABETIS INSIPIDUS (DI)

– The hyposecretion of ADH
• Disorder w/ massive polyuria d/t either lack of ADH or kidney’s insensitivity to it
Cause: Idiopathic/ unknown

Predisposing factor: “PITT”
1. Pituitary surgery
2. Inflammation
3. Trauma
4. Tumor
Pathophysiology: Diabetes Insipidus
Disorder of H20 metabolism
ADH * Alcohol inhibits release of ADH
Prevents renal tubules from reabsorbing H20
S &Sx: POLYURIA (excessive urine output 5-29 L/24 hrs.)
Polydipsia F & E imbalance Diluted Urine Urine Specific gravity Dehydration
Other S & Sx:

2. Sx of Dehydration: Excessive thirst, Agitation, Poor skin turgor, Dry mucus membrane
3. Weakness & Fatigue
4. Hypotension – if left untreated
5. Hypovolemic shock *Anuria – Late sign hypovolemic shock
6. Weight loss
Dx:
1. Decrease urine specific gravity- concentrated urine (N = 1.015 – 1.035)
2. Serum Na = Increase d/t compensation to attract more H2o (N =135 -145 meq/L)
Mgt:
1. Force fluid 2,000 – 3,000ml/day
2. Administer IV fluid replacement as ordered ( Isotonic fluid solution)
3. Monitor VS, I&O
4. Administer meds as ordered (Commercially-Prepared ADH)
a. Pitressin Tannate Oily preparation: Give deep I.M.
b. Vasopressin Tannate May cause lipodystrophy , rotate site of administration
Will cause vasoconstriction--Monitor BP before & after

c. Desmopressin Acetate Given by Nasal Spray
d. Lypressin
5. Prevent complications: Most feared complication – Hypovolemic shock
2. SYNDROME OF INAPPROPRIATE ANTI-DIURETIC HORMONE (SIADH)
- An increase production of ADH or Hypersecretion of ADH

- Idiopathic/ unknown
1. Head injury
2. R/T Bronchogenic cancer or lung cancer-
Early Sign of Lung Ca : Cough – productive, non productive
3. Hyperplasia of Pituitary gland

4. Increase size of organ d/t increase # of cells
S&Sx
1. Fluid Retention
2. Increase BP – HPN
3. Edema
4. Wt gain
5. Danger of Water Intoxication (The only Endocrine Gland with Water Intoxication)
Cerebral Edema Increase ICP

Complications of SIADH
Seizure Activity
Dx :
1. Urine specific gravity increase: Reveals a diluted urine
2. Serum Na ----Decrease
3. Low serum osmolality
4. High urine osmolality (urine osmolality >100 mosmol/kg)
5. Normal renal function (low BUN <10 mg/dL), absence of hypothyroidism & glucocorticoid deficiency &
recent diuretic therapy.
Nsg Mgt:
1. Restrict fluid. (<1,000 ml/day)
Takes 3-10 days to work
2. Administer meds as ordered
If the patient has evidence of fluid overloading, a history of CHF, or is resistant to treatment, loop diuretics
(Furosemide) may be added as well.
a. Diuretics-----both ----Osmotic (Mannitol)---for the Increase ICP (side-drip)

----Loop (Lasix)---------for edema----IV push
b. Chronic treatment: lithium or demeclocycline which inhibit ADH action.
3. Monitor strictly V/S, I&O, neuro check – increase ICP

4. Weigh daily
5. Assess for presence edema
6. Provide meticulous skin care
7. Prevent complications : Increase ICP & Seizure
8. Maintain sodium balance

– Increase sodium intake
– If the serum sodium is below 120 or if the patient is seizing, emergency treatment: 3% NaCl.
May be followed by Furosemide.
– Excessively rapid correction of hyponatremia may cause central pontine myelinolysis.
– Patients with a plasma sodium concentration greater than 125 mmol/l rarely need specific therapy
for hyponatremia.
III. ADRENAL GLAND
 Located at the top of the kidney

2 Parts:
A. Adrenal Cortex (Outermost layer)
1. Zona Fasiculata – secrets glucocorticoids

Ex. Cortisol, Corticosterone
--Controls glucose metabolism (SUGAR)
• Increase blood glucose levels by increasing rate of gluconeogenesis
• Increase protein catabolism
• Increase mobilization of fatty acids
• Promote sodium and water retention
• Anti-inflammatory effect
• Aid the body in coping with stress
2. Zona Reticularis – secrets traces of glucocorticoids & androgenic hormones

M – Testosterone
F – Estrogen & progesterone
Fx: Promotes development of secondary sexual characteristics
3. Zona Glomerulosa - secretes mineralocortisone/mineralocorticoids

Ex. Aldosterone, corticosterone, Deoxycorticosterone
Fx: Promotes Na & H2O reabsorption & excretion of potassium (SALT)
Regulate fluid and electrolyte balance
Stimulate reabsorption of sodium, chloride and water
Stimulate potassium excretion
Under the control of the Renin-Angiotensin-Aldosterone system
Summary: Adrenal Cortex Hormones

• Sugar
• Salt
• Sex
B. Adrenal Medulla (Innermost layer)
 Secrets cathecolamines
a. Epinephrine
b. Norephinephrine (Potent vasoconstrictor)
Released during “fight or flight” situations  SYMPATHETIC effect
DISORDERS OF THE ADRENAL CORTEX:
CODE: 3 S’s
S
Addison’s Disease ugar Cushing’s Syndrome
alt
ex
Hypoglycemia Glucocorticoid Hyperglycemia

Hyponatermia Mineralcoritcoid Hypernatremia
Loss of pubic Androgen Hirsutism
CONN’S DISEASE
1. ADDISON’S DISEASE
- Hyposecretion of adrenocortical hormones leading to:

a. Metabolic Disturbances (sugar)
b. F&E Imbalances- Na, H2O, K
c. Deficiency of neuromuscular function (salt & sex)
1. Atrophy of adrenal gland
2. Fungal infections Sx of Hypoglycemia
3. Tubercular infections
T – tremors, tachycardia
I – irritability
Pathophysiology : R - restlessness
E – extreme fatigue
S
D – diaphoresis & depression
- Hypoglycemia
- Decreased Plasma cortisol Tolerance To Stress ---- Addisonian’s Crisis

Sugar
- Melanocyte secreting hormone Hyperpigmentation (discoloration of skin & m. m.)
Tan = BRONZE-SKINNED
- Decreased Volume Hypovolemia --- Hypotension
Salt - Hyponatremia ---- Dehydration (Extreme thirst & agitation)----Weight Loss
- Hyperkalemia
Sx of Hyperkalemia
influence cardiac polarization
I – irritability
D – diarrhea
Arrythmia ---Cardiac Arrest
A – arrhythmia ( T wave )
Sex - Decrease sexual hormone ---- libido & sexual urge

Loss of axillary & pubic hair
Breast atrophy
S & Sx:
1. Hypoglycemia
2. Hyponatremia
Hypovolemia
a. Hypotension
b. Dehydration
c. Weight loss
3. Hyperkalemia
4. Decrease libido & loss pf pubic hair/axilla
* Pathognomonic Sign = Bronze-like skin pigmentation d/t decrease cortisol w/c will stimulate pituitary gland to release MSH
Dx :
1. FBS – decrease FBS (N 80 – 120 mg/dL)
2. Plasma cortisol – decreased Normal
3. Serum Na – decreased Na = 135 -145 meq/L
4. Serum K – increased K = 3.5 – 5.5 meq/L
Nsg Mgt:
1. Monitor VS, I&O – to determine presence of Addisonian crisis
2. Administer isotonic fluid as ordered
3. Diet – increase calorie or CHO
Increase Na, Increase CHON, Decrease K
4. Force fluid d/t hyponatremia & dehydration
5. Meticulous skin care – d/t bronze-like skin
6. Maintain patent IV line
a.) Steroids supplementation : Corticosteroids - (Decadron) or Dexamethazone

Hydrocortisone (cortisone)- Prednisone
Betamedasone
Nsg. Mgt. with Steroids
1. Administer 2/3 dose in AM & 1/3 dose in PM in order to mimic the normal diurnal rhythm.
2. Give on full stomach, after meal or w/ milk or w/ antacid ( gastric irritants)
3. Monitor blood sugar level ( will cause hyperglycemia)
4. Limit fluid intake ( will cause retention of water)
5. Monitor body weight at least once a day
6. Give calcium preparation ( can cause osteoporosis)
7. Avoid any form of skin trauma/injury ( Steroids increases capillary fragility-----ecchymosis)
8. Not given to children---can cause growth retardation
9. Monitor S/E (Cushing’s syndrome S/Sx)
a. HPN
b. Hirsutism
c. Edema
d. Moon face & buffalo hump
10. Taper the dose (withdraw gradually from drug) to prevent complication of Addison’s Crisis
Sudden withdrawal--------- Acute exacerbation of Addison’s Crisis characterized by :
Sudden hypoglycemia, severe

Hypotension
Hypovolemia, severe
Hypocalcemia
Weight loss
Sudden severe Hypokalemia------ Arrhythmia
Cardiac arrest
Leads to progressive stupor & coma
Nsg Mgt: Addisonian Crisis (Coma)

1. Assist in mechanical ventilation
2. Administer steroids
3. Force fluids
11. Can suppress immune response-------prone to infection

Avoid sources of infection
Avoid crowded areas, people with RTI
Place on reverse isolation
b.) Mineralocorticoids. Ex. Flurocortisone
8. HT & Discharge planning
a. Avoid precipitating factors leading to Addisonian crisis
1. Sudden withdrawal crisis

2. Stress
3. Infection
b. Prevent complications
1. Addisonian crisis
2. Hypovolemic shock
9. Hormonal Replacement Therapy – lifetime

10. Important follow up care
2. CUSHING’S SYNDROME
– Hypersecretion/ increase secretion of adrenocortical hormone

1. Hyperplasia of adrenal gland
2. Tubercular infection: spread of infection to adjacent organs – Milliary TB (TB of the Adrenal Gland)
Pathophysiology: Hyperglycemia (3
P’s)
P polyuria
S
polydipsia
- Hyperglycemia polyphagia Lead to DM
Sugar Buffalo Hump & Moon Face d/t abnormal fat distribution
- Increase steroids w/c WBC Increase susceptibility to infection (reverse isolation)
Sx of Hypokalemia
W – eakness & Fatigue
Salt - Hypokalemia
C – constipation
A – arrhythmia ( U wave )
Arrythmia ---Cardiac Arrest
- Hypernatremia--- fluid retention Hypervolemia (Increase intravascular volume)
Edema HPN
1
Anasarca
Obese Trunk w/ thin extremities
Sex - Virility, Hirsutism, Muscularity of female

Striae & Acne, Enlarged clitoris
S & Sx:
1. Hyperglycemia ( Difference From DM: 3 P’s + Glycosuria + Weight Loss)---Complication of Cushings: DM

2. Hypernatremia
a. HPN
b. Edema
c. Wt gain
d. Moon face (oily w/ acne)
Buffalo hump
Obese trunk Classic Signs
Pendulous abdomen
Thin extremities
3. Hypokalemia
4. Easy Bruising
Dx:
1. FBS – increase↑
2. Plasma cortisol increase
3. Na – increase
4. K - decrease
Nsg Mgt:
1. Monitor VS, I&O
2. Weigh patient daily & assess presence of edema
3. Reverse isolation
4. Restrict Na
a. K- Sparing Diuretics (Aldactone) spironolactone
- Promotes excretion of NA while conserving potassium
- Not lasix due to S/E hypoK & Hyperglycemia!
6. Provide Dietary intake – Low in CHO, low in Na & fats

High in CHON & K
7. Skin care – d/t acne & striae
8. Prevent complication
- Most feared – arrhythmia & DM
- Endocrine disorder lead to MI – Hypothyroidism & DM
9. Hormonal Replacement Therapy : Lifetime

Receive Cortisol Inhibitor
Ex. Aminogluthetemide
Metotane
Trilostane
*Metyrapone
10. Surgery:
a. Surgical Removal: Bilateral Adrenolectomy
b. Destruction: Cobalt Therapy
3. CONN’S DISEASE/ PRIMARY ALDOSTERONISM
- Results from adenoma ( benign tumor of the adrenal cortex)
Increase aldosterone
HPN, Increase ADH, General Edema
DISORDER OF THE ADRENAL MEDULLA:
4. PHEOCHROMOCYTOMA
- Benign tumor of the adrenal medulla
Hyperactive Increase catecholamines Epi/Nore SNS response
All lead to 5 H’s
H
Hypertension
Headache
Hyperglycemia
Hypermetabolism
Hyperhidrosis & Other S/Sx
Goal:
1. Cobalt Therapy
2. Adrenalectomy
Dx :
VMA ( Vanillylmandellic Acid)
Done to evaluate the level of catecholamines in the blood & urine
Normal: Blood – 0.2 – 0.9 mg %

Urine – 0.2 – 7 mg % for 24 hrs. urine sample
IV. THYROID GLAND
Abnormal Physical Findings: Normal:

a. With tenderness – Not tender
b. No nodular consistency - With nodular consistency
c. Marked asymmetry - Only 1
d. Palpable upon swallowing - Never palpable unless with goiter

Anatomy:
Thyroid Glands secretes 3 hormones:
T3 T4 Thyrocalcitonin
Tri-indotyronine -Tetraiodothyronine/ Tyroxine Function: Inhibits effects of parathormone
Promotes Calcium reabsorption
3 molecules of iodine 4 molecules of iodine
Function: Metabolic or Calorigenic hormone
Effects: CNS: Increase metabolism brain

GIT: Motility
Physiology:
Essential Elements In The Production Of Thyroid Hormones
Plasma Iodide (iodine iodized in plasma by active transport)

+
Tyrosine (derived from CHON in diet + amino acid)
Thyroglobulin (in storage form)

Released in blood circulation in the form of
T3 & T4
Through the Feedback mechanism
Ex. APG ------secretes Trophic Hormones ( any hormone that stimulate a target organ)
TSH ------target organ-----Thyroid gland------- T3 & T4
ACTH---------------target organ-----Adrenal cortex------ Steroids

(Adrenocothropic hormone)
Normal:
T3 = 70 -170 % mg
T4 = 4.7 – 11 ug%
THYROID DISORDERS
1. SIMPLE GOITER
– Enlargement of the thyroid gland d/t iodine deficiency *A non-toxic goiter can lead to Toxic goiter
- No increase in T3 T4, below or Normal anytime if:
> Prolonged exposure to cold weather
Toxic Goiter : If there is an increase in T3 T4 > Stress
> Infection
Created by Niňa E. Tubio All can cause an increase in T3 T4 44
1. Goiter Belt area ------ “ Endemic Goiter” ---cause by goiter belt area
a. Place far from sea – no iodine seafood’s rich in iodine
2. Mountainous area results to an increase intake of goitrogenic foods Ex. Baguio/Cordilllera

Ex. Turnips (singkamas) radish, peas, strawberries, sweet potato, beans, kamote, cassava (root crops), nuts, broccoli
3. Goitrogenic Drugs that contains progoitrin--- an anti-thyroid agent that has no iodine
Ex. Anti thyroid agents
(PTU) prephyl thiupil
Lithium carbonate, Aspirin PASA, Cobalt, Phenyl butasone
“Sporadic Goiter –“ if caused by goitrogenic drugs or from an increase intake of goitrogenic foods
S & Sx :
1. Enlarged TG
2. Mild restlessness
3. Mild dysphagia
Dx.
1. Thyroid Scanning – Reveals enlarged TG
Done to evaluate the amount of Iodine 131 accumulated by the thyroid gland
2. *Serum Thyroid Stimulating Hormone (TSH)
Result: Increase (Confirmatory Dx of Goiter)
3. T3, T4 Determination
More reliable test, more potent & rapid effect on metabolism
Result : Serum T3, T4 will Normal or below N
Nsg Mgt:
1. Administer meds as ordered:
a. Iodine solution – Logol’s solution or Saturated Solution of K iodide (SSKI)
- Violet/Purple Color
Nsg Mgt For Lugol’s Solution
1. Use straw to prevent staining of teeth Drugs Given Using Straw To Prevent Staining
2. Prophylaxis 2 -3 drops , Treatment – 5 to 6 drops
1. Tetracycline
b. Thyroid Hormone / Agents 2. Iron preparation
1. Levothyroxine (Synthroid) 3. Nitrofurantoin (Macrodantin)
2. Liothyronine (cytomel) 4. Logul’s Solution
3. Thyroid extract
Nsg Mgt for Thyroid Hormones/agents
1.
Monitor VS – HR d/t tachycardia & palpation
2.
Take it early AM – S/E : Insomnia
3.
Monitor S/E:
Tachycardia, palpations
Insomnia Signs of Hyperthyroidism
Restlessness agitation
Heat intolerance
HPN
4. Encourage increase intake iodine
1. Seaweeds – highest source 99%
2. Seafood: Highest iodine content: 1st: Oysters 2nd: Crabs 3rd: Lobster Least iodine: Shrimps
3. Iodized salt –easily destroyed by heat, take it raw not cooked
5. Assist surgery: Sub-Total Thyroidectomy
2. HYPOTHROIDISM
– The Hyposecretion of T3, T4 leading to MI, Atherosclerosis, HPN & stroke.
Classified According To Onset of S & Sx:
1. CRETINISM – appear during childhood / only endocrine d/o that leads to mental retardation
2. MYXEDEMA – appear in adulthood (both pitting & non-pitting edema)

Classified According To Cause:
1. PRIMARY – failure of thyroid to secrete T3 T4

2. SECONDARY – failure of APG to secrete TSH
3. TERTIARY - failure of Hypothalamus to secrete TRH (Thyroid Releasing Hormone)
1. Iatrogenic causes – disease caused by medical intervention or surgery

2. Atrophy of TG d/t:
a. Irradiation
b. Trauma
c. Tumor & Inflammation
3. Iodine deficiency
4. Autoimmune – “ Hashimoto disease”
Pathophysiology:
Hypothalamus APG secretes-----TSH---stimulate----Thyroid Gland---secrete--- T3 T4
Any disorder of T.G. will decrease T3 T4
Leading to Tertiary causes or Hypothyroidism
Altered Metabolism
Hypometabolic Memory Impairment

Hypoactive Decrease O2 in metabolism
Weight Gain
Decrease VS
Unable to tolerate Cold weather
S&Sx:
Everything decreased except weight gain & menstruation w/c are both increase
Early Sx : Weakness & Fatigue

Loss of appetite
Weight gain
Cold Intolerance – Myxedema - Coma
Constipation
Dry skin
Late Sx : Brittle hair/ nails

Non pitting edema d/t increase accumulation of mucopolysacharide in SQ tissue
Hoarseness of voice – only endocrine d/o that can be Dx thru telephone conversation
Decrease libido
Decrease VS – Hypotension, Bradycardia, Bradypnea & Hypothermia
Lethargy
Memory Impairment leading to Psychosis
Menorrhagia (high)
Dx:
1. T3 T4 Determination: Serum T3 T4 Decrease
2. Serum Cholesterol: Increase – can lead to MI
3. Radio Iodine Uptake (RAIU): Decrease
- Use to evaluate the amount of radiation RAI 131 accumulated by the T.G. & excreted by the kidneys
- Most reliable Diagnostic Test
Normal Uptake : 15 - 40 % of the administered dose

Urine : 40 – 80% Result: Directly proportional to Uptake, inversely proportional to urine

2 Endocrine D/O that leads to Cardiac Complications
Nsg Mgt In RAIU:
1. DM
1. No iodine in diet prior to test
2. Hypothyroidism
2. Taken P.O. RAI 131 cocktail (liquid)
Nsg Mgt:
1. Monitor strictly V/S. I&O – to determine presence of Myxedema Coma
A severe form of hypothyroidism

Characterized by:
Hypotension
Hypoventilation
Bradycardia
Bradypnea, Hyponatremia & Hypoglycemia
That can lead to progressive stupor & coma
Important Mgt For Myxedema Coma:
1. Assist in mechanical ventilator

2. Administer thyroid hormone
3. Administer IVF replacement
2. Monitor VS, I&O

3. Provide dietary intake : Low in calories d/t weight gain
4. Skin care d/t dry skin
5. Comfortable & warm environment d/ to cold intolerance that can lead to Coma
6. Administer IVF replacements
7. Force fluid
8. Administer meds as ordered – Take AM
Supplement Thyroid Hormones/Extract
Synthetic: Levothyroxine S/E: Constipation
Thyroid Extracts: Proloid ( Thyroglobulin)

Cytomel
Synthroid
Euthroid
Thyrolar
Eltroxime
9. Health teaching & discharge plan

a. Avoidance precipitating factors leading to myxedema coma:
1. Exposure to cold environment
2. Stress
3. Infection
4. Use of sedative, narcotics, anesthetics not allowed – CNS depressants V/S already down
b. Prevent Complications: Hypovolemic shock, Myxedema coma, HPN, LHF, MI, Stroke
c. Hormonal replacement therapy - lifetime
d. Importance of follow up care
3. HYPERTHYROIDISM “GRAVE’S DISEASE” or “THYROTOXICOSIS”
“TOXIC GOITER/ BASEDOU/ PARRY’S DISEASE”
- The hypersecretion of T3 & T4
1. Autoimmune Disease – Release of LATS

Exopthalmos
Enopthalmos – severe dehydration depressed eye
2. Excessive iodine intake
3. Hyperplasia of TG d/t increase # of cells
Pathophysiology: 1. Theory Of LATS: (Long Acting Thyroid Stimulator)
In blood, there is gamma globulin that causes Iodine Accumulation

Thyroid Hyperplasia
W/c will manifest the TRIAD SYMPTOMS:
1. GOITER d/t iodine accumulation

2. EXOPTHALMOS (eye signs seen in EPS)
3. HYPERTHYROIDISM (seen in EPS)
2. EPS ( Exopthalmus Producing Substance)
APG -----releases EPS----responsible for the Triad S & Sx
Proptosis (downward displacement of eyeball)

Lid lag (sleepy eyes)
Infrequent blinking
Fixed stare DALYRIMPLE SIGN
Peri-orbital Edema
Von Graefe ------------ failure of eyelids to follow movement of eyes when looking down
3. Hyperthyroidism ---------- Hyperactive, Voracious but losing weight, hypermetabolic
T3 T4 ------the cause is over-excitability of SNS
Tremors Hallucinations Diaphoresis Palpitation Nervousness Irritability Insomnia
S & Sx:
1. Increase appetite : Hyperphagia but weight loss d/t increase metabolism

2. Skin is moist
3. Heat intolerance
4. Diarrhea – most common gastric complications of Grave’s Disease
5. All VS increase = HPN, Tachycardia, Tachypnea, Hyperthermia
6. CNS changes
7. Goiter
8. Exopthalmos Constipation – common in advanced graves disease
9. Amenorrhea d/t constant increase in T3 T4
Dx:
1. Serum T3 & T4 - Increased
2. RAIU : Increase
3. Thyroid Scanning: Reveals an enlarged TG
Nsg Mgt:
1. Monitor VS & I & O – To determine presence of thyroid storm or most feared complication: Thyrotoxicosis
a. Antithyroid Agents
1. Prophylthiouracil (PTU)
2. Methimazole (Tapazole)
3. Neomercazole ( Carbimazole)
Most Toxic S/E for prolonged Used: Agranulocytosis
Common S/S: Complications R/T infections

- Fever, Sore throat, Mild Leukocytosis

Dx Test To Check For Toxicity: Differential Platelet Count
If not available, Monitor CBC
Throat Swab & Culture
Most feared complication : Thrombosis ----Stroke CVS
b. Adrenergic Blocking
To control the symptoms brought about by the over-excitability of SNS
- Propanolol, Inderal, Betaloc, Neobloc, Metoprolol, Nadol, Visken, Aptin, Sotalex, Corgard
3. Diet – Increase caloric intake to correct weight loss

4. Skin care
5. Comfy & cool environment
6. Maintain siderails d/t restlessness
7. Provide bilateral eye patch (dry material) – to prevent drying of eyes
8. Hormonal Replacement Therapy
10. Importance of follow-up care
11. Assist in surgery – Subtotal Thyroidectomy
Tx:
1. RAI 131
To reduce size of T.G.
Isotope: Risk of genetic abnormalities or genetic mutation
2. Surgery : Subtotal Thyroidectomy

Nsg Mgt: Peri-Operative
1. Administer Lugol’s solution (SSKI) K iodide

Function: To decrease vascularity of TG
To prevent bleeding & hemorrhage during & after surgery
To increase firmness
Promote T3 T4 storage
2. Diet :
a. High in calories Increase CHO
Increase CHON
Increase in polyunsaturated fats
To satisfy increase in appetite & restore loss of glycogen reserve
b. Avoid stimulant in diet (No colas, caffeine)
c. Increase fluid intake
d. Monitor body weight
e. Provide physical & mental rest to reduce metabolism
f. Provide quiet & calm environment to decrease irritability
3. If (+) for exopthalmus -----dryness of the cornea ----corneal ulceration---blindness
Nsg Mgt:
1. Cover eyes w/ bilateral eye patch
2. Instill saline to moisten eyes ( Drug: Methylcellulose OD)
3. Elevate head on pillow to promote drainage & reduce peri-orbital edema
4. Give psychological preparation by telling pt. that eye signs will remain
even after surgery
Nsg Mgt: Post-Operative Thyroidectomy
Complication: 1. Watch out for signs of Thyroid Storm or Thyrotoxicosis

- If no emotional preparation pre-operative: Stress
- Post-opt wound infection
Pathphysiology: Pre-opt (euthyroid state----post-opt----thyroid compensates for T3 T4 production

(Hyperthyroid d/t stress, infection)
Increase PR, Increase BP

Triad Signs of Thyroid Storm: “HAT”
a. Hyperthermia
b. Agitation
c. Tachycardia ----------Early Sign: Fever w/ Tachycardia
Nsg Mgt Thyroid Storm:
1. Monitor VS & neuro check

Agitated might decrease LOC
2. Antipyretic – fever/ TSB
Tachycardia -  blockers (-lol)
3. Siderails – agitated
Complication 2. Watch for inadvertent (accidental) removal of parathyroid gland
Secretes Parathormone (Calcium Reabsorption)
TETANY : Hypocalcemia
If 1 removed – No sign of tetany

If 2 removed – Mild signs of tetany
If 3 or more removed - Classic Sx of Tetany:
(+) Trousseau sign & (+) Chvosteck’s sign
(Twitching of fingers) (Facial paralysis)
Nsg Mgt:
1. Administer calcium gluconate
Slowly – to prevent arrhythmia
Ca gluconate toxicity – antidote – MsSO4
Complication 3. Watch out for accidental Laryngeal nerve damage
Sx: Hoarseness of Voice 2 recurrent laryngeal nerves that control vocal cords (bilateral laryngeal)
Aphonia (no voice) Responsible for voice production
If 1 removed – whispery, hoarseness

If Trauma only – Whispery, Hoarseness
Edema on glottis – Whispery, Hoarseness
If 2 removed – Aphonia -----start speech therapy
Nsg Mgt:
1. Encourage pt to talk or speak postoperatively
2. Notify physician immediately
4. Watch out for Signs of Laryngeal Spasm--------- Inflammation of Larynx
Sx: DOB Narrow opening ---- O2 cannot enter

SOB
Laryngeal Spasm
Nsg Mgt:
1. Prepare at bedside tracheostomy
5. Watch Out for Signs of bleeding Post-Subtotal Thyroidectomy
D/T : Failure to administer Logul’s Solution (SSKI) pre-opt
Failure to tie/ ligate blood vessels --------bring back to OR for emergency operation
Sx:
“Feeling of fullness” at incision site
“ Feeling of Choking sensation”
- BP -------- Rapid, feeble, thready pulse
Rapid but shallow respiration
Cold, Clammy diaphoretic skin
Nsg Mgt:
1. Check soiled dressing at nape area (Slip hand under neck to check for dampness)
2. Evaluate VS
3. Notify Physician immediately

Bleeding can lead to-------------- 1. Respiratory Obstruction
D/T blood occlusion & Hematoma
Accumulation of Tracheobronchial secretions
Can also lead to Laryngospsam/Laryngoedema

Prepare for Emergency Tracheostomy
OTH ER DIAGNOSTIC TEST FOR THYROID DISORDERS:
1. Protein Bound Iodine (PBI)

- Done to evaluate amount of iodine attached to protein molecule of the blood
Normal: 4-8 ug %
Nsg. Care:
1. 2-3 days prior to test, no taking of foods & drugs containing iodine
Ex. Seafoods, iodized salt,
No cough syrup, ASA
Estrogenic Preparations: Pills, Dyes, X-ray
2. Basal Metabolic Rate (BMR)

- Done to evaluate O2 consumption when client is at rest
Nsg Mgt:
1. At night, NPO for 12 hrs.
2. Ensure client had a good night sleep to decrease anxiety level
Procedure:
1. When client no activity yet, no food yet
2. Clamp nose, breathe through tube connected to a tank w/ machine evaluating O2 consumption
3. TBMR (Theoretical)
- Compute pulse pressure + PR/ minute – 111 ( Normal: 20-30)
- Not conclusive, but if s/s submit to other test
Summary:
HYPOTHYROIDISM HYPERTHYROIDISM
Lethargy
Memory Impairment
Diarrhea
Decrease VS
T3 Agitation & Restlessness
Hallucination
Constipation
Increase VS
T4
ALL DECREASE ALL INCREASE
Except: Except:
Wt: Weight Gain Weight Loss
Menstruation: Menorrhagia Amenorrhea
V. PARATHYROID GLAND
– A pair of small nodules located behind the Thyroid Gland

– There are 4 Parathyroid glands
Anatomy: PTH------secretes---- PARATHORMONE
Function: Essential to the absorption of Calcium & secretion of Phosphorus by renal tubules
Promotes reabsorption of Calcium
Regulates cardiac rythmicity
Essential for blood coagulation
*Thyrocalcitonin – Antagonizes secretion of parathyroid hormone

CODE: CALCIUM

DISORDERS OF THE PARATHYROID GLAND
1. HYPOPARATHYROIDISM
– Hypoactive PTH or a decreased secretion of parathormones
HYPOCALCEMIA HYPERPHOSPHOTEMIA
(TETANY)
[If Ca decreases, phosphate increases]
Uncontrolled spasm/Hyperactivity
1. Following subtotal thyroidectomy d/t accidental removal of PTH

2. Atrophy of parathyroid gland due to
a. Inflammation
b. Tumor
S&Sx:
1. Acute Tetany
a. Tingling sensation
b. Paresthesia
c. Dysphagia
d. Laryngospasm
e. Bronchospasm
f. Seizure Most feared complications
g. Arrhythmia
Pathognomonic Sign of Tetany:
a. (+) Chvosteck’s Sign : Tap facial nerve, if facial spasm of facial muscle (+)
b. (+) Trousseau’s /Carpopedial spasm: Occlude blood flow to vascular extremity (legs)
Use tourniquet Test for 1-2 min. & observe for carpopedial spasm
2. Chronic tetany
a. Loss of tooth enamel
b. Photophobia & cataract formation
c. GIT changes : Anorexia, N/V & generalized body malaise
d. CNS changes : Memory impairment, Irritability
Dx:
1. Serum Calcium – Decrease (N 8.5 – 11 mg/100ml or 4.5 -5.5 mEq/L)
2. Serum Phosphate – Increase (N 2.5 – 4.5 mg/100ml)
3. X - ray of long bone – Increase bone density
4. CT Scan – Reveals degeneration of basal ganglia
Nsg Mgt:
1. Administration of meds:
a. Acute Tetany:
Administer Ca gluconate – IV, slowly to prevent cardiac arrest
b. Chronic tetany
1. Give Oral Ca supplements
Ex. Ca gluconate - Calci-aid

Ca carbonate - Calsan
Ca lactate
Ca chloride 10% - Caltrate
2. Give Vit. D for calcium to be readily absorb

Vitamin D (Cholecalceferol)
Drug Diet Sunlight
Cholecalceferol Calcidiol Calcitriol 7am – 9am
Commercially-Prepared: *Calciferol
Hytakerol
Calcidiol
*Rocatriol
Dihydrotachysterol
3. Give Phosphate binder for excretion of phosphate
Ex. Aluminum OH gel (ampho gel) S/E: Constipation
Antacid
AAC MAD
Aluminum Containing Acids Magnesium Containing Antacids
Aluminum OH gel Milk or Magnesia
Constipation Diarrhea
*Maalox: Magnesium & Aluminum – With Lesser S/E
2. Avoid precipitating stimulus such as bright lights & noise to prevent seizure
3. Diet : Increase Ca & decrease phosphorus

- Don’t give milk – due to increase phosphorus
Diet : Also For Osteoporosis

a. Baked Salmon
b. Dilis/Anchovies
c. Green Turnips (Singkamas)
4. Bedside: Tracheostomy set d/t laryngospasm

5. Encourage to breath with paper bag in order to produce mild respiratory acidosis
– To promote increase ionized Ca levels
6. Most feared complication : Seizure & arrhythmia
7. Hormonal Replacement Therapy: Lifetime
8. Institute Seizure & safety precautions
9. Important follow up care
2. HYPERPARATHYROIDISM / “Von Reclinghausen”
- Increase secretion of parathormones

- HYPERCALCEMIA -------- w/c can lead to Hypophosphotemia
Pathophysiology:
PTH Increase bone resorption Calcium loss from bones
Normal: Ca – 99% bones Reverse effect: Ca in bone goes to blood

1% blood
Hypercalcemia Bone Demineralization Hypercalciuria
Hypophospotemia bones are brittle Formation of Calcium crystals in Urine
Leads to bone fracture Nidus/ Nucleus

Forms Kidney Stones
1. Hyperplasia of the parathyroid gland
2. Over compensation of PTG d/t Vit D deficiency
Children – Rickets
Adults – Osteomalacia Vitamin D deficiency
*Sippy’s diet – Vit D diet – not good for pt with ulcer: 2 -4 cups of milk & butter
*Karrel’s diet – Vit D diet – not good for pt with ulcer: 6 cups of milk & whole cream
*Food rich in CHON – eggnog – combination of egg & milk
S/Sx:
1. Bone fracture
a. Bone pain (especially at back)
2. Kidney Stones
a. Renal colic
b. Cool moist skin & body malaise
3. GIT changes: Anorexia, N/V, Ulcerations ----- only endocrine D/O that causes ulceration
4. CNS involvement: Irritability, Memory impairment
Dx :
1. Serum Ca: Increase
2. Serum phosphorus: Decreases Hypo : Replacement w/ commercial preparation
3. X-ray of long bones : Reveals bone demineralization Hyper: Removal or Destruction of the gland
Tx:
1. Removal of the gland - Parathyroidectomy
2. Destruction of the gland – Cobalt Therapy
3. Drug of Choice: Calcitonin ---- inhibits resorption ACID-ASH DIET
Nsg Mgt: Kidney Stone 3 C’s Cranberry
Calamansi
1.
Force fluids : 2,000 – 3,000/day or 2-3L/day Vit. C
2.
Isotonic solution 1G Grapefruit
3.
Warm sitz bath – for comfort 1P Plum
4.
Strain all urine with gauze pad
5.
Acid Ash diet to acidify urine
6.
Adm meds as ordered
a. Narcotic analgesic – Morphine SO4, Demerol
S/E – Respiratory Depression
Antidote - Narcan/ Naloxone
Naloxone toxicity – Tremors
7. Siderails
8. Assist in ambulation
9. Diet – low in Ca, increase phosphorus lean meat
10. Prevent complication of Parathyroidectomy : Most Feared – Renal Failure
11. Hormonal Replacement Therapy: Lifetime
12. Importance of follow up care
VI. PANCREAS
- Located behind the stomach , a mixed gland
Pancreas: Consists of
Acinar Cells (Exocrine gland) Islets of Langerhans (Endocrine Gland: Ductless)
Secrete Pancreatic juices Secretes 3 Types of Cells
Flows in the pancreatic duct

 Cells  Cells Delta Cells
Aids in digestion (in stomach) Secretes Glucagon Secretes Insulin Secretes Somatostatin
Fx: Hyperglycemia Fx: Hypoglycemia Fx: Antagonizes Growth Hormones

DISORDER OF THE PANCREAS
1. PANCREATITIS
– Acute inflammation of the pancreas leading to Pancreatic Edema, Hemorrhage & Necrosis d/t Autodigestion
(Self-digestion )
Cause: Unknown/idiopathic
Alcoholism
Obstruction in the pancreatic duct ---- backflow of pancreatic juice to the pancreas
Will cause autodigestion
Pathognomonic Sign: (+) Cullen’s Sign - Ecchymosis of umbilicus (bluish color)

(+) Grey Turner’s Spots - Ecchymosis of flank area
Both Signs Means Hemorrhage
2. CHRONIC HEMORRHAGIC PANCREATITIS “Bangugot”
Predisposing Factors: Unknown
Risk factor:
1.
History of hepatobiliary disorder
Alcohol 2.
Drugs: 3.
Thiazide diuretics
Oral contraceptives
Aspirin
Penthan
4. Obesity
5. Hyperlipidemia
6. Hyperthyroidism
7. High intake of fatty food – Saturated fats
3. DIABETES MELLITUS
- A metabolic disorder characterized by non-utilization of CHO, CHON,& fat metabolism

d/t
1. Absolute Insulin Deficiency

- Cause is unknown but the islets of langerhans do not produce insulin
- Congenital
- Beta-Cell damage by VIRUS ----- Human Leukoantigin----Human Leuko Antibodies
(Chicken Pox)
Autoimmune: Destroys B-cells
2. Relative Insulin Deficiency
- Capable of producing insulin but not used efficiently d/t
Blocked by chemical antagonist at site of production
Epinephrine Thyroxin Glucogen Glucagon All causes Glucogenolysis
Physiology:
Pancreas → glucose → ATP (Main fuel of cell) (reserve glucose – glycogen)
Glucogenesis ( synthesis of glucagons)
Glycogenolysis ( breakdown of glucagons)
Liver will undergo Gluconeogenesis (formation of glucose from CHO sources – CHON & fats)
Pathphysiology:
DIABETES MELLITUS
Little or No Supply of Insulin
CHO Metabolism CHON metabolism Lipolysis
CHO utilization of glucose breakdown of stored glucose
Cell Starvation Cell to Tissue Starvation Oxidation of fatty acid
Cell weakness Hyperglycemia Stimulate Satiety Center

d/t (Hypothalamus)
cellular starvation Glucose go to blood Hyperlipidemia Ketone Production
POLYPHAGIA
Weight loss (excessive hunger)
Blood Osmolarity DKA (Diabetic
Ketoacidosis)
(result from increase breakdown of fats)
kidney
Kidney’s tubular secretion POLYURIA Death Diabetic Coma

Stimulate thirst center (needs O2)
Glucose in blood ECF dehydration

DKA
Act as osmotic diuretic (Increase) POLYDIPSIA Early Sx:
(excessive thirst) Weight loss
Renal tubules fail to reabsorb glucose Weakness
HONKC Late Sx:
GLYCOSURIA Acetone-breath odor
Kausmaul’s Respiration
Irritate perineal area (rapid, shallow
Fungi in the area breathing)
(-) Nitrogen Balance
Pruritus Tissue Wasting (Cachexia)

A. CLASSIFICATION:
1. TYPE 1 2. TYPE II
IDDM NIDDM
“ Brittle Disease”
Juvenile Onset Adult/ Maturity onset
Common among children 40 y/o & Above
Non- obese Obese
Weight loss Weight gain
Symptomatic Asymptomatic
Absolute Deficiency Relative Deficiency
Tx: Insulin Administration Tx: OHA (Oral Hypoglycemic Agents)
Diet Diet Regimen
Exercise Exercise

Complications: Complication: H – hyper
Diabetic Ketoacidosis (DKA) O – osmolar
Metabolic Acidosis N – non
Tx: Sodium Bicarbonate K – ketotic
C – coma
Incidence Rate: Incidence Rate:
- 10% of population with DM have Type I - 90% of population w/ DM have Type II

Mid 1980’s increase in type II d/t fast food chains
Predisposing Factor: Predisposing Factors:
1. 90% hereditary – total destruction of pancreatic dells 1. Obesity – lack insulin receptors binding site
2. Virus - # 1 cause of Type 2 DM
3. Toxicity to carbon tetrachloride (CC14) 2. Hereditary
4. Drugs – Steroids
Lasix - Loop diuretics
DIABETES MELLITUS
P
S/Sx: S/Sx:
Polyuria
1. 3 P’S + G Polydipsia 1. 3 P’s + G
2. Weight loss Polyphagia 2. Asymptomatic
3. Anorexia +
4. N/V Glycosuria
5. Blurring of Vision
6. Increase susceptibility to infection
7. Delayed/ poor wound healing
3. GESTATIONAL DM
– Occurs during pregnancy & terminates upon delivery of child
1. Unknown/ idiopathic
2. Influence of maternal hormones
S/Sx :
Same as type II –
1. Asymptomatic
2. 3 P’s & 1G
Mgt:
1. Type of delivery: CS d/t macrosomia (large baby)
Sx of Hypoglycemia on Newborn:
1. High pitched shrill cry
2. Poor sucking reflex
B. COMPLICATIONS OF DIABETES MELLITUS
1. HYPERLIPIDEMIA
Formation of atheromatous plaques (atherosclerosis) in the arteries
Narrowed arterial lumen ( blood flow) -----result to thickening of BV--- inelastic blood vessels
Formation of vascular lesion ( micro/macro-angiopathy)
Vascular Degeneration
Cerebral blood flow Coronary arteries Retinal Blood Vessels Renal blood vessels Peripheral blood vessels
Brain Heart Eyes Kidney Lower extremities

CVA Myocardial Ischemia Retinopathy Nephropathy Tissue Ischemia
(Kimmiel-Stiel Wilson Syndrome)
In 30 minutes Cataract Peripheral Neuritis
Irreversible M.I. RENAL FAILURE Tissue Necrosis
Retinal Hemorrhage Diabetic Gangrene

Exudation
Aggregation of CHON Hardening of renal tubules

In Retinal Molecules
Opacified Ischemia 1st d/t Ischemia

3 Pathies of DM
Nephropathy Diabetic Cataract
Retinopathy KSW PERIPHERAL NEURITIS
Pyelopathy Sx: Sx:
Proteinuria Numbness of exremity
Edema Coldness of extremity
Puffiness of eyelids Tingling sensation of extremity
HPN
Sx of Nephropathy is a progressive destruction of glomeruli --RF
2. DIABETIC KETOACIDOSIS (DKA)

- Acute complication of Type I DM due to severe hyperglycemia leading to CNS depression & Diabetic Coma.
1. Stress ------ # 1 cause of DKA Nsg Mgt:
2. Hyperglycemia
3. Infection 1. Can lead to coma: assist in mechanical ventilation
4. Missed dose/Omitting dose of insulin 2. Administer .9NaCl – isotonic solution
Sx: 3 P’s & 1 G Followed by .45 NaCl hypotonic solution
Early Sx: To counteract dehydration.
Weight loss 3. Monitor VS, I&O, blood sugar levels
Weakness 4. Administer meds as ordered:
Late Sx: a. Insulin therapy – IV push
Anorexia, N/V, Dim Vision Regular Acting Insulin : Clear
Acetone-breath odor (2-4hrs, peak action)
Kausmaul’s Respiration b. To counteract acidosis – Na HCO3
(rapid, shallow breathing)
CNS depression, Coma 5. Antibiotic to prevent infection
“Cherry Red Lips”
Dx :
1. FBS: Increase
2. Hct: Increase (compensate d/t dehydration)
C. DIAGNOSTIC PROCEDURES FOR DIABETES MELLITUS:
1. FBS/ FPG (Fasting Plasma Glucose)
- NPO 6-8 hrs. or NPO 12 hrs. with sips of water
2. RBS (Random Blood Sugar)
- No NPO, anytime
3. PPBS ( Post Prandial Blood Sugar) Determination Test 1-5 Use to Diagnosed Glycemia

- NPO 2 hrs. after diet of 100 gm CHO
4. Hgt (Hemaglukotest)
- Finger prick or Capillary Blood Glucose Determination (CBg)
5. OGTT ( Oral Glucose Tolerance Test)
- NPO 6-8 hrs. then collect fasting specimen (am)
Administer p.o. 100 gms: Urine Blood

Glucose + fruit juice
After 1 hr. -----extract venous blood ---- Rise glucose Increase BS (Normal)
2 hrs. --- next extraction ---- start to normalized Decreased BS
Final 3 hrs. --- next extraction ---- w/in normal BS
(+) Diabetic if: Rise glucose till the 3rd extraction still not normal & there is sugar in urine
6. BT, CT (Benedict’s Test) (Clini Test) Test For Glycosuria
- Double voided or 2nd voided specimen = accurately test presence of glucose in urine
- Discard 1st void, offer 1-2 glass of H20 after 1 hr. or 30 minutes collect urine
7. Acetest
- To test for presence of ketone bodies in urine (Ketonuria) (Result from incomplete breakdown of fats)
How? Get acutest tablet (creamy/white/ off-white in color) ---drop in urine

If there is no change (-), if color changes to purple (+) for ketonuria
8. Glycosylated HgB (HgBAC)
- To evaluate the amount of glucose attached to the hemoglobin of the blood for the previous 120 days---lifespan of HgB
D. MANAGEMENT OF DIABETES MELLITUS: Supportive & Palliative
1. TYPE 1 DM
INSULIN THERAPY
A. Sources:
1. Animal source – beef/ pork : rarely given because it causes allergic reaction
2. Human – has less antigenetic property
Ex. Humulin – most commonly used
If kid is allergic to chicken – don’t give measles vaccine, it comes from chicken embryo.
3. Artificially compound
B. Types of Insulin

Types of Insulin Onset Peak Given Color & Duration
Consistency
1. Rapid Acting Insulin 30 minutes after 2-4 hrs. 3x/day Clear 6-8 hrs.
administration
- Regular Acting
- Humulin R
- Semi-Lente
- Crystallized Zinc
- Velosulin
- Novolin R
- MC Actrapid
2. Intermediate Insulin 1-2 hrs 8-16 hrs. OD Cloudy 24 hrs.
- NPH (Non-protamine Hagedorn

1)
- Humulin N
- Monotard
- Lente
- Globin
- Novolin L
3. Long Acting Insulin 3-4 hrs. 16-24 hrs. Cloudy, Mixed 36 hrs.
- Ultra Lente
- PZI (Protamine Zinc Insulin)
- Humulin U
5 R’s Of Insulin Administration
1. Right Patient: Give insulin only if there are signs of glycosuria & hypergylcemia
2. Right Drug : Administer right type of Insulin
3. Right Route: Not given P.O., insulin destroyed in the GIT by proteinase
Given: SQ, IM, I.V.
Humulin R
Crystalline Zinc Incorporated w/ water, given by drip (IVF)
Regular Insulin
4. Right Time:
Best time given – 60-90 minutes before meal or an hour before meal
Physiologic effect of insulin will parallel the absorption of glucose
5.Right Dose: Know stock dose of insulin

10 ml vial
40 units/ml or 80 units/ml or 100 units/ml
Nsg Mgt For Insulin Therapy:
1. Administer insulin at room temperature. Do not expose to sunlight

 Refrigerate insulin once opened only
 Before administration, gently roll vial between palms. Avoid shaking to prevent formation of
bubbles
2. Use gauge 25 – 26 needle : Tuberculin syringe

3. Administer insulin at either 45 or 90 depending on the client tissue deposit.
5. Don’t aspirate after injection
 Rotate injection site to prevent lipodystrophy (atrophy/ hypertrophy of SQ tissue)
Deltoid Upper Arm R & L

Rectus Femoris R & L IM Below breast
Vastus Lateralis Lower Central Abdominal Wall SQ
Gluteus Maximus Lateral thigh R & L
Below scapula R & L
Buttocks R & L
6. Most accessible site – abdomen

7. When mixing 2 types of insulin, aspirate
1st regular/ clear – before cloudy to prevent contaminating clear insulin & to promote accurate calibration.
8. In giving insulin:
Before meals but if pt. eating already: Give insulin
If pt. already eaten 2 hrs. : Do not give, repeat CBC> MD will adjust the dose
9. 1ml or cc of tuberculin = 100 units of insulin
- - 1 cc = 10 units = 100 units
- - .5cc = 5 units = 50 units
- - .1 cc = 1 unit = 10 units
6 units RA
10. Monitor for signs of complications:
a. Allergic reactions
b. Lipodystrophy
c. Somogyi’s Phenomenon
– Rebound Effect of Insulin characterized by hypoglycemia followed by periods of hyperglycemia
(Insulin Shock, Hyperinsulinism, Insulin Overdose, Hyperglycemia)
d/t
 Occurs w/ insulin overdose

 Prolonged NPO, vomiting
 Long interval of insulin from the serving of food
* If allowed to eat, give anything to eat an hour after administration of insulin
Sx: Hunger Pangs

Double Vision 4-8 ounces of softdrinks
Pallor, cold clammy skin 4-8 ounces of fruitjuice
Tremors 1 tbs. of sugar ---best alternative, put in oral cavity
Mgt: 5 ml of honey
1. Give 20-30 gm of carbo 5 ml of karo syrup
2-4 pcs. Of candies
2. Drugs 2 slices of graham crackers
Epinephrine 1.1000 SQ
Glucagon 1-2 mg IM
*IV glucose H20 ---- D50% by IV push
---- D5W by venoclysis
2. TYPE 2 DIABETES MELLITUS
Most Feared Complication of Type II DM
Hyper ↑ osmolarity = severe dehydration

Osmolar
Non - absence of lipolysis
Ketotic - no ketosis
Coma – S/Sx: headache, restlessness, seizure, decrease LOC
Normal: BUN = 10-20 mg/100ml
Dx : Creatinine = .8 – 1 mg/100ml
1. FBS: N 80 – 120 mg/dl Hgb:

Increase , 3 consecutive times Female = 12-14 gm %
3 P’s & 1G = confirmed DM Male = 14-16 gm%
Hct: Average = 42 %
Female = 36-42 %
Male = 42 – 48 %
2. Oral Glucose Tolerance (OGTT)
Most sensitive test
3. Random Blood Sugar : Increased
4. Alpha Glucosylated Hgb : Elevated
(Normal: <9 %)
Nsg Mgt:
- Same as DKA except don’t give NaHCO3!
1. Can lead to coma – assist mechanical ventilation

2. Administer .9NaCl – isotonic solution, followed by .45NaCl hypotonic solution to counteract dehydration.
3.Monitor VS, I&O, blood sugar levels
4.Administer meds
a.) Insulin therapy – IV

Regular Acting Insulin – clear
b.) Antibiotic to prevent infection
Tx:
1. Give OHA
O ral
H ypoglycemic Fx: Stimulates pancreas to secrete insulin
A gents
Classifications of OHA:
1. 1st Generation Sulfonylureas

Fx: Given to stimulate B-cell to secrete endogenous insulin
a. Chlorpropamide (Diabenase) C/I:

b. *Tolbutamide (Orinase) Pregnant Women
c. Tolazamide (Tolinase) Monitor For:
Surgery
d. *Acetonexamide (Dymelor) Allergy
e. Glibenclamide (Euglucon) GI upset
Infection
f. Gliclazide (Diamicron) Headache
Stress
g. Glipizide (Minidiab) Paresthesia
Kidney/liver damage
Weakness
*Presence of any of these
2. 2nd Generation Sulfonylureas Tinnitus
even if pt. is NIDDM insulin
a. Diabeta (Micronase) is required
b. Glipside (Glucotrol)
3. Biquanides
- Increase uptake of glucose by the cell but prolonged use may cause lactic acidosis
Ex. Metformin
Glucophage
Nsg Mgt or OHA:
1. Administer with meals – to lessen GIT irritation & prevent hypoglycemia
2. Avoid alcohol (alcohol + OHA = severe hypoglycemic reaction) ---leads to antabuse (Disulfiram) toxicity
Nsg Mgt For DM:
1. Monitor for PEAK action of OHA & insulin

3. Monitor VS, I&O, neurocheck, blood sugar levels.
4. Administer insulin & OHA therapy as ordered.
5. Monitor signs of hyperglycemia & hypoglycemia.
-Pt DM –“ hinimatay”
- You don’t know if hypo or hyperglycemia - Give simple sugar
(Brain can tolerate high sugar, but brain can’t tolerate low sugar!)
*Cold, clammy skin – Hypoglycemia – Orange Juice or simple sugar
*Warm to touch, dry – Hyperglycemia – Administer insulin
DIABETIC DIET
6. Provide nutritional intake of Diabetic Diet:
CHO = 50%
-Or offer alternative food products or beverage.
CHON = 30%
-Lots of orange juice.
Fats = 20%
7. Exercise – after meals to promote increase glucose utilization
- After strenuous exercise, glucose is already consumed even w/o insulin
Pre-breakfast insulin: For pt. who exercised already—decrease dose of insulin
Athletes: Take snacks in between exercise
8. Monitor complications of DM
a. Atherosclerosis – HPN, MI, CVA
b. Can affect the small minute capillaries of eyes & kidney leading to : Microangiopathies (thickening)
c. Eyes – Diabetic retinopathy , Premature cataract & blindness
d. Kidneys – Recurrent pyelonephritis & Renal Failure
e. Gangrene formation 2 Major Cause of Renal
f. Peripheral Neuropathy Failure
- Diarrhea/ Constipation
- Sexual impotence (Complication of HPN & DM) 1. DM
g. Shock
9. Foot Care Mgt d/t delayed wound healing especially of extremities

a. Avoid waking barefooted
b. Cut toe nails straight
c. Apply lanolin lotion – prevent skin breakdown
d. Avoid wearing constrictive garments
e. No Crossing of legs
f. Avoid local cold application in extremities
g. Never elevate legs on pillow to prevent tissue ischemia unless there are sx of leg edema
10. Encourage annual eye & kidney exam

11. Avoid smoking d/t vasoconstriction
12. Monitor urinalysis for presence of ketones or Blood or serum – more accurate
13. Assist in surgical wound debridement
14. Monitor signs of DKA & HONKC
15. Assist surgical procedure: BKA or above knee amputation
D. DM ASSOCIATED WITH OTHER DISORDER
a.) Pancreatic tumor

b.) Cancer 3 Main Food Groups
c.) Cushing’s syndrome Anabolism Catabolism
1. CHON Glucose Glycogen
Increase Fat Catabolism 2. CHON Amino Acids Nitrogen
3. FATS Fatty Acid Free Fatty Acid
Free Fatty Acids (Cholesterol &
Ketones)
Cholesterol Ketones DKA
Atherosclerosis Coma
HPN Death
MI Stroke
HEMATOLOGICAL SYSTEMS
Overview:
I . BLOOD-FORMING ORGANS
1.Thymus – removed myasthenia gravis

2. Liver – largest gland (occupies most of the right hypochondriac region)
3. Lymph nodes
4. Lymphoid organs – Payer’s Patches (located between the small intestine- site of salmonella thypi)
5. Bone marrow
6. Spleen
Ex.
Varicosities
Deep Vein Thromboplehbities
II. BLOOD VESSELS
1. Veins –SVC, IVC, Jugular vein, superficial – blood towards the heart
2. Artery – deep seated, carries blood away from the

- 2 largest artery : Aorta, carotid Ex.
Aneurysm
3. Capillaries Buerger’s Disease
Raynaud’s Disease
III. BLOOD
Blood
Formed Elements 45 % 55% Plasma & Serum
Cellular Components: Plasma CHON’s (Liver)
1. RBC (Erythrocytes) 1. Albumin - largest, most abundant plasma

- largest
(Normal: 4 – 6 M/mm3) Fx: Maintains osmotic pressure preventing edema,
- Anucleated (no nucleus) If decrease albumin- Ascites
- Biconcave discs Promotes skin integrity
- Has molecules of Hgb (red cell pigment)
- Transports & carries O2 2. Globulins
a. Alpha – Transports steroids, hormones & bilirubin

b.  - Transports iron & copper
c. Gamma – Transport immunoglobulins or antibodies
Hgb:
F = 12-14 gms% 3. Prothrombin (CF2)– Fibrinogen (CF1)
M = 14-16 gms % – Clotting factor to prevent bleeding
- Spleen life span = 120 days
Hct : 3x Hgb
F = 36-42 %
M = 42-48 %
Average = 42 %
CLOTTING FACTOR 1-13
CF 1 = Fibrinogen From
CF 2 = Prothombin Pakistan
CF 3 = Thrombin To
CF 4 = Ca # China
CF 5/6 = Proaccelerin - Labile factor People
CF 7 = Procenvertion - Stable Factor Power
CF 8 = Anti- HFA Against
CF 9 = Christmas Factor/ Anti-hemophilia Communism

CF 10 = Stuart-Prower Start
CF 11 = Plasma Thromboplastin Peace
CF 12 = Hageman Hate
CF 13 = Fibrin Stabilizing Factor Fire
COAGULATION PATHWAY/CASCADE
Intrinsic Factor Stage 1 Extrinsic Factor
EF TF TF (CF3)
CF 12
CF 9 F
CF 11
CF 9--------------------------------------------------CF 10 ------------------------------------------ CFS
Creates------Prothrombinase----------------- CF 2 Stage 2
Product of Stage 1
Thrombin
Stage 3
CF 1
Fibrin
Clot -------- --Clot dissolved
Tissue Plasminogen Activator
Plasminogen
Plasmin Stage 4
I. DISORDERS OF THE BLOOD
Pathophysiology:
BLOOD DYSCRASIA
Production of blood cells Production of both normal Spleen Disorder Defect in Coagulation
(PANCYTOPENIA) & defective cells Mechanism
Life span of RBC

8-120 days
1. ANEMIA
- A condition in which the hemoglobin concentration is lower than normal
- Results from :
1. Decreased Erythropoiesis (Formation-maturation process of RBC)
2. Increased Hemolysis
3. Bone Marrow Depression
4. Blood loss 1 st Sign of ANEMIA:
Weakness &
Pathophysiology: Hgb Count
Reduction in the O2 carrying capacity of the blood Hallmark & Basis of Anemia
All symptoms cause by this
TISSUE HYPOXIA
Brain Restlessness Heart Respiratory GIT Skin

Headache, Irritability Anginal Pain RR Anorexia Mucus Membrane
Syncope, Vertigo PR Dyspnea Angular Cheilosis
Fatigability
Lesions at the
Palpitation
corner of the mouth
D/T compensation of the

body D/T decreased Hgb that Pallor
gives color to skin
Brittle nails & hair

KOILONYCHIA (Spoon-shaped nails)
d/t atrophy of epidermal
cells
Intolerance to Cold
D/T decreased
RBC
Normal shape of nails = Biconcave & 180
CAUSES: Substances Needed For Maturation Of RBC:

I. DECREASED ERYTHROPOIESIS 1. CHON – formation of all tructure/membrane
2. Iron/Fe - formation of pigment hemoglobin
Production maturation of RBC 3. Vit. B 12 - responsible for synthesis of nucleic acid
4. Folic Acid - matures the cell
5. Vit. C - catalyst for iron/absorption of iron
Absence of any one of the factors 6. Vit. B6
For RBC maturation will cause 7. Intrinsic Factor
Type I:
A. IRON DEFECIENCY ANEMIA
- Cells are microcytic (small) & hypochronic d/t inadequate absorption of iron leading to hypoxemic injury
“HYPOCHROMIC ANEMIA” “HYPOPROLIFERATIVE ANEMIA”
Pathophysiology: The body stores of iron decrease, leading to depletion of hemoglobin synthesis
Incidence Rate: Common:

Suicide - common in teenager
1. Common in developed country d/t high cereal intake & accidents Poisoning – common in children (aspirin)
2. Common in tropical countries – blood sucking insects Aspiration – common in infant
3. Women – 15 – 45 y/o of reproductive yrs Accidents – common in adults
4. Common among the poor d/t poor nutritional intake Choking – common in toddler
SIDS – common in infant in US
1. Chronic blood loss- most common cause Bleeding:

a. Trauma Hematemesis – vomiting of blood
b. Menstruation Melena – passage of dark stool
c. GIT bleeding - Bleeding in Upper GIT
- Doudenal Cancer
2. Inadequate intake of food rich in iron Hematochezia –passage of fresh blood
- Bleeding in Lower GIT
3. Inadequate absorption or iron d/t : - large intestine
a. Chronic diarrhea (Metabolic Acidosis)
b. Malabsorption syndrome (Celiac Disease)
c. High cereal intake with low animal CHON ingestion Decreased O2
d. Subtotal gastrectomy
4. Improper cooking of food/ Alcoholism Atrophy of cells
S/Sx: Cerebral Hypoxia
1. Asymptomatic PICA
2. General body malaise
3. All Sx of Anemia + PICA – abnormal appetite or craving for non-edible food Ex. Chalk
+ “PLUMMER VINSON’S SYNDROME Atropic Glossitis – inflammation of tongue

Stomatitis – mouth sores
Dysphagia
Dx :
1. RBC
2. Hgb Nsg Dx:
3. Reticulocyte Activity Intolerance
4. Hct
5. Iron
6. Ferritin
7. Bone Marrow Aspiration = Most Definitive
Tx:
1. Blood Transfusion = Packed RBC
Nsg Mgt:
IRON-RICH FOOD:
1. Monitor signs of bleeding of all hematologic test including urine, stool & GIT 1 ST : organ meat, liver
2. Complete bed rest – don’t overtire pt 2nd: eggyolk
3. Encourage – iron rich food 3rd: raisins, legumes
4. Instruct the pt to avoid taking tea (Tannates - impairs iron absorption) dried fruits
5. Administer meds: Hematinic Agents or drugs that will increase blood heme nuts
4th: green leafy vegetables
a.) Oral iron preparation
Ferrous SO4
Fe gluconate 300 mg OD
Fe Fumarate
Fortifier
Fergon, Feorol, Iberet
*Liquid Preparations: W/ brassy taste, disguise by chilling
Nsg Mgt Of Oral Iron Medication: IRON Side-Effects:

Anorexia
1. Administer w/ meals – to lessen GIT irritation/or 0ne hours before meals N/V
Abdominal Pain
Diarrhea/ Constipation
Melena
2. If diluting in iron liquid prep –administer w/ straw
3. Give Orange juice – for absorption
4. Monitor & inform pts S/E
5. If pt can’t tolerate oral iron preparation

– Administer parenteral iron preparation
1. Iron dextran (IV, IM)
2. Sorbitex (IM only)
3. Inferon, Jectofer
Nsg Mgt Parenteral Iron Preparation:
1. Administer using Z tract method to prevent discomfort, discoloration leakage to tissues.

2. Don’t massage injection site. Ambulate to facilitate absorption.
3. Monitor S/E:
a.) Pain at injury site
b.) Localized abscess (“nana”)
c.) Lymphadenopathy
d.) Fever/ chills
e.) Urticaria – itchiness
f.) If (+) to Hypotension ------------Anaphylactic shock
Give epinephrine (SNS Effect)
B. FOLATE DEFICIENCY ANEMIA
- Cell is macrocytic, hypochromic anemia

- A form of “MEGALOBLASTIC ANEMIA”
- Anemia’s characterized by abnormal large RBC 2nd to impaired DNA synthesis d/t deficiency of Folic acid
Pathophysiology:
Folic acid impaired DNA synthesis in the bone marrow impaired RBC development, impaired nuclear
maturation but cytoplasmic maturation continues large size
Causative Factors:
1. Alcoholism
2. Mal-absorption
3. Diet deficient in uncooked vegetables
Sx: All symptoms of Anemia
C. PERNICIOUS ANEMIA
- A megaloblastic chronic anemia characterized by deficiency of intrinsic factor secreted by the parietal cells
leading to Hypochlorhydria---------decrease Hcl acid secretion
- A Vit. B12 deficiency
1. Subtotal Gastrectomy – partial removal of the stomach
2. Atrophy of gastric mucosa (elderly) ------ # 1 cause Largest part of GIT = Large Intestine
3. Hereditary Widest part of GIT = Stomach
4. Inflammatory disorder of ileum
5. Autoimmune
6. Strict vegetarian diet
7. Gastrointestinal malabsorption----Crohn’s Disease/ Cancer of stomach
Pathophysiology: STOMACH (composed of different cells)
Parietal or ergentaffen Oxyntic cells

Function: Produce Intrinsic Factor Function: Secrets Hcl acid
INTRINSIC FACTOR HYDROCHLORIC ACID
Binds w/ Vit. B12 to promote absorption Aids in digestion
For maturation of RBC Decreased Digestion ----- Dyspepsia & Weight Loss
Disorder in the Process

Diet: High caloric Intake to correct Wt loss
Immature RBC
Killed by Spleen
Heme----Globin
Ferroes------------Ferretin = Bilirubin ----- Jaundice
S/Sx:
1. All Sx of Anemia +
2. GIT changes
a. RED –BEEFY TONGUE = PATHOGNOMONIC SIGN
b. Dyspepsia – indigestion
c. Wt loss, mild diarrhea
d. Jaundice
3. CNS – Most dangerous anemia d/t neurologic involvement d/t deficiency in Vit. B 12
a. Tingling sensation
b. Paresthesia (numbness) in extremities
c. (+) Romberg’s test = Ataxia
d. Psychosis
Dx:
1. Peripheral Blood Smear = shows giant RBCs, WBCs w/ giant hypersegmented nuclei
2. Very High MCV
3. Shilling’s Test = reveals inadequate absorption of Vit. B 12
4. Intrinsic Factor Antibody Test
Common Route: Dorso-gluteal
Tx:
Ventro-gluteal
1. Vit. Supplementation : Folic Acid 1 mg daily
2. Diet Supplementation
3. Lifetime monthly injection of IM Vit. B 12 as ordered -----not oral---pt. may developed drug tolerance—No S/E
Nsg Mgt :
1. Enforce CBR
2. Diet – high calorie or CHO----Increase CHON, iron & Vit C
3. Avoid irritating mouthwashes. Use of soft bristled toothbrush is encourage
4. Avoid applying electric heating pads – can lead to burns
II. INCREASE HEMOLYSIS/ “HEMOLYTIC ANEMIA”
- Destruction of RBC greater than the rate of formation

----all + Hyperbilirubinemia-----JAUNDICE + TEA-COLORED URINE
Causes:
1. Post-viral injection
2. Exposure to ionizing radiation
3. Prolong use of toxic drugs & medications (penicillin, chloramphenicol)
Type II:
A. SICKLE CELL ANEMIA

- A severe chronic incurable hemolytic anemia that results from heritance of the sickle hemoglobin gene.
Causative Factor:
1. Genetic inheritance of the sickle gene- HbS gene
Pathophysiology:
Decreased O2, Cold, Vasoconstriction can precipitate sickling process
Factors cause defective Hgb to acquire a rigid, crystal-like C-shaped configuration
Sickled RBCs adhere to endothelium pile up & plug the vessels ischemia results pain, swelling & fever
Sx:
1. Jaundice
2. Enlarged skull & facial bones
3. Tachycardia, murmurs & cardiomegaly
Primary sites of thrombotic occlusion: spleen, lungs & CNS
4. Chest pain, dyspnea
Complications:
1. Sickle Cell Crises = Results from tissue hypoxia & necrosis

2. Acute Chest Syndrome = Manifested by a rapidly falling Hgb level, tachycardia, fever & chest infiltrates in the CXR
Tx:
1. Bone marrow transplant
2. Hydroxyurea = Increases the Hgb
3. Long term RBC transfusion = Packed RBC
Surgery For Hemolytic anemia = Spleenectomy
Nsg Mngt:
1. Manage the pain 3 Nursing Priority:

Support & elevate acutely inflamed joint
Relaxation techniques 1. A/W – Avoid deoxygenating activities
Analgesics - High altitude is bad
2. Prevent and manage infection 2. Fluid Deficit – Promote hydration
Monitor status of patient 3. Pain & Comfort
Initiate prompt antibiotic therapy
3. Promote coping skills
Provide accurate information
Allow patient to verbalize her concerns about medication, prognosis & future pregnancy
4. Monitor and prevent potential complications
Provide always adequate hydration
Avoid cold, temperature that may cause vasoconstriction
5. Monitor and prevent potential complications
Leg ulcer
Aseptic technique
Priapism = Sudden painful erection
Instruct patient to empty bladder, then take a warm bath
B. POLYCYTHEMIA
- Refers to an INCREASE volume of RBCs -----reverse of sickle cell anemia

- The hematocrit is ELEVATED to more than 55%
Classified as Primary or Secondary
1. POLYCYTHEMIA VERA
- Primary Polycythemia
- A proliferative disorder in which the myeloid stem cells become uncontrolled
Causative Factor: Unknown
Pathophysiology:
The stem cells grow uncontrollably
The bone marrow becomes HYPERcellular & all the blood cells are increased in number
The spleen resumes its function of hematopoiesis and enlarges
Blood becomes thick & viscous causing sluggish circulation
Overtime, the bone marrow becomes fibrotic
Sx:
1. Skin is ruddy
2. Splenomegaly POLYCYTHEMIA
3. Dizziness, blurred vision, HA Earliest Sign : Headache
5. Angina, dyspnea & thrombophlebitis Late Sign: Pruritus
Dx: Complication: Stroke, Thrombosis

1. CBC- shows elevated RBC mass
2. Normal oxygen saturation
3 Elevated WBC & Platelets
Complications:
1. Increased risk for thrombophlebitis, CVA MI

2. Bleeding d/t dysfunctional blood cells
Tx:
1. To reduce the high blood cell mass- PHLEBOTOMY
2. Allopurinol
3. Dipyridamole
4. Chemotherapy to suppress bone marrow
Nsg Mngt:
1. Primary role of the nurse is EDUCATOR
2. Regularly assess for the development of complications
3. Assist in weekly phlebotomy
4. Advise to avoid alcohol & aspirin
5. Advise tepid sponge bath or cool water to manage pruritus
III. BONE MARROW DEPRESSION/ HYPOPLASTIC ANEMIA
- Inadequate abnormal cells-------Hypoplastic anemia/Aplastic Anemia

- All Sx + decreased WBC --------------Leukopenia ----------risk for infection
+ decreased PLATELETS--- Thrombocytopenia----- bleeding
when all 3 are present ----- PANCYTOPENIA
WBC
(Leucocytes 5,000 – 10,000/mm3)
GRANULOCYTES NON-GRANULOCYTES
3 Types:
1. Polymorphonuclearneutrophils (PMNs) A. Monocytes (Macrophage)
-Largest WBC

- Most abundant 60-70% WBC - Involved in long term phagocytosis
- Lifespan of 24-48 hrs. - For chronic inflammation
Function: Short-term Phagocytosis - Other name macrophage
For acute inflammation
2. Polymorphous Basophils (PMBa) Macrophage in CNS- Microglia

Macrophage in skin – Histiocytes
-Involved in Parasitic infection Macrophage in lungs – Alveolar macrophage
- Release of chemical mediator for inflammation Macrophage in Kidneys – Kupffer cells
(Serotonin, Histamine, Prostaglandin, Bradykinins)
-Absorbs large fat particles after ingestion of high fat meal B. Lymphocytes
3 Types:
3. Polymorphous Eosinophils (PMEo)
1. B Cell – L
- Involved in Allergic reactions – Bone marrow or bursa dependent
- Arises from bone marrow
HIV
2. T Cell
Window Period: 6 months
– Dev’t of immunity
Incubation: 6 months to 5 yrs.
- From thymus
Sx: Kaposi Sarcoma
- Target cell of HIV
Dx Test: Western Blot Test
Drug of Choice:
3. NK Cell
Zidovudine ( AZT or Retrovir)
– Natural killer cell
Standar Precaution:
-Have both antiviral & anti-tumor properties
Gloves, Gown, Goggles & Mask
C. Platelets (Thrombocytes)
SIGNS OF PLATELET DYFUNCTION (Normal: 150,000 – 450, 000/ mm3)
1. Petecchiae - Promotes homeostasis – prevention of blood loss by
2. Ecchymosis/bruises activating clotting
3. Oozing of blood from venipuncture site - Consists of immature or baby platelets known as
Megakaryocytes – Target of Dengue Virus
- Normal lifespan 9 – 12 days
A. APLASTIC ANEMIA
– A condition characterized by decreased number of RBC as well as WBC & platelets
- Common among clients undergoing chemotherapy, Cobalt therapy, Radiation therapy
- Stem cell disorder d/t bone marrow depression leading to pancytopenia – all RBC are decreased
Decrease RBC Decrease WBC Decrease platelets

Anemia Leucopenia Thrombocytopenia
Susceptibility to infection No clotting
Fever Bleeding
Petechia Ecchymosis Bruising

(Purpura)
Predisposing Factors :
1. Environmental Toxins & Chemicals – Pesticides, Benzene & its derivatives
2. radiation

3. Immunologic injury
4. Certain drugs –causes bone marrow depression
a. Chemotherapeutic agents, = Methotrexate, Nitrogen Mustard (anti-metabolite), Vincristine
b. Broad Spectrum antibiotic =Chlorampenicol, Sulfonamides – bactrim
(Pt – severe isolation)
c. Phenybutazones
5. Heavy Metals
Pathophysiology:
Toxins cause a direct bone marrow depression acellular bone marrow decreased production of blood elements
Sx:
1. All Sx of Anemia +
2. Leucopenia – increase susceptibility to infection
3. Thrombocytopenia
4. Splenomegaly
5. Retinal hemorrhages
Dx:
1. CBC- decreased blood cell numbers
2. Bone marrow aspiration at posterior iliac crest: Confirms the anemia- hypoplastic or acellular marrow replaced by fats
Fatty streaks in bone marrow
Tx:
1. Bone Marrow Transplantation Bone Marrow Transplantation
2. Immunosuppressant drugs 1. Syngeneic BMT
3. Rarely, steroids – donor from twins
4. Blood transfusion = Fresh Whole blood 2. Allogenic BMT
Nsg Mgt: – Related or unrelated as long
1. Removal of underlying cause as compatible (Human leukocyte antigen)
2. Blood transfusion as ordered 3. Autologous BMT
3. CBR – Own self
4. O2 inhalation - harvest marrow during remission
5. Reverse isolation d/t leukopenia
6. Monitor signs of infection
7. Avoid SQ, IM or any venipuncture site
8. Use electric razor when shaving to prevent bleeding
9. Administer meds:
Immunosuppressant
Anti lymphocyte globulin (Alg) given via central venous catheter, 6 days – 3 weeks to achieve max therapeutic effect of
drug.
IV. BLOOD LOSS

- Cells are normocytic (normal size), normochronic (normal content) but d/t surgery, menstruation------anemia
- All Sx + Hypovolemia
- Blood Transfusion = Fresh Whole blood
OTHER BLOOD RELATED PROBLEMS
1. DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
- Acute hemorrhagic syndrome characterized by wide spread bleeding & thrombosis d/t a deficiency of clotting
factors (Prothrombin & Fibrinogen).
1. Rapid BT d/t hemolysis

2. Massive trauma
3. Massive burns
4. Septicemia
5. R/T Hemolytic reaction & Anaphylaxis
6. Neoplasia – new growth of new tissue (tumor)
7. Pregnancy
8. Septicemia
S/Sx:

1. Petechiae – widespread & systemic (lungs, lower & upper trunk)
2. Ecchymosis – widespread
3. Oozing of blood from venipunctured site
4. Hemoptysis – cough blood
5. Hemorrhage
6. Oliguria---------------LATE SIGN
Dx :
1. CBC – reveals decrease platelets

2. Stool for occult blood (+)
Specimen – stool
3. Opthalmoscopic exam – sub retinal hemorrhage
4. ABG analysis – metabolic acidosis
Nsg Mgt:
1. Monitor signs of bleeding – All hematologic test + urine, stool, GIT

2. Administer isotonic fluid solution
3. Administer O2 inhalation
4. Administer meds:
a. Vit K aquamephyton
b. Pitressin or vasopressin -----t o conserve H20 & has vasoconstriction effect----Most Common S/E: Chest Pain
5. NGT – lavage
- Use iced saline lavage 1st to induce vasoconstriction inside the stomach
6. Monitor NGT output

7. Provide heplock
8. Prevent complication: Hypovolemic shock----Early Sign: Restlessness & Cool moist Skin
Late Sign of hypovolemic shock : Anuria
9. Give Heparin-----short-acting
DIAGNOSTIC TEST FOR BLOOD DYSCRASIAS
1. CBC, Hgb, Hct
2. BT, CT, PT
3. ERYTHROCYTE INDEX
MCV = Mean Corpuscolar Volume -----to evaluate size of RBC

MCH = Mean corpuscular Hgb -----------to evaluate the Hgb content of RBC
MCHC = Mean corpuscular Hgb Concentration—to evaluate Hgb content of Pack RBC (in grams /100ml)
(Normal: 30-36 grams/100ml)
4. COOMB’S TEST RBC

Normal Size: 80-94 cu micron
- To evaluate the presence of immune bodies that adheres to < 80 ---- Microcytic Cell ANISOCYTOSIS
RBC causing hemolysis/agglutinization of RBC > 94 ----- Macrocytic Cell (abnormal size)
(Rh Incompatibility, ABO Incompatibility)
Normal Hgb content of RBC: 22-28 micromicrogram
Created by Niňa E. Tubio < 22 >28 74

Hypochromic Hyperchromic
5. SCHILLING TEST
- To evaluate rate of absorption of Vit. B12 (Cyanocobalamine)

- Use to diagnosed Pernicious Anemia
Procedure: Administer P.O. radioactive Vit. B12 ------24 hr. urine

Check (+) (-) of Vit. B12 ------ if (-) Pernicious Anemia (do not give P.O. give parenterally)
------ if (+) in urine ---normal
Common in Pts. Who undergone gastrectomy/ cancer----they do not have intrinsic factor
6. BONE MARROW ASPIRATION/PUNCTURE/TAP

POIKILOCYTOSIS = abnormality in shape of RBC
METARUBRICYTE = abnormal RBC w/ nucleated
- To evaluate size, shape, character of RBC cells

- Invasive (consent)
- Local anesthesia (lidocaine 1-2%)
- Sites: Sternum ------ Position: Supine
A & P Iliac Crest ------ Position: Supine (A) & Prone/Lateral (P)
- Pediatric pts. --- use the long bones (femur, humerus)-----as we grow older the # of marrows in long bones decreases
- Apply pressure dressing over site to prevent bleeding
7. LYMPH NODE BIOPSY
- Site : Cervical LN, Axilla LN, Inguinal LN
IV. BLOOD TRANSFUSION:
Objectives:
Packed RBC = 250 ml
Refrigerated = 3-5 days
1. To replace circulating blood volume
Platelet = 3-6 days
2. To increase O2 carrying capacity of blood
3. To combat infection if there’s decrease WBC
4. To prevent bleeding if there’s platelet deficiency
Nsg Mgt & Principles in Blood Transfusion
1. Proper refrigeration
2. Proper typing & cross matching
Type O – universal donor
AB – universal recipient
85% of people are RH (+)
3. Aseptically assemble all materials needed:
a.) Filter set
b.) Isotonic or PNSS or .9NaClfor flushing to prevent Hemolysis
Hypotonic solution – Cell swells or burst

Hypertonic solution – Cell will shrink or crenate
c.) Needle gauge 18 - 19 or large bore needle to prevent hemolysis.
d.) Instruct another RN to recheck the following .
Pts name, blood typing & cross typing expiration date, serial number – Most important
e.) Check blood unit for bubbles, cloudiness, dark in color & sediments – indicates bacterial contamination.
Return to blood bank, do not dispose
f.) Never warm blood products – may destroy vital factors in blood.
- Warming is done if with warming device – only in EMERGENCY!
- Within 30 mins room temp only!
g.) Blood transfusion should be completed < 4hrs because blood that is exposed at room temp for > 2h causes blood
deterioration------can lead to bacterial contamination
h.) Avoid mixing or administering drug at BT line – leads to hemolysis
i.) Regulate BT 10 – 12 gtts/min KVO or 100cc/hr to prevent circulatory overload
j.) Monitor VS before, during & after BT especially q15 mins for 1st hour
- Majority of BT reaction occurs within 1h.
BLOOD TRANSFUSION REACTIONS:

BT REACTIONS:
1. HEMOLYTIC REACTION
H - Hemolytic Reaction
Sx: A - Allergic Reaction
Headache P - Pyrogenic Reaction
Dizziness C - Circulatory Reaction
Dyspnea A - Air Embolism
Palpitation T - Thrombocytopenia
Lumbar/Sternal flank pain C - Citrate Intoxication
Hypotension, Flushed Skin---red port wine urine H - Hyperkalemia d/t expired blood
Nsg Mgt:
1. Stop BT
2. Notify Doc
3. Flush with plain NSS
4. Administer isotonic fluid sol – to prevent acute tubular necrosis & counteract shock
5. Send blood unit to blood bank for reexamination
6. Obtain urine & blood samples of pt & send to lab for reexamination
7. Monitor VS & Allergic Rxn
2. ALLERGIC REACTION
S/Sx:
1. Fever/ chills
2. Urticaria/ pruritus
3. Dyspnea
4. Laryngospasm/ bronchospasm
5. Bronchial wheezing
Nsg Mgt:
1. Stop BT
2. Notify Doc
3. Flush with PNSS
4. Administer antihistamine – diphenhydramine Hcl (Benadryl)
If (+) Hypotension – anaphylactic shock administer – epinephrine
5. Send blood unit to blood bank
6. Obtain urine & blood samples – send to lab
7. Monitor VS & IO
8. Adm. Antihistamine as ordered for Allergic Rxn, if (+) to hypotension – indicates anaphylactic shock
Shock -----administer epinephrine
9. Administer antipyretic & antibiotic for pyrogenic Rxn & TSB

3. PYROGENIC REACTION:
S/Sx:
a.) Fever/ chills d.) Tachycardia

b.) Headache e.) Palpitations
c.) Dyspnea f.) Diaphoresis
(Pyrogens -----fever-producing agents)
Nsg Mgt:
1. Stop BT
2. Notify Doc
3. Flush with PNSS
4. Administer antipyretics, antibiotics
5. Send blood unit to blood bank
6. Obtain urine & blood samples – send to lab
7. Monitor VS & IO
8. Tepid sponge bath – offer hypothermic blanket
4. CIRCULATORY OVERLOAD
PRIORITY CASES
Sx:
- Dyspnea Hemolytic Reaction = 1st
- Orthopnea d/t Hypotension---attend to destruction of Hgb
- Rales or crackles ------ O2----- Brain Damage
- Exertional discomfort
Circulatory Reaction = 2 nd
Nsg Mgt: Allergic Reaction = 3 rd
Pyrogenic Reaction = 4 th
1. Stop BT
2. Notify Doc But:
3. Administer diuretics Anaphylactic = 1st priority
Hemolytic = 2nd
ONCOLOGIC NURSING
Oncology – study of neoplasia –new growth
Benign (tumor) Malignancy (cancer)
Well differentiated Poorly or undifferentiated

Encapulation – (+) (-)
Metastasis – (-) (+)
Prognosis – good Poor prognosis
Surgery 1. Chemotherapy Many S/E
2. Radiation
3. Surgery most preferred treatment
4. Bone marrow transplant - Leukemia only
Predisposing Factors: (Carcinogenesis)

G – genetic factors
I – immunologic factors
V – viral factors
a. Human Papiloma Virus – causing warts
b. Epstein Barr Virus
E – environmental Factors 90%
a. Physical – irradiation, UV rays, nuclear explosion, chronic irritation, direct trauma
b. Chemical factors –
- Food additives (nitrates
- Hydrocarbon vesicants, alkalies
- Drugs (stillbestrol) Warning / Danger Sx of CANCER
- Urethane
- Hormones C – change in bowel /bladder habits
- Smoking A – a sore that doesn’t heal
Male: U – unusual bleeding/ Discharge
st
1 Lung Cancer – Bronchogenic d/t smoking T – thickening of lump – breast or elsewhere
nd
2 Liver Cancer – Hepatic d/t alcohol I – indigestion/Dysphagia
rd
3 Prostate cancer – 40 y/o & above (middle age & above) O – obvious change in wart/ mole
th
4 Testicular Cancer – 30 y/o N – nagging cough/ hoarseness
BPH – 50 & above U – unexplained anemia
A - anemia
Female: S – sudden wt loss
st
1 Breast Cancer – 40 yrs old & up
– Mammography 15 – 20 mins (SBE – 7 days after mens)
2nd Cervical Cancer – 90% Multi-sexual partners
5% Early Pregnancy
3rd Ovarian Cancer – common to squamous cell type 3 L’S TRIAD Sx
4th Uterine Cancer
Large
Lump
Loaded
CLASSES OF CANCER:
Tissue Typing:
1. Carcinoma – arises from surface epithelium & glandular tissues
2. Sarcoma- from connective tissue or bones
3. Multiple myeloma – from bone marrow

Pathological fracture of ribs & back pain
4. Lymphoma – from lymph glands
5. Leukemia – from blood
1. LEUKEMIA
- Cancer of the WBC
Pathology: Uncontrolled abnormal proliferation ---------------immature WBC known as Blast Cells
activity of cell cellular metabolism Temperature
Proliferation of BLAST CELLS prone to infection
Invade/Infiltrate vital organs Crowd/ Congest/Accumulate
Spleen Liver Kidney Brain Joint Pain, Swell
Spleenomegaly Hepatomegaly RF ICP Hinder/Prevent Production of Cells
RBC Platelets

CLASSIFICATION:
ONSET DURATION CELLS
1. ACUTE LEUKEMIA Sudden Short < 6 months Immature blast cells
2. CHRONIC LEUKEMIA Gradual long duration Mature WBC

- Characterized by periods of remission (absence) & exacerbation (recurrence)
PREDOMINANT CELLS PRESENT IN BLOOD:
1. Acute/Chronic Lymphocytic Leukemia = Lymphocytes & monocytes ---- ALL (common to children)
2. Acute/ Chronic Myelocytic Leukemia = myeloblasts ----- CML (common to Adult)
Cells Derived
1. Bone Marrow 2. Lymphoid Tissue
Granulocyte Agranulocyte Agranulocyte
Immature immature immature
Myeloblast Monoblast mature
Myelocyctes Monocyte Lymphocyte
2. BREAST CANCER
1. Family Hx (mother/sister)
2. Obesity
3. Unmarried at age 40 y/o
4. Married w/o children
5. Married w/ children but did not breastfeed Early Sign of Breast Ca:
6. Women w/ prolonged menstruation Non-tender
7. Early menarche at 11 y/o Non-mobile
8. Late menopause at 52 y/o Painless breast mass/lump
9. 1st pregnancy at age 35 y/o
Prevention: SBE = 7-10 days after menstruation

= after menopause----- 1x/month
Sx: Late Sign of Breast Ca:

1. Dimpling of skin
2. Orange skin MASTOIDYNA = breast pain
3. Asymmetry of breast
4. Discharges of nipple
Dx: Common Site Of Breast Ca

1. Mammography
Created by Niňa E. Tubio UPPER OUTER QUADRANT LEFT 79
2. Breast Biopsy = Best confirmatory Dx
Tx:
1. Surgery:
Lumpectomy
Modified Mastectomy – mass, tissue, pectoralis major or minor at axillary
Radical Mastectomy - leave either pectoralis major or minor muscle
3. ONCOLOGIC EMERGENCIES
1. Obstructive or Compressive Disorders

PROGNOSIS
– Superior vena cava syndrome Lung = 6 yrs
– Pericardial effusion/cardiac tamponade Breast = 2-6 yrs.
– Leukostasis Colon = 2-6 yrs.
– Spinal Cord Compression Pancreatic = 3-6 months
Liver = 3 mnths
2. Metabolic Disorders
– Hypercalcemia
– Symptoms of SIADH
– Tumor lysis syndrome
3. Disruptions of hematologic/im-munologic function
– DIC
– Septic shock
3. BRAIN TUMOR
Location:
1. Supratentorial – Cerebrum, anterior 2/3 of the brain
2. Infratentorial – Cerebellum, brainstem, posterior 1/3 of the brain

Early Sign of Brain Tumor:
*Both will manifest Increased ICP PAPILLEDEMA
(tumor compress on optic chiasm)
Both will undergo Brain Surgery:
a. CRANIOTOMY/CRANIECTOMY
- Use general endotracheal anesthesia (For all brain surgery)
If surgery lasts for more than 2 hrs, assured of patent airway
- Type of incision: Coronal or Butterfly
- Skin Preparation: Shaving of head done at stage 3 of anesthesia
Nursing Management:
DONT’S POST-OPERATIVE:
1. Do not put client on Trendelenberg position---- it will increase ICP & abdominal content will compress stomach
2. If pt. in shock: Supine w/ pillow, head turned to one side
3. If pt. not in shock: Supratentorial---- elevate head 45 degrees (SF) ---- to promote venous return to heart
Infratentorial ---- elevate head 10-15 degrees ------ to prevent compression of brain stem
--- turn head to one side, unoperated side especially if bone flap not returned
--- allowed on affected side but not more than 20 minutes to prevent ischemia
4. Do not give narcotic agent/analgesic

No Demerol------ respiratory depressant
5. No suctioning---- mere suction will trigger coughing----- Increased ICP

--- If needed: Oropharyngeal suctioning only
--- Nasal suctioning will damaged nasal mucosa---leakage of CSF
6. Do not restrain client

-- Makes client agitated --- Increased ICP
7. No rectal tube, rectal movement or manual extraction of feces.

-- Vagal stimulation------Bradycardia
Treatment Modality:
1. Radiotherapy
Classification of Cytotoxic Agents: Classification of Cytotoxic Agents: Classification of Cytotoxic Agents
Cell-Cycle Non-specific Cell-Cycle Specific 1. Hormones & Steroids
1. Alkylating Agents 1. Antimetabolite Action:

(S phase) Reduces cellular metabolism by
Action: providing a non-favorable
Therapeutic Modality: environment for growth of Ca cells
Action: Foster cell death by
Binds w/ DNA & prevents cell replication interfering w/ the cellular metabolic
1. CHEMOTHERAPY
process • Estrogens
– Nitrogen Mustard – DES (Post-menopausal)
• Cyclophosphamide (Cytoxan) – Cytarabine (Cytosar/Ara C) (Diethylstibestrol)
– Use various chemotherapeutic agents that kills cancer cells & kills normal rapidly producing cells – GIT, bone
• Chlorambucil (Leukeran) – 5-fluorouracil (5-FU) – Ethinyl estridiol
marrow, and hair follicle.
– Nitrosureas – Hydroxyurea
• Carmustine • Antiestrogens
– 6-mercaptopurine – Tamoxifen
• Lomustine (Purinethol)
– Alkylating-like agents – Raloxifene
– Methotrexate (Mexate)
• Busulfan (Myeleran)
• Carboplatin • Others
• Cisplatin (Platinol)* common – Aminogluthetimide
Thiotepa – Asparaginase
Ifex (Ifosfamide) – Leuprolide
2. Vinca/Plant Alkaloids – Mitotane
2. Antitumor/Anti-Neoplastics Antibiotics (M phase)
• Androgens (Pre-menopausal)
Action: Inhibits cell division by interfering Action: Mitotic Inhibitors – Fluoxymesterone
w/ synthesis of nucleic acid – Testosterone Propionate
– Docetaxel – Halotestin
– Bleomycin – Etoposide (Toposar)
– Doxorubicin – Vinblastine (Velban,Velbie) • Antiandrogens
– Dactinomycin – Bicalutamide
– Vincristine (Oncovin)
– Mitomycin – Flutamide
– Idarubicin
– Adriamycine (Doxorubicin) • Progestins
Created–byMithramycin
Niňa E. Tubio 81
– Medroxyprogesterone
– Plimcamycin – Megestrol acetate
– Actinomycin
Side-Effects: PROTOCOL IN THERAPY
1. GIT - -Nausea & Vomiting 6 cycle of Chemotherapy
Interval of 28 days
Nsg Mgt:
1. Administer anti-emetic (Plasil) 4 – 6h before start of chemotherapy

Ex. Ondansetrone – Zofran
Alprazolan - Zanax
2. Withhold food/ fluid before start of chemo
3. Provide bland diet post chemotherapy: Avoid spic foods---irritants
Ex. Non irritating / non spicy
4. Avoid bulky course diet
5. Advise Neutropenic Diet : Avoid raw foods, raw vegetable
- Diarrhea
Doxorubicin
1. Administer anti diarrhea 4 – 6h before start of chemo
2. Monitor urine, I&O qh -Toxic to myocardium
- Do not give if client is not hooked up
- Stomatitis/ Mouth Sores to a cardiac monitor
1. Oral care – offer ice chips/ popsickles

Use alkalanizer for mouth sores
2. Inform patient that 10-15 days after chemotherapy there will be hair loss – Temporary Alopecia
- Loss from other hair of the body
- Hair will grow back after 4 – 6 months post chemo.
-Bone Marrow Depression --------Leukopenia/Anemia
1. Enforce CBR
2. O2 inhalation
4. Monitor signs of bleeding
5. Inform pt. it will last only for 21 days
2. Reproductive Organ – Sterility
1. Do sperm banking before start of chemo
3. Renal System – Increase uric acid
1. Administer allopurinol/ xyloprin (gout)

Fx: Inhibits uric acid
Acute gout – colchicines
Increase secretion of uric acid
3. Neurological Changes – peristalsis – paralytic ileus
Most feared complication following any abdominal surgery

Vincristine – plant alkaloid causes peripheral neuropathy
Mngt:
1. Cancer drugs can be very potent------- it can destroy normal cells

2. Protect yourself from Ca drugs that can destroy the skin: cover everything
3. Increase fluid intake post-chemo d/t drugs are hepato-toxic
4. Avoid exposure of Ca drugs to light----reduces the potency of the drug---cover w/ carbon paper, dim lights
REVERSE ISOLATION TECHNIQUE
1. Private room, laminar air flow (positive pressure room)

2. Sterile linen, sterile hygiene equipment
3. Dedicated equipment
4. Put on shoe covers, mask & cap, sterile gown & gloves.
5. Low bacteria diet: no fresh fruits & vegetables; avoid drinking water allowed to stand for more than 15 min.
6. No fresh flowers or potted plants
7. Institute prophylactic oral hygiene regimen before, within 30 minutes after each meal & q2H–q4H during waking hours
8. May use ¼ tsp salt, pinch of baking soda & 8 oz. of H2O or saline
9. Avoid alcohol- or glycerine-based mouthwash
10. Use soft–bristled toothbrush
11. Use foam stick moistened with mouthwash to remove debris from mucosa
12. May apply topical anesthetic, as prescribed
13. Encourage fluid intake of 2000 ml/day
14. Encourage bland diet high in CHON to promote healing.
– Avoid hard or spicy food
– Avoid citrus juices
15. If patient has difficulty in eating & maintaining fluid intake, parenteral nutrition may be necessary
16. Assess the need for use of antifungal or antibacterial agents
2. RADIATION THERAPY
– Involves use of ionizing radiation that kills cancer cells & inhibit their growth & kill rapidly producing cells.
Types of Energy Emitted:
1. Alpha rays – rarely used – doesn’t penetrate skin tissues

2. Beta rays – internal radiation – more penetration
3. Gamma ray – external radiation – penetrates deeper underlying tissues
2 Methods of Delivery:
1. External Radiation - Involves electro magnetic waves

Ex. Cobalt Therapy, Teletherapy, External Beam Radiation
Nursing Responsibility:
a. Explain that it is a painless procedure

b. During procedure: “Pencil Markings “ on skin indicating area to be radiated
c. Tell pt. not to erase markings & cleanse area only w/ H2O. No soap. Pat dry.
d. Avoid sunlight over site
e. Avoid pressure over the site
f. Avoid hot/cold application over site
g. Avoid use of oil cream solution/lotion to prevent skin reaction
h. Observed for S/S of RADIATION SICKNESS
Locally Manifested Systematically

- Erythema - Leukopenia—bone marrow
- Dryness of skin - Sterility---- Gonads—both sensitive to radiation
- Loss of skin hair
- Blister formation
- Skin desquamation
2. Internal Radiation – Injection/ implantation of radioisotopes proximal to CA site for a specific period of time.
- Form of wire, seed, needle
- Isotope inside client’s body
Administering ISOTOPE:
a. Implant or “Intracavitary Implantation

- Insert isotope into body cavity
- Radium seed/Radom seed (sealed)
b. Brachytherapy
- Intralesion/ intratumor
- Cesium 135 (sealed)
c. P.O.
- RAI 135, RAI 131 (unsealed liquid)
d. Intra-arterial Perfusion
- RA Gold 198 (liver cancer)
- RA Phosphorus (bone cancer)
2 Types:
a. Sealed Implant – Radioisotope with a container & doesn’t contaminate body fluid.
Ex. Radium Seed, Radom Seed, Cesium 135
b. Unsealed Implant – Radioisotope without a container & contaminates body fluid.

- Liquid given either P.O. or Intra-arterial
Ex. Phosphorus 32, RAI, RA
Nursing Responsibility:
1. Isolate patient.
2. Offer diversional therapy
3. Post at door radiation sign
4. Separate set of utensils
5. articles not needed in room should be removed
6. In Unsealed: All excreta, vomitus are considered contaminated. Throw directly to toilet bowl
7. Observe for Time:
Longer exposure means more radiation
Not more than 5 minutes/exposure, 30 minutes/shift
Distance: 3-8 ft. from site
Shielding: Stay at the farthest part/ use lead apron
8. Prevent accidental dislodgement of the radium:

Place on CBR
NO bed pan, insert indwelling catheter
Give diet constipation: Decreased fiber & roughage
Once dislodge, pick-up w/ long forcep, put in lead container
9. Use scanner, Geiger counter to detect remaining traces of radiation

10. Tell partner to resume sex, once edema has subsided
11. Tell pt. if dysuria & burning in urination: SUSPECT URETHRAL ATHROPHY
Meatus, Urinary bladder---- CYSTITIS, HEMATURIA
3 Factors Affecting Exposure:
a. Half life –Time period required for half of radioisotopes to decay.

- At end of half life – less exposure
b. Distance – The farther the distance – lesser exposure
c. Time – The shorter the time, the lesser exposure
d. Shielding – Rays can be shielded or blocked by using rubber gloves –  &  gamma – use thick lead on concrete.
S/E & Mgt:
a.) Skin errythema, redness, sloughing
1. Assist in bathing pt
2. Force fluid – 2,000 – 3,000 ml/day
3. Avoid lotion or talcum powder – skin irritation
4. Apply cornstarch or olive oil
b.) GIT –Nausea / Vomiting / Stomatitis
1. Administer antiemetic 4 – 6h before start of chemo - Plasil

2 Withhold food/ fluid before start of chemo
3. Provide bland diet post chemo
Non irritating / non spicy
Dysglusia – decrease taste sensitivity
-When atrophy papilla (taste buds) – 40 y/o
c.) Bone Marrow Depression
1. Enforce CBR
2. O2 inhalation
4. Monitor signs of bleeding
CARDIOVASCULAR SYSTEM
OVERVIEW:
HEART:
- Muscular, pumping organ of the body Cardio Physiology:

- Occupies most of the Left mediastinum
- Weigh 300 – 400 grams • The main functions of this system are:
- Microscopic – To transport oxygen, hormones &
- Resembles a closed fist nutrients to the tissues
- Covered by a serous membrane – Pericardium
2 Parts
– To transport waste products to
the lungs & kidneys for excretion
Parietal layer Pericardial Space Visceral layer

Fluid – prevent Friction rub
CONSISTS OF 3 LAYERS:
1. Epicardium – Outermost - ( Essential, coronary arteries arelocated here) --------- M.I. & AP
2. Myocardium – Inner – Responsible for pumping action/ Most dangerous layer -- Cardiogenic shock & RHD
3. Endocardium –Innermost layer – Connected to Tunica Intica ------------------------ Endocarditis
2 CHAMBERS:
1. Upper – Collecting/ Receiving chamber - Atria

2. Lower – Pumping/ Contracting chamber – Ventricles
VALVES & HEART SOUNDS:
1. Atrioventricular Valves - Tricuspid & Mitral Valve

Closure of AV valves – gives rise to 1st heart sound or S1 or “lub”
2. Semi-lunar Valve – Pulmonic & Aortic

Closure of semilunar valve – gives rise to 2nd heart sound or S2 or “dub”
Extra heart Sound:
S3 – d/t Increased Ventricular Filling -Ventricular Gallop – Left CHF, Left ventricular hypertrophy
S4 – d/t Forceful Atrial Contraction - Atrial Gallop – MI, HPN, Pulmonic Stenosis, Aging
CORONARY ARTERIES:
The Blood supply of the heart comes from the Coronary arteries
a. Right coronary artery

b. Left coronary artery
Both supply the myocardium with blood

1.Arises from the base of the aorta : RMCA & LMCA
CONDUCTION SYSTEM OF THE HEART:
1. Sino atrial node (SA node) (or Keith-Flock node)

Location: Junction of SVC & Right Atrium
Function: Primary pace maker of heart
Initiates electric impulse of 60 – 100 bpm
2. Atrioventicular Node (AV node or Tawara node)

Location: Inter atrial septum
Delay of electric impulse to allow ventricular filling of 0.8 milliseconds
Slowest conduction
3. Bundle of His
Location: Interventricular septum
Branches out into: Rt main Bundle Branch & Lt main Bundle Branch
4. Purkenjie Fiber
Location: Walls of ventricles-- Ventricular contractions
Fastest conduction
Physiology
• The intrinsic conduction system causes the heart muscle to depolarize in one direction
• The rate of depolarization is around 75 beats per minute (60-100/min)
• The SA node sets the pace of the conduction
• This electrical activity is recorded by the Electrocardiogram (ECG)

• Sympathetic system INCREASES HR
• Parasympathetic system (Vagus) DECREASES HR
ANATOMY OF THE HEART
SA node
AV
Septum
Purkenjie Fibers
Bundle of His
BLOOD SUPPLY:
Amount of blood the heart pumps out in each beat
Stroke Vol. X HR/min (Normal C.O: 4-6 L/min)
Cardiac Output X Total Peripheral Resistance = Blood Pressure
Factors in Cardiac Output:
1. Systole - Contraction
2. Diastole - Relaxation
• The PRELOAD refers to the amount of blood contained in the ventricle at the end of a diastole.
Degree of stretching of the heart muscle when it is filled-up with blood
(reduced with hypovolemia)
• The AFTERLOAD force that LV has to exert in order to pump blood to the aorta.
The resistance to which the heart must pump to eject the blood
(increased with HPN)
• Control is neural (central & peripheral) & hormonal

• Baroreceptors in the carotid & aorta
• Hormones- ADH, Adrenergic hormones, Aldosterone & ANF
– ADH increases water retention
– Aldosterone increases sodium retention & water retention secondarily
– Epinephrine & NE increase HR & BP
– ANF= causes sodium excretion
• The vascular system consists of the arteries, veins & capillaries

• The arteries are vessels that carry blood away from the heart to the periphery
• The veins are the vessels that carry blood to the heart
• The capillaries are lined with squamos cells, they connect the veins & arteries
• The lymphatic system also is part of the vascular system & the function of this system is to collect the extravagated fluid from
the tissues & returns it to the blood
IRREGULARITIES:
1. Complete Heart Block – Insertion of pacemaker at Bundle Branch

Metal – Pace Maker – change q3 – 5 y/o
2. ECG Tracings
Prolonged PR – Atrial Fibrillation

ST segment Depression – Angina Pectoris
ST elevated – MI
T wave inversion – MI
Widening QRS – Arrhythmia
3. Coronary Artery Disease
Atherosclerosis – Myocardial Injury

Angina Pectoris – Myocardial Ischemia
MI - Myocardial Necrosis
DISORDERS OF THE HEART
I. CORONARY ARTERY DISEASE/ ISCHEMIC HEART DISEASE
– Results from the focal narrowing of the large & medium-sized coronary arteries d/t deposition of atheromatous plaque in
the vessel wall
If 50% of the left coronary arterial lumen is reduced or 75% of the other coronary artery, becomes significant
Pathophysiology:
Fatty streak formation in the vascular intima

T-cells & monocytes ingest lipids in the area of deposition
Potential For:
Atherosclerosis Thrombosis
Embolism
Narrowed arterial lumen
Reduced coronary blood flow
With Coronary occlusion Without Coronary Occlusion
Myocardial Ischemia ( 8-10 seconds : Anginal Pain)

Chest Pain Myocardial Necrosis
Akinesia/Dyskinesia of the myocardium

“SAVERS”
*DECREASED CARDIAC OUTPUT
S – sudden onset
(myocardial & anginal)
CARDIOGENIC SHOCK PULMONARY EDEMA
A – anterior or
substernal Renal Damage Right Ventricular
(Acute Renal Failure) Hypertrophy
V – vague discomfort
Electrical Failure Right Ventricular
E – exercise Hypertrophy
Dysrrythmia Rales
R – rest Cough
Ventricular Fibrillation Hemoptysis
S – short Orthopnea
Sudden Heart Arrest Excertional dyspnea
Easy fatigability
Cyanosis
Sx of Right
CHF Pitting Edema Weight Gain Ascites Hepatomegaly (+) Hepato-Jugular Reflux
Dyskinesia Sx of Left CHF

- difficult contraction
of the myocardium
Akinesia
-temporary paralysis
of the myocardium
1. ATHEROSCLEROSIS
ATHEROSCLEROSIS ARTEROSCLEROSIS
- Narrowing of artery d/t fat/ lipid deposits at tunica - Hardening of artery d/t calcium & CHON deposits at tunica media.
intima.
Predisposing Factor: LAYERS OF THE ARTERY

1. Sex – male
2. Black race TUNICA ADVENTITIA – outer
3. Hyperlipidemia - Genetic TUNICA INTIMA - innermost
4. Smoking TUNICA MEDIA - middle
5. HPN
6. DM
7. Oral contraceptive/Steroids - prolonged use
9. Obesity >20 % of Body weight
10. Hypothyroidism
Sx:
1. Chest pain
2. Dyspnea
3. Tachycardia
4. Palpitations
5. Diaphoresis
Tx:
1. PTCA
2. CABG
(Refer to MI for management)
2. ANGINA PECTORIS
- A clinical syndrome characterized by paroxysmal chest pain d/t temporary myocardial ischemia usually relieved by
REST or NGT nitroglycerin
- Reversible, no dead cells yet
- Chest pain resulting from coronary atherosclerosis or myocardial ischemia (tissue ischemia)
3 COMMON TYPES OF ANGINA
1. Stable Angina
- The typical angina that occurs during exertion

- Relieved by rest and drugs & the severity does not change Variant Angina – From smoking
- < 15 minutes Angina Decubitus – pain when lying-down
2. Unstable Angina
-Occurs unpredictably during exertion & emotion

- Severity increases with time & pain may not be relieved by rest & drug
- Mimics M.I.
3. Variant angina
- Prinzmetal angina, results from coronary artery VASOSPASMS

- May occur at rest
Pathophysiology:
STERLING LAW = the greater the myocardium fiber stretch

= the greater the pressure on contraction
For Myocardium to survive: Supply = Demand
If < then it will suffer ISCHEMIA
If blood supply decreased or 8-10 seconds (partially occluded)
Suffer Ischemia
CHEST PAIN (Anginal Pain)
If more than 30 minutes, the heart cannot withstand
Myocardial Infarction/Necrosis
CHEST PAIN
Angina Pectoris:
Precipitating Factors: 4 E’s
1. Sex – male
2. Black raise 1. Excessive physical exertion
3. Hyperlipidemia 2. Exposure to cold environment (vasoconstriction)
Created by Niňa E. Tubio 3. Extreme emotional response 90
4. Excessive intake of foods high in saturated fats
4. Smoking
5. HPN
6. DM
7. Oral contraceptive prolonged
Angina Sx:
9. Obesity
S – sudden onset
10. Hypothyroidism
1 st: Levine’s Sx: hand clutching chest
A – anterior or substernal pain

Sx:
Type: sharp, stabbing, excruciating pain
Others:
Radiates to back, shoulders, axilla, arms & jaw muscles
1. Dyspnea
2. Tachycardia
E – exercise will intensify the pain
3. Palpitation
R – rest
6. Diaphoresis
Relieved by rest or NGT
Dx:
S – short (10-15 minutes only)
1.History taking & PE
2. ECG – ST segment depression
3. Stress test – treadmill = abnormal ECG
If chest pain does not radiate:
4. Serum cholesterol & uric acid - increase.
5. Cardiac Catherization
Cause: Pulmonary Embolism
Pneumonia
Nsg Mngt: To decrease Myocardial Demand
1. Administer prescribed medications

• Nitrates- to dilate the venous vessels decreasing venous return and to some extent dilate the coronary arteries
NTG – small doses – Venodilator (sublingual)

Large dose – vasodilator
1st dose NTG – give 3 – 5 min
2nd dose NTG – 3 – 5 min Given 3x at 3-5 minutes interval
3rd & last dose – 3 – 5 min
Still painful after 3rd dose – notify doc. MI!
Exercise:
55 yrs old with chest pain:
1st question to ask pt: what did you do before you had chest pain.
2nd question: does pain radiate? If radiate – heart in nature. If not radiate – pulmonary origin
Venodilator – veins of lower ext – increase venous pooling lead to decrease venous return.
Nsg Mgt For NGT:

1. Keep in a dry place. Avoid moisture & heat, may inactivate the drug.
2. Monitor S/E:
Vasodilation
Orthostatic hypotension
Transient headache
Dizziness
3. Rise slowly from sitting position
4. Assist in ambulation.
5. If giving NTG via Patch:
a. Avoid placing it near hairy areas-will decrease drug absorption

b. Avoid rotating transdermal patches- will decrease drug absorption
c. Avoid placing near microwave oven or during defibrillation-will burn pt d/t aluminum foil in patch
(color: blue & white)

• Aspirin- to prevent thrombus formation
• Beta-blockers- to reduce BP & HR (Propanolol)
• Calcium-channel blockers- to dilate coronary artery & reduce vasospasm
• ACE inhibitors – Captopril
• Ca antagonist – Nefedipine (anti-hypertensive)
Nursing Diagnoses For Angina Pectoris:
2. Teach the patient management of anginal attacks
• Advise patient to stop all activities Decreased cardiac output
Altered comfort
Impaired gas exchange
3. Enforce CBR
Activity intolerance
4. Administer O2 inhalation
Anxiety
5. Semi-fowler
6. Diet- Decrease Na & saturated fats, low caffeine
7. Monitor VS, I&O, ECG
8. HT:
Discharge Planning:
a. Avoid precipitating factors – 4 E’s

b. Prevent complications – MI
c. Instruct client to take meds before physical exertion-to achieve maximum therapeutic effect of drug
d. Importance of follow-up care.
3. MYOCARDIAL INFARCTION (MI)
– A terminal stage of CAD characterized by necrosis & scarring leading to permanent mal-occlusion
Anatomy: Coronary Artery
1. Right CA ---supply blood------ RA, RV, Posterior Wall

2. Left CA
i. Anterior Descending LCA --- supply--- RV, LV, Septum, Anterior Wall
j. Circumflex LCA -------------- supply --- LA, LV, Lateral Wall
2 Blood vessels supplying ventricles------ventricles receive higher blood than atria
LV – needs more blood to pump to pulmonary circulation

RV – pump blood to systemic
Ex. If occlusion is in Circumflex LCA-------affected LA, LV so basis of nursing DX----- systemic Circumflex---- CO2
TYPES OF MI:
Zone ECG
1. Clot RCA RA, RV Inferior Wall MI
Posterior Wall Posterior Wall MI
2. Anterior Descending LCA RV, LV Anterior Wall MI
3. Circumflex LCA Septum Antero-Septal MI

LA Lateral Wall MI
LV lateral wall
TYPES OF MI BY LAYERS:
1. Sub-endocardial MI – Mal-occlusion of either R & L coronary artery, Ischemia of the inner part
2. Myocardial Infarction – muscle layer affected: most common
3. Trasmural MI – Most dangerous MI – Mal-occlusion of both R&L coronary artery, Involves all layers
PATHOLOGY OF CHEST PAIN IN MI & Sx:
Myocardial Ischemia reverse effect if occluded (KREB’s CYCLE) Anaerobic Metabolism
causes Metabolite will release enzyme
Increased BP Vasodilation LACTIC ACID
Alters conduction of electrical impulses
Dysrrythmia Irritate sensory nerve endings
Weakness: PR or PR CHEST PAIN
Ensuing inflammatory process
Causes release of increased neutrophils (1st cells to migrate when inflammation occurs)
LEUKOCYTOSIS
LOW GRADE FEVER (38 degree C) lasts for 3-5 days---best indicator for monitoring of MI progression or healing
If responding to treatment & N.I.
Neutrophils will be replaced by fibroblastic cells----result to scarring/fibrolysis---- the healing process---- Normal Temperature
MYOCARDIAL INFARCTION
Predisposing Factors S/Sx Dx Exam

1. Cardiac Enzymes
- Sex – male 1. CHEST PAIN Go to blood following cardiac death
- Black raise
- Hyperlipidemia S – sudden onset of pain a. CPK – MB – Creatinine Phosphokinase
- Smoking
- HPN A – anterior/substernal/precordial area b. LDH – lactic acid dehydrogenase
- DM Excruciating, vice like, visceral pain
- Oral contraceptive Radiates back, arm, shoulders, axilla, jaw c. SGPT – (ALT)
- Sedentary lifestyle Serum Glutamic Pyruvate Transaminase
- Obesity via afferent nerve cells
- Hypothyroidism d. SGOT (AST) – Serum Glutamic Oxalo-acetic
w/ referred epigastric pain
2. Troponin test – increase
Feeling of tightness or heavy chest 3. ECG Tracing – ST segment elevation,
Widening of QRS complexes – means arrhythmia in MI
E – exercise increases pain indicating PVC
R – rest does not relieved the pain or by NGT 4. Serum Cholesterol & Uric acid
5. CBC – increase WBC
2. Dyspnea
3. Erthermia
4. Initial increase in BP Myocardial Infarction
5. Mild restlessness & apprehensions Nursing Diagnoses
6. Cool, moist, ashen skin Pain (Altered comfort)
Decreased cardiac output
Impaired gas exchange
Activity intolerance
Altered tissue perfusion
7. Occasional findings
a. Split S1 & S2
b. Pericardial friction rub (inspiration)
c. Rales /crackles
d. S4 (atrial gallop)
*Most critical period after Dx of MI – 6-8 hrs. d/t arrhythmia, a type of PVC premature ventricular contraction.
COMPLICATIONS:
(Refer to Pathophysiology of Atherosclerosis)
1. Cardiogenic Shock – d/t poor contraction/akinesia .

2. Renal Failure – decreased CO2----decreased renal failure---renal ischemia----cessation—RF
3. Ventricular Fibrillation--- heart beat very irregular, erratic & very rapid 180 bpm
4. Pulmonary Edema
5. Right Ventricular Hypertrophy
6. Left-sided HF
7. Right-sided HF Late Sx of Cardiogenic Shock In MI
8. Thrombophlebitis – DVT Oliguria
9. Arrhythmias – PVC
10. Dressler’s Syndrome – post MI syndrome
- Non-resistant to Pharmacological agents
-Administer 150,000 – 450,000 units of streptokinase
Management of Myocardial Infarction:
1. Increase Myocardial O2 supply

- Administer O2 inhalation (low-flow)
- Also to prevent extension of necrosis
- Monitor VS, I&O & ECG tracings
2. Relieve pt. of chest pain

- Give drug of choice: Narcotic Analgesic
Morphine SO4 ------ Action: Decreased preload & afterload through vasodilation
Decrease level of anxiety
Relieves severe intensity of pain
Longer sustained effect
If not available: Demerol but S/E: Hypotension
3. Relieve pt. of anginal pain

- *Give NITRITES or NITRATES
Action: Relax smooth muscles of the coronary artery/ also as vasodilators
Ex. a. Isosorbade (Isordil)

b. Isosorbide Mononitirite (Indur)
c. NGT (Nitroglycerine)
5 mg – SL Ex. Nitrostatic
10 mg - P.O.
Patch, cream – Topical Ex> Nitral Patch, Transderm
Nsg. Mgnt For Nitroglycerine:
1. Explain that drug may cause S/E :

Throbbing headache
Flushing of skin *continue taking the drug s/s will
Warm sensation & stringing, biting disappear w/ the continued
Burning sensation under tongue if taken SL medication
2. S/E : Postural hypotension d/t vasodilation

Give drugs while on bed or in a sitting position
3. Keep drug in dark, opaque container because exposure to light/sun will reduce potency of nitrates
4. If topical administration: Cleanse area w/ H2O only, Avoid hairy areas, rotate administration
Place on precardium: 5th ICS or site of pain
5. If SL : Advise pt. to place under tongue, allow to dissolve, swallow saliva
NEVER follow it w/ H2O (interrupt sustained effect)
6. Keep away from your own skin, causes vasodilation & headache
4. R - rest
- To decrease cardiac workload
- To decrease work for breathing
- To decrease myocardial O2 demand
- To increase cardiac reserve
- Enforce CBR without BRP
- Provide Bedside commode
- Abstain from sexual activity (4-6 wks. After MI attack)
- Take nitrate prior to sex & if w/ insomnia, chest pain, SOB-----seek medical advice
- Avoid valsalva maneuver
- Semi fowler
- Resume ADL – activity
- Post-cardiac rehab:
1.)Sex as an appetizer rather then dessert
Before meals not after, after meals increase metabolism – heart is pumping hard after meals.
2.) Assume a non-weight bearing position.
*When to resume sex/ act: When pt can already use staircase, then he can resume sex.
5. D – diet
- To decreased caloric intake in order to decrease cardiac load

- General liquid to soft diet
- Low in Na 2-4 grams/day to get rid of ECF fluid excess
- Avoid food high in saturated fat & avoid gas-forming foods
- Avoid drugs w/ high Na like laxative
- Avoid cardiac stimulant (caffeine, colas)
- Increase fiber intake to avoid constipation
- Avoid too hot drinks ------abdominal distention----- SOB
- Avoid too cold drinks------ vagal stimulation-------- Decreased PR (Bradycardia)
- Take 20 – 30 ml/week – wine, brandy/whisky to induce vasodilation
6. D- diuretic
- To prevent reabsorption of H20 by the renal tubules-----absorption---Hypokalemia----Use K-sparing diuretics

Ex. Aldactone
Spironolactone
Ex. Furosemide (lasix)

Sign that diuretic is effective?
Frusema
Diuret
*Absence of rales indicates (+) effect of diuretics
Edecrine
Mercuhydrin
7. D- digitalis
- Drug categorized as “CARDIAC GLYCOSIDES
Ex. Digitoxin, Digoxin, Lanoxin, Gdiranid
3-FOLD ACTION OF DIGITALIS
1. Strengthen myocardial contraction-----------(+) Inotropic Effect

Any drug that influences myocardial contraction has an inotropic effect
2. Increase cardiac output -------- Increase renal blood flow/renal perfusion

Increase urinary output (secondary effect: Diuretic)
3. Decrease Cardiac Rate --------- (-) Chronotropic Effect

Any drug that influences cardiac rate has a chronotropic effect (- or +)
Nursing Management in Giving Digitalis:
1. Check CR, if below 60 do not give drug

2. Monitor serum potassium d/t its secondary effect as a diuretic
3. Check for DIGITALIS Toxicity:
Anorexia-----------------most common complaint

Headache w/ N/V------ Early Sx of toxicity
Diarrhea
Photophobia
Dysrrythmia
Yellow spots in eyes
Gynecomastia ----- Late Sx of Toxicity
Antidote: DIGIBIND or DIGOXIN IMMUNE Fab ---------bind w/ lanoxin to decrease toxicity of lanoxin
8. If patient undergoes CARDIOGENIC SHOCK:
a. Prepare for vasopressor------ BP Ex. Dopamine

Intropine
Aramine --- Metaraminol Bitartrate
Levophed – Levartenenol
Adrenalin /Epinephrine
b. Increase rate of impulse formation in SA node

Ex. Lidocaine 1-2%
Pronestyl --------Procainamide HCI
Quinidine SO4 -- Quinidex
Brethylium ------blocks release of norepenephrine
c. Dysrrythmia ----------- Give anti-arrhythmic drugs

Ex.
1. Lydocaine blocks release of norepenephrine
2. Brithylium S/E: Confusion & Agitation
If not corrected by medications:
- Install artificial pacemaker or when SA node is damaged
- Equipped with wire electrode & pulse generator
PACEMAKER
Type Insertion Wire/Electrode Pulse Generator
1. Temporary Antecubital basilic vein Tip rest on RA or RV Outside
2. Permanent:
Epicardial-------- thru Thoracotomy RV Implanted in abdominal wall

Endocardial------ Thoracotomy RV Implanted subcutaneously
(5-6 yrs. ) Permanent SA so attach to chamber w/ thicker myocardium below the device
(subclavicular)
Nursing Management:
1. Temporary: Avoid toying w/ the pulse generator

Wrapped w/ rubber gloves
2. Permanent: Avoid vigorous arm & shoulder movements

Avoid lifting heavy objects
Both: Do not come closer to a microwave oven, cell site, electrical power
Or any apparatus emitting power voltage
Do not go through X-rays, scanner
Teach pt. how to monitor PR for 1 whole minute
S/S of malfunctioning pacemaker:
HICCUP
Bradycardia
Palpitation
Syncope
9. Prevent other complications. Give medications
a. Beta-blockers – “lol”
1. Propanolol (inderal)
b. ACE inhibitors - pril
1. Captopril – (enalapril)
c. Ca – antagonist
1. Nifedipine
d. Anti platelet PASA (aspirin)
e. Thrombolitics or fibrinolytics– to dissolve clots/ thrombus

S/E allergic reactions/ uticaria
Ex. 1. Streptokinase--------most common

2. Urokinase ----------- S/E: Hypotension
3. Tissue Plasminogen Activating Factor (TPAF) ------- S/E: Chest Pain
Monitor for bleeding:

Anticoagulants
1. Heparin 2. Coumadin – delayed reaction 2 – 3 days
PTT PT
If prolonged bleeding Prolonged bleeding
Antidote : Protamine Sulfate Antidote Vit K
10. For patient w/ VENTRICULAR FIBRILLATION
a. Administer:
DEFIBRILLATION
– To terminate a life-threatening dysrrythmia thru unsynchoronous application (anytime) at
any rate (200-360 joules)
CARDIOVERSION
- To correct dangerous dysrrythmia (sinus tachycardia) thru a synchronous application during
R wave w/ 50-200 joules
11. Relieve patient of Sx of PULMONARY EDEMA:
a. Rotating Tourniquet/ Dry, bloodless Phlebotomy Indicative of too tight Tourniquet:

- To reduce right atrial flow Absence of Peripheral Pulses
Nursing Management:
1. Only 3 extremities should be pressed at the same time

2. Tourniquet should not be applied too tight
3. Rotate tourniquet every 15 minutes
4. Rotate clockwise ---use BP cuff if not available (at Pulse pressure)
5. Remove at interval of 15 minutes
6. No single extremity should be compressed for more than 45 minutes
Cause VENOUS STASIS ----- stagnation of blood in 3 extremities
Decrease blood to enter RA---- pulmonary system---- blood will edema
12. Treatment for patient with CORONARY ARTERY DISEASE:
1. Prepare for Revascularization Surgery to restore myocardial blood flow
a. PTCA PTCA
–Done to pt with single occluded vessel/simple vessel P – percutaneous
- Done under direct fluoroscopic guidance T – transluminar
- Indicated for Angina less than 1 year & coronary artery not calcified C – coronary
A - angioplasty
Objective of PTCA:
1. To revascularize the myocardium

2. To prevent angina
3. Increase survival rate
4. To compress plaque against vessel wall increasing arterial lumen
Procedure: Balloon-tipped catheter to/from femoral to CA to dilate CA or dislodge an atheroma/plaque

b. CABG
- For Multiple occluded vessels:
- Done to improve blood flow to myocardial tissue
- Uses saphinous vein/mammary artery
- Done on an “open heart technique” & jump-graft from lower extremities
Nsg Mgt Before CABG:

CABAG Feared Complications
1. Deep breathing cough exercises C – coronary
2. Use of incentive spirometer A – arterial 2 P’s Pneumonia
3. Leg exercises B – bypass Pulmonary Embolism
4. Cut at sigmoid process to umbilicus G – graft surgery
- Once thoracic is opened, change in normal pressure (-) intrapleural pressure
lungs will collapse
Prepare for 1 way or 3 way Chest drainage
13. CHEST DRAINAGE
-Done to restore (-) intrapleural pressure of lungs to prevent collapse
a. One-way H20 Sealed Chest Drainage System

- Maintain an air-tight water-sealed system
To patient Air vent, above H2O level

(Emerson/Steidmann’s Pump)
Glass rod 2-3 cm.

Tip below H2O level H2O
b. 3-Way Chest Drainage

To suction
provides (-) pressure

To patient
H2O H2O H2O
Output Bottle H2O Sealed Bottle Vacuum Controlled
Nursing Management For Chest Drainage:
1. The 3 bottles should be below chest level (18 inches) to prevent backflow
2. Bottles should be taped to the floor to prevent accidental leakage
3. Observe for OSCILLATION fluctuation, Tidalling---- rise & fall of H2O
Important that there is constant communication bet. thoracic cavity & output bottle
a. Observe for OSCILLATION
- Favorable ---- indicates that the lungs has re-expanded

Non-Favorable ---- Absence may mean:
Turn client side to side, if still (-) (To dislodge adhesion to wall)
Tell client to do deep breathing exercise, if still (-)
Stripping/Milking of the tube----an occlusion/clot will come out
b. Observe for BUBBLING
- Normal in vacuum bottle connected to suction machine

- If present in H2O sealed bottle----- indicates PLEURAL LEAKAGE/DAMAGE
- Measure output correctly. Put tape on bottle

- Change bottle when empty
- Do not clamp when changing bottle---- Tension Pneumothorax
- For accidental breakage: Immediately get a bottle w/ sterile H2O & immersed tube
If none available----clamp
- In any set-up: 1st bottle is always the output bottle
- Observe aseptic technique
- Removal:
Do not remove test tube during inhalation.
Inhale deeply then pull during expiratory phase to prevent entry of air & suction residual fluid
Apply petrolatum gauze dressing (non-porous dressing0
After removal, continue observing for S/S of hypoxia
4. CONGESTIVE HEART FAILURE
- Inability of the heart to pump blood towards systemic circulation d/t obstruction.
- Backflow
- A syndrome of congestion of both pulmonary & systemic circulation caused by inadequate cardiac function &
inadequate cardiac output to meet the metabolic demands of tissues
- Inability of the heart to pump sufficiently
- The heart is unable to maintain adequate circulation to meet the metabolic needs of the body
This can happen acutely or chronically

• Acute as in Myocardial infarction
• Chronic as in cardiomyopathies
Classified according to the major ventricular dysfunction-

1.Left Ventricular failure
2. Right ventricular failure

Etiology of CHF
1. CAD
2. Valvular heart diseases
3. Hypertension
4. MI
5. Cardiomyopathy
6. Lung diseases
7. Post-partum
8. Pericarditis & cardiac tamponade
Systemic Circulation
*Inferior Vena Cava & Superior Vena cava
UnO2 Aorta
Right Atrium Left Ventricles
Tricuspid Valve Mitral Valve LSHF blood goes

RSHF back to PV
Blood goes back Right Ventricles Left Atrium
to TV-circulation
Pulmonary Artery Lungs Pulmonary Veins
(For Oxygenation)
A. RIGHT-SIDED HF B. LEFT-SIDED HF
-#1 Cause: Tricuspid Valve Stenosis -#1 Cause: Mitral Valve Stenosis
S/S: S/S:
Jugular Vein Distention Pulmonary Edema/ congestion
Pitting Edema---IVC from toes Dyspnea
Ascites Paroxysmal Nocturnal Dyspnea –2 pillows/High-fowlers
Weight Gain Orthopnea
Hepatospleenomegaly Productive Cough (blood-tinged sputum)
Jaundice Frothy Salivation
Pruritus---Urticaria Rales/Crackles
Esophageal Varices Bronchial Wheezing
Anorexia Pulsus Alterans (weak-strong pulse)
Anorexia & generalized body malaise
S3 (Ventricular Gallop)
Cyanosis
PMI is displaced laterally : 4th -5th ICSMCL
-----if below 5th ---cardiomegaly
1. LEFT-SIDED HEART FAILURE:
1. 90% Mitral Valve Stenosis – d/t RHD, Aging

RHD affects mitral valve – streptococcal infection
Dx:
1. ASO Titer (Anti-Streptolysine O) > 300 total units
- Steroids
- Penicillin
- Aspirin
Complication:
RS-CHF
Aging – degeneration / calcification of mitral valve
Ischemic heart disease
HPN, MI, Aortic stenosis
Dx:
1. CXR – Reveals Cardiomegaly
2. PAP – Pulmonary Arterial Pressure
3. PCWP – Pulmonary Capillary Wedge Pressure
PAP – Measures pressure of R ventricle. Indicates cardiac status.

PCWP – Measures end systolic/ diastolic pressure
PAP & PCWP:

Swan – Ganz Catheterization – cardiac catheterization is done at bedside at ICU
(Tracheostomy – bedside) - Done 5 – 20 mins – scalpel & tracheostomy set
CVP – Indicates fluid or hydration status

Increase CVP – decrease flow rate of IV
Decrease CVP – increase flow rate of IV
4. Echocardiography – Reveals enlarged heart chamber or cardiomayopathy
5. ABG – PCO2 increase, PO2 decrease = = hypoxemia = respiratory acidosis
Tx:
M - Morphine SO4 (to induce vasodilation)
A - Aminophylline
D - Digoxin
D - Diuretics
O - O2
G - Monitor Blood Gases ----------- PO2
Respiratory Acidosis
Hypoxemia
Cyanosis
2. RIGHT-SIDED HEART FAILURE
1. 90% - Tricuspid Stenosis

2. COPD
3. Pulmonary embolism
4. Pulmonic stenosis
5. Left sided heart failure
S/Sx:
Venous Congestion
- Neck or jugular vein distension
- Pitting edema
- Ascites
- Wt gain
- Hepatomegaly/ Splenomegaly
- Jaundice
- Pruritus
- Esophageal Varices----- Dilation of the veins of the esophagus
- Anorexia, General body malaise, Nausea
Pulsus alternans
Nocturia = urination at night at frequent intervals as the blood moves from interstitial space to
the intravascular space & is excreted
Dx:
- CXR – Reveals Cardiomegaly
- CVP – Measures the pressure at R atrium
Normal: 4 to 10 cm of water
Increase CVP > 10 – hypervolemia
Decrease CVP < 4 – hypovolemia
Flat on bed – post of pt when giving CVP
Position during CVP insertion – Trendelenburg to prevent pulmonary embolism & promote ventricular
filling.
3. Echocardiography – enlarged heart chamber / cardiomyopathy
4.Liver enzyme
SGPT ( ALT)
SGOT AST
Nsg mgt: Increase force of myocardial contraction = increase CO

3 – 6L of CO
1. Administer meds:
M – morphine SO4 to induce vasodilatation
A – aminophylline & decrease anxiety
D – digitalis (digoxin)
D - diuretics
O - oxygen
G - gases
a.) Cardiac Glycosides

Increase myocardial = increase CO
Digoxin (Lanoxin)
Antidote: digivine
Digitoxin: metabolizes in liver not in kidneys not given if with kidney failure.
b.) Loop diuretics: Lasix – effect with in 10-15 min. Max = 6 hrs
c.) Bronchodilators: Aminophylline (Theophyllin). Avoid giving caffeine
d.) Narcotic analgesic: Morphine SO4 - induce vasodilator & decrease anxiety
e.) Vasodilators – NTG
f.) Anti-arrhythmic – Lidocaine
2. Administer O2 inhalation – high! @ 3 -4L/min via nasal cannula
3. High –Fowlers (2-3 pillows)
4. Restrict Na
5. Provide meticulous skin care
6. Weigh pt daily. Assess for pitting edema.
Measure abdominal girth daily & notify MD
7. Monitor V/S, I&O, breath sounds
8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venous
return
9. Diet – decrease salt, fats & caffeine
10. HT:
a) Prevent Complications :
Shock
Arrhythmia
Thrombophlebitis
MI
Cor Pulmonale – RT ventricular hypertrophy
b.) Dietary modifications

c.) Adherence to meds
CLASSIFICATION BASED ON New York Heart Association
Class 1
• Ordinary physical activity does NOT cause chest pain & fatigue
• No pulmonary congestion
• Asymptomatic
• NO limitation of ADLs
Class 2
• SLIGHT limitation of ADLs
• NO symptom at rest
• Symptoms with INCREASED activity
• Basilar crackles and S3
Class 3
• Markedly limitation on ADLs

• Comfortable at rest BUT symptoms present in LESS than ordinary activity
Class 4
• SYMPTOMS are present at rest
OTHER PROBLEMS ASSOCIATED WITH THE CARDIOVASCULAR SYSTEM
1. CARDIAC TAMPONADE
- A condition where the heart is unable to pump blood d/T accumulation of fluid in the pericardial sac
(pericardial effusion)
- This condition restricts ventricular filling resulting to decreased cardiac output

- Acute tamponade happens when there is a sudden accumulation of more than 50 ml fluid in the pericardial sac
Causative Factors:
1. Cardiac trauma
2. Complication of Myocardial infarction
3. Pericarditis
4. Cancer metastasis

ASSESSMENT FINDINGS
1. BECK’s Triad- Jugular vein distention, hypotension & distant/muffled heart sound
2. Pulsus paradoxus
3. Increased CVP
4. Decreased cardiac output
5. Syncope
6. Anxiety
7. Dyspnea
8. Percussion- Flatness across the anterior chest
Laboratory FINDINGS
1. Echocardiogram= shows accumulate fluid in the pericardial sac

2. Chest X-ray
NURSING INTERVENTIONS
1. Assist in PERICARDIOCENTESIS
2. Administer IVF
3. Monitor ECG, urine output & BP
4. Monitor for recurrence of tamponade
Pericardiocentesis
1. Patient is monitored by ECG

2. Maintain emergency equipments
3. Elevate head of bed 45-60 degrees
4. Monitor for complications- coronary artery rupture, dysrhythmias, pleural laceration & myocardial trauma
2. CARDIOGENIC SHOCK
- Heart fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion
- This shock occurs when the heart’s ability to contract & to pump blood is impaired & the supply of oxygen is
inadequate for the heart & tissues
• Risk factors: Coronary factor- Myocardial infarction

• Risks factors: NON coronary:
– Cardiomyopathies
– Valvular damage
– Cardiac tamponade
– Dysrhythmias
– Severe CHF
Pathophysiology:
• Precipitating factors will cause decreased cardiac contractility Decreased stroke volume & cardiac output
leading to 3 things:
• Damming up of blood in the pulmonary vein will cause pulmonary congestion
• Decreased blood pressure will cause decreased systemic perfusion
• Decreased pressure causes decreased perfusion of the coronary arteries leading to weaker contractility of the heart
ASSESSMENT FINDINGS
1. HYPOTENSION
2. Oliguria (less than 30 ml/hour)
3. Tachycardia
4. Narrow pulse pressure
5. Weak peripheral pulses
6. Cold clammy skin
7. Changes in sensorium/LOC
8. Pulmonary congestion
LABORATORY FINDINGS
1. Increased CVP due to pooling of blood in the venous system

– Normal is 4-10 cmH2O
2. Metabolic acidosis
1. Place patient in a modified Trendelenburg (shock ) position
2. Administer IVF, vasopressors and inotropics such as DOPAMINE and DOBUTAMINE

– These drugs will increase cardiac contractility
3. Administer O2
4. Morphine is administered to decreased pulmonary congestion & to relieve pain, relieve anxiety
5. Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganz catherization & IABP
6. Monitor urinary output, BP & pulses
7. Cautiously administer diuretics & nitrates
DIAGNOSTIC PROCEDURES FOR CARDIOVASCULAR DISORDERS
1. ECG/EKG
-Done To measure the electrical impulses of the heart to Dx heart rate & rhythm
Pathology:
SA node------starts myocardial contractions
Initiates electrical (+) impulses (emikts 60-100 bpm)

Goes into
Intra-atrial Track-------- A-V Node (located at right side of intra-atrial septum)
Bundle of His (L & R)
Purkinje Fibers
Ventricular Contraction
 If below 60---- Sinus Bradycardia

 If above 100--- Sinus Tachycardia
 If 60-100 ------ Normal Sinus Rhythm
 DEPOLARIZATION – is the myocardial contraction

 REPOLARIZATION – Refractory Period/relaxation –regaining its (-) charge
Normal Refractory Period

0.15-0.30 seconds
SA NODE ----- located at posterior wall of RA close to the entrance to Vena Cava
 During depolarization ---- permeable to entry of Na & Cal----- influencing myocardial contraction
 During repolarization----- permeable to entry of K & Cl
 P Wave – Atrial depolarization or contraction
 PR interval – travel time of impulse from atria to ventricle ( Normal: 0.12-0.20 seconds)
Any delay in flow of impulse ------heart block
 QRS Complex – Ventricular Repolarization

(From ventricular contraction A---V to time it will be (+) charged
After a brief period of resting----- (-) charge refractory period
 ST Segment - completion of depolarization & beginning if repolarization

 T Wave – ventricular repolarization
 QT Interval – entire duration of depolarization & repolarization ( lasts for 0.42-0.43 seconds)
(From QRS to T)
5 IMPORTANT ECG TRACINGS
1. MYOCARDIAL INFARCTION
- Inverted T wave area of ischemia ---- reversible with time
- Elevated ST
-Pathological prominent T wave area of infarction ----- irreversible, will always appear for life
2. HYPERKALEMIA
- Peaked T wave
- Prolonged PR Interval
- Widened QRS complex
3. HYPOKALEMIA
- Flat T wave
- Depressed ST
- Prominent U wave ----- Pathological--- influences myocardial repolarization

Decreased K ---- weakened contraction or repolarization
Prolonged T wave
Forming an abnormal U wave
4. HYPERCALCEMIA
- Shortened QT interval
5. HYPOCALCEMIA
- Prologed QT interval
2. 24 HOUR HOLTER MONITORING/DYNAMIC ECG
- Done to monitor 24 hrs. cardiac activity

- Given pen & paper to record 24 hrs.
- Non-invasive
3. STRESS TEST/ THREADMILL TEST/BICYCLE/ERGOMETRIC TEST
- Done to evaluate amount of activities that the heart can tolerate
Nsg Responsibility:
- Avoid smoking the night before the threadmill
- Wear comfortable light material
- Wear rubber-soled shoes
- Avoid heavy meal prior to test
- Allowed light snack 2 hrs. before test
- Avoid hot shower 2 hrs. after test to prevent syncope
- Rest after the exercise
4. PHONO-ECHOCARDIOGRAPHY
- Non-invasive
- Use to detect any abnormal anatomical structure & abnormal heart sounds
5. ECHOCARDIOGRAPHY
- Use to evaluate changes in the cardiac dimension during the cardiac cycle
6. ELECTROLYTE STUDIES
- No NPO
- Na & Ca ------- Depolarization
- K & Cl ------- Repolarization
7. BLOOD TEST
- Use to evaluate atheromatous changes
Serum Cholesterol ------ NPO 6-8 hrs.

Serum Triglyceride ----- NPO 12 hrs
Serum Lipids -------- NPO 12 hrs.
Nsg. Responsibility:
- No lipid forming drugs
Ex. Salicylates
Estrogen
Steroids
No alcohol----- influence
8. ENZYMATIC TEST
- No NPO------ it is normally released by the myocardium---- if elevated enzymes----problem to the myocardium
a. SGOT (Serum Glutamic Oxaloacitic Aminotransferase)

SGOT/AST : 5-40 u/L
or
AST (Serum Aspartate Aminotransferase)
b. SGPT (Serum Glutamic Pyruvic Transaminase) SGPT/ALT : 4-36 u/L

or
ALT ( Serum Alanine Amintransfirase)
c. CPK mb ( Creatinine Phosphokinase )
3 Isoenzymes
MB BB MM
Increases myocardial insult/damage Increased brain, bladder, bowel Increased skeletal muscle
d. SLDH (Serum Lactic Dehydrogenase)
1&2 3 4&5
Myocardial insult lung parenchymal damage liver damage
*BEST CONFIRM MI -------- SGOT
* BEST DIAGNOSED MI -------- CPKmb
*Nsg Intervention prior to blood extraction ----- No IM injection------- Increased CPK when skeletal muscle injury
CARDIOVASCULAR ASSESSMENT
Assessment:
I. During Interview:
1. (+) Family History
2. Smoking
Pathology:
a.) Nicotine -----stimulates release of Catecholamines--------------------------Epinephrine
Platelet Increased Myocardial O2 demand Vasoconstrictor

Aggregation
Increased cardiac workload HPN
Risk for thrombus formation
Increased cardiac workload

b.) Carbon Monoxide ------ + Hgb (blood) ------interfere w/ O2 transport (carboxyhgb)
Tissue hypoxia/hypoxemia
3. Stress
4. DM------can lead to MI
5. Atherosclerosis
6. HPN
7. Age ------- above 40 y/o
8. Sex ------- M: high risk
F: high risk after menopause
9. Personality ---- high among Type A individual
10. Assess for history of easy fatigability----- 1st sign of poor cardiac reserve
Ability of the heart to adjust to cardiac demand

11. History of Palpitations
2 Types:
a. Physiologic ------ diet (coffee), strenuous activity, strong emotion, after eating
b. Pathologic ------- clients w/ hyperthyroidism

clients w/ cardiomegaly ( enlarged heart)
contractions----hit cardiac wall----- palpitations

Palpitations---pounding, jumping sensations for every myocardial contractions
12. Listen for normal & abnormal sounds
S1 – lubb ----systole Best heard at PMI ( Point of Maximum Impulse) on the 4th-5th ICSMCLL
S2 – dub ----- diastole
Abnormal: S3 sound -----heard on early part of diastole------ Sign of Ventricular Dysfunction

Sign of Left Ventricular Hypertension
S4 sound ----- heard on late part of diastole------- Seen in MI, HPN, Pulmonic Stenosis
*S3 sound-----normal to children
Assess for audible sound: Murmur ------ audible vibration

Thrill --------- palpable vibration Stenotic Valvular Opening/narrowing
Heave --------- visible vibration
Increased velocity of bloodflow
Abnormal vibrations
13. Lifestyle----- Diet ----- High in calories, saturated fats, Na & heart stimulant like caffeine, alcohol
---- Exercise—Sedentary lifestyle----venous stasis---- Risk for thrombus formation
14. Assess for history of chest pain
15. Assess for Dyspnea & its cause

--- Positioning: Orthopnea
Time : Night (Paroxysmal Nocturnal Dyspnea)
16. Check for history of CYANOSIS

2 Types:
a. Central Cyanosis----- circum-oral (lips, oral mucus membrane)
Sign of decreased arterial O2 saturation (Normal: 95-100%)
b. Peripheral Cyanosis---- cyanosis of nail beds, earlobes
Sign of decreased cardiac output

17. Assess for pitting edema:
a. Elevate 1st the legs w/ edema, if still (+)
b. Press skin, if indentation is present = (+) Pitting Edema
18. Assess for HPN:
Systole---- Atrio-ventricular contraction & closure of the A-V valves—-----TV & BV
Strength of Myocardial contractions
Diastole – Atrio-ventricular relaxation & closure of Semi-lunar valves---- PV & AV
More dangerous because it is systematic Degree of systolic arterial resistance
TYPES OF HPN:
1. Systolic HPN & Diastolic HPN
2. Primary/Essential/Idiopathic
- Unknown cause
2 Theory:
a. R-A-A
Pathology: Juxtaglomerular Cells (kidney)
Renin releases
Angiotensin I (activated by enzymes that converts it to)
Angiotensin II ------- stimulates adrenal cortex to release aldosterone
Potent vasoconstrictor Fx: Fluid & Na retention & K excretion
HPN Increased IV volume
Hypovolemic Shock
3. Secondary HPN
- Due to pregnancy related to toxemia
- Children w/ coarctation of the aorta
- Pheochromocytoma ( 5 H)
4. Accelerated HPN ----- persistent high BP with signs of retinal hemorrhages + epistaxis
5. Malignant HPN ----- persistent high BP with signs of papilledema (Increased ICP)
FLUIDS & ELECTROLYTES
1. WATER
Adult: 50-60% TBS

Child: 70-80% TBS
*Volume of Distribution Depends On:
1. Age - H2O decreases with age
2. Sex – Male with more muscles so increase H2O
3. Adipose Tissues – More Obese so more H2O

*Fluid Intake: 2 – 2.5 L/day 24 hrs.
Fluid: 1 -1.5 L/24 hrs.

Food 1 L/24 hrs.
By-product of oxidation-nitrogen process = 100 ml/24 hrs.
*Avenues Of Losses/Routes:
1. Kidney = 1-1.5 L/24 hrs

2. Skin = 600-700 ml/24 hrs
3. Lungs = 400-500 ml/24 hrs
4. GIT = 100 ml/24 hrs
CELLS BLOOD
Intracellular ICF = 2/3 of BF 70 % Intravascular (blood, lymph vessels)

Extravascular ECF = 1/3 of BF 30 % Intercellular ( interstitial space)
2. ELECTROLYTES
1. CATION (+) = Sodium Na Homeostasis--- continuous shifting of fluids in Intravascular compartment

Potassium K
Calcium Cal
Magnesium Mg
2. ANION (-) = Chloride Cl

Phosphorus PO4
Sulfate SO4
Bicarbonate HCO3
3. ICF = K & PO4

ECF = Na & Cl
FLUID SHIFTING
1. IV-ITS-IV (Normally exercised by circulatory blood)
Arteriolar End COP = 22 mmHg Venular End
HP = 40 mmHg HP = 12 mmHg
Start: Fluid pushed into ITS

COP> HP
Fluid drawn back into capillaries
ITS
 HP greater than COP so that fluid movement occurs
2 Governing forces for IV-ITS Shifting
1. COLLOID OSMOTIC PRESSURE

- Pressure exerted by plasma protein/albumin on semi-permeable membrane
2. HYDROSTATIC PRESSURE
- Pressure exerted by fluid against wall of BV
Example:
1. MALNUTRITION (Protein)
Less COP----venous HPN congestion-----fluids remains in ITS---Edema, Anasarca, Ascites
2. ABNORMAL
If HP less than COP---fluid stays in the VC------ Circulatory Overload------ Hypovolemia
3. BLOOD TRANSFUSION
BT/Protein/Albumin----- High COP----fluid stays in capillary---- Circulatory Overload
4. FLUID SHIFTING IC ----TO----- EC
*Movement of fluids governed by Osmosis & Diffusion
Solvent (H2O) Solute (Electrolyte)
* High H2O EC------ Low Na concentration-------- H2O will enter the cell
If continues
Cell will Swell/Burst
H2O Intoxication/ Hypo-Osmolar Imbalance
* Less H20 E ----- High Na-----leave the cell-----cell shrink-----Dehydration
3. BURNS
– Direct tissue injury caused by thermal, electric, chemical & smoke inhalation (TECS)
Nursing Priority – infection (all kinds of burns)
Head burn-priority- a/w

2nd priority for 1st & 2nd  - pain
2nd priority for 3rd  - F&E
CLASSIFICATION:
1. CAUSE
a. Thermal - direct contact – flames, hot grease, sunburn. -- wrapped

b. Electric – wires
c. Chemical – direct contact – corrosive materials acids-------flush with saline solution
4. Smoke – gas / fume inhalation

2. DEPTH OF TISSUE DAMAGE & AREA
I. Partial Thickness Burn
1. 1st degree
– Superficial Partial Thickness Burns

- Affects epidermis
- Cause: Thermal burn/sun burn
- Painful
-No edema
- Redness (erythema) & (+) blanching upon pressure with no fluid filled vesicles
- Healing Duration : 1-2 wks. w/ any residual evidence of tissue damage
2. 2nd degree
– Deep Partial Thickness Burns

- Affects epidermis & dermis
- Cause –chem. Burns
- With edema
- (+) Very painful
- (+) Erythema & fluid filled vesicles (blisters)
- Mottled (bluish & reddish)
- Healing duration: 2-3 wks. w/ signs of minimal scarring
II . Full Thickness Burns
1. Third & 4th Degrees Burn
- Affects all layers of skin, muscles, bones

- Cause – electrical
- Without pain or less painful
- Blanched, pale, charred
- Dry, thick, leathery wound surface – known as ESCHAR – devitalized or necrotic tissue.
- Healing duration: No exact time-frame. Depends on the actual depth of tissue damage, infection
3. ACCORDING TO EXTENT OF BODY SURFACE BURNED
Rule of 9
Head & Neck & Face = 9%
Upper Anterior Trunk/Chest = 18%
Upper Posterior Trunk/Chest = 18%
@ Arm 9+9 = 18%
Lower Anterior Extremity (leg) = 18%
Upper Posterior Extremity (leg) = 18 %
Genitalia/ perineum = 1%
Total 100%
4. CLASSIFICATION AS MINOR & MAJOR
1. Minor :
2nd Degree : 10-20% BSA (C)
2nd Degree: 15-25 % BSA (A)
3rd Degree: 2-10 % BSA
2. Major:
2nd Degree: 10-20 % (C)
2nd Degree: 15-25 % (A)
3rd Degree: 2-10 %
3. Critical:
2nd Degree: > 21 % ( C)
2nd Degree: > 25 % (A)
3rd Degree > 10 %
STAGES:
1. Emergent Phase – Removal of pt from cause of burn. Determine source or loc or burn
2. Shock Phase – 24 - 48. Characterized by shifting of fluids from intravascular to interstitial space = Hypovolemia
S/Sx:
- BP Decrease
- Urine output Priority To All Types of Burn:
- HR Increase INFECTION
- Hct Elevated
- Serum Na Decrease
- Serum K Increase
- Metabolic Acidosis
3. Diuretic/ Fluid Remobilization Phase - 3 to 5 days. Return of fluid from interstitial to intravascular space
4. Recovery/ Convalescent Phase – complete diuresis. Wound healing starts immediately after burn injury.
Pathophysiology Of THERMAL BURN:
(2ND Stage in the 1st 24-48 hrs.)
Intense heat ------------- activates a sympatho-adrenal medullary response
Tissue Trauma
Release of Histamine
Vasodilation
Increased Capillary Permeability
Fluid shifts from IV to ITS (seepage of plasma fluid to ITS)
1 2
Edema formation Hyponatremia HYPOVOLEMIA 3
Decreased Cardiac Output Sluggish BF
Thrombus Formation
Hypovolemic Shock Renal Perfusion Tissue Ischemia
Evaluate:
1. Decreased BP
Hourly Urine Output BUN Creatinine Hematuria Hyperkalemia 2. Increase Hct
(Evaluate vol. % of RBC in
Ventricular Fibrillation plasma hemoconcentration)
3. Decreased CVP
Sudden Cardiac Arrest
Tissue Starvation Anaerobic Metabolism
(-) Nitrogen balance Lactic Acid Production
METABOLIC ACIDOSIS
Weight loss Weakness (Common problem)
Legend:
1 - Stage of Neurogenic Shock
2 – Stage of Hypovolemic Shock/ Oligenic Shock
3 – Stage of Diuresis
4 – Stage of Repair
COMPLICATIONS OF BURNS:
1. SODIUM (Na) (Normal: 135-145 mEq/L)

a. Decrease Na system of burn victim d/t Hyponatremia
Edema----- trapping of Na----------------- Na activated in 3 Ways/Causes
Hyponatremia 1. R-A—Aldosterone --- Na reabsorption & K excretion

2. Prostaglandin-Renin
S/Sx: - Decreased BP 3. Kallikreen---Kinin--- Increase urination, Na excretion
- Increased rapid, weak pulse
- Diaphoresis Distal tubules of the kidneys
- Poor memory
- Hypoactive
- (-) reflexes
- Oliguria-Anuria
b. Hypernatremia
S/Sx:
- Thirst
- Flushed Skin Normal CVP
- Increase temperature
- Dry tongue 6-12 mmHg
- Dry & sticky mucus membrane
- Hyperactive reflexes
c. Hypovolemia
- Assess for BP, Hct, CVP
d. CVP
- Pressure exerted by blood appropriately at the right atrium of the heart
- Done to evaluate cardiac efficiency
- Done to evaluate state of hydration
- CVP: decrease in burn victims
-If CVP, prepare for Cut-down or Venesection------prior insert 3-way polyethylene tubing
e. Hypovolemic Shock (Oligenic)

- Evaluate BP, Hct, CVP Normal Hourly Urine Output:
- LOC decreased 30 – 60 ml/hour
- PR increased
- RR increased but shallow
- Skin cold & clammy (Hypo, Tachy, Tachy)
BUN ------ 10-20 mg% w/ NPO

Creatinine ------ 0.9 -1.5 mg % w/o NPO--- Reliable indicator of renal function
Not influenced by protein content & diet
Product of muscle metabolism
2. POTASSIUM (K) (Normal: 3-5 – 5.5 mEq/L)
causes
b. R-A-A
c. Insulin/Glucose/ Glucagon ----- Increase Uptake of K----- cell
Ex. In DM pt.--- insulin decrease or none--- potassium will leave the cell (EC to IV)--- K in blood (Hyperkalemia)
a. Increased K in Burns
S/Sx:
- Decreased PR
- Abdominal cramps
- Diarrhea
- Muscular weakness
- ECG changes
b. Decreased K in Diarrhea
S/Sx:
- Increased PR followed by decreased PR
- Weakness
- Weak respiratory muscle
- Shallow respiration------- Paralytic Ileus
Hypo-active bowel sound Abdominal distention

(K influences intestinal tone)
3. Evaluate METABOLIC ACIDOSIS: ABG Interpretation

S/Sx:
Acidosis = CNS depression + Increased K
Alkalosis = CNS excitability + Decreased K
MANAGEMENT OF BURN VICTIMS:
1. Extinguish the flame

- Roll over the pt.
- If burn w/in the eyes, irrigate the eyes.
- Remove clothing that can impede circulation
- Get piece of cloth & place on wound
2. Hospital:
- Establish patent airway

- Make initial assessment including body weight---needed for fluid replacement
- If (+) for hypokalemia: hook patient to a cardiac monitor
- Get an open IV line for cardiac replacement
- If veins are collapsed, do a cut-down or venisection
- Prepare for insertion of indwelling catheter to monitor urine output
- Prepare for NGT ----- to evacuate/decompress gastric content to prevent aspiration
3. Administer isotonic fluid solution

4. Strict aseptic technique
5. Diet – increase CHO, increase CHON, increase Vit C, and increase K- orange
6. If (+) to burns on head, neck, face - Assist in intubation
7. Assist in surgical wound debridement. Administer analgesic 15 – 30 minutes before debridement
8. Prevent Complications:
1. Infection ------ Increase anerobic circulation, risk for anaerobic infection
a. Prepare Tetanus Toxoid Injection------ .5 ml IM

- Prevent Tetanus: Burn surface area is source of anaerobic growth – Clostridium tetany
Tetanus
Tetanolysin Tetanospasmin
Hemolysis Muscle Spasm
b. Morphine SO4
2. Hypovolemic Shock
- Replace fluid losses. Use solution
a. EVAN’S FORMULA
 Colloid – 1 ml x kgBW x % BSA

Ex. Isotonic solution---- NSS, LRS
 Non-Electrolyte - 2,000 ml of glucose in H2O
 Electrolyte - 1 ml x Kg BW x % BSA
b. BROOKE’S FORMULA
 Colloid - 0.5 ml x Kg BW x % BSA

 Electrolyte - 1.5 ml x kg BW x % BSA
c. PARKLAND/BAXTER FORMULA
 4 ml LRS x KgBW x % BSA
Ex. Colloid – Plasma Expanders ------ will increase IV volume

Dextran
Polyrpan
Electrolyte - Isotonic solution--- NSS, LRS------ will increase IV volume
Non- Electrolyte - Glucose in H2O

- D5 in H2O
INDICATIONS FOR FLUID RESUSCITATION/REPLACEMENT
1. Child below 2 y/o ----- resuscitate ---- Increase 10 % BSA

2. Adult 60 y/o ------ resuscitate ------- Increase 10 % BSA
Ex.
Face & Neck = 45
Abdomen =9
Posterior forearm = 2.25
Whole RLE = 18
Buttocks =6
Perineum =1
Total 40.75 = 41%
33 y/o with BW 60
Using Evan’s Formula: Colloid = 1 x 60 x 41 = 2,460 ml/24 hrs.

Electrolyte = 1 x 60 x 41 = 2,460 ml/24 hrs.
Non-electrolyte = 2,000 ml/24 hrs.
*Replace losses 1 hr. after incident to prevent hypovolemic shock
Time % Colloid Electrolyte Non-Electrolyte

12-8pm 1st 8 hrs. – 50% 1,230 ml 1,230 ml 1,000 ml
8-4 pm 2nd 8 hrs. – 25 % 615 615 500
4-12 3rd 8 hrs. – 25 % 615 615 500
*If only 1 IV line (cut-down) ---- transfuse LRS, NSS---- piggyback glucose H2O
*Maximum volume in 24 hrs. is only 10 liters (divided)

* Should replaced only 50 % of body losses
* No plasma in cut-down
* WBC---- FWB given only to burn pt. 1 unit = 500 ml to run for 4 hrs. to prevent hemolysis
3. Paralytic ileus – d/t hypovolemia & hypokalemia

4. Curling’s ulcer – H2 receptor antagonist
5. Septicemia blood poisoning
6. Surgery: Skin grafting
9. Management to promote wound healing:
a. Diet : Increase CHON replacements & K-orange for repair of tissue damage &o promote wound healing
Vitamin C ----- for formation of collagen fibers
Granulation of tissue
Scarring/ fibrosis
Healing Process
b. Cleanse wound/ dress

- Use aseptic technique, use betadine or NSS
c. Apply ointment as anti-microbic agent
Topical antibiotic :
1. Silver Sulfadiazine (silvadene) ----- anti-microbic---promote re-epithelization of wound tissue
2. Sulfamylon
3. Silver nitrate
4. Povidone iodine (betadine)
d. Systemic Antibiotic
Ex.
1. Ampicillin
2. Cephalosporin
3. Tetracycline
e. Dressing
1. Open/Exposure Method
2. Closed/Occlusive
*Reverse isolation if open wound/method (bed cradle)
f. Do hydrotherapy/Tubbing ------ to loosen the eschar
- In Hubbard Tank
Done only when VS are stable & level of electrolyte is normal
2 to 3x/day for 15-20 minutes
Prior to tubbing, check temperature of solution
Give analgesic 30 minutes before tubbing
Take VS prior to tubbing
While pt. in tub, encourage ROM exercises to prevent contracture deformity
If wound is severely infected, mix betadine solution
4. RELATED TO F & E BALANCE
1. BLOOD GASES
pH HCO3
R pH PCO2 Respiratory Alkalosis
O ph PCO2 Respiratory Acidosis
M ph HCO3 Metabolic Alkalosis
E ph HCO3 Metabolic Acidosis
RESPIRATORY RESPIRATORY METABOLIC METABOLIC

ALKALOSIS ACIDOSIS ALKALOSIS ACIDOSIS
Chronic Bronchitis Vomiting Ileostomy
Pyloric Stenosis Intestinal Tubing
Cushing DM
Diarrhea
VASCULAR DISEASES
I. HYPERTENSION
CLASSIFICATION OF HYPERTENSION by JNC-VII
Pathophysiology:
Multi-factorial etiology
BP= CO (SV X HR) x TPR
Any increase in the above parameters will increase BP
1. Increased sympathetic activity
2. Increased absorption of Sodium & water in the kidney
3. Increased activity of the RAAS
4. Increased vasoconstriction of the peripheral vessels
5. Insulin resistance
Risk factors for Cardiovascular Problems in
ASSESSMENT FINDINGS Hypertensive patients
1. Headache Major Risk factors

2. Visual changes
3. chest pain 1. Smoking
4. dizziness 2. Hyperlipidemia
5. N/V 3. DM
Created by Niňa E. Tubio 4. Age older than 60 120
5. Gender- Male & post menopausal Women
6. Family History
DIAGNOSTIC STUDIES
1. Health history & PE

2. Routine laboratory
- Urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS
3. Other lab- CXR, creatinine clearance, 24-huour urine protein
MEDICAL MANAGEMENT
1. Lifestyle modification Drug Therapy For HPN:

2. Drug therapy
3. Diet therapy Diuretics
4. Drug therapy Beta blockers
Calcium channel blockers
ACE inhibitors
NURSING INTERVENTIONS A2 Receptor blockers
Vasodilators
1. Provide health teaching to patient
Teach about the disease process

Elaborate on lifestyle changes
Assist in meal planning to lose weight
Provide list of LOW fat , LOW sodium diet of less than 2-3 grams of Na/day
Limit alcohol intake to 30 ml/day
Regular aerobic exercise
Advise to completely Stop smoking
2. Provide information about anti-hypertensive drugs

Instruct proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition
Instruct to avoid over-the-counter drugs that may interfere with the current medication
3. Promote Home care management

Instruct regular monitoring of BP
Involve family members in care
Instruct regular follow-up
4. Manage hypertensive emergency & urgency properly

II. ANEURYSM
- Dilation involving an artery formed at a weak point in the vessel wall
Types:
1. Saccular= when one side of the vessel is affected
2. Fusiform= when the entire segment becomes dilated
RISK FACTORS
1. Atherosclerosis
2. Infection= syphilis
3. Connective tissue disorder
4. Genetic disorder= Marfan’s Syndrome
PATHOPHYSIOLOGY
Damage to the intima and media weakness outpouching
Dissecting aneurysm tear in the intima and media with dissection of blood through the layers
ASSESSMENT

1. Asymptomatic
2. Pulsatile sensation on the abdomen
3. Palpable bruit
LABORATORY:
1. CT scan
2. Ultrasound
3. X-ray
4. Aortography
Medical Management:
1. Anti-hypertensives
2. Synthetic graft
Nursing Management:
1. Administer medications
2. Emphasize the need to avoid increased abdominal pressure
3. No deep abdominal palpation
4. Remind patient the need for serial ultrasound to detect diameter changes
III. PERIPHERAL VALVULAR DISEASES
A. PERIPHERAL ARTERIAL OCCLUSIVE DISEASE (PAOD)
- Refers to arterial insufficiency of the extremities usually secondary to peripheral atherosclerosis.

- Found in males age 50 & above
- The legs are most often affected
Risk factors for Peripheral Arterial occlusive disease

Non-Modifiable
1. Age
2. gender
3. family predisposition
Risk factors for Peripheral Arterial occlusive disease

Modifiable
1. Smoking
2. HPN
3. Obesity
5. DM
6. Stress
ASSESSMENT FINDINGS:
1. INTERMITTENT CLAUDICATION- the hallmark of PAOD

This is PAIN described as aching, cramping or fatiguing discomfort consistently reproduced with the same
degree of exercise or activity
This pain is RELIEVED by REST
This commonly affects the muscle group below the arterial occlusion
2. Progressive pain on the extremity as the disease advances

3. Sensation of cold and numbness of the extremities
4. Skin is pale when elevated and cyanotic/ruddy when placed on a dependent position
5. Muscle atrophy, leg ulceration and gangrene
Diagnostic Findings
1. Unequal pulses between the extremities
2. Duplex ultrasonography
3. Doppler flow studies
Medical Management
1. Drug therapy
Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles
Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation
2. Surgery- Bypass graft and anastomoses
Nursing Interventions
1. Maintain Circulation to the extremity

Evaluate regularly peripheral pulses, temperature, sensation, motor function and capillary refill time
Administer post-operative care to patient who underwent surgery
2. Monitor and manage complications
Note for bleeding, hematoma, decreased urine output
Elevate the legs to diminish edema
Encourage exercise of the extremity while on bed
Teach patient to avoid leg-crossing
3. Promote Home management

Encourage lifestyle changes
Instruct to AVOID smoking
Instruct to avoid leg crossing
B. ARTERIAL ULCERS
1. BUERGER’S DISEASE / THROMBOANGIITIS OBLITERANS
-Acute inflammatory disorder characterized by recurring inflammation of the medium sized small arteries & veins of the
lower extremities
- Occurs in MEN ages 30 y/o /FEET

- SMOKING!
Pathophysiology:
Cause is UNKNOWN
Probably an Autoimmune disease
 Inflammation of the arteries thrombus formation occlusion of the vessels
Sx:
1. INTERMITTENT CLAUDICATION
Leg PAIN upon walking but relieved by rest
Foot cramps in the arch (instep claudication) after exercise
Aggravated by smoking, emotional disturbance & cold chilling
2. Digital rest pain not changed by activity or rest
3. Cold sensitivity & skin color changes

Intense RUBOR (reddish-blue discoloration), progresses to CYANOSIS as disease advances
FEET----becomes White Bluish Red (W-B-R)

Pallor Cyanosis Rubor – with dependency (+) especially post-smoking
d/t vasoconstriction d/t pooling of deoxygenated blood d/t exaggerated reflow/hyperemia
4. Paresthesia
5. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis
6. Tropic changes
7. Ulcerations
8. Gangrene formation
Dx:
1. Oscillometry – Reveals a decrease peripheral pulse volume.
2. Doppler UTZ – (Duplex ultrasnography) Reveals a decrease blood flow to affected extremities.
3. Angiography (Contrast angiography) – reveals site & extent of mal-occulsion.
Nsg Mgt:
1. Encourage a slow but progressive physical activity
a.) Walk 3 -4 x / day
b.) Out of bed 2 – 3 x a / day
2. Meds
a.) Analgesic
b.) Vasodilator
c.) Anticoagulant
3. Foot care mgt like DM to prevent gangrene formation–
a.) Avoid walking barefoot
b.) Cut toe nails straight
c.) Apply lanolin lotion – prevent skin breakdown
d.) Avoid wearing constrictive garments
4. Avoid smoking & exposure to cold environment
5. Assist in the medical and surgical management
Surgery: BKA (Below the knee amputation) Bypass graft/amputation
Post-operative care: after amputation
Elevate stump for the FIRST 24 HOURS to minimize edema & promote venous return
Place patient on PRONE position after 24 hours
Assess skin for bleeding and hematoma
Wrap the extremity with elastic bandage
2. RAYNAUD’S DISEASE/
- A form of intermittent arteriolar VASOCONSTRICTION that results in coldness, pain & pallor of the fingertips or toes
- Acute episodes of arterial spasm affecting digits of hands & fingers
Cause : UNKNOWN
Predisposing Factors: 1. SLE – Pathognomonic sign – butterfly rash on face

Chipmunk face – bulimia nervosa
1. WOMEN 16- 40 yrs Cherry red skin – carbon monoxide poisoning
2. Smoking Spider angioma – liver cirrhosis
3. Collagen Disease Caput medusae – leg & trunk umbilicus- Liver cirrhosis
Lion face – leprosy
2. Rheumatoid Arthritis - Direct hand trauma

(Piano playing, excessive typing, operating chainsaw)
Sx:
1. RAYNAUD’S PHENOMENON
- A localized episode of vasoconstriction of the small arteries of the hands that causes color & temperature
changes

2. Intermittent claudication - leg pain upon walking - Relieved by rest
3. Cold sensitivity (same with buerger’s) W-B-R
4. Paresthesia
5. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis
6. Ulcerations
7. Gangrene formation
8. Tingling sensation
9. Burning pain on the hands and feet
Nsg Mgt:
a. Analgesics to relieve pain
b. Vasodilators -----CALCIUM channel blockers
To prevent vasospasms
c. Encourage to wear gloves especially when opening a refrigerator.
d. Avoid smoking & exposure to cold environment
e. Instruct patient to avoid situations that may be stressful
f. Instruct to avoid exposure to cold & remain indoors when the climate is cold
g. Instruct to avoid all kinds of nicotine
h. Instruct about safety. Careful handling of sharp objects
DIFFERENTIATION:
PERIPHERAL VALVULAR DISEASE
Arterial Ulcers Venous Ulcer

1. Thromboangiitis Obliterans – male/ feet 1. Varicose veins
2. Raynauds – female/ hands 2. Thrombophlebitis
C. VENOUS ULCERS
1. VARICOSE VEINS / Varicosities
- Abnormal dilation of veins usually in the lower extremities & trunk
Pathophysiology
Veins in valve
Factors  venous stasis increased hydrostatic pressure  edema Fx: To increase venous return
Due to: If incompetent valve

a.) Incompetent valves leading to
Pump blood down
b.) Increase venous pooling & stasis leading to
Pooling of blood in veins
c.) Decrease venous return Cannot return to heart
Distention of veins
Predisposing Factors: Sx: Warm to touch/ heavy legs
a. Hereditary
b. Congenital weakness of veins
c. Thrombophlebitis
d. Cardiac diseases
e. Pregnancy
f. Obesity
g. Prolonged immobility - Prolonged standing/sitting -------dorsiflex feet
h. Constipation (for hemorrhoids)
i. Incompetent venous valves
Sx:
- Pain especially after prolonged standing
- Dilated tortuous superficial skin veins on the legs
- Warm to touch
- Leg pain & Heaviness in legs
- Dependent edema
Dx:
1. Venography
2. Trendelenberg’s Test – Reveals that veins distends quickly in < 35 secs.
How: Elevate legs in 45 degrees angle. After 15-30 minutes, let pt. stand & see the varicosities
Medical Management:
1. Pharmacological therapy
2. Leg vein stripping/ligation
Sclerotherapy----------Spider Wed Varicosities (small-like)
(Cold-solution injection)
S/E: Thrombosis
3. Anti-embolic stockings
Nsg Mgt: “Consistent to all venous ulcers”
1. Elevate legs above heart level – to promote venous return – 1 to 2 pillows

2. Measure circumference of leg muscles to determine if swollen.
3. Wear anti embolic or knee high stockings. Women – full panty hose
4. Meds: Analgesics for pain
5. Caution patient to avoid prolonged standing or sitting
6. Provide high-fiber foods to prevent constipation
7. Teach simple exercise to promote venous return
8. Caution patient to avoid knee-length stockings & constrictive clothings
9. Avoid massage on the affected area
2. THROMBOPHLEBITIS / DVT- Deep Vein Thrombosis
- Inflammation of the deep veins of the lower extremities & the pelvic veins
- The inflammation results to formation of blood clots in the area
1. Smoking
2. Obesity
2. Hyperlipedemia
4. Prolonged use of oral contraceptives
- Chronic anemia
- DM
- MI
- CHF
- Post-surgical complications
- Post cannulation – insertion of various cardiac catheters
- Prolonged immobility
- Varicosities
- Traumatic procedures
- Diet high in saturated fats
Complication:
 Pulmonary Embolism:
Sx:
- Sudden sharp chest pain
- Dyspnea
- Tachycardia
- Palpitation
- Diaphoresis
- Mild restlessness
Sx:
1. Pain at affected extremities
2. Cyanosis
3. (+) HOMAN’S SIGN - Pain at leg muscles upon dorsiflexion of foot ---- Pathognomonic sign
4. Leg tenderness
5. Leg pain & edema
6. Dilated tortous vein
Dx:
1. Angiography
2. Doppler UTZ
3. Duplex Scan
Medical Management:
Antiplatelets
Vein stripping & grafting
Anti-embolic stockings
Analgesics.
Anticoagulant: Heparin
Nsg Mgt:
1. Elevate legs above heart level.
2. Apply warm, moist packs to reduce lymphatic congestion.
3. Measure circumference of leg muscles to detect if swollen.
4. Use anti embolic stockings.
5. Provide measures to avoid prolonged immobility
Repositioning Q2
Provide passive ROM
Early ambulation
6. Provide skin care to prevent the complication of leg ulcers
7. Monitor for signs of pulmonary embolism (sudden respiratory distress)
GASTROINTESTINAL TRACT
Overview:
The GIT is composed of two general parts
The main GIT starts from the mouthEsophagusStomachSILI
I. Upper Alimentary Canal: Function for digestion
a. Mouth ------------------------ where digestion starts

• Contains the lips, cheeks, palate, tongue, teeth, salivary glands, masticatory/facial muscles & bones
• Anteriorly bounded by the lips
• Posteriorly bounded by the oropharynx
Important for the mechanical digestion of food
The saliva contains SALIVARY AMYLASE or PTYALIN that starts the INITIAL digestion of CHO
b. Pharynx (throat)
c. Esophagus
A hollow collapsible tube
• Length- 10 inches
• Made up of stratified squamos epithelium
• The upper third contains skeletal muscles
• The middle third contains mixed skeletal and smooth muscles
• The lower third contains smooth muscles and the esophago-gastric/ cardiac sphincter is found here
Functions to carry or propel foods from the oropharynx to the stomach
d. Stomach ---------------------- widest section of UAC: Digestion ends here

e. 1st half of duodenum
II. Middle Alimentary canal – Function: For Absorption
* Small Intestine – Absorption starts

* Large Intestine - Complete absorption / 90% of water absorbed
a. 2nd half of duodenum
b. Jejunum
c. Ileum
d. 1st half of ascending colon
III. Lower Alimentary Canal – Function: Elimination
a. 2nd half of ascending colon

b. Transverse
c. Descending colon
d. Sigmoid
e. Rectum
IV. Accessory Organ
a. Salivary Gland
b. Verniform Appendix ---------------------- commonly inflammed
c. Liver ---------------------- site of bile production
d. Pancreas – auto digestion
e. Gallbladder – storage of bile
The GIT Physiology
• Absorbs water
• Eliminates wastes
• Bacteria in the colon synthesize Vitamin K
• Appendix participates in the immune system
SYMPATHETIC
• Generally INHIBITORY!
• Decreased gastric secretions
• Decreased GIT motility
• But: Increased sphincteric tone and constriction of blood vessels
PARASYMPATHETIC
• Generally EXCITATORY!
• Increased gastric secretions
• Increased gastric motility
• But: Decreased sphincteric tone and dilation of blood vessels

Gastrointestinal Assessment : Physical Exam Sequence
• Inspection
• Auscultation
• Percussion
• Palpation
The ABDOMINAL examination
The sequence to follow is:
• Inspection
• Auscultation
• Percussion
• Palpation
COMMON LABORATORY PROCEDURES
1. FECALYSIS
Examination of stool consistency, color and the presence of occult blood.
Special tests for fat, nitrogen, parasites, ova, pathogens and others
FECALYSIS: Occult Blood Testing
Instruct the patient to adhere to a 3-day meatless diet
No intake of NSAIDS, aspirin and anti-coagulant
Screening test for colonic cancer
2. Upper GIT study: barium swallow

Examines the upper GI tract
Barium sulfate is usually used as contrast
Pre-test: NPO post-midnight
Post-test: increase pt fluid intake, instruct that stools will turn white, monitor for obstruction, laxative is also
ordered
3. Lower GIT study: barium enema

Examines the lower GI tract
Pre-test: Clear liquid diet and laxatives, NPO post-midnight, cleansing enema prior to the test
Post-test: Laxative is ordered, increase patient fluid intake, instruct that stools will turn white, monitor for obstruction
4. Gastric analysis
Aspiration of gastric juice to measure pH, appearance, volume and contents
Pre-test: NPO 8 hours, avoidance of stimulants, drugs and smoking

Post-test: resume normal activities
5. EGD (Esophagogastroduodenoscopy)
Visualization of the upper GIT by endoscope
Pre-test: ensure consent, NPO 8 hours, pre-medications like atropine and anxiolytics
Intra-test: position : LEFT lateral to facilitate salivary drainage and easy access
Post-test: NPO until gag reflex returns, place patient in SIMS position until he awakens, monitor for complications,
saline gargles for mild oral discomfort
6. Lower GI- scopy

Use of endoscope to visualize the anus, rectum, sigmoid and colon
Pre-test: consent, NPO 8 hours, cleansing enema until return is clear
Intra-test: position is LEFT lateral, right leg is bent and placed anteriorly
Post-test: bed rest, monitor for complications like bleeding and perforation
7. Cholecystography
Examination of the gallbladder to detect stones, its ability to concentrate, store and release the bile
Pre-test: ensure consent, ask allergies to iodine, seafood and dyes; contrast medium is administered the night prior, NPO
after contrast administration
Post-test: Advise that dysuria is common as the dye is excreted in the urine, resume normal activities
8. Paracentesis
Removal of peritoneal fluid for analysis
Pre-test: ensure consent, instruct to VOID and empty bladder, measure abdominal girth
Intra-test: Upright on the edge of the bed, back supported and feet resting on a foot stool
9. Liver biopsy
Pretest
Consent
NPO
Check for the bleeding parameters
Intratest
– Position: Semi fowler’s LEFT lateral to expose right side of abdomen
Post-test: position on RIGHT lateral with pillow underneath, monitor VS and complications like bleeding, perforation.
Instruct to avoid lifting objects for 1 week
I. ACCESSORY ORGANS DISORDER
SALIVARY GLANDS
Function: Produces saliva for mechanical digestion

1200 -1500 ml/day - saliva produced
3 Types of Saliva produced:

Parotid – below & front of ear
Sublingual
Submaxillary
1. PAROTITIS
- “ Endemic Mumps”
- Inflammation of the parotid gland
- Contagious
Causative Agent: Paramyxo Virus --------- Target: Parotid Glands, Respiratory Glands & Meninges
Swollen Parotid Glands

Ear Ache Fever Dysphagia
(Otalgia)
S/Sx:
1. Fever, chills anorexia, gen body malaise
2. Swelling of parotid gland
3. Dysphagia
4. Ear ache – Otalgia
MOT: Direct transmission & droplet nuclei
Incubation Period: 14 – 21 days
Period of Communicability – 1 week before swelling & immediately when swelling begins.
Nsg Mgt:
1. CBR
2. Strict isolation (Gentan Violet for aesthetic purposes only)
3. Meds: Analgesic
Antipyretic
Antibiotics – to prevent 2 complications
4. Alternate warm & cold compress at affected part
5. General liquid to soft diet
6. Prevent Complications :
1.Women – Cervicitis, Vaginitis, Oophoritis
2.Both sexes – meningitis & encephalitis/ reason why antibiotics is needed
3. Men – Orchitis (inflammation of testes) might lead to sterility if it occur during / after puberty.
VERNIFORM APPENDIX
Location: Right Iliac or Right Inguinal area

Function : As a Lymphatic organ that produces WBC during fetal life - ceases to function upon birth of baby
1. APENDICITIS
– Inflamation of verniform appendix
1. Microbial infection cause by bacteria

2. Fecalith – undigested food particles – Ex. Tomato seeds, guava seeds
3. Intestinal obstruction, lymphoid hyperplasia, foreign body & helminthic obstruction
4. Kinking & external occlusion by adhesions, fibrous conditions of abdomen
Pathophysiology:
• Obstruction of lumen increased pressure decreased blood supply bacterial proliferation and mucosal inflammation
ischemia necrosis rupture
• Stages: 1. Congestive
2. Suppurative
3. Gangenous
4. Perforation

S/Sx:
1. Pathognomonic sign: (+) REBOUND TENDERNESS
2. Low grade fever, anorexia, n/v
3. Diarrhea / & or constipation
4. Pain at Rt iliac region
5. Late sign : Tachycardia D/T pain
6. Abdominal pain: begins in the umbilicus then localizes in the RLQ (Mc Burney’s point)
7. Abdominal rigidity (if perforated)
Dx:
1. CBC : Reveals mild leukocytosis – increase WBC---------- Confirmatory DX
2. PE : (+) Rebound Tenderness (flexion of Rightt leg, palpate Rt iliac area – rebound)
3. Urinalysis --- Reveals (+) to acetone
4. Ultrasound
5. Abdominal X-ray
Treatment:
1. Surgical Intervention
Appendectomy- Should be operated 24 – 48 to prevent rupture---- Peritonitis
* MC BURNEY’S POINT – site of surgical incision for appendectomy
Nsg Mgt: PRE- OPERATIVE
1. Consent PAIN sensation an important parameter:

2. Notify MD----- local anesthesia
3. Routinary nursing measures: (-) to pain : Ruptured appendix
a.) Skin preparation
b.) NPO (+) to pain : Inflammation
c.) Avoid enema – lead to rupture of appendix
4. Meds:
Antipyretic
Antibiotics to prevent secondary infection
*Don’t give analgesic – will mask the pain
- Presence of pain means appendix has not ruptured.
4. Avoid heat application, enemas & laxative – will rupture appendix.
5. Monitor VS, I&O bowel sound, fever & hydration status
6. Monitor for perforation and signs of shock
7. POSITION of Comfort: RIGHT SIDELYING in a low FOWLER’S
Nursing Mgt: POST-OPERATIVE
1. If (+) to Pendrose Drain – indicates rupture of appendix

Position- affected side to drain
If no Penrose Drain, position based on pt. comfort
2. Meds: analgesic due post op pain

Antibiotics, Antipyretics PRN
3. Monitor VS, I&O, bowel sound
4. Maintain patent IV line
5. Complications: Peritonitis & Septicemia
6. Monitor VS and signs of surgical complications
7. Maintain NPO until bowel function returns
8. If rupture occurred, expect drains and IV antibiotics
9. POSITION post-op: RIGHT side-lying, SEMI- FOWLER’S to decrease tension on incision & legs flexed to promote
drainage
10. Administer prescribed pain medications
COMMON GIT SYMPTOMS AND MANAGEMENT
1. CONSTIPATION
- An abnormal infrequency and irregularity of defecation
- Multiple causations
Pathophysiology
• Interference with three functions of the colon

1. Mucosal transport
2. Myoelectric activity
3. Process of defecation
1. Assist physician in treating the underlying cause of constipation

2. Encourage to eat HIGH fiber diet to increase the bulk
3. Increase fluid intake
4. Administer prescribed laxatives, stool softeners
5. Assist in relieving stress
2. DIARRHEA
-Abnormal fluidity of the stool
• Multiple causes
– Gastrointestinal Diseases
– Hyperthyroidism
– Food poisoning
Nursing Interventions
1. Increase fluid intake- ORESOL is the most important treatment!
2. Determine and manage the cause
3. Anti-diarrheal drugs
LIVER In locating organs of the abdomen:

Use the 9 regions
• The largest internal organ

• Located in the right upper quadrant/ Right Hypochondriac Region
• Contains two lobes- the right & the left
• Color: Scarlet Red
• Covered by a fibrous capsule--------- GLISSON’S CAPSULE
• The hepatic ducts join together with the cystic duct to become the common bile duct
• Functions to store excess glucose, fats and amino acids
• Also stores the fat soluble vitamins- A, D and the water soluble- Vitamin B12
• Produces the BILE for normal fat digestion
• The Von Kupffer cells remove bacteria in the portal blood
• Detoxifies ammonia into urea
• Functional Unit – Liver Lobules
Precursor: Cholesterol
Function:
Created by Niňa E. Tubio Bile salt + water 133
Bile
1. Produces bile
Bile: Function is to emulsifies fats
Gives color to urine – Urobilin (light yellow)
Stool – Stircobilin (brown)
2. Detoxifies toxic substances from drugs Vitamin A = Retinol

Vitamin D = Cholecalciferol
3. Promotes synthesis of Vit A, D, E, K Vitamin E = Tococalciferol
(Fat soluble vitamins) Vitamin K = Phetione
Excess Vit. D & K = Hypervitaminosis

4. It destroys excess estrogen hormone Deficiency Vit. A = Night Blindness
Deficiency Vit. D = Rickets
= Osteoarthritis
5. For metabolism of:
A. CHO
1. Glycogenesis – synthesis of glycogens
2. Glycogenolysis – breakdown of glycogen
3. Gluconeogenesis – formation of glucose from non- CHO sources
B. CHON
1. Promotes synthesis of albumin & globulin
Cirrhosis – decrease albumin
Albumin – maintains osmotic pressure, prevents edema
2. Promotes synthesis of prothrombin & fibrinogen
3. Promotes conversion of ammonia to urea.
Ammonia like breath – fetor hepaticus
C. FATS
1. Promotes synthesis of cholesterol to neutral fats – called triglycerides
1. LIVER CIRRHOSIS / “Laennec’s Cirrhosis”
 Lost of architectural design of liver leading to fat necrosis & scarring

 A chronic, progressive disease characterized by a diffuse damage to the hepatic cells
 The liver heals with scarring, fibrosis and nodular regeneration
Laennac’s Cirrhosis – caused by alcoholism

1. Chronic alcoholism ------ Common Cause
2. Malnutrition – DecreaseVit B- Thiamine - main cause
3. Virus
4. Toxicity to Carbon Tetrachloride
5. Use of hepatotoxic agents
6. Post-infection
7. Cardiac diseases
8. Schistosomiasis
9. Biliary obstruction
10. Portal Hypertension
Compression of the intra-liver vessels
Decreased protein (colloid pressure)
Increased hydrostatic pressure

S/Sx:
Early signs:
a.) Weakness & Fatigue
b.) Anorexia, Early mornig Nausea & vomiting, Weight loss
c.) Stomatitis
d.) Urine – Tea color / Stool – Clay color
e.) Amenorrhea
f.) Decrease sexual urge
g.) Loss of pubic & axilla hair
h.) Hepatomegaly
i.) Jaundice
j.) Pruritus or Urticaria
k.) RUQ abdominal pain
2. Late signs
a.) Hematological changes – all blood cells decrease---- Pancytopenia
Leukopenia- decrease
Thrombocytopenia- decrease
Anemia- decrease
b.) Endocrine changes
Spider Angiomas (Teleangectasis---nose), Gynecomastia
Caput medusae (Abdomen—loss of tortousity of the umbilicus) , Palmar errythema (redness)
c.) GIT changes
Ascitis, bleeding esophageal varices – due to portal HPN
d.) Neurological Changes: Hepatic Encephalopathy
Dx:
1. Liver enzymes- increase
SGPT (ALT)
SGOT (AST)
2. Serum cholesterol & ammonia = Iincrease
3. Indirect Bilirubin or Unconjugated Bilirubin = Increase
4. CBC = Pancytopenia
5. PTT = Prolonged
6. Hepatic Ultrasonogram = Reveals fat necrosis of liver lobules
Pathophysiology:
CIRRHOSIS
* 1-3 : Complications
HEPATIC ENCEPHALOPATHY
No production of albumin (accumulation
No convertionof of
ammonia-a
Ammoniacerebral
to urea No Prothrombin & Firinogen
toxin)
Decreases Osmotic Pressure Ammonia reabsorb back to blood No clotting Factor
1st Sign: Asterixis BLEEDING ESOPHAGEAL VARICES
(Flapping Hand Tremors) (d/t Portal HPN—dilation of esophageal
Edema to Liver HEPATIC ENCEPHALOPATHY 1 BLEEDING 3
veins)
2
Late Signs: Sx:
ASCITES
ASCITES Headache Vomiting---- accompanied by blood
(Fluid Accumulation in the Peritoneal Fetor Hepaticus
cavity) Restlessness Nsg Mgt:
Disorientation/ Confusion
Nsg Mgt: Decrease LOC—can lead to 1. Medication:
Hepatic Coma Vit. K
1. Medication: Pitressin or Vasopressin (IM)
Loop Diuretics (10-15 minutes) Nsg. Priortity:
K- sparing diuretics Assist In Mechanical Ventilation 2. NGT Decompression- Lavage
Give before lavage
2. Assist in abdominal Paracentesis Nsg. Mgt: - ice or cold saline solution
(Aspiration of fluid in the 1. Assist in mechanical ventilation d/t Monitor NGT output
peritoneum) coma
*Void before paracentesis to prevent 2. Monitor VS, neuro check
Created by Niňa E. Tubio 3.Assist in Mechanical decompression 135
accidental puncture of bladder as 3. Siderails – d/t restless - Insertion of Sangtaken-Blackemore
trochar is inserted 4. Meds: tube (3 lumen-typed catheter)
Laxatives – to excrete ammonia - Scissors at bedside to deflate balloon
Liver cirrhosis – bedside scissor – if pt
complaints of DOB
Cut cystachean tube to deflate balloon

Nsg Mgt:
1. CBR ---- Elevate the head of the bed to minimize dyspnea
2. Restrict Na before fluids
3. Monitor VS, I&O, weight, LOC & bleeding
4. With pt daily & assess pitting edema
5. Measure abdominal girth daily – notify MD
6. Meticulous skin care
7. Provide Moderate to LOW-protein (1 g/kg/day) & LOW-sodium diet
DIET
8. Diet – Increase CHO, Vit. & minerals. Moderate fats. Well balanced diet
Early Stage
9. Provide supplemental Vit. (especially K) & minerals
10. Administer prescribed:
High in: CHO
Diuretics= to reduce ascites & edema
CHON
Lactulose= to reduce NH4 in the bowel
Vitamins
Antacids= to prevent ulcer & bleeding
Minerals
Neomycin= to kill bacterial flora that cause NH production
Low in : Fats
11. Avoid hepatotoxic drugs
Paracetamol Late Stage:
Anti-tubercular drugs High in: CHO
12. Reduce the risk of injury Vit. & Minerals
Side rails reorientation Low in : CHON
Assistance in ambulation Fats
Use of electric razor & soft-bristled toothbrush
13. Keep equipments ready including Sengstaken-Blakemore tube, IV fluids, Medications to treat hemorrhage
PANCREAS
- Mixed gland (Functions as an exocrine & endocrine gland)

- A retroperitoneal gland
• The pancreatic duct (major) joins the common bile duct in the sphincter of Oddi
• The exocrine function of the pancreas is the secretion of digestive enzymes for carbohydrates, fats &
proteins
• Pancreatic amylase carbohydrates
• Pancreatic lipase (steapsin) fats
• Trypsin, Chymotrypsin and Peptidases proteins
• Bicarbonate to neutralize the acidic chyme. Stimulated by SECRETIN!
Pancreas----- with acinar cells----secretes pancreatic juice going to--- pancreatic duct--- to--stomach
1. PANCREATITIS
– An Inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto digestion
– Can be acute or chronic
Cullen’s Sign at the Umbilicus:
Bleeding of the
Pancreas
1. Chronic alcoholism
2. Hepatobilary disease
3. Obesity
4. Hyperlipidemia
5. Hypoparathyroidism
6. Drugs – Thiazide diuretics, pills, Pentamidine HCL (Pentam)---for AIDS
7. Diet – increase saturated fats
8. Hypercalcemia
9. Trauma
10. Biliary tract disease - cholelithiasis
11. Bacterial disease
12. PUD
13. Mumps
Pathophysiology of Acute Pancreatitis:

 Self-digestion of the pancreas by its own digestive enzymes principally TRYPSIN
 Spasm, edema or block in the Ampulla of Vater reflux of proteolytic enzymes Auto digestion of the Pancreatic Tissue
INFLAMMATION
Hemorrhage----- Necrosis
KININ ACTIVATION will result to increased permeability
Loss of Protein-rich fluid into the peritoneum
HYPOVOLEMIA
S/Sx:
1. Severe Left epigastric pain – radiates from back &flank area
2. Abdominal pain- acute onset, occurring after a heavy meal or alcohol intake
2. Aggravated by eating, with DOB---- rest the GIT
3. N/V, Jaundice, Anorexia
4. Tachycardia
5. Palpitation due to pain
6. Dyspepsia – indigestion
7. Decrease bowel sounds
8. (+) Cullen’s sign - ecchymosis of umbilicus Hemorrhage------ Chronic Hemorrhagic Pancreatitis
9. (+) Grey Turner’s spots – ecchymosis of flank area Confirmatory Dx
10. Hypocalcemia
11. Hypotension & Hypovolemia
12. Signs of Shock
Dx:
1. Serum amylase & lipase – Increase---- Confirm the presence of pancreatitis
2. Urine lipase – Increase
3. Serum Ca – Decrease
4. Ultrasound
5. WBC
6. CT scan
7. Hemoglobin and hematocrit
Nursing Mgt:
1. Meds:
Assist in pain management. Usually, Demerol is given. Morphine is AVOIDED
a.) Narcotic analgesic - Meperidine Hcl (Demerol)

Don’t give Morphine SO4 –will cause spasm of sphincter.
b.) Smooth muscle relaxant/ anti cholinergic

Ex. Papavarine Hcl
Prophantheline Bromide (Profanthene)
c.) Vasodilator – NTG
d.) Antacid – Maalox
e.) H2 receptor antagonist - Ranitidine (Zantac) To decrease pancreatic stimulation
*Ranitidine ---- more common & with less S/E
f.) Ca – gluconate
A Phosphate binder---- Antacid-----Constipation---- Amphogel
2. Withold food & fluid – aggravates pain
3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentation
Complications of TPN:
1. Infection
2. Air Embolism -----Tape all connections to the system
3. Hyperglycemia
4. Hyponatremia
4. Institute stress mgt tech

a.) DBE
b.) Biofeedback
5. Comfy position - Knee chest or fetal like position to decrease pain

Position patient in SEMI-FOWLER’s to decrease pressure on the diaphragm
6. If pt can tolerate food, give increase CHO, decrease fats, and increase CHON
7. Assist in correction of Fluid and Blood loss
8. lace patient on NPO to inhibit pancreatic stimulation
9. NGT insertion to decompress distention and remove gastric secretions

10. Maintain on bed rest
11. Deep breathing and coughing exercises
12. Introduce oral feedings gradually- HIGH carbo, LOW FAT

13. Maintain skin integrity
14. Manage shock and other complications:
Chronic hemorrhagic pancreatitis
Shock
Pulmonary Complications---- Pneumonia, Air embolism & Pleural effusion
GALLBLADDER
• Located below the liver

• The cystic duct joins the hepatic duct to become the bile duct
• The common bile duct joins the pancreatic duct in the sphincter of Oddi in the first part of the duodenum
• Storage of bile (made of cholesterol) & concentrates bile
• Contracts during the digestion of fats to deliver the bile
• Cholecystokinin is released by the duodenal cells, causing the contraction of the gallbladder & relaxation of the
sphincter of Oddi
DISORDER OF THE GALLBLADDER
1. CHOLECYSTITIS
– Inflammation of the gallbladder
Can be acute or chronic:

1. Acute cholecystitis usually is due to gallbladder stones
2. Chronic cholecystitis is usually due to long standing gall bladder inflammation

CHOLELITHIASIS
- Inflammation of the gallbladder with Formation of GALLSTONES in the biliary apparatus
Predisposing FACTORS:
1. 5 “F”
Female
Fat (Obesity)
Forty (High Risk : 40 y/o)
Fertile
Fair
2. Post menopausal women – undergoing estrogen therapy

4. Hyperlipidemia
5. Neoplasm
Pathophysiology:
Supersaturated bile, Biliary stasis
Stone formation
Blockage of Gallbladder
Inflammation, Mucosal Damage and WBC infiltration
S/Sx:
1. Severe Right abdominal pain (after eating fatty food). Occurring especially at night
Epigastric pain that radiates to the scapula or localized at the RUQ
Mass at the RUQ
2. Fatty intolerance
3. Anorexia, n/v
4. Jaundice
5. Pruritus
6. Easy bruising
7. Tea colored urine / Dark-orange & foamy urine
8. Steatorrhea
9. Indigestion, belching and flatulence
10. Murphy’s sign
Dx:
1. Oral cholecystogram (or gallbladder series)- Confirms presence of stones but cannot visualize the gallbladder
2. Ultrasonography- can detect the stones
3. Abdominal X-ray
4. Cholecystography
5. WBC count increased
6. ERCP: Revaels inflamed gallbladder with gallstone
7. Serum Lipase – Increase
8. Indirect Bilirubin - Increase
Tx:
Analgesic- Meperidine
Chenodeoxycholic acid= to dissolve the gallstones
Antacids
Anti-emetics
Nursing Mgt:
1. Medications:
Administer prescribed medications to relieve pain.

a.) Narcotic Analgesic - Usually Demerol (MEPERIDINE)
NOT Codeine & Morphine may cause spasm of the Sphincter increased pain.
Morphine cause MOREPAIN
b.) Anti cholinergic - Atropine SO4
c.) Anti emetic – Metoclopramide (Plasil)

Phenergan – Phenothiazide with anti emetic properties
2. Diet – increase CHO, moderate CHON, decrease fats

3. Meticulous skin care d/t Urticaria
4. Maintain NPO in the active phase
5. Maintain NGT decompression
6. Instruct patient to AVOID HIGH- fat diet & GAS-forming foods
7. Surgical Procedures :
Cholecystectomy---removal of gallbladder
Choledochotomy
Laparoscopy
Post-operative Nursing Interventions Cholecystectomy:
1. Monitor for surgical complications

2. Post-operative position after recovery from anesthesia- LOW FOWLER’s
3. Encourage early ambulation
4. Administer medication before coughing and deep breathing exercises
5. Advise client to splint the abdomen to prevent discomfort during coughing
6. Administer analgesics, antiemetics, antacids
7. Care of the biliary drainage or T-tube drainage
8. Fat restriction is only limited to 4-6 weeks. Normal diet is resumed
IMPORTANT:
-Maintain patency of T-tube . Check if intact & drain to prevent infection

Purpose: To prevent entry of bile into the peritoneal cavity
STOMACH
- A J-shaped structure organ in the epigastrium

- Capacity is 1,500 ml
• Contains 4 Parts:
1. Fundus/ Anthrum
2. Cardia
3. Body
4. Pylorus
 Valves ------ prevents reflux or regurgitation of food
1. Cardiac Sphincter - prevents the reflux of the contents into the esophagus (bet. esophagus & stomach)
2. Pyloric Sphincter - regulates the rate of gastric emptying into the duodenum (bet. stomach & half of pylorus)
• The glands & cells in the stomach secrete digestive enzymes:
1. Parietal / Oxyntic Cells

Function:
a. Produces intrinsic factor - promotes reabsorption of Vit. B12 – promotes maturation of RBC
b. HCl Acid - Aids in digestion

Ph of Hydrocholoric Acid: 1-2
2. Chief Cells/ Zymogenic Cells : Secretes
a. Gastric amylase - digest CHO

b. Gastric lipase – digest fats
c. Pepsin – digests PROTEIN
d. Rennin – digests milk products
3. Antral G-cells- gastrin
4. Argentaffin cells- serotonin
5. Mucus neck cells- mucus
6. Endocrine cells - Secrets gastrin – increase Hcl acid secretion
• Function of the Stomach:
Generally to digest the food (proteins) & to propel the digested materials into the SI for final digestion
1.Mechanical
2.Chemical Digestion
3.Storage of food
CHO & CHON : Stored in the stomach for 1 -2 hrs.
FATS : Stored in stomach for 2 – 3 hrs
DISORDERS OF THE STOMACH
1. PEPTIC ULCER DISEASE (PUD)
– An ulceration of the gastric & duodenal lining characterized by excoriation / erosion of submucosa &
mucosal lining due to:
a.) Hypercecretion of acid – pepsin
b.) Decrease resistance of mucosal barrier to HCl acid secretion
- May be referred as to location as Gastric ulcer in the stomach, or Duodenal ulcer in the duodenum
- Most common Peptic ulceration: anterior part of the upper duodenum
Incidence Rate:
1. Men : 40 – 55 yrs old

2. Aggressive persons
PATHOPHYSIOLOGY of PUD:
Disturbance in acid secretion & mucosal protection
Increased acidity or decreased mucosal resistance erosion & ulceration
Infection with H. pylori------ # 1 cause of ULCER
1. Hereditary
2. Emotional Stress
3. Smoking – vasoconstriction – GIT ischemia---lead to resistance of HCl----- ulceration
4. Alcoholism – stimulates release of histamine = stimulates Parietal cell release Hcl acid = Hypersecretion ----Ulceration
5. Caffeine – tea, soda, chocolate
6. Irregular diet
7. Rapid eating
8. Ulcerogenic drugs – NSAIDS, aspirin, steroids, indomethacin, ibuprofen
Indomethacin - S/E corneal cloudiness. Needs annual eye check up.
9. Gastrin producing tumor or Gastrinoma “ Zollinger Ellison’ Syndrome”
10. Microbial invasion R/T helicobacter pylori. Metromidazole (Flagyl)
TYPES OF ULCERS Most feared complications of

I. Ascending to severity: Bruns in GIT : Curling’s Ulcer
1. Acute – affects submucosal lining
2. Chronic – affects underlying tissue – heals & forms a scar
II. According to location:
1. Stress ulcer ---common among critically-ill patients

2. Gastric ulcer
3. Duodenal ulcer – most common----- 90% of ulcers because it has less bicarbonate ions
Buffers that neutralizes acidity
A. STRESS ULCER
2 Types Of Stress Ulcer
1. CURLING’S ULCER : 2. CUSHING’S ULCER:

Cause: Trauma & Burns
Cause: Stroke/ CVA / Head Injury
Bleeding
Increase vagal stimulation
Hypovolemia
Hyperacidity
GIT schemia
Ulcerations
Decrease resistance of mucosal barriers to Hcl acid
Ulcerations
Drug Of Choice: Ranitidine (Zantax)
B. GASTRIC ULCER DUODENAL ULCER
DEFINITION - Ulceration of the gastric mucosa, submucosa & rarely - Ulceration of duodenal mucosa & submucosa
the muscularis d/t break in the mucosal barrier - Usually d/t increased gastric acidity
w/ reduced production 2nd to incompetent
pylorus.
- Hypoperfusion-ischemia to gastric mucosa is also a

factor. H.pylori in >90% cases
RISK FACTORS Stress Helicobacter pylori infection

(same) Smoking NSAIDS abuse
Alcohol Type A personality
History of gastritis
PATHOLOGY Decreased mucosal protection----------Infection with H. Increased gastric acidity------Infection with H pylori
pylori-----Decreased blood supply to the stomach
SITE Antrum or lesser curvature Duodenal bulb
Other Sx 1. Nausea
2. Vomiting is more common
3. Hematemesis>melena
4. Weight loss

EPIGASTRIC PAIN -30 min – 1 hr AFTER EATING -2-4 hrs after eating or during the night
- epigastrium - mid epigastrium
- Hot , gaseous & burning - Cramping & Burning PAIN
- not usually relieved by food & antacid - usually relieved by food intake & antacid
- Gnawing, sharp pain in the mid-epigastrium - 12 MN – 3am pain
- NOT RELIEVED by food intake, sometimes
AGGRAVATING the pain!
GASTRIC Normal gastric acid secretion Increased gastric acid secretion
SECRETION
VOMITING common Not common
HEMORRHAGE Hematemesis Melena
WT Wt loss Wt gain
COMPLICATIONS a. Stomach Cancer a. Perforation

b. Hemorrhage
HIGH RISK 40 - 60 y/o 20 y/o
Incidence is high in older adults, male>female,
Dx
1. EGD to visualize the ulceration 1. EGD & Biopsy
2. Urea breath test for H. pylori infection 2. Endoscopic exam
3. Biopsy- to rule out gastric cancer d/t malignancy risk 3.Stool from occult blood
4. Barium swallow 4.Gastric analysis = INCREASE
5. Gastric analysis = NORMAL 5. Upper GI series – confirms presence of ulceration
NURSING INTERVENTIONS:
1. Give BLAND diet, small frequent meals during the active phase of the disease
a. Diet – bland, non irritating, non spicy

b. Avoid caffeine & milk/ milk products, carbonated drinks
Increase gastric acid secretion
2. Administer prescribed medications- H2 blockers, Protein pump inhibitor, mucosal barrier protectants & antacids
a.) Antacids
ACA MA
Aluminum Containing Antacids Magnesium Containing Antacids
Ex. Aluminum OH gel Ex. Milk Of Magnesia
(Ampho-gel) S/E diarrhea
S/E constipation
Maalox (fewer S/E)
b.) H2 Receptor Antagonist

Ex.
1. Ranitidine (Zantac) – lesser S/E---- Best given if OD = AM
or BID = AM & Nightime to prevent nocturnal acid gastric secretion
2. Cimetidine (Tagamet) – more S/E
3. Famotidine (Pepcid)
3. Avoid smoking – decrease effectiveness of drug
Nursing Mgt For Both:

1. Administer antacid & H2 receptor antagonist – 1hr apart
-Cimetidine decrease antacid absorption & vise versa
- Instruct client to avoid smoking because it decreases effectiveness of the drug
c.) Cytoprotective Agents
Ex.
1. Sucralfate (Carafate) - Provides a paste-like substance that coats mucosal lining of stomach
2. Cytotec - causes severe spasm ( abortive effect)
d.) Sedatives/ Tranquilizers - Valium, lithium
e.)Anticholinergics / Anti-spasmodic Agent

1. Atropine SO4
2. Prophantheline Bromide (Probanthine)
(Pt has history of HPN crisis With peptic ulcer disease. Rn should not administer alka seltzer- has large amount of Na.
4. Provide teaching about stress reduction & relaxation techniques
5. Surgery: Subtotal Gastrectomy - Partial removal of stomach
Billroth I (Gastroduodenostomy) Billroth II (Gastrojejunostomy)

-Removal of 1/3 of stomach & anastomoses of gastric - Removal of 1/2 -3/4 of stomach & duodenal bulb & anastomostosis
stump to the duodenum. of gastric stump to jejunum.
Before surgery for BI or BII - Do vagotomy (severing of vagus nerve) & pyloroplasty (drainage) first.
` Nursing Mgt For B1 or B II: SURGICAL PROCEDURES FOR PUD

Total gastrectomy, vagotomy, gastric resection,
1. Monitor NGT output Billroth I & II, pyloroplasty
a.) Immediately post op should be bright red drainage Post-operative Nursing management
b.) Within 6-8 hrs – output is greenish in color 1. Monitor VS
c.) After 24h – output is dark red d/t influence of HCI acid 2. Post-op position: FOWLER’S
2. Administer meds: 3. NPO until peristalsis returns
a.) Narcotic Analgesic 4. Monitor for bowel sounds
b.) Antibiotic 5. Monitor for complications of surgery
c.) Antiemetics 6. Monitor I & O- report U.O:<.5cc/kg/hr, IVF,
3. Maintain patent IV line hydrate
4. VS, I&O & bowel sounds 7. Maintain NGT
5. Monitor for Complications: 8. Diet progress: clear liquid full liquid six
bland meals
a. HEMORRHAGE – Hypovolemic shock
Late signs – anuria
Nsg Interventions For BLEEDING:
1. Maintain on NPO
2. Administer IVF & medications
3. Monitor hydration status, Hct & Hgb
4. Assist with room temperature SALINE lavage
(iced may lead to more mucosal damage via severe vasoconstriction-ischemia,vagal stimulation)
5. Insert NGT for decompression & lavage & assessment of GI bleeding
6. Prepare to administer blood transfusion
7. Prepare to give VASOPRESSIN to induce vasoconstriction to reduce bleeding
8. Prepare patient for SURGERY if warranted
b. PERITONITIS
c. PARALYTIC ILEUS – Most feared complication in all types of abdominal surgery (absence of peristalsis)
d. Hypokalemia
e. Thromobphlebitis
f. Pernicious anemia

g. DUMPING SYNDROME
– Common complication
– Rapid gastric emptying of hypertonic food solutions – CHYME leading to hypovolemia.
A postprandial condition of rapid emptying of the gastric contents into the small intestine (jejunum) usually
after a gastric surgery (gastrojejunostomy) without proper mixing of chyme & the normal duodenal
digestive process
- Symptoms occur 5-30 minutes after eating
Pathophysiology:
Foods high in CHO & electrolytes must be diluted in the jejunum before absorption takes place.
The rapid influx of stomach contents will cause distention of the jejunum early symptoms
The hypertonic chyme will draw fluid from the blood vessels to dilute the high concentrations of CHO and electrolytes
Later, there is increased blood glucose stimulating the increased secretion of insulin
Then, blood glucose will fall causing reactive hypoglycemia
Sx of Dumping syndrome:
EARLY Sx: d/t rapid movement of extracellular fluids into the bowel to convert the hypertonic bolus to isotonic
1. Nausea and Vomiting, syncope
2. Abdominal fullness
3. Abdominal cramping
4. Palpitation, tachycardia
5. Diaphoresis, Pallor
LATE Sx:
1. Drowsiness
2. Weakness & Dizziness
3. Hypoglycemia
4. Diarrhea
Nursing Mgt:
1.
Avoid fluids in chilled solutions
2.
Instruct to eat SMALL frequent meals, include MORE dry food items in 6 equally divided
feedings
3. Advise patient to eat LOW-carbohydrate HIGH-fat and HIGH-protein diet
4. Flat on bed 15 -30 minutes after q feeding
5. Instruct to AVOID consuming FLUIDS 1 hr before, with, 2 hrs after meals
6. Instruct to eat in semi recumbent position, LIE DOWN after meals
7. Administer sedative, anti-spasmodic medications to delay gastric emptying
2. GASTRO-ESOPHAGEAL REFLUX DISEASE (GERD)
- Backflow of gastric contents into the esophagus
FACTORS:
- Usually due to incompetent lower esophageal sphincter , pyloric stenosis or motility disorder
- Symptoms may mimic ANGINA or MI
Pathophysiology:
incompetent lower esophageal sphincter
regurgitation of acidic contents
Erosion of esophageal mucosa
Pain
Sx: Heartburn
Dyspepsia
Regurgitation
Epigastric pain
Difficulty swallowing
Ptyalism
Dx:
1. Endoscopy or barium swallow
2.Gastric ambulatory pH analysis
– Note for the pH of the esophagus, usually done for 24 hours
– The pH probe is located 5 inches above the lower esophageal sphincter
– The machine registers the different pH of the refluxed material into the esophagus
1. Instruct the patient to AVOID stimulus that increases stomach pressure & decreases GES pressure
2. Instruct to avoid alcohol , spices, coffee, tobacco & carbonated drinks
3. Instruct to eat LOW-FAT, HIGH-FIBER diet, BLAND DIET
4. Avoid foods and drinks TWO hours before bedtime
5. Elevate the head of the bed with an approximately 8-inch block
6. Administer prescribed H2-blockers & prokinetic meds like cisapride, metochlopromide
7. Advise proper weight reduction
3. GASTRITIS
- Inflammation of the gastric mucosa
May be Acute or Chronic
Etiology:
Acute- bacteria, irritating foods, NSAIDS, alcohol, bile & radiation
Chronic- Ulceration, bacteria, Autoimmune disease, diet, alcohol, smoking
Pathophysiology:
Insults cause gastric mucosal damage inflammation, hyperemia and edema superficial erosions  decreased
gastric secretions, ulcerations & bleeding
Dx:
Sx: 1. EGD- to visualize the gastric mucosa for
(Acute) inflammation
Dyspepsia 2. Low levels of HCl
3. Biopsy to establish correct diagnosis whether
Headache
acute or chronic
Anorexia
Nausea/Vomiting NURSING INTERVENTIONS
Chronic) 1. Give BLAND diet
Pyrosis 2. Monitor for signs of complications like bleeding,
Singultus obstruction and pernicious anemia
Sour taste in the mouth 3. Instruct to avoid spicy foods, irritating foods,
Dyspepsia, N/V/anorexia, Pernicious anemia alcohol and caffeine
4. Administer prescribed medications- H2 blockers,
antibiotics, mucosal protectants (sucralfate)
UPPER GIT 5. Inform the need for Vitamin B12 injection if
deficiency is present

1. HERNIATIONS
- Abnormal protrusion of an organ/tissue/part of an organ through a structure that normally contains it through
a congenital or acquired weakness of the enclosing wall
(eg. Abdominal musculature) with accompanying increased pressure (valsalva, lifting, crying).
Wall defect
Intraabdominal
Pressure
Tissue/organ
Protrusion
Types:
Descriptors: - Reducible
- Incarcerated/Irreducible
- Strangulated (emergency)
Medical management:
- Truss
Surgery:
- Herniorrhapy, mesh
- Laparoscopic ExtraPeritoneal herniorrhapy
Nursing Management:
- Preop: Health instructions, consent, let patient void
- Postop: Vital signs, urine output & urine bladder status
- Scrotal swelling. Ice pack over the incision.
- General diet as soon tolerated by the patient. Advise no lifting for 4-6 wks
- Postop Scrotal support.
ESOPHAGUS
1. ESOPHAGEAL VARICES
- Dilation &tortuosity of the submucosal veins in the distal esophagus
ETIOLOGY: commonly caused by PORTAL hypertension secondary to liver cirrhosis

This is an Emergency condition!
Sx:
1. Hematemesis
2. Melena
3. Ascites
4. Jaundice
5. Hepatomegaly/splenomegaly
Signs of Shock- tachycardia, hypotension, tachypnea, cold clammy skin, narrowed pulse pressure
Dx: 1. Esophagoscopy
NURSING INTERVENTIONS FOR EV
1. Monitor VS strictly. Note for signs of shock

2. Monitor for LOC
3. Maintain NPO
4. Monitor blood studies
5. Administer O2
6. Prepare for blood transfusion
7. Prepare to administer Vasopressin and Nitroglycerin
8. Assist in NGT and Sengstaken-Blakemore tube insertion for balloon tamponade (scissors pls!)
9. Prepare to assist in surgical management: Endoscopic sclerotherapy, Variceal ligation, Shunt procedures
2. HIATAL HERNIA (Diaphragmatic Hernia)

-Protrusion of the esophagus into the diaphragm thru an opening (esophageal hiatus)
Two types:
- Sliding hiatal hernia ( most common)
- Axial hiatal hernia
Factors:
History: >/=60 y/o, female>male, history of trauma, increased intraabdominal pressure conditions
Sx:
1. Heartburn (30-60min after meal) in sliding type, (-) in rolling type.
2. Regurgitation
3. Dysphagia, chestpain
4. 50%- without symptoms
Pathophysiology:
Weakness/ Enlarged Esophagial hiatus
Increased intraabdominal pressure
Protrusion of the stomach
sliding hernia rolling hernia
LES exposed to low Obstruction

thoracic pressure Strangulation
Volvulus
Reflux/regurgitation &
motor dysfunction
manifestations
Dx:
1. Barium swallow & Fluoroscopy
1. Provide small frequent feedings

2. AVOID supine position for 1 hour after eating
3. Elevate the head of the bed on 8-inch block
4. Provide pre-op and post-op care
Surgical Management: -Nissen fundoplication (suturing the fundus around esophagus, most common procedure)
- Angelchick prosthesis insertion
Pre-op nursing: Health teaching, consent
Post-op nursing:
Monitor respi distress especially if chest tubes are in place.
Instruct coughing and deep breathing exercises, ambulation
Assess for bleeding, thrombosis and infection
NGT maintained patent
Diet transition, starts with fluids after 24hrs, then small frequent feeding,
avoid carbonated beverages
LOWER GIT

The Small Intestine
• Grossly divided into the Duodenum, Jejunum & Ileum
• The duodenum contains the two openings for the bile & pancreatic ducts
• The ileum is the longest part (about 12 feet)
• The intestinal glands secrete digestive enzymes that finalize the digestion of all foodstuff
• Enzymes for carbohydrates disaccharidases
• Enzymes for proteins dipeptidases & aminopeptidases
• Enzyme for lipids intestinal lipase
The Large intestine

• Approximately 5 feet long, with parts:
• 1. The cecum widest diameter, prone to rupture
• 2. The appendix
• 3. The ascending colon
• 4. The transverse colon
• 5. The descending colon
• 6. The sigmoid most mobile, prone to twisting
• 7. The rectum
1. CROHN’S DISEASE
-Also called Regional Enteritis

- An inflammatory disease of the GIT affecting usually the small intestine
Inflammatory Bowel Disease

• ETIOLOGY: unknown, genetics,environmental, immune defect
1. CROHN’S DISEASE
• The terminal ileum thickens, with scarring, ulcerations, abscess formation and narrowing of the lumen
Sx:
1. Fever
2. Abdominal distention
3. Diarrhea
4. Colicky abdominal pain
5. Anorexia/N/V
6. Weight loss
7. Anemia
CONDITIONS OF THE LARGE INTESTINE
2. ULCERATIVE COLITIS
- Ulcerative and inflammatory condition of the GIT usually affecting the large intestine
- The colon becomes edematous and develops bleeding ulcerations
- Scarring develops overtime with impaired water absorption and loss of elasticity
Sx:
1. Anorexia
2. Weight loss
3. Fever
4. SEVERE diarrhea with Rectal bleeding
5. Anemia
6. Dehydration
7. Abdominal pain and cramping
NURSING INTERVENTIONS for CD & UC

1. Maintain NPO during the active phase
2. Monitor for complications like severe bleeding, dehydration, electrolyte imbalance
3. Monitor bowel sounds, stool and blood studies
4. Restrict activities= rest and comfort
5. Administer IVF, electrolytes and TPN if prescribed
Monitor complications of diarrhea
6. Instruct the patient to AVOID gas-forming foods, MILK products and foods such as whole grains, nuts, RAW fruits and
vegetables especially SPINACH, pepper, alcohol and caffeine
7. Diet progression- clear liquid LOW residue, high protein diet
8. Administer drugs- anti-inflammatory, antibiotics, steroids, bulk-forming agents and vitamin/iron supplements
3. HEMORRHOIDS
- Abnormal dilation and weakness of the veins of the anal canal

- Variously classified as Internal or External, Prolapsed, Thrombosed and Reducible
PATHOPHYSIOLOGY
-Increased pressure in the hemorrhoidal tissue due to straining, pregnancy, etc dilatation of veins
Internal hemorrhoids
These dilated veins lie above the internal anal sphincter
Usually, the condition is PAINLESS
External hemorrhoids
These dilated veins lie below the internal anal sphincter
Usually, the condition is PAINFUL
Sx:
1. Internal hemorrhoids- cannot be seen on the peri-anal area

2. External hemorrhoids- can be seen
3. Bright red bleeding with each defecation
4. Rectal/ perianal pain
5. Rectal itching
6. Skin tags
Dx:
1. Anoscopy
2. Digital rectal examination
1. Advise patient to apply cold packs to the anal/rectal area followed by a SITZ bath
2. Apply astringent like witch hazel soaks
3. Encourage HIGH-fiber diet and fluids
4. Administer stool softener as prescribed
Post-operative care for hemorrhoidectomy
1. Position: Prone or Side-lying

2. Maintain dressing over the surgical site
3. Monitor for bleeding
4. Administer analgesics and stool softeners
5. Advise the use of SITZ bath 3-4 times a day
BOWEL OBSTRUCTION
• Condition where the segment of the intestine is obstructed by:

– Tumors
– Paralysis
– Volvolus
Signs and Symptoms
– Abdominal pain
– Abdominal rigidity
– Increased BOWEL sound in early stage and ABSENT BOWEL sound in late stage
– Abdominal distention
– Vomiting and fluid imbalance
DX:
1. Abdominal x-ray
Management:
Surgery
Nursing care of abdominal surgery
Quick Summary
• Peptic Ulcer
– Ulceration of mucosa; In the stomach or duodenum
– Outstanding Symptom: PAIN
– Nursing Goal: Allow ulcer to heal, prevent complication
– Rest: physical and Mental
– Eliminate certain foods
– Medications: antacid, H2 blockers, Proton Pump inhibitors, antibiotics, mucosal protectants
– Surgery: Vagotomy, Billroth 1 and 2
Quick Summary
• Liver Cirrhosis
– Destruction of liver with replacement by scars
– Common causes: alcoholism, post-hepatitic
– Manifestations related to liver derangements
– Jaundice, Ascites, splenomegaly, bleeding, enceph
– Nursing goal: Control manifestations and maximize liver function
GENITO-URINARY TRACT
Overview:
Function:
1. Promote excretion of nitrogenous waste products
2. Maintain F&E & acid base balance
I. KIDNEYS:
– Pair of bean shaped organ

- Located Retro peritonially (back of peritoneum) on either side of vertebral column. Encased in Bowmans’s Capsule.
Parts:
1. Renal pelvis --------If there’s inflammation----Pyelonephritis
2. Cortex
3. Medulla
* Nephrons = Basic living unit

* Glomerulus = Filters blood going to kidneys
Function of Kidneys:
1. Urine formation
Urine formation – 25% of total CO (Cardiac Output) is received by kidneys
1. Filtration -------------any disorder affecting filtration results to decreased renal output
*Normal GFR/ min is 125 ml of blood /minute filtered by glomerulus
2. Tubular Reabsorption
Tubular reabsorption – 124ml of ultra infiltrates (Na,K,Mg,Cl, H2O)
(H2O & electrolytes is for reabsorption)
3. Tubular Excretion
Tubular Excretion – 1 ml is excreted in urine/minute
2. Regulation of BP:
Ex. CS – hypovolemia – decrease BP going to kidneys

Activation of RAAS
Release of Renin (hydrolytic enzyme) at juxtaglomerular apparatus
Angiotensin I mild vasoconstrictor
Angiotensin II Vasoconstrictor
Adrenal cortex increase CO increase PR
Aldosterone
Increase BP
Increase Na &
H2O reabsorption
Hypervolemia
II. URETERS
– 25 – 30 cm long, passageway of urine to bladder
– Capable of peristalis movement
III. BLADDER
– Located behind the symphysis pubis. Consists of muscular & elastic tissue that is distensible
Function: Reservoir of urine
Maximum capacity: 1200 – 1800 ml – Normal adult can hold

250 – 500 ml – needed to initiate micturition reflex
NORMAL COMPOSITION OF URINE:
Color = Pale yellow toAmber

Odor = Faint Aromatic
Consistency = Clear or slightly turbid
Ph = 4–8
Specific Gravity = 1.015 – 1.030
WBC/ RBC = (-)
Albumin = (-)
E coli = (-)
Mucus thread = few
Amorphous urate = (-)
CHON = None
Catheters:
Pediatric = 8-10 french

Female = 12-14 french
Male = 16-18 french
IV. URETHRA
– Extends to external surface of body. Passage of urine, seminal & vaginal fluids.
Female : 3 – 5 cm or 1 to 1 ½ “
Male: 20 cm or 8”
Urological Assessment
I. Nursing History
Reason for seeking care
Current illness
Previous illness
Family History
Social History
Sexual history
II. Key Signs & Symptoms of Urological Problems
1. EDEMA
Associated with fluid retention
Renal dysfunctions usually produce ANASARCA
2. PAIN
Suprapubic pain= bladder
Colicky pain on the flank= kidney
3. HEMATURIA
Painless hematuria may indicate URINARY CANCER!
Initial/Early-stream hematuria= urethral lesion,prostatic,seminal vesicle
Terminal/Late-stream hematuria= bladder lesion,post urethra
Throughout: glomerulonephritis
Pneumaturia: gas in urine;bladder-bowel fistula
4. DYSURIA
Pain with urination= lower UTI
Normal urine output: 1cc/kg/hr or 800-1800ml/24hr

5.POLYURIA
More than 2 Liters urine per day
6. OLIGURIA
100- 400 mL per day
7. ANURIA
Less than 100 mL per day
8. Urinary Urgency: sudden controllable strong desire to void

Urinary retention: sense of incomplete bladder emptying(100ml left)
Urinary frequency: voiding more often than every 2hrs
Urinary Hesitancy: at least 10 sec delay in initiation of urination
Urinary incontinence: involuntary loss of urine
Nocturia: excessive urination at night
Implementation Steps for selected problems
III. PHYSICAL EXAMINATION
1. Provide PAIN relief
Inspection a. Assess the level of pain
Auscultation b. Administer medications usually narcotic
Percussion ANALGESICS
Palpation
2. Maintain Fluid and Electrolyte Balance
a. Encourage to consume at least 2 liters of fluid
IV. Laboratory examination per day
Urinalysis b. In cases of ARF, limit fluid as directed
BUN and Creatinine levels of the serum c. Weigh client daily to detect fluid retention
Serum electrolytes
Radiographic 3. Ensure Adequate urinary elimination
IVP a. Encourage to void at least every 2-3 hours
KUB x-ray b. Promote measures to relieve urinary retention:
KUB ultrasound Alternating warm and cold compress
CT and MRI Bedpan
Cystography Open faucet
Provide privacy
Catheterization if indicated
DISORDERS OF THE GUT
1. URINARY TRACK INFECTION (UTI)
- Bacterial invasion of the kidneys or bladder (CYSTITIS) usually caused by Escherichia coli
- Bacteria (+) 10 to the 5th in culture
 Poor hygiene
 Irritation from bubble baths
 Urinary reflux
 Instrumentation
 Residual urine, urinary stasis
 Dehydration
Pathophysiology:
The invading organism ascends the urinary tract, irritating the mucosa & causing characteristic symptoms:
 Ureter= ureteritis
 Bladder= cystitis
 Urethra=Urethritis
 Pelvis= Pyelonephritis
Sx:
Low-grade fever
Abdominal pain
Enuresis
Pain/burning on urination
Urinary frequency
Hematuria
Upper UTI
Fever and CHIILS
Flank pain
Costovertebral angle tenderness
Laboratory Examination
Urinalysis
Urine Culture
Nursing interventions:
Administer antibiotics as ordered

Provide warm baths and allow client to void in water to alleviate painful voiding.
Force fluids. Nurses may give 3-4 liters of fluid per day if not contraindicated
Encourage measures to acidify urine (cranberry juice, acid-ash diet).
Provide client teaching and discharge planning concerning
a. Avoidance of tub baths
b. Avoidance of bubble baths that might irritate urethra
c. Importance for girls to wipe perineum from front to back
d. Increase in foods/fluids that acidify urine.
Pharmacology for urine bacteria >100,000/ml
1. Sulfa drugs
 Highly concentrated in the urine
 Effective against E. coli!
 Can cause CRYSTALLURIA
2. Quinolones
 Not given to less than 18 because they can cause cartilage degradation
3. Pyridium= urinary antiseptic

 Can cause urine discoloration
a. CYSTITIS
– Inflammation of bladder
1. Microbial invasion – E. coli

2. High risk – women
3. Obstruction
4. Urinary retention/stagnation
5. Increase estrogen levels
6. Sexual intercourse
S/Sx:
1. Hypogastric Pain – flank area
2. Urinary frequency & urgency
3. Burning upon urination
4. Dysuria & hematuria
5. Fever, chills, anorexia, gen body malaise
Dx:
1. Urine culture & sensitivity = (+) to E. coli (80-90% cause)
Nursing Mgt:
1. Force fluid = 2000 ml-3000 ml/day

2. Warm sitz bath – to promote comfort
3. Monitor & assess for gross hematuria, assess odor of urine
4. Acid Ash Diet – cranberry, vit C -OJ to acidify urine & prevent bacterial multiplication
5. Meds:
a. Systemic antibiotics
Ampicillin
Cephalosporin
b. Sulfonamides – cotrimaxazole (Bactrim)
- Gantrism (ganthanol)
c. Urinary Antiseptics – Nitrofurantoin (Macrodantin)
S/E: Staining of Teeth
Peripheral Nephropathy
GIT irritants
Hemolytic Anemia ----- 1st Sign: Fever
d. Urinary analgesic- Pyridum
6. Health Teaching
a.) Importance of Hydration

b.) Void after sex
c.) Female – avoids cleaning front to back
Do not use Bubble bath, Tissue paper, Powder, perfume----alters the ph of vagina & irritants
d.) Complications:
Pyelonephritis *Ph = measures acidity of solution
b. PYELONEPHRITIS
- Acute/Cchronic inflammation of 1 or 2 renal pelvis of kidneys leading to tubular destruction, interstitial abscess
formation & can leadt to Renal Failure
1. Microbial invasion
a. E. Coli
b. Streptococcus
2. Urinary retention /obstruction
3. Pregnancy
4. DM
5. Exposure to renal toxins
S/Sx:
Acute Pyelonephritis:
a. Costovertibral angle pain & tenderness “FLANK PAIN”

b. Fever, anorexia, gen body malaise
c. Urinary frequency, urgency
d. Nocturia, dsyuria, hematuria
e. Burning on urination
Chronic Pyelonephritis:
a. Fatigue, wt loss
b. Polyuuria, polydypsia
c. HPN
Dx:
1. Urine culture & sensitivity – (+) E. coli & streptococcus---- (+) Cultured Microorganisms
2. Urinalysis
Increase WBC, CHON & pus cells
3. Cystoscopic exam – Reveals urinary obstruction
Nursing Mgt:
1. Provide CBR – acute phase. Especially during acute attack

2. Force fluid
3. Acid ash diet
4. Meds:
a.) Urinary antiseptic – nitrofurantoin (macrodantin)

SE: peripheral neuropathy
GI irritation
Hemolytic anemia
Staining of teeth
b.) Urinary analgesic – Pyridium
2. Complication- Renal Failure
2. NEPHROLITHIASIS/ UROLITHIASIS
- Formation/ Presence of stones elsewhere in the urinary tract
3 Major Types of Stone
1. Calcium 2. Oxalate 3. Uric Acid
Milk Cabbage Anchovies

Cranberries Organ meat
Nuts tea Nuts
Chocolates Sardines
1. Diet – large amounts of Ca & oxalate

2. Hereditary – gout
3. Obesity
4. Sedentary lifestyle, immobility
5. Hyperparathyroidism
6. Increased uric acid levels(diet)
7. Dehydration,urinary stasis
Pathophysiology:
Supersaturation of crystals due to stasis
Stone formation
May pass through the urinary tract
OBSTRUCTION, INFECTION & HYDRONEPHROSIS
S/Sx:
1. Renal Colic radiating to the groin
2. Cool moist skin (shock)
3. Burning upon urination
4. Hematuria
5. Anorexia, n/v
6. Abdominal or flank pain
Dx:
1. IVP (Intravenous Pyelography) = Identifies site of obstruction and presence of non-radiopaque stones
2. KUB Ultrasound & X-ray = Reveals location of stone, number & size
3. Cytoscopic exam = Reveals urinary obstruction
4. Stone analysis = Reveals composition & type of stone
5. Urinalysis = Indicates presence of bacteria, increased protein, increased WBC and RBC (hematuria)
Medical Mgt:
1. Surgery
a. Percutaneous Nephrostomy: tube is inserted through skin & underlying tissues into renal pelvis to remove calculi.
b. Percutaneous Nephrostolithotomy: delivers ultrasound waves through a probe placed on the calculus.
2. Extracorporeal shock-wave lithotripsy: delivers shock waves from outside the body to the stone, causing pulverization
- Non-invasive
- Dissolves stone through shock wave application
Pain management : Morphine or Meperidine
Diet modification
3. Nephrectomy – Removal of affected kidney

4. Litholapoxy – removal of 1/3 of stones- Stones will recur. Not advised for pt with big stones
Nursing interventions
1. Strain all urine through gauze to detect stones and crush all clots.
2. Force fluids (3000—4000 cc/day).
3. Encourage ambulation to prevent stasis.
4. Relieve pain by administration of analgesics as ordered and application of moist heat to flank area.
5. Monitor I & O
6. Warm sitz bath – for comfort
7. Alternate warm compress at flank area
8. Medications:
a.) Narcotic analgesic- Morphine SO4
b.) Allopurinol (Zyloprim) to decrease uric acid production
S/E : Allergic Reactions-----rashes, nasal congestion
9. Patent IV line
10. Provide modified diet, depending upon stone consistency: Calcium, Oxalate and Uric acid stones
1. Calcium Stones
Limit milk/dairy products
Acid-Ash Diet to acidify urine (cranberry or prune juice, meat, eggs, poultry, fish, grapes & whole grains)
2. Oxalate Stones
Avoid excess intake of foods/ fluids high in oxalate (tea, chocolate, rhubarb, spinach)
Alkaline-Ash Diet to alkalinize urine (Milk, milk products, vegetables; fruits except prunes, cranberries &
plums)
3. Uric Acid Stones

Reduce foods high in purine (liver, beans, kidneys, venison, shellfish, meat soups, gravies, legumes)
Maintain alkaline urine
11. Provide client teaching and discharge planning concerning

Prevention of Urinary stasis by maintaining increased fluid intake especially in hot weather & during illness; mobility;
voiding whenever the urge is felt and at least twice during the night
12. Provide client teaching & discharge planning concerning:

Adherence to prescribed diet
Need for routine urinalysis (at least every 3—4 months)
Need to recognize and report signs/ symptoms of recurrence (hematuria, flank pain).
3. ACUTE RENAL FAILURE (ARF)
– Sudden inability of the kidneys to excrete nitrogenous waste products & maintain F&E balance d/t a decrease in GFR.
Most important manifestation: OLIGURIA
Pathophysiology: Normal GFR = 125 ml/min

3 Stages/Causes:

1. Pre-Renal Cause:
Decrease in GFR
Causes:
1. Septic shock
2. Hypovolemia
3. Hypotension Decrease flow to kidneys
4. CHF
5. Hemorrhage
6. Chronic Diarrhea
7. Burns
8. Cardiogenic Shock
9. Anaphylaxis
2. Intra-Renal Cause:
Involves renal pathology – Kidney Problem
Conditions that cause damage to the nephrons:
1. Acute tubular necrosis (ATN

2. Endocarditis
3. DM
4. Malignant HPN
5. AGN
6. Ttumors
7. BT Reactions
8. Hypercalcemia
9. Nephrotoxins (certain antibiotics, x-ray dyes, pesticides, anesthetics)
10. Pyelonephritis
3. Post-Renal Cause:
Mechanical Obstruction anywhere from the tubules to the urethra
1. Calculi
2. BPH
3. Tumors
4. Strictures
5. Blood clots
6. Trauma
7. Anatomic malformation
8. Urolithiasis
Laboratory Findings:
1. Urinalysis: Urine osmo and sodium

2. BUN & Creatinine levels increased
3. Hyperkalemia
4. Anemia
5. ABG: Metabolic Acidosis
3 Phases of Acute Renal Failure
1. Oliguric Phase
 Urine output less than 400 cc/24 hours 4 Phases of Acute Renal Failure
 Duration 1—2 weeks (Brunner & Suddarth)
 Manifested by 1. Initiation phase ( 0-2 days)
2. Oliguric phase
a. Dilutional Hyponatremia 3. Diuretic phase
b. Hyperkalemia 4. Convalescence or recovery phase
c. Hyperphosphatemia
d. Hypocalcemia
e. Hypermagnesemia
f. Metabolic Acidosis
Dx: BUN & creatinine elevated
2. Diuretic Phase
 Diuresis may occur (output 3—5 liters/day) d/t partially regenerated tubule’s inability to concentrate urine
 Duration: 2—3 week
 Manifested by:
a. Hyponatremia
b.Hyperkalemia
c. Hypovolemia
d. Metabolic Acidosis
Dx: BUN & Creatinine slightly elevated
3. Convalescence or Recovery Phase

 Renal function stabilizes with gradual improvement over next 3—12 months. Complete Diuresis
Nursing Interventions:
1. Monitor & maintain fluid & electrolyte balance.
Measure l & O every hour. note excessive losses in diuretic phase
Administer IV F & E supplements as ordered.
Weigh daily & report gains.
Monitor lab values; assess/treat F & E & acid-base imbalances as needed
2. Monitor alteration in fluid volume.
Monitor vital signs, PAP, PCWP, CVP as needed.
Weigh client daily.
Maintain strict I & O records.
3. Assess every hour for hypervolemia
Maintain adequate ventilation.
Restrict FLUID intake
Administer diuretics & antihypertensives
4. Promote optimal nutritional status.
Administer TPN as ordered.
With enteral feedings, check for residual & notify physician if residual volume increases.
Restrict protein intake to 1 g/kg/day
Restrict POTASSIUM intake
HIGH CARBOHYDRATE DIET, calcium supplements
5. Prevent complications from impaired mobility (pulmonary embolism, skin breakdown & atelectasis)
6. Prevent fever/infection.
Assess for signs of infection.
Use strict aseptic technique for wound & catheter care.
7. Support client/significant others & reduce/ relieve anxiety.
Explain pathophysiology & relationship to symptoms.
Explain all procedures and answer all questions in easy-to-understand terms
Refer to counseling services as needed
8. Provide care for the client receiving dialysis
9. Provide client teaching & discharge planning concerning
Adherence to prescribed dietary regimen
Signs and symptoms of recurrent renal disease
Importance of planned rest periods
Use of prescribed drugs only: Sx of UTI or respiratory infection need to report to physician immediately
4. CHRONIC RENAL FAILURE (CRF)
– Irreversible loss of kidney function

- Gradual, Progressive irreversible destruction of the kidneys causing severe renal dysfunction.
The result is azotemia to UREMIA
1. DM – worldwide leading cause Hallmark of Renal Failure:
2. HPN -2nd cause
3. Recurrent UTI/ Pyelonephritis AZOTEMIA & OLIGURIA
4. Exposure to renal toxins
5. Recurrent infections
6. Urinary tract obstruction
Pathophysiology: As renal functions decline
Retention of end-products of metabolism
STAGE 1= Reduced renal reserve volume (Asymptomatic) 40-75% loss of nephron function
Normal BUN & Creatinine
GFR <10-30%
STAGE 2= Renal insufficiency, 75-90% loss of nephron function
STAGE 3= End-stage renal disease, more than 90% loss. DIALYSIS IS THE TREATMENT!
S/Sx:
1. Urinary System 2. Metabolic disturbances
a. Polyuria a. Azotemia (increase BUN & Crea)
b. Nocturia b. Hyperglycemia
c. Hematuria c. Hyperinulinemia
d. Dysuria
e. Oliguria
3. CNS 4. GIT
a. Headache a. N/V, Anorexia
b. Lethargy b. Stomatitis
c. Disorientation/Confusion c. Uremic breath
d. Restlessness d. Diarrhea/ constipation
e. Memory impairment
5. Respiratory 6. Hematological
a. Kassmaul’s resp a. Normocytic anemia
b. Decrease cough reflex bleeding tendencies
c. Pericardial Friction rub Pancytopenia/ Leukopenia
7. Fluid & Electrolytes 8. Integumentary
a. Hyperkalemia a. Itchiness/ pruritus
b. Hypernatermia b. Uremic frost – accumulation of urea in the
c. Hypermagnesemia skin
d. Hyperposphatemia 9. Cardiovascular
e. Hypocalcemia a. Pulmonary HPN
f. Metabolic Acidosis b. CHF
c. Pericarditis
Diagnostic Tests:
a. 24 hour creatinine clearance urinalysis
b. Protein, sodium, BUN, Crea and WBC elevated
c. Specific gravity, platelets, and calcium decreased
d. CBC = Aanemia
Medical Mgt:
1. Diet restrictions
2. Multivitamins
3. Hematinics and erythropoietin
4. Aluminum hydroxide gels
5. Anti-hypertensive
6. Anti-seizures
7. Assist in DIALYSIS
DIALYSIS
- A procedure that is used to remove fluid & uremic wastes from the body when the kidneys cannot function
Two Methods:
1. Hemodialysis Weight:
2. Peritoneal dialysis An important parameter
that indicates effective
hemodialysis
Process of: Diffusion / Osmosis / Ultrafiltration
Nsg. Responsibility:
1. Assist in Hemodialysis
1.) Consent/ explain procedure
2.) Obtain baseline data & monitor VS, I&O, wt, blood exam
3.) Strict aseptic technique
4.) Monitor for signs of complications: DISEQUILIBRIUM SYNDROME:
-Results from rapid removal of urea &
nitrogenous waste prod leading to:
B – bleeding 1. N/V
E – embolism 2. HPN
D – disequilibrium syndrome 3. Leg cramps
S – septicemia 4. Disorientation
S – shock – decrease in tissue perfusion 5. Paresthesia
6. Headache
5.) Avoid BP taking, blood extraction, IV, at side of shunt or fistula.

Can lead to compression of fistula.
6.) Maintain patency of shunt by:

Palpate for thrills & auscultate for bruits if (+) patent shunt!
Bedside- Bulldog Clip to prevent embolism
- If with accidental removal of fistula to prevent embolism.
- Infersole (Diastole) – Most common type of dialysate used
7. Meet the patient's psychosocial needs

8. Remember to avoid any procedure on the arm with the fistula (HEMO)
9. Monitor WEIGHT, blood pressure & fistula site for bleeding
10. Monitor symptoms of uremia
11. Detect complications like infection, bleeding (Hepatitis B/C and HIV infection in Hemodialysis)
Peritonitis in peritoneal dialysis
12. Warm the solution to increase diffusion of waste products (PERITONEAL)
13. Manage discomfort & pain
14. To determine effectiveness, check serum creatinine, BUN & electrolytes
15. Inform client that minimal bleeding is expected because blood has been heparinized
Nursing Mgt For Chronic Renal Failure:

DIET:
1. Enforce CBR
CHO = Increased
2. Monitor VS, I&O
CHON = Decreased
3. Meticulous skin care. Uremic frost – assist in bathing pt
FATS = Decreased
4. Meds:
a.) Na HCO3 = to correct acidosis

b.) Kayexelate Enema = to promote excretion of potassium
c.) Anti HPN = Hydralazine
d.) Vit & minerals
e.) Phosphate binder
(Amphogel) Al OH gel - S/E constipation
f.) To Decrease Ca – Ca gluconate
g.) Hematinics
5. Assist in surgery: Renal transplantation : Complication – rejection. Reverse isolation: Lifetime steroids
6. Complication
- Peritonitis -------Early Sign: Cloudy Output
- Shock
Additional Nsg. Interventions For Chronic Renal Failure:

1. Prevent neurological complications.
 Assess every hour for signs of uremia (fatigue, loss of appetite, decreased urine output, apathy, confusion, elevated blood
pressure, edema of face and feet, itchy skin, restlessness, seizures).
 Assess for changes in mental functioning.
 Orient confused client to time, place, date, and persons
 Institute safety measures to protect client from falling out of bed.
2. Promote optimal GI function.

 Assess/provide care for stomatitis
 Monitor nausea, vomiting, anorexia
 Administer antiemetics as ordered.
 Assess for signs of Gl bleeding
3. Monitor/prevent alteration in fluid and electrolyte balance
4. Assess for hyperphosphatemia (paresthesias, muscle cramps, seizures, abnormal reflexes), and administer aluminum
hydroxide gels (Amphojel) as ordered
5. Promote maintenance of skin integrity.

 Assess/provide care for pruritus.
 Assess for uremic frost (urea crystallization on the skin) and bathe in plain water
6. Monitor for bleeding complications, prevent injury to client.

 Monitor Hgb, hct, platelets, RBC.
 Hematest all secretions.
 Administer hematinics as ordered.
 Avoid lM injections
7. Promote/maintain maximal cardiovascular function.

 Monitor blood pressure and report significant changes.
 Auscultate for pericardial friction rub.
 Perform circulation checks routinely.
Administer diuretics as ordered and monitor output.
 Modify drug doses
8. Provide care for client receiving dialysis
MALE REPRODUCTIVE DISORDERS
1. BPH
2. Prostatic cancer
DIAGNOSTIC PROCEDURES:
1. DIGITAL RECTAL EXAMINATION- DRE

Recommended for men annually with age over 40 years
Screening test for cancer
Ask patient to BEAR DOWN
2. TESTICULAR EXAMINATION
Palpation of scrotum for nodules and masses or inflammation
BEGINS DURING ADOLESCENCE
3. Prostate specific antigen (PSA)

Elevated in prostate cancer
Normal is 0.2 to 4 nanograms/mL
Cancer= over 4
1. BENIGN PROSTATIC HYPERPLASIA (BPH)
Enlargement of the prostate gland that causes outflow obstruction leading to :
1. Hydro ureters – dilation of ureters

2. Hydronephrosis – dilation of renal pelvis
3. Kidney stones
4. Renal failure
1. High Risk – Men 50 years old & above

60 – 70 – (3 to 4 x at risk)
2. Influence of male hormone
S/Sx:
1.Nocturia - Decrease in the volume & force of urinary stream
2.Dysuria
3.Hematuria
4.Burning upon urination
5.Terminal bubbling
6.Backache
7.Sciatica
8. Increased frequency, urgency & hesitancy
Diagnosis:
1. Digital rectal exam – enlarged prostate gland that is rubbery, large & NON-TENDER
2. KUB – urinary obstruction
3. Cystoscopic exam – obstruction
4. Urinalysis – increase WBC, CHON
Medical Mgt:
1. Immediate catheterization
2. Prostatectomy
3. TRANSURETHRAL RESECTION of the PROSTATE (TURP)
4. Pharmacology: alpha-blockers, alpha-reductase inhibitors. SAW palmetto
NURSING INTERVENTION: TURP

Maintain the three way bladder irrigation to prevent hemorrhage
Only initially the drainage is pink-tinged and never reddish
Administer anti-spasmodic to prevent bladder spasms
NURSING INTERVENTION
Nursing Mgt:
1. Prostatic message – promotes evacuation of prostatic fluid

2. Limit fluid intake
3. Provide catheterization
4. Meds:
a. Alpha-Adrenergic Blockers
b. Terazozine (hytrin) - Relaxes bladder sphincter
c. Finasteride (Proscar) - Atrophy of Prostate Gland
5. Avoid anticholinergics
6. Prepare for surgery or TURP
7. Teach the patient perineal muscle exercises. Avoid valsalva until healing
8. Surgery: Prostatectomy – TURP- Transurethral resection of Prostate- No incision
-Assist in cystoclysis or continuous bladder irrigation.
Nursing Mgt:
1. Monitor symptoms of infection
2. Monitor symptoms gross/ flank bleeding. Normal bleeding within 24h.
9. Maintain irrigation or tube patent to flush out clots - to prevent bladder spasm & distention
2. PROSTATE CANCER
- A slow growing malignancy of the prostate gland

- Usually an adenocarcinoma
-This usualy spread via blood stream to the vertebrae
Predisposing Factor: Age
Assessment:
1. DRE: hard, pea-sized nodules on the anterior rectum

2. Hematuria
3. Urinary obstruction
4. Pain on the perineum radiating to the leg
Dx:
1. Prostatic specific antigen (PSA)

2. Elevated SERUM ACID PHOSPHATASE indicates SPREAD or Metastasis
Medical & Surgical Mgt:
1.Prostatectomy
2. TURP
3. Chemotherapy: hormonal therapy to slow the rate of tumor growth
4. Radiation therapy
Nursing Interventions:
1.Prepare patient for chemotherapy

2. Prepare for surgery
Nursing Interventions: Post-prostatectomy:
1. Maintain continuous bladder irrigation. Note that drainage is pink tinged w/in 24 hours
2. Monitor urine for the presence of blood clots and hemorrhage
3. Ambulate the patient as soon as urine begins to clear in color
OVERVIEW OF RESPIRATORY SYSTEM:

I. Upper respiratory tract:
Fx:
1. Filtering of air
2. Warming & moistening
3. Humidification
a. Nose – cartilage
- Parts: Rt nostril separated by septum
Lt nostril
2. Consists of anastomosis of capillaries –

Kessel – Bach Plexus – site of epistaxis
b. Pharynx (throat) – muscular passageway for air& food
Branches:
1. Oropharynx
2. Nasopharynx
3. Layngopharynx
c. Larynx – voice box

Fx:
1. For phonation
2. Cough reflex
Glottis – opening
Opens to allow passage of air
Closes to allow passage of food
II. Lower Rt – Fx for gas exchange

a. Trachea – windpipe
- has cartillagenous rings
- site for permanent/ artificial a/w – tracheostomy
b. Bronchus – R & L main bronchus
c. Lungs – R – 3 lobes = 10 segments
L – 2 lobes – 8 segments
Post pneumonectomy - position affected side to promote expansion of lungs

Post segmental lobectomy – position unaffected side to promote drainage
Lungs – covered by pleural cavity, parietal lobe & visceral lobe

Alveoli – acinar cells
3. site of gas exchange (O2 & CO2)
4. diffusion: Daltons law of partial pressure of gases
Ventilation – movement of air in & out of lungs

Respiration – movement of air into cells
Type II cells of alveoli – secrets surfactant

Surfactant - decrease surface tension of alveoli
Lecithin & spinogometer

L/S ratio 2:1 – indicator of lung maturity
If 1:2 – adm O2 - < 40% Concentration to prevent atelectasis & retinopathy or blindness.
I. PNEUMONIA – inflammation of lung parenchyma leading to pulmonary consolidation as alveoli is filled with exudates.
Etiologic agents:
1. Streptococcus pneumoniae (pnemococcal pneumonia)
2. Hemophilus pneumoniae(Bronchopneumonia)
3. Escherichia coli
4. Klebsiella P.
5. Diplococcus P.
High risk elderly & children below 5 yo

1. Smoking
2. Air pollution
3. Immuno-compromised
a. AIDS – PLP
b. Bronchogenic CA - Non-productive to productive cough
4. Prolonged immobility – CVA- hypostatic pneumonia
5. Aspiration of food
6. Over fatigue
S/Sx:
1. Productive cough – pathognomonic: greenish to rusty sputum
2. Dyspnea with prolonged respiratory grunt
3. Fever, chills, anorexia, gen body malaise
4. Wt loss
5. Pleuritic friction rub
6. Rales/ crackles
7. Cyanosis
8. Abdominal distension leading to paralytic ileus
Sputum exam – could confirm presence of TB & pneumonia
Dx:
1. Sputum GSCS- gram staining & culture sensitivity - Reveals (+) cultured microorganism.
2. CXR – pulmo consolidation
Erythrocyte sedimentation rate
4. ABG – PO2 decrease
Nsg Mgt:
1. Enforce CBR
2. Strict respiratory isolation
3. Meds:
1. Broad spectrum antibiotics
Penicillin or tetracycline
Macrolides – ex azythromycin (zythromax)
2. Anti pyretics
3. Mucolytics or expectorants
4. Force fluids – 2 to 3 L/day
5. Institute pulmonary toilet-
1. Deep breathing exercise
2. Coughing exercise
3. Chest physiotherapy – cupping
4. Turning & reposition - Promote expectoration of secretions
6. Semi-fowler
7. Nebulize & suction
8. Comfy & humid environment
9. Diet: increase CHO or calories, CHON & vit C
10. Postural drainage - To drain secretions using gravity
Mgt for postural drainage:
a.) Best done before meals or 2 – 4 hrs after meals to prevent Gastroesophageal Reflux
b.) Monitor VS & breath sounds
Normal breath sound – bronchovesicular
c.) Deep breathing exercises
d.) Adm bronchodilators 15 – 30 min before procedure
e.) Stop if pt can’t tolerate procedure
f.) Provide oral care – it may alter taste sensation
g.) C/I – pt with unstable VS & hemoptysis, increase ICP, increase IOP (glaucoma)
Normal IOP – 12 – 21 mmHg
11. HT:
a.) Avoidance of precipitating factors
b.) Complication: Atelectacies & meningitis
c.) Compliance to meds

2. PULMONARY TUBERCULOSIS (KOCH DSE) - Inflammation of lung tissue caused by invasion of mycobacterium TB or
tubercle bacilli or acid fast bacilli – gram (+) aerobic, motile & easily destroyed by heat or sunlight.
1. Malnutrition
2. Overcrowding
3. Alcoholism
4. Ingestion of infected cattle (mycobacterium BOVIS)
5. Virulence
6. Over fatigue
S/Sx:
1. Productive cough – yellowish
2. Low fever
3. Night sweats
4. Dyspnea
5. Anorexia, general body malaise, wt loss
6. Chest/ back pain
7. Hempotysis
Diagnosis:
1. Skin test – mantoux test – infection of Purified CHON Derivative PPD
DOH – 8-10 mm induration
WHO – 10-14 mm induration
Result within 48 – 72h
(+) Mantoux test – previous exposure to tubercle bacilli
Mode of transmission – droplet infection

2. Sputum AFB – (+) to cultured microorganism
3. CXR – pulmonary infiltrate caseosis necrosis
Nursing Mgt:
1. CBR
2. Strict resp isolation
3. O2 inhalation
4. Semi fowler
5. Force fluid to liquefy secretions
6. DBCE
8. Comfy & humid environment
9. Diet – increase CHO & calories, CHON, Vit, minerals
10. Short course chemotherapy
5. Intensive phase
INH – isoniazide - give before meals for absorption

Rifampicin - given within 4 months, given simultaneously to prevent resistance
-S/E: peripheral neutitis – vit B6
Rifampicin -All body secretions turn to red orange color urine, stool, saliva, sweat & tears.
PZA – Pyrazinamide – given 2 mos/ after meals. S/E: allergic rxn, nephrotoxicity & hepatoxicity
Standard regimen
1. Injection of streptomycin – aminoglycoside
Ex. Kanamycin, gentamycin, neomycin
S/E:
a.) Ototoxicity – damage CN # 8 – tinnitus – hearing loss
b.) Nephrotoxicicity – monitor BUN & Crea
HT:
a.) Avoid pred factors
b.) Complications:
1.) Atelectasis
2.) Miliary TB – spread of Tb to other system
b.) Compliance to meds
- Religiously take meds
3. HISTOPLASMOSIS- acute fungal infection caused by inhalation of contaminated dust with histoplasma capsulatum
transmitted to birds manure.
S/Sx: Same as pneumonia & PTB – like
1. Productive cough
2. Dyspnea
3. Chest & joint pains
4. Cyanosis
5. Anorexia, gen body malaise, wt loss
6. Hemoptysis
Dx:
1. Histoplasmin skin test = (+)
2. ABG – pO2 decrease
Nsg Mgt:
1. CBR
2. Meds:
a.) Anti fungal agents
Amphotericin B (Fungizone)
S/E :
a.) Nephrotoxcicity check BUN
b.) Hypokalemia
b.)Corticosteroids
c.) Mucolytic/ or expectorants
3. O2 – force fluids
4. Nebulize, suction
5. Complications:
a.) Atelectasis
b.) Bronchiectasis COPD
6. Prevent spread of histoplasmosis:
a.) Spray breading places or kill the bird.
4. COPD – Chronic Obstructive Pulmonary Disease

1. Chronic bronchitis
2. Bronchial asthma
3. Bronchiectasis
4. Pulmonary emphysema – terminal stage
CHRONIC BRONCHITIS - called BLUE BLOATERS inflammation of bronchus due to hypertrophy or hyperplasia of goblet
mucus producing cells leading to narrowing of smaller airways.
1. Smoking – all COPD types
2. Air pollution
S/Sx:
1. Prod cough
2. Dyspnea on exertion
3. Prolonged expiratory grunt
4. Scattered rales/ rhonchi
5. Cyanosis
6. Pulmo HPN – a.)Leading to peripheral edema
b.) Cor pulmonary – respiratory in origin
7. Anorexia, gen body malaise
Dx:
1. ABG
PO2 PCO2 Resp acidosis
Hypoxemia – causing cyanosis

Nsg Mgt:
(Same as emphysema)
2.) BRONCHIAL ASTHMA- reversible inflammation lung condition due to hyerpsensitivity leading to narrowing of smaller
airway.
1. Extrinsic Asthma – called Atropic/ allergic asthma
a.) Pallor
b.) Dust
c.) Gases
d.) Smoke
e.) Dander
f.) Lints
2. Intrinsic Asthma-
Cause:
Herediatary
Drugs – aspirin, penicillin,  blockers
Food additives – nitrites
Foods – seafood, chicken, eggs, chocolates, milk
Physical/ emotional stress
Sudden change of temp, humidity &air pressure
3. mixed type: combi of both ext & intr. Asthma
90% cause of asthma
S/Sx:
1. C – cough – non productive to productive
2. D – dyspnea
3. W – wheezing on expiration
4. Cyanosis
5. Mild apprehension & restlessness
6. Tachycardia & palpitation
7. Diaphoresis
Dx:
1. Pulmo function test – decrease lung capacity
2. ABG – PO2 decrease
Nsg Mgt:
1. CBR – all COPD
2. Meds-
a.) Bronchodilator through inhalation or metered dose inhaled / pump. Give 1st before corticosteroids
b.) Corticosteroids – due inflammatory. Given 10 min after adm bronchodilator
c.) Mucolytic/ expectorant
d.) Mucomist – at bedside put suction machine.
e.) Antihistamine
2. Force fluid
3. O2 – all COPD low inflow to prevent resp distress
5. Semifowler – all COPD except emphysema due late stage
6. HT
a.) Avoid pred factors
b.) Complications:
6. Status astmaticus- give epinephrine & bronchodilators
7. Emphysema
c.) Adherence to med
BRONCHIECTASIS – abnormal permanent dilation of bronchus resulting to destruction of muscular & elastic tissues of alveoli.
1. Recurrent upper & lower RI
2. Congenital anomalies
3. Tumors
4. Trauma
S/Sx:
1. Productive cough
2. Dyspnea
3. Anorexia, gen body malaise- all energy are used to increase respiration.
4. Cyanosis
5. Hemoptisis
Dx:
1.
ABG – PO2 decrease
2.
Bronchoscopy – direct visualization of bronchus using fiberscope.
Nsg Mgt: before bronchoscopy
1. Consent, explain procedure – MD/ lab explain RN
2. NPO
3. Monitor VS
Nsg Mgt after bronchoscopy
1. Feeding after return of gag reflex
2. Instruct client to avoid talking, smoking or coughing
3. Monitor signs of frank or gross bleeding
4. Monitor of laryngeal spasm
8. DOB
9. Prepare at bedside tracheostomy set
Mgt: same as emphysema except Surgery

Pneumonectomy – removal of affected lung
Segmental lobectomy – position of pt – unaffected side
PULMONARY EMPHYSEMA – irreversible terminal stage of COPD

10. Characterized by inelasticity of alveolar wall leading to air trapping, leading to maldistribution of gases.
11. Body will compensate over distension of thoracic cavity
12. Barrel chest
1. Smoking
2. Allergy
3. Air pollution
4. High risk – elderly
5. Hereditary -  1 anti trypsin to release elastase for recoil of alveoli.
S/Sx:
1. Productive cough
2. Dyspnea at rest – due terminal
3. Anorexia & gen body malaise
4. Rales/ rhonchi
5. Bronchial wheezing
6. Decrease tactile fremitus (should have vibration)– palpation – “99”. Decreased - with air or fluid
7. Resonance to hyperresonance – percussion
8. Decreased or diminished breath sounds
9. Pathognomonic: barrel chest – increase post/ anterior diameter of chest
10. Purse lip breathing – to eliminated PCO2
11. Flaring of alai nares
Diagnosis:
1. Pulmonary function test – decrease vital lung capacity
2. ABG –
1. Panlobular / centrolobular emphysema
pCO2 increase
pO2 decrease – hypoxema resp acidosis Blue bloaters
2. Panacinar/ Centracinar
pCO2 decrease
pO2 increase – hyperaxemia resp alkalosis Pink puffers
Nursing Mgt:
1. CBR
2. Meds –
a.) Bronchodilators
b.) Corticosteroids
c.) Antimicrobial agents
d.) Mucolytics/ expectorants
3. O2 – Low inflow
4. Force fluids
5. High fowlers
6. Neb & suction
7. Institute
P – posture
E – end
E – expiratory to prevent collapse of alveoli
P – pressure
8. HT
a.) Avoid smoking
b.) Prevent complications
1.) Cor pulmonary – R ventricular hypertrophy
2.) CO2 narcosis – lead to coma
3.) Atelectasis
4.) Pneumothorax – air in pleural space
9. Adherence to meds
5. RESTRICTIVE LUNG DISORDER
PNEUMOTHORAX – partial / or complete collapse of lungs due to entry or air in pleural space.
Types:
1. Spontaneous pneumothorax – entry of air in pleural space without obvious cause.
Eg. rupture of bleb (alveoli filled sacs) in pt with inflammed lung conditions
Eg. open pneumothorax – air enters pleural space through an opening in chest wall
-Stab/ gun shot wound
2. Tension Pneumothorax – air enters plural space with @ inspiration & can’t escape leading to over distension of thoracic
cavity resulting to shifting of mediastinum content to unaffected side.
Eg. flail chest – “paradoxical breathing”
1.Chest trauma
2.Inflammatory lung conditions
3.Tumor
S/Sx:
1. Sudden sharp chest pain
2. Dyspnea
3. Cyanosis
4. Diminished breath sound of affected lung
5. Cool moist skin
6. Mild restlessness/ apprehension
7. Resonance to hyper resonance
Diagnosis:
1. ABG – pO2 decrease –
2. CXR – confirms pneumothorax
Nursing Mgt:
1. Endotracheal intubation
2. Thoracenthesis
3. Meds – Morphine SO4
13. Anti microbial agents
4. Assist in test tube thoracotomy
Nursing Mgt if pt is on CPT attached to H2O drainage
1. Maintain strict aseptic technique
2. DBE
3. At bedside
1. Petroleum gauze pad if dislodged Hemostan
2. If with air leakage – clamp
3. Extra bottle
4. Meds – Morphine SO4
Antimicrobial
5. Monitor & assess for oscillation fluctuations or bubbling
1. If (+) to intermittent bubbling means normal or intact
- H2O rises upon inspiration
- H2o goes down upon expiration
b.) If (+) to continuous, remittent bubbling
1. Check for air leakage
2. Clamp towards chest tube
3. Notify MD
c.) If (-) to bubbling
1. Check for loop, clots, and kink
2. Milk towards H2O seal
3. Indicates re-expansion of lungs
When will MD remove chest tube:
1. If (-) fluctuations
2. (+) Breath sounds
3. CXR – full expansion of lungs
Nursing Mgt of removal of chest tube

2. DBE
3. Instruct to perform Valsalva maneuver for easy removal, to prevent entry of air in pleural space.
4. Apply vaselinated air occlusive dressing
14. Maintain dressing dry & intact
EAR –
1. Hearing
2. Balance (Kinesthesia or position sense)
Parts:
1. Outer-
a.) Pinna/ auricle – protects ear from direct trauma
b.) Ext. auditory meatus – has ceruminous gland. Cerumen
c.) Tympanic membrane – transmits sound waves to middle ear
Disorders of outer ear

Entry of insects – put flashlight to give route of exit
Foreign objects – beans (bring to MD)
H2O - drain
2. Middle ear
a.) Ear osssicle

1. Hammer -malleus
2. Anvil -Incus for bone conduction disorder conductive hearing loss
3. Stirrups -stapes
b. Eustachian tube - Opens to allow equalization of pressure on both ears

- Yawn, chew, and swallow
Children – straight, wide, short
9. Otitis media
Adult – long, narrow & slanted
c. Muscles
1. Stapedius
2. Tensor tympani
3. Inner ear
a. Bony labyrinth – for balance, vestibule
Utricle & succule
Otolithe or ear stone – has Ca carbonate
Movement of head = Righting reflex = Kinesthesia

b. Membranous Labyrinth
1. Cochlea – ( function for hearing) has organ of corti
2. Endolymph & perilymph – for static equilibrium
3. Mastoid air cells – air filled spaces in temporal bone in skull
Complications of Mastoditis – meningitis
Types of hearing loss:

1. Conductive hearing loss – transmission hearing loss
Causes:
a.) Impacted cerumen – tinnitus & conduction hearing loss- assist in ear irrigaton
b.) Immobility of stapes – OTOSCLEROSIS
10. Middle ear disease char by formation of spongy bone in the inner ear causing fixation or immobility of stapes
11. Stapes can’t transmit sound waves
Surgery
Stapedectomy – removal of stapes, spongy bone & implantation of graft/ ear prosthesis
1. Familiar tendency
2. Ear trauma & surgery
S/Sx:
1. Tinnitus
2. Conductive hearing loss
Diagnosis:
1. Audiometry – various sound stimulates (+) conductive hearing loss
2. Weber’s test – Normal AC> BC
result BC > AC
Stapedectomy
Nursing Mgt post op
1. Position pt unaffected side
2. DBE
No coughing & blowing of nose
- Night lead to removal of graft
3. Meds:
a.) Analgesic
b.) Antiemetic
c.) Antimotion sickness agent. Ex. meclesine Hcl (Bonamine)
4. Assess – motor function – facial nerve - (Smile, frown, raise eyebrow)
5. Avoid shampoo hair for 1 to 2 weeks. Use shower cap
SENSORY NEURAL HEARING LOSS/ NERVE DEAFNESS

Cause:
1. Tumor on cocheal
2. Loud noises (gun shot)
3. Presbycusis – bilateral progressive hearing loss especially at high frequencies – elderly
Face elderly to promote lip reading
4. Meniere’s disease – endolymphatic hydrops
12. Inner ear disease char by dilation of endo – lympathic system leading to increase volume of endolin
Predisposing factor of MENIERE’S DISEASE

Smoking
Hyperlipidemia
30 years old
Obesity – (+) chosesteatoma
Allergy
Ear trauma & infection
S/Sx:
1. TRIAD symptoms of Meniere’s disease
a.) Tinnitus
b.) Vertigo
c.) Sensory neural hearing loss
2. Nystagmus
3. n/v
4. Mild apprehension, anxiety
5. Tachycardia
6. Palpitations
7. Diaphoresis
Diagnosis:
1. Audiometry – (+) sensory hearing loss
Nursing mgt:
1. Comfy & darkened environment
2. Siderails
3. Emetic basin
4. Meds:
a.) Diuretics –to remove endolymph
b.) Vasodilator
c.) Antihistamine
d.) Antiemetic
e.) Antimotion sickness agent
f.) Sedatives/ tranquilizers
5. Restrict Na
6. Limit fluid intake
7. Avoid smoking
8. Surgery – endolymphatic sac decompression- Shunt
*Kawasaki : Drug of Choice : Aspirin, IgG
Common to children 5 y/o below
(desquamation of palms & toes)
*Anatomy : URT LRT

 Nose Trachea

 Pharynx Bronchos
 Larynx

Understanding the Nervous System

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Understanding the Nervous System

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MEDICAL SURGICAL

OVERVIEW OF THE STRUCTURES & FUNCTIONS OF THE NERVOUS SYSTEM

3 PARTS OF THE NERVOUS SYSTEM

1. Central NS 2. Peripheral NS 3. Autonomic NS C-8

I. Autonomic Nervous System

4. Adrenergic or Parasympatholitic Response

Adrenergic Agents a. Epinephrine (Adrenaline) S/E : SNS Effects

Bodily Effects of PNS

a. Meiosis = constriction of pupils

4. Cholinergic or Vagal or Sympatholitic Response

a. Beta-Adrenergic Blocking Agents (Beta-Blockers) (all end in –‘lol’)

II. CNS (Brain & Spinal Cord)

A. Cells – neurons = Basic living units

3 Types of Cells According To Its Regenerative Capacity:

B. Neuroglia : can cause brain tumors

Hepatic encephalopathy (liver cirrhosis) = death of liver d/t necrosis

others: Bilivedrin = green pigment

* Carotenemia = yellowish discoloration of the skin

b. Carbon Monoxide :Tx for Carbon monoxide poisoning

Parkinson’s Disease Seizure

d. Lead = Antidote for lead poisoning ------ Calcium EDTA

e. Ketones - acids, CNS depressant

Cholesterol Ketones ----- DKA : Early Signs = Weakness/ Weight Loss

Created by Niňa E. Tubio 3

3. Ependymal Cells = acts as a defense in the CNS along with microglia

secretes a glue ------ Chemoattractants

4. Oligodendrocytes = produces myelin sheath: acts as a cover for neurons

2. MULTIPLE SCLEROSIS (MS) -Chronic intermittent disorder of CNS

Normal Resident Antibodies: 5 types

1.) Administer Meds as ordered

b. Baclopen (Lioresol) or Dantrolene Na (Dantrene) : To muscle spasticity

h. Anti-spasmodic (Prophanthelene Bromide) Pro-banthene & anti-cholinergic

2. Maintain side rails

*3 Causes of UTI In Women

PART II: Compositions of Cord & Spinal cord

1st: Brain mass

A. CEREBRUM– Largest Part - Connects Right & Left cerebral hemisphere

3.) Parietal lobe – appreciation & discrimination of sensory impulses

5.) Insula/island of reil/ Central lobe- controls visceral fx

6.) Rhinencephalon/ Limbic

Dopamine :Parkinson’s or Huntington’s Dopamine : Schizophrenia

B. MID BRAIN/ MESENCEPHALON

C. DIENCEPHALON -------between brain

a. PONS – Pneumotaxic center – controls rate & depth of respiration

b. MEDULLA OBLONGATA- lowest portion of the brain

E. CEREBELLUM – smallest part of the brain

2nd: CerebroSpinal Fluid (CSF)

1. INCREASED ICP – increase IC bulk is due to increase in 1 of the IC components

DIFFERENCE BET. SHOCK : & INCREASE ICP:

f. Uncal herniation – unilateral dilation of pupil

stimulate lungs to Hyperventilate

2.) Loop diuretic - Lasix (Furosemide) in ampule

Mg SO4 toxicity– administer Ca gluconate : “BURP” B – BP decrease

3. Hyponatremia (Normal Na level = 135 – 145 meg/L)

4. Hyperglycemia – Increase blood sugar level

5. Hyperurecemia – increase serum uric acid = by product of purine metabolism

Gouty arthritis kidney stones- renal colic (pain)

Nsg Mgt of Gouty Arthritis

S/E of Morphine SO4 toxicity

Cont. Increase ICP meds

3.) Corticosteroids - Dexamethsone – decrease cerebral edema (Decadrone)

Magic 2’s of Drug Monitoring Toxicity Level: “DLADA”