2011

1. Dr. Mahmoud Alsheyab:

Child presented with pallor and jaundice

Q1: whats your initial diagnosis?
Hemolytic anaemia
Q2: what is the most important questions you would like to ask in the history?
Family history of splenectomy (one of the clinical features)
Q3: what's the most important in physical examination?
Splenomegaly and weight/height (mild growth retardation)
Q4: what investigations you would like to do?
CBC: Hb/MCV/MCHC , Hb electrophoresis, Blood film
Q5: You found spherocytosis in the blood film, whats your diagnosis?
Hereditary spherocytosis (ad: defect in red cell membrane protein spectrin)
Q6: what specific test you would like to do?
Osmotic fragility test
Q7: His HB level is 4, how you will treat him?
Blood transfusion and consider splenectomy
Q8: how much blood you will give him
15 mL/kg
Q9: how you will give him the blood; the rate and why?
Lower rate to prevent heart failure
Q10: what are the complications of blood transfusion?
Hemochromatosis, transmission of infections
Q11: when to do splenectomy and how to prepare for him?
Usually after the age of 5 years (to decrease the incidence of invasive disease caused
by encapsulated bacteria); we give him prophylactic vaccination two weeks before
the surgery

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Q12: what you will give him after surgery?
Prophylactic antibiotics
Q13: the parents ask you what is the risk of recurrence for this disease?
50%

2. Dr. Azhar Dawood:

A 6 y/o girl came to the ED with jaundice and pallor of 2 months duration; she also
has
tachypnea and tachycardia.

Q1: What to ask in the relevant history?

Family history of splenectomy
Q2: Her brother has removed the spleen previously, what is your diagnosis?
Hereditary spherocytosis
Q3: Shes having frequent attacks of pallor and jaundice, what it is your
treatment?
Blood transfusion; with low rate of 15 mL/kg every 3-4 weeks with iron chelating
agents.
Q4: Adverse effects of transfusion?
Hemocrhomatosis (iron overloaded), Blood borne infections, acute immune
hemolytic reaction or delayed hemolytic reaction (due to non-matching blood
type)
Q5: Now she needs blood transfusion every 1 week; increase frequency and this
mean
hypersplenism, what to do?
Splenectomy.

3. Dr. Faisal Qteesh:

Q1: A 9 years old female diagnosed as asthma came to the ER they told me ana 3a
2sas ene dr:P eno she has un controlled asthma how do i make sure???bte7kolo ele
maktobeen b mo7adret elbateny!!b3den be2olak tayeb belbeet 3shan 23melha
controll sho ba3teeha

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??bet2olo inhaled steroid,long acting b2 agonist,leukotriens inhibiters ,short acting as
needed..ma t2olo mast cell stabilizer leno alli ghaalat m3 ene 2oltelo enha maktobe
belkotb alli ew3ek ta3teeha la7ada...then alli tyeb 3m ta5od hay el2dweye o ma 3m
tet7san sho y3ne??2oltello m3nato she's not complianet alli 2- 2oltelo ma 3m
test5demo el inhaler mne7 ali 3- ali wrong dose..ma talab mene aktar
then he told me e7ki 3l sree3 keef b3alega bel ER kan bdo hek
:o2,nebulizer salbutamol,ibratropium bromide,sys steroid,ketamine o
a5er she intubation
Q2: Treatment for status epilepticus:
1. 2 IV cannula
2. Maintain ABC
3. Place patient on the left lateral position and pull his tongue out
4. Lorazepam (but the recommended anti-seizure medication in Jordan is
Diazepam; alternative for Diazepam is Valproate sodium)
Lorazepam (0.05 0.1)
mg/kg IV Diazepam (0.25)
mg/kg
Rectal Diazepam (0.3 0.5) mg/kg
Give it slowly over 2-3 mins because if given rapidly it will cause respiratory
arrest
5. Wait for 10 mins to see if the seizure has stop, if not then repeat the dose for
the second and third time
6. If still persist, give phenytoin as a bolus dose 20mg/kg
7. Treat fever with paracetamol / NSAIDS / fanning / removing clothes
8. If still persist, give Phenobarbitol 15 20mg/kg
9. If still persist, add additional dose of 5mg/kg over 15 30 mins
10.If still persist, induce general anesthesia in ICU by Phenobarbitol or
Propafol or Medazolam (avoid paralytic agents)

4. Dr. Faisal Qteesh:

11 y/o male patient referred from PRH after having seizures of 20 mins duration
which was aborted. In the ED, KAUH the patient was drowsy and found to have BP
of 200/110 mmhg
Q1: What is your diagnosis?
Hypertensive encephalopathy

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Q2: Management?
Na nitroprusside, hydralazine.
Q3: Investigations?
CBC, electrolytes, KFT, LFT.
Q4: KFT was abnormal and results were showing renal failure, how to
differentiate
between chronic and acute renal failure?
Metabolic & electrolyte changes and by renal U/S and the changes you see in U/S
Q5: What other investigations?
non-contrast head CT scan
Q6: Treatment?
ACEI

5. Dr. Iyad Al-Omari from Jordanian University:

A 3 y/o male patient presented to the ED with fever, drowsiness and skin rash of
2 days duration
Q1: Approach?
History, P/E & investigations focusing mainly on meningitis and
meningococcemia Hx:
- Headache / Neck stiffness / Lethargy / Drowsiness / Decreases
consciousness / Photophobia / Phonophobia.
- Young children: sudden onset of fever and lethargy + vomiting / convulsion.
- DDX: Recent URTI / hx of trauma / bleeding from other site / joint pain
PE: Brudzinski / Kernig / Nuchal rigidity
Q2: vitals: [HR; 120bpm] [BP; 70/50] whats the diagnosis?
Septic shock
Q3: CSF results going with bacterial infections what other specific test that
confirms your diagnosis? Would you like to order other than PCR?
5
Skin biopsy and gram stain (?)
Q4: Management?
Resuscitation with IV fluid, clotting factors or platelets if bleeding developed. IV
antibiotic:
Q5: Inherited disease causing meningococcemia?
Inherited terminal complement deficiency
Q6: The nurse in the ER is pregnant, what antibiotic would you offer her?
IV Ceftriaxone
(If not pregnant: Rifampicin / Ciprofloxacin / Ceftriaxone) chemoprophylaxis for anyone who has
direct contact for at least 4 hours

meningococcemia
Pg 16 2013
Dr Mahmood Sheyab

Hx; 4 years old,last night he was hypoactive, today he is having fever and skin rash

-what do you think? Meningococcemia

-What cause of meningococcemia? Neisseria meningitidis

-What is the type of rash? Patechial rash (star-like shape) non blanchable

-Where do u see this rash? characteristic petechial skin rash is usually located
on the trunk and legs and may rapidly evolve into purpura

-How is the mechanism of the rash in general? release of toxins into the blood that break down the
walls of blood vessels. A rash can develop under the skindue to blood leakage that may leave red or
brownish pinprick spots

-other ddx? Acute- acute hypersensitivity vasculitides, septic vasculitis due to acute bacteremia or
endocarditis, toxic shock syndrome, and purpura fulminans.
Chronic- chronic gonococcemia, Henoch-Schnlein purpura, rat-bite fever, Sweet syndrome,
erythema multiforme, and subacute bacterial endocarditis.

-then he asked what do u want to do for him in the ER?

Antibiotics given through a vein immediately
 Breathing support
Clotting factors or platelet replacement, if bleeding disorders develop
Fluids through a vein
Medicines to treat low blood pressure
Wound care for areas of skin with blood clots

-How can u be sure this is meningococcemia?

hx-non specific + rash
p/e-rash + meningeal sign?
Lab-cbc, blood culture, blood clotting studies, skin bx & gram staining, U/A

-What is ur management?
Antibiotics recommended for the treatment of meningococcemia include the following:
Third-generation cephalosporins such as ceftriaxone (2 g IV q24h) or cefotaxime (2 g IV q4-
6h) are the preferred antibiotics
Alternative agents include (1) ampicillin 12 g/d either by continuous infusion or by divided
dosing q4h or (2) moxifloxacin 6-8 g/d IV
The course of therapy is 7-10 days

Note: Meningococci are resistant to vancomycin and the aminoglycosides

Chloramphenicol may be considered in patients who are allergic to beta-lactam antibiotics. It

appears to be most useful when administrated as a single IM injection during epidemics in
developed countries.

(Every answer and every word u say, he will ask u about it!!! So do not make my mistake and only
answer things u know!!!)

nephrotic
pg 16 2013 Dr rola

-what do u know about nephrotic syndrome?

protein in the urine, low blood protein levels, high cholesterol levels, high triglyceride levels,
and swelling.

-what is the cause?(decrease production, decrease intake(what is this disease called...!!), increase
excretion by stool)<<jawapan student
The most common cause in children is minimal change disease 2-6y/o atau
loss of protein through the kidneys (proteinuria) leads to low protein levels in the blood
(hypoalbuminemia), which causes water to be drawn into soft tissues (edema)

-Is hypoalbuminemia a dangerous condition?

Very low hypoalbuminemia can also cause a variety of secondary problems, such as water in the
abdominal cavity (ascites), around the heart or lung (pericardial effusion, pleural effusion),
high cholesterol (hence hyperlipidemia), loss of molecules regulating coagulation (hence increased
risk of thrombosis)
-How does the albumin affect your body if it was low(mechanism)? Rasanya sama dengan jawapan
kat atas.

Om
acute otitis media dose & duration ? 90 mg/kg/day amoxicillin for 10 days

iron

regarding the dose of Iron I give the patient.In the past years Qs Once he talks about elemental iron
and how much iron sulphate contains elemental iron?
and in another time he says it's 5 mg/Kg ferrous sulphate, so which one to answer with?

Ferrous sulphate 300mg = 60mg elemental iron

Ferrous sulphate dried 200mg = 65mg elemental iron
The recommended dose of elemental iron for iron-deficiency anaemia is 100mg to 200mg daily. ie.
1 of either the above tablets 2 to three times a day
The RDA of elemental iron for females 19 to 50 years old is 18 mg Iron per day ie. 1/4 of a tablet
daily.
The dose of Iron will depend on what you are taking it for.
Some iron tablets are marketed for RDA allowances (low dose iron supplements) and others for Iron
deficiency anaemias (high dose) .

-the increase in Hg level after giving iron , is it 2 g/week or 1g/week? dose recommended for
children is 3 to 6 mg/kg/day of elemental iron ( in dr hala's lecture ) ,each 325 mg ferrous sulfate
contains 65 mg elemental iron , therapeutic doses of iron should increase hemoglobin levels by 0.7-
1.0 g/dL per week.
-What is the cause of improved symptoms shortly after Iron supplementation of IDA patient?
according to the lecture appetite improved by 24 hours due to replacement of intracellular iron
enzymes

2012

1.in the ER 3 yrs boy with history of stridor and wheeze.

2. 3 yrs old male brought to u, complaining of stridor of an acute onset.

-What do u want to ask in the history ?
Age of onset, duration, severity, and progression of the stridor

Precipitating events (eg, crying or feeding)

Positioning (eg, prone, supine, or sitting)

Quality and nature of crying

Presence of aphonia

Other associated symptoms (eg, paroxysms of cough, aspiration, difficulty in feeding,

 drooling, or sleep-disordered breathing)
Other respt sx, cough, horseness voice, resp distress, fever, rapid breathing etc

-What are your ddx ?

Croup, epiglotitis, tonsillitis, FBA, GERD,diphtheria, anaphylaxis blab la bla hahha -.-

-What is your first line TT ?

ABC?? entah
epiglottitis and bacterial tracheitis, bact croup, antibiotic therapy
others steroid might be helpful
epiglotitis intubation, o2
viral croup, akan hilang sendiri?
-How are you going to treat him ?

3. A 6 year-old girl came to the ER WITH JAUNDICE AND PALLOR OF 2 months duration, she
has also tachypnea and tachycardea.
(Acute cases can threaten to cause hypoxia through anemia and acute kernicterus through high
blood levels of bilirubin)
- Ask relevant hx?
-Then it appears to u that it's hereditary spherocytosis because her brother has removed the spleen.
you tell him it's HS .
-He is telling u now that she's having frequent attacks of pallor and jaundice what it is your tt?
bte7kilo blood transfusion u have to tell him the rate 15 ml/kg every 3-4 weeks..and iron chelating
agents..bes2lak sho eladverse effects of transfusion they are 3!! (Transfusion reaction symptoms
include: back pain, blood in your urine, chills, fainting or dizziness, fever, flank pain, skin flushing)
(risk: Allergic reaction and hives, fever, acute immune hemolytic reaction, lung injury, blood borne
infection, delayed hemolytic reaction, iron overload, graft-versus-host disease)
-then she's now needs blood trans.every 1 week y3ne increase bel freqeuncy sho y3ne
>>hyperspleenism what to do>>spleenectomy what to do b4 it and after it (before- take
immunization such as pneumococcal, meningococcal, Haemophilus influenza, flu vaccines. After-
children may need to take antibiotics)
4. GE .. HYPOnatremia -RX in details
Depend on etiology and vol status
If symptomatic, vol depleted, and sodiul <120meq/L administer 3%normal saline (usually 2mL/kg)
until sodium rises above 120 meq/L then switch to normal saline if seizure occur gv barbiturate iv or
rectally
5. ITP HSP dif. ??
The differential diagnosis of purpura includes:
Acute hemorrhagic edema of infancy For more information about AHEI
Acute streptococcal glomerulonephritis
Blood clotting disorders
Drugs particularly which may cause fragile blood vessels or platelet problems
Hemolytic-uremic syndrome
Henoch-Schnlein or anaphalactoid purpura for more information about HSP
Hypersensitivity vasculitis
Hypertension malignant, pre-eclampsia and similar gestational problems
Immune thrombocytopenic purpura
Infection
Disseminated intravascular coagulation / Sepsis
Purpura fulminans from Neisseria meningiditis
Congenital infections such as cytomegalovirus and rubella
Rickettsial diseases
Polyarteritis nodosa
Thrombotic thrombocytopenic purpura
Scurvy
Urticarial vasculitis
Trauma

6. A 14 or whatever year old female, a known patient of liver disease comes to the hospital pouring
blood from the mouth. how do u like to approach her?? . then give DDx & proceed to investigations
that may help u to know the cause.
Resuscitation (colloid/crystalloid, blood transfusion, endoscopy)
Hepatitis B was the leading cause of chronic liver disease in children followed by Wilson's disease
and autoimmune liver disease/ extra hepatic portal htn/ hemolytic anemia?
Ix:LFT, PT serum albumin, u/s, copper in urine, virals marker?
7. A 1 year old child with fever, tugging his ear :
-diffrential? OM
-ask more questions to confirm ur diagnosis.Ear discharge, URTI, flu, fever, irritability, loss
appetite, vomit, dirrhea etc
- what do u want to do next (examination : using otoscope, explain what do u expect to see with
otoscope) bulging of the tympanic membrane, redness, othorea
what most common cause for otitis media Streptococcus pneumoniae, Haemophilus
influenzae, Moraxella catarrhalis, and Staphylococcus aureus
treatment : doses and duration amoxicillin 40-50mg/kg for 10 days
15. 2 yrs old male with fever , pulling his ear and u suspect he has otitis media , wut r things u look
for in the history to support ur diagnosis ? wut r the invs. u'll order ? wuts ur mang. ? y u did u chose
this antibiotic in particular ? , to cover wich bacteria ? if this was the 5th episode of OM wut will u
suspect the pnt has ??
Top of Form
Acute otitis media:
*Hx that support dx==> hotness, activity, sleep, oral intake, irritability, otorrhea, recent URI in him
or contact, daycare, bottlefeeding, passive smoking, family hx, previous episodes of OM, vaccines
...
*Exam==> Check for dehydration. Otoscope: erythematous membrane (normally pink/white), full
or bulging membrane, lost light reflex, purulent discharge or a hole in membrane if perforation...
*Investigations==> NONE. Do tympanocentesis and culture of exudate if immunocompromised,
neonate, or not responding to therapy.
*Mx:
- Fever: acetaminophen, profen.
- Dehydrated: oral rehydration or IV fluids, 7asab how severe - OM: Amoxicillin high dose (90
mg/kg/day) P.O for 10 days, with food, covers S. pneumonia and H. influenzae (weakly). If no
response at 3 days of Abx, suspect resistance, give Amoxiclav high dose (90 mg/kg/day) or
Cefuroxime P.O. - in case of vomiting and can't take oral meds, IM ceftriaxone. - give yogurt to
prevent antibiotic diarrhea
* Recurrent OM: >=6 episodes in the first 6 yrs of life. indicates craniofacial anomaly (cleft) or
immunodeficiency. But most are otherwise healthy!
8. Hematurea .....
hx sx of acute hemolytic anemia, pallor, jaundice, abd pain, vomit, diarrhea, low grade fever,
hemoglobinuria (cola colored urine), fatigue
-> G6bd deficiency ,
-PE, hepatosplenomegally, jaundice/icterus,
- Investigation- quantitative assay G6PD electrophoresis, CBC, retics count, pheripheral smear,
LFT, U/A
- treatment-education, avoid inciting agent, hydration, FA, blood transfusion if severe
9. inhibitor of cell wall synthesis : *B-lactam AB : 1- penicillin : -amoxicillin -ampicillin -
dicloxacillin -penicillin G & penicillin V

10. Cephalosporins :
*1st:cefadroxil , cefazolin , cephalexin
*2nd: cefaclor , cefoxitin , cefuroxime
*3rd: ceftriaxone , cefotaxime , cefixime
*4th : cefepime

11. protin synthesis inhibitor :

1- tetracycline : Doxycycline , demeclocycline , tetracycline
2- aminoglycoside : Amikacin , gentamycin , streptomycin ,neomycin
3- macrolides: Azithromycin , clarithromycin , erythromycin
4- chloramphenicol 5- clindamycin
12.family brings her 9 year old female who was shaking, i mean seizing for 20 minutes. how do u
approach her?
(copy/paste) From 2008 nicely written:
Dx: Status epilepticus
-What will you do first? ABC What is ABC? Airway, breathing and circulation if ABC is OK,
-what will you do as management ? gluco-check if blood glucose is normal,
-what is your next step? if I have an IV access I will give lorazepam 0.1mg \kg we don't have
lorazaepam,
-what will you give him? Diazepam 0.5mg\kg per rectum
-if there was no response , what will you do? repeat the dose after 10 min
-no response till now, you next step? Paraldhydehyde 0.4mg PR
-no response ? Phenobarbital 18 mg \kg
-no response ? call anesthetist and consider intubation and referral to PIC
repeat diazepam 2-3 times 10 mins apart then if no response give phenytoin 20mg/kg as a bolus then
phenobarb then aesthesia
13. 2.5 year old boy, with stridor:
-mention 5 causes for stridor? differentiate by history b\w each of them? if it was sudden stridor,
without fever?what is ur diagnosis? what do u want to do next? - what is ur next step?
-Epiglottitis: acute rapid onset, toxic looking, drooling, sniffing position
-Laryngomalacia: starts in first 2 weeks of life and progressive during first 6 months. Most will
outgrow the condition by age 2 years. In Down syndrome it may persist.
-Foreign body: sudden, hx of playing with toys or eating when it started
-Croup: barking cough, worse at night if sudden without fever:
-foreign body aspiration next step: rigid bronchoscopy pulse oximetry and oxygen if required
14. non blanchable rash .. DDX .. . investigation ?? how would you differentiate between them in hx
and exam ?? HSP AND ITP what is the rx for ITP ?? ? how does IVIG work ?? would u give steriod
..
A:
*DDx: ITP, HSP, HUS, Acute leukemia, meningococcemia, viral infex
*Investigations depend on situation; -regardless u need--> CBC, blood film, PT, PTT -if toxic,
febrile, hypotensive--> CRP, meningococcal PCR, blood culture -Hx of vomiting, diarrhea; bloody-
-> KFT, U analysis, stool culture -Fatigue, fever, wt loss, anorexia, abd pain/discomfort, bone pain,
enlarged nodes--> LFT, serum electrolytes, BONE MARROW BIOPSY, +-LP, +-CXR, +-CT
abdomen...
*Differentiation:
- HSP=> ill child, classical distribution of purpura, bruising and urticaria on the buttocks and
extensor surfaces of the limbs, sometimes associated with joint or abdominal pain, hematochezia
and hematuria are possible.
- ITP=> well child, with multiple bruises and petechiae noted over several days, epistaxis common
*Treatment of ITP:
-generalization : ABC, +-IV fluid, steroids, IVIg, Anti-D (for Rh+ only), platelet transfusion,
splenectomy (if life threatening).
-known case of ITP || IF serious bleeding (e.g. SAH) &/or plt <10000 => admit, IV fluids, IV
steroid, IVIg, send blood for type&screen, platelets transfusion!
-known case of ITP || IF just rash, otherwise well child, platelets>30000 => outpatient is
appropriate, P.O steroid+- IVIg and close follow up...
-u suspected ITP=> admit always, la2enno ITP is a dx of exclusion, so he
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needs further tests.
*IVIg works by blocking receptors found on platelets surface, on which autoimmune IgG's work;
decreasing destruction. Anti-D, works the same as IVIg plus it decreases phagocytosis of opsonized
platelets. Steroids work by decreasing production of autoimmune IgG's.
*NO I won't give steroids. Leukemia needs to be excluded first. Leukemia+steroids= severely
immunodeficient= die of an overwhelming infection. *Leukemia never presents with isolated
thrombocytopenia! *Platelets transfusion only in emergency, destruction of these is delayed by co-
administration of IVIg..................
16. HYPEROXIA TEST
important clinical test - If the pt is cyanotic & you can overcome his cyanosis by giving him O2
then more likely he has respiratory illness rather than a shunt. If there is a shunt, means blue blood
going to the body so it won't be corrected by O2 .
- We give the pt 100% O2 for 15 min. then take arterial sample for ABG then look at the partial
pressure of O2 (PO2) . PO2 is > 250 so more likely to be a pulmonary disease; overcome by O2
PO2 is < 150 so more likely to be a shunt ; cardiac PO2 is 150-250 gray zone
17. swelling, wheezes & a history of bee sting , what's ur diagnosis ? why did he have the wheeze ?
what's the coz of his airways obstruction ? what type of allergic reaction is this ? what's ur
management ? what's ur advise 2 the family ?
8
*Dx: anaphylaxis
*Wheeze --> bronchial muscle spasms
*Obstruction--> spasms+edema/swelling
*type I; IgE-mediated
*Airway, breathing, O2 mask, IM epinephrine +- IV steroid (to prevent biphasic anaphylaxis, not
gonna change this episode), +- Salbutamol nebulizer
*iza 3endhom na7il ebe3ooh, la2enno this can recur m3 another sting, and the best thing to prevent
it is to avoid the trigger. labsoo bracelet. if same scenario occurs again, call 911, rush to ER............
18. Top of Form
stages of neonatal encephaopathy :
-stage 1 : Duration < 24 hours with hyperalertness Uninhibited Moro and stretch reflexes
Sympathetic effects Normal electroencephalogram.
-stage 2 : Obtundation Hypotonia Decreased spontaneous movements with or without seizures.
-stage 3 : Stupor Flaccidity Seizures Suppressed brain stem and autonomic functions The EEG may
be isopotential or have infrequent periodic discharges.
19. a child with history of bee sting with symptoms and signs of anaphylaxis came to the ER
- Massive release of mediators from mast cells and basophils , IgE mediated .
- lead to crease vascular permeability , vasodilatation and respiratory smooth
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muscle contraction .
- symptoms within 5-60 min of exposure to antigen ... urticaria , wheeze, upper airway obstruction ,
hypotension .
- Management : Remove the precipitating cause ABC , IV access Epinephrine ( 0.01 ml/kg of
1/1000 solution ) repeat after 5 min if no improvement High concentration oxygen Antihistamine
Corticosteroid Nebulized salbutamol (if respiratory symptoms) IV fluids
- Patients who at risk of developing another attack should carry a preloaded syringe of epinephrine
for subcutaneous self-administration and wear a medical bracelet .
20. Meningitis .... hx , ph. exam & treatment

- Hx : poor feeding , lethargy , irritability , seziure jaundice, rash , fever diarrhea , vomiting
photophobia , headache , projectile vomiting (in >2 yrs) family history travels symptoms of other
causes of fever (UTI , Pneumonia , OM ...) and the rest of the usual hx
- PE : Vital signs , Head circumferance , Fontanells , in case closed fontanells look for (sunset eyes ,
diplopia , papilledema ) , Meningeal signs (Neck stiffness , Kernig , Brudziniski ... those will be in
child >2 yrs ) , Rash .
- tt : according to kaplan Emperic ( vancomycin + 3rd gen. ceph. )
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After Cx result : strep. pneumonia (pencillin 10-14 days) ... HiB (ampicillin 7-10 days) ...
N.meningitids (pencillin 5-7 d) ... if pretreated (ceftriaxone 7-10 d) ... gram -ve (ceftriaxone 3 wks)
cushing's triad of increased ICP ( hypertension , bradycardia , irregular breathing) treat by Mannitol
and hyperventilation
21. ToA 3 Years old girl ,previously well, presented with sudden onset of fever for one day,after
walking from sleep she could not walk ..
1)what imp questions in the history ? 2)what DDX? 3)in physical examination you fin that BP
110/70 ,Temp 39c,what the examination you well do in the Right involved Leg? 4)if you find
flaccidity in the exam what is your dx? 5)How to differntiated b/w Gillian Barre and Polio?

Q1)Analysis of CC: onset ,Duration,Pain*,symmetry*,site*,progression and its nature y3ne

Ascending or not *,previous similar attack . then Hotness,tenderness, warmth ,descrese mobilty
,limbing and skin rash* . b)Ask about trauma c) ask about GIT symptoms (diarrhea*) d) RENAL
symptoms (hematuria,dysurea) e) Sore throat * f)family history of joint disorder

Q2)DDX: SEPTIC ARTHRITIS ,Poliomyelitis, Guillian Barre, SLE, HSP,Brucellosis

Q3)look for sign of inflamation first :swelling ,hotness,rednees ,tenderness,mobility, BOTH LEGS.
Tone, Power, TENDON REFLEXES*........etc.

Q4)Guillian Barre, Polio.

Q5) to differntiated 1)symmetry of involvment 2) sensation loose on Gullian 3) LP Leukocytosis is

in in Poilo 4)serological testing for viral serology demonstarting 4- fold rise in IgG . and IgM
antibodies is diagnostic for POILO

22. Counseling about the benefits of breast feeding over bottle feeding.
-promote immunity -more sterile -bonding
-contain less amount of protein but high quality so less chance for protein allergy
-contain more fat long chain PUFA which imp. for brain and reital development -less amount
of iron but more bioavailability
-contain grow factor .imp for intestine maturation
-contain lactoferine decrease chance of infx
-avoid over/under feeding
-they tend to produce stool more with breastfed
-they are smarter (3-5 more IQ)
Assessed by : **voiding 6-8 times**weight gain**sleep after feeding.

Contraindication for breastfeeding :

-radioactive compound
-galactosemia -alcoholic mother
-some psychiatric ptns (some anticonvulsant *)
-HIV ---if the baby delivered in poor endemic area and the risk of contaminated formula high
there is indication of breastfeeding means to die later by HIV better than death early by viral
infx.

BENEFITS
For the mother :
a- enhances mother child relationship .
b- decrease risk of post partium hemorrhage, longer period of amenorrhea,reduce risk of ovarian &
pre menopausal breast CA , & possibly reduce risk of osteoporosis.
c- contraceptive although not reliable.
d- reduce health care cost owing to lower incidence of illness in BF infants. e- reduce employee
absenteeism for care attributable for infant illness.

For the baby :

a) decrease the incidence or severity of diarrhea , resp. illnesses ,otitis media, bacteremia , Bacterial
meningitis , necrotizing enterocolitis. Decrease the incidence of food allergy & eczema .
b) Contains protective bacterial & viral ABs (secretory IgA) & non specific immune factors
(macrophages & nucleotides),which help limit infections.
C ) Improve cognitive development.
d) Reduce the risk of insulin dependent diabetes , IBD, sudden infant death syndrome (unproven)
Later on in life.
23. A child has a VP shunt, presented with nausea, vomiting, and fever, he also has sunset eyes
(the case was infected VP shunt) what is the commonest microorganism?
-Most common organisms are S. epidermidis and S. aureus and gram negative organisms.
-tt: Antibiotics including Vancomycin and Gentamycin
-Removal of the shunt.
-External Ventricular Drainage
24. A child with chronic shortness of breath, take a history (the case was CHF due to VSD).
Analysis of cc, ask about tachypnea, tachycardia,sweating during feeding, feeding difficulty ,
respiratory distres, FTT, recurrent LRTI,
By exam: displaced apex beat, pansystolic murmur,hepatomegaly cardiomegaly, increase vascular
marking.
echo diagnostic.
asymptomtic =no need for tt spontaneous closure no restricion of activity no SBE prophylaxis
if symptomatic =surgical tt
25. 11year old male patient refered from PRH after having seizure of 20 min duration which
was aborted , in ER - KAUH the patient was drowsy and found to have BP of 200/110
*What ur diagnosis? Hypertensive encephalopathy
*Managment? Na nitroprusside , hydralazine,labetolol ....

*Investigation? CBC,urinalysis, KFT,LFT, electrolyte

*KFT was abnornal and result show renal failure how to deffrentiated btween chronic and acute
renal failure?
Metabolic and electrolyte change and renal ultrasond
-Hx :long standing renal disease &HTN....family hx of PCKD...chronic drug use.
-U/S : Acute >>large kidney...Chronic>>small kidney except in MM ,PCKD,DM & amylidosis

* Other investigation ? Non contrast head CT scan

* Treatment ? ACEI

26. 9 year diagnose as have asthma came to ER ..

*How to make sure enno un controlled asthma??

1- daytime symptome more than twice/week
2-limitation of activity
3-nocturnal symptom
4-need for reliever more than twice /week
5- abnormal lung function

* how to make it controlled ?

Inhaled steroid , long acting B agonist , leukotriens inhibitor .....

* if she took drug but not improve what u think??

1-not compliant
2-she dont use inhaler properly
3- wrong dose

*how u manage in ER?

O2, nebulizer salbutamol , ipratropium bromide , sys steroid , ketamine , ..... Intubation
my mneumonic for status asthamticus 'O SIC SAMI'
O- O2 S- salbutamol I-ipratropium bromide C-cortisone (iv hydrocortisone)
S-salbutamol continuous A- aminophylline
M- Magnesium sulphate I- intubation
27. Common antidotes :
Acetaminophine ... N-acetylcysteine
Organophosphate ... Atropine
Benzodiazepine ... Flumazenil
Heparin .... Protamine sulfate
Iron ... Defuroxamine Isonizide ...
Pyrodixine Methanol ... Ethanol
Opioid .... Naloxone
hydrochloride TCA/Salicylate ... Sodium bicarbonate
28. 1.5 year old baby, his mother noticed that he is pale, he is exclusively breast feed:
ask relevant questions what do u want to do investigation? what is ur diagnosis? what is the
treatment? oral iron sulphate? dose? duration? what do u expect the first thing to improve? and
why? when does the retics increase? when does the hemoglobin increase back to normal? any
further advice to the mother? about nutrition
1- iron deficiency anemia
2- 2- ferrous salts (sulfate, fumarate, gluconate) orally.. for 8 weeks after Hb normalize dose (1-
2 mg/kg/day elemental iron ..... each 325 mg ferrous sulfate contains 65 mg elemental iron)
3- 3- appetite .. due to increase demand because the bone morrow is working
4- 4- within 72-96 hrs
5- it increase by max of 1 g/dl/week (usually within 2 months)
6- advice her to introduce food.. with the supplement avoid milk and give it with orange juice or
so
30. 30 months old male brought 2 u by his mother complaining of pallor , u suspect a case of
anemia .
what do u want 2 know about his history ? he was exclusively breast fed till 14 months old , & he
had a history of cow's milk allergy , what do u think the cause of his anemia is ? what investigations
will u order ? what will u look for in the lab results ?

ANEMIA
30. 30 months old male brought to you by his mother complaining of pallor, you suspect a case
of anemia, what do you want to know about his history?
Questions to ask:
Prenatal history (infants) Premature? Low birth weight? Congenital conditions?
Diet Breastfeeding? If over 6months, iron fortified cereal? Cows milk?
Developmental assessment Any concerns of delay, possibly attributable to iron deficiency
Symptoms Fatigue? Irritable? Pallor? Disturbed sleep? Loose, pale stool? Activity, weight
changes, Pica, other bloos loss, any chronic illness
Differential Thalasemia (family history), lead exposure
He was exclusively breast fed till 14 months old, had a history of cows milk allergy, what do
you think the cause of anemia is?
1. The most common cause of anemia in children is poor intake of iron, premature infants at
increased risk due to low iron endowment at birth.
2. Cows milk causes iron deficiency in several ways: (1) slow, continuos GI bleeding due to
intolerance to milk protein; (2) competition with iron-rich foods (milk is low in ironand its
iron is poorly absorbed; (3) cows milk binds iron and prevents absorption from other sources
Answers from d previous editor: The cause likely the combination of poor intake (exclusively breast
fed till 14 months!) & blood loss (cows milkallergycause GI bleeding).
What investigation will you order?
The gold standard test for IDA is a bone marrow aspirate to test for iron stores, however this is an
invasive test.
CBC, retics count, blood film, serum iron, ferritin transferrin saturation, stool guaiac
Differentiate b/w other hypochromic, microcytic anemias:
Lead poisoning will present with basophilic stippling of RBCs
Thalassemia will have a normal RDW
Anemia of chronic disease: Increased transferrin, decreased TIBC, elevated ferritin level
What you will look for in the lab?
Test Finding
Ferritin Decreased
CBC Decreased hb (<10), decreased MCV
(<80), low MCHC (<32)
RDW Increased (>15)
Peripheral smear Hypochromic microcytosis
Fe Decreased
TIBC Increased
Transferrin saturation (serum Fe/ Decreased
TIBC)
POSITIVE STOOLL GUAIAC
CONFIRMS GI BLOOD LOSS

What is your treatment?

Iron supplements (ferrous sulphate, feroous gluconate, ferrous fumarate)*Ferrous sulphate is
preferred as it is least expensive , however more side effect (constipation).
Dosage dependent on age of child, but generally 3-6mgkg/day of elemental iron divided in 2 to 3
doses is a therapeutic dose. Continue for 3 months after normalization of lab results. Supplemet
should be taken with vitamin C to enhance absorption. It should be given in between meals and not
with milk.
When do you suspect the symptoms to improve? Why?
After initiating iron therapy, reticulocytes will increase after one week. HB will normalize by about
10g/L per week. Follow-up after therapy (repeat blood work) should be done about 4 weeks after
initiating iron supplementation.
Answer fr d prev editor: Symptoms improve within 24-48hoursof Fe supplements. Better body
oxygenation.
When do you think the Hb level wud be normal? Do you know the rate by week?
Answer fr d prev editor: within 1 month Hb will be normal, shud start to increase after 2 weeks, an
increase by ~2g/dLHb per week. (1% Hct increase/ day 1g/ dLHb increase/ 3 days)
What other things will you tell the mother?
Tell the mother enno r7 e9eeer more active, more playful within 24-48 hours. Teltizimbldawaa. El
dwamomken ye3mallo GI upset, constipation, black stool. Terja b3d 2 weeks, for some tests (CBC+
film, aiming to check if theres response or not).
Increase intake of iron rich foods (liver, pork, beef, veal, spinach, sweet potatoes, strawberries).
JAUNDICE
2 days old boy with jaundice
Hx, Invx, Tx, Counselling
Hx:
Full term? Breast fed? Maternal blood group (ABO & Rh .. if Rh ve, should ask if this the
first baby or not, paternal bl group)
Any hx of dark, tea colored urine, or pale stools
Any yellowing of the whites of the eyes?
Abdominal pain? Pruritis?
Exclude sepsis: hypo/ hyperthermia, poor feeding, hypoactivityetc
Family hx of hemolytic dz, G6PD, jaundice, previous kid who had exchange transfusion, fhx
of consangruity may suggest inherited dz
Maternal drug hx acetaminophen abuse
Recent travel
Ix
Answer fr d prev editor:
1. CBC (Hb for hemolysis, WBC, platelet for sepsis)
2. Blood film: Spherocytosis
3. Bilirubin: total & direct
4. If the mtherbl group O, Rh ve: Bl group & direct Coomb test
5. G6PD screen
6. If d baby has hyperbilirubinemia + hypoglycemia: exclude galactosemia
7. If d baby has hyperbilirubinemia + dysmorphic feature: exclude Alagillis syndrome
Answer fr d book (BRS Series)
1. Jaundice shud be olways be evaluated under d following circumstances:
Jaundice appears at < 24 hrs of age.
Bilirubin rises > 5-8 mg/dL in a 24 hour period.
The rate of rise of bilirubin exceeds 0.5 mg/dL per hour (suggestive of hemolysis).
2. To evaluate indirect hyperbilirubinemia, CBC, retc count, and smear (for hemolysis).
Evaluation for sepis may be indicatd.
3. To evaluate direct hyperbilirubinemia, hepatic ultrasound (to evaluate for choledochal cyst),
serologies for viral hepatitis, and radioisotope scans of the hepatobiliary tree are necessary.
Evaluation for sepsis may be needed.
Tx
1. Serial bilirubin assessment, observation, and reassurance for physiological jaundis.
2. Phototherapy, creates water soluble photoisomers of indirect bilirubin that are more readily
excreted. Contraindicated for porphyria.
3. Exchange transfusion, performed for rapidly rising bilirubin levels secondary to hemolytic dz.
Counsellng
Answer fr d prev editor
I hv no idea about this except >> nursing at least 8-12 times/ day for d 1st several day to prevent
severe jaundis. I think counsellng based on the cause of jaundis, if Rh incompatibilitystthen counsel
her about anti D for the future pregnancies, if breastfeeding jaudis (typically occurs 1 week of life,
usually related to suboptimal milk intake), increase freq of breastfeeding, if breast milk jaundis,
continue breastfe, if galactosemia is contraindicated.
Examination (started at 2nd day)
Physical examination (olwys including vital sign, growth parameter)
General appearance: Jaundis, sclera icterus, pallor, malnutrition
Signs of chronic liver dis: palmar erythema, spider nevi on chest, upper extremities
Generalizing lymphadenopathy, pharyngitis: EBV infxn
Eyes: Kayser-Fleischer (KF) rings; Wilsons dz
Liver: careful palpation & percussion to assess texture & size
o Nodular shrunken liver suggest cirrhosis
o Tender, hepatomegaly suggest acute hepatit
Spleen: splenomegaly (hemolysis, EBV infn)
Abdomen: distention, ascites
Neurologic: confusion, asterixis, hyperreflexia, features of hep, encephalopathy
STATUS ASTHMATICUS
10 yrs old, 1 day hx of cough, SOB, approach (be6la3 status asthmaticus w sa2alu 3n el
management, wl indications for ICU admission, w ..etc bar9o 7asab el dr)
History
A. Previous history of wheezing?
B. If known asthmatic, what are maintenance meds? Compliance? Time of last aerosol?
C. Previous office/clinic/ED visits?
D. Previous hospitalizations, intubations, last steroid course?
E. When did this exacerbation begin?
F. Precipitating factors?
G. General medical history, including any medications.
Management
Initial Evaluation: As for all patients, the initial evaluation should center around the ABCs.
History taking and a more detailed examination can occur after you assure adequate airway,
breathing, and circulation. This need only takes a few seconds to minutes, but is essential.
A. Airway: Can the patient maintain his/her airway? Is the mental status adequate to protect the
airway?
B. Breathing: What is the degree of air exchange? Is the patient cyanotic?
C. Circulation: How is the perfusion? The pulses?
Pharmacology treatment
Indication for ICU admis
If the patient does not respond to appropriate therapy in the emergency department
If the frequency of required aerosol treatments is greater than can be administered on the
ward (usually q1 hour)
If the patient is deteriorating significantly despite appropriate therapy
Source, check it out! http://pedsccm.org/FILE-CABINET/Practical/Akron_pdfs/7ASTHMAP.PDF
STATUS EPILEPTICUS
STATION 1, Dr Faisal Qteesh
*ya doctor, you are in the ER, and you have this 9 year boy, who hv been seizing for the last 30
minutes, parents describe shaking of body and all limbs.
Dr: What is urmanagemenet?
Me: This is likely status epilepticus. I start with brief history
Dr: No doctor, blaashHx! Proper Mx.
Me: Put the patient on bed, left lateral position, the I start with ABCs. Check his airway; inpect the
mouth, for example pull the tongue iza suffocating, remove any foodif he was eating, put mouth
piece. Then make sure hes breathing; inspect chest movement, auscultate bilaterally. Check BP and
pulses. Draw blood and do CBC, check for glucose and electrolytes (8alle 3edhom; Na, K, Mg, Ca),
serum antiepileptic meds concentration. (hay not sure. E5tara3tha bl exam)
Dr: keef y3ne 3milt hal f7o9aat kolhabdoncanula?!! (layazam)
Me: hahaha, yeekeefnseet a7keeha hay :P
Then in order to stop the seizure I give him BZD like Diazepam or Lorazepam either IV or rectally,
and wait for 10 minutes for response. He didnt ask for doses.
Dr: Still seizing
Me: Another dose.
Dr: Still seizing
Me: Another dose.
Dr: Still seizing
Me: Now I need to give Phenytoin.
Dr: Still seizing
Me: Phenobarbital.
Dr: Still seizing
Me: Mg sulphate
Dr: Still seizing
Me: Call for anesthesia for intubation & induction of anesthesia.
Dr: Ok the seizure now stopped. What made it stop?
Me: The anesthetic!
Dr: What do you think the cause of his condition?
Me: Likely hes epileptic and non compliant to medications, infections, drugs, metabolic
disturbances
Okay, seriously donno how to edit this information.
From BRS: Treatment of status epilepticus requires IV anticonvulsants, such as BDZ (eg
lorazepam, diazepam) followed by a loading dose of either phenobarbital or phenytoin.
2013
1st station: Dr wa2el hayajneh... (the same scenario was repeated for 2 students) a 6 years old
boy came to ER with fever 39 of one day duration.. consider me the patient take a hx, do
physical exam and order investigations....
in hx.. (all normal except vomiting and bloody diarrhea ( 6 times per day)...
DDx... Gastroenteritis what are the 5 types of E coli?
Escherichia coli
Enteropathogenic (EPEC) Adherence, effacement
Enterotoxigenic (ETEC) (traveler's diarrhea) Enterotoxins (heat-stable or heat-
labile)
Enteroinvasive (EIEC) Invasion of mucosa
Enterohemorrhagic (EHEC) (includes O157:H7 causing Adherence, effacement, cytotoxin
HUS)
Enteroaggregative (EAEC) Adherence, mucosal damage

Only certain strains of E. coli produce diarrhea. E. coli strains associated with enteritis are classified
by the mechanism of diarrhea: enteropathogenic (EPEC), enterotoxigenic (ETEC), enteroinvasive
(EIEC), entero-hemorrhagic (EHEC), or enteroaggregative (EAEC). EPEC is responsible for many
of the epidemics of diarrhea in newborn nurseries and in daycare centers. ETEC produce heat-labile
(cholera-like) enterotoxin, heat-stable enterotoxin, or both. ETEC causes 40% to 60% of cases of
traveler's diarrhea. EPEC and ETEC adhere to the epithelial cells in the upper small intestine and
produce disease by liberating toxins that induce intestinal secretion and limit absorption. EIEC
invades the colonic mucosa, producing widespread mucosal damage with acute inflammation,
similar to Shigella. EHEC, especially the E. coli O157:H7 strain, produce a Shiga-like toxin that is
responsible for a hemorrhagic colitis and most cases of hemolytic uremic syndrome (HUS), which
is a syndrome of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure (see
Chapter 164). EHEC is associated with contaminated food, including unpasteurized fruit juices and
especially undercooked beef. EHEC is associated with a self-limited form of gastroenteritis, usually
with bloody diarrhea, but production of this toxin blocks host cell protein synthesis and affects
vascular endothelial cells and the glomeruli, resulting in the clinical manifestations of HUS.
types of shigella?
Shigella dysenteriae may cause disease by producing Shiga toxin, either alone or combined with
tissue invasion. The incubation period is 1 to 7 days, and infected adults may shed organisms for 1
month. Infection is spread by person-to-person contact or by the ingestion of contaminated food
with 10 to 100 organisms. The colon is selectively affected. High fever and seizures may occur, in
addition to diarrhea
-Nelson essential of pediatrics 5E- pages 512 - 515
Second station; Dr Rula... (the same scenario was repeated for 2 students)
what is the most common cause of genetic disease in jordan? (consanguinity marriage)
what are the types of inheritance..?
In evaluating children with congenital malformations, the clinical geneticist attempts to classify the
patient's condition into one of five different categories:
1. Single gene mutations, accounting for 6% of children with congenital anomalies
2. Chromosomal disorders, accounting for approximately 7.5%
3. Multifactorially inherited conditions, accounting for 20%
4. Disorders that show an unusual pattern of inheritance, accounting for 2% to 3%
5. Teratogenically caused conditions, accounting for 6%
(Mendelian / non Mendelian) - how many types do we have in Mendelian inheritance? ( autosomal
recessive, dominant, x-linked)
Single gene inheritance is also referred to as Mendelian inheritance as they follow transmission
patterns he observed in his research on peas. There are four types of Mendelian inheritance patterns:

Autosomal dominant X-linked recessive

Autosomal recessive X-linked dominant
Autosomal: the gene responsible for the phenotype is located on one of the 22 pairs of
autosomes (non-sex determining chromosomes).
X-linked: the gene that encodes for the trait is located on the X chromosome.
Dominant: conditions that are manifest in heterozygotes (individuals with just one copy
of the mutant allele).
Recessive: conditions are only manifest in individuals who have two copies of the mutant
allele (are homozygous).
http://www.uvm.edu/~cgep/Education/Inheritance2.html
- which type of them is what we see in consanguinity marriages? (recessive)
if two copies of the gene must have the mutation for disease to result, the condition is termed AR
- Examples?
Table 47-2. Autosomal Recessive Diseases
Disease
Adrenal hyperplasia, congenital (CAH, 21-hydroxylase deficiency, CA21H, CYP21, cytochrome
P450, subfamily XXI)
Phenylketonuria (PKU, phenylalanine hydroxylase deficiency, PAH)
Cystic fibrosis (CF)
Friedreich ataxia (FA, frataxin)
Gaucher disease, all types (glucocerebrosidase deficiency, acid -glucosidase deficiency) (a
lysosomal storage disease)
Sickle cell disease (hemoglobin beta locus, beta 6 gluval mutation)

is thalasemia - types? alfa and beta

the most common type in jordan? beta
-Thalassemia is common in South East Asia. Individuals of South East Asian descent are also at
risk of having three or four genes deleted, resulting in hemoglobin H disease ( 4) or hydrops
fetalis with only Bart (4) hemoglobin. -Thalassemia occurs in 1.5% of African Americans and is a
common cause of microcytosis, either without anemia or with a mild hypochromic, microcytic
anemia.

types of beta? major and minor

-Thalassemia minor is prevalent throughout the Mediterranean region, the Middle East, India, and
South East Asia.

-Thalassemia Major (Cooley Anemia)

Etiology and Epidemiology.
-Thalassemia major is a hemoglobinopathy caused by mutations that impair beta chain synthesis.
Excess gamma and beta chains do not damage the RBCs, whereas excess alpha chain tetramers are
toxic. Because of unbalanced synthesis of alpha and beta chains, alpha chains precipitate within the
cells, resulting in RBC destruction either in the bone marrow or in the spleen when the cell is
released. Beta-Thalassemia major is seen most commonly in individuals of Mediterranean or Asian
descent. The clinical severity of the illness varies on the basis of the molecular defect.

- - presentations, symptoms of each?.....

Clinical Manifestations.
Signs and symptoms of -thalassemia major result from the combination of chronic hemolytic
disease, decrease in or absent production of normal hemoglobin A, and ineffective erythropoiesis in
the marrow. The anemia is severe and leads to growth failure and high output heart failure.
Ineffective erythropoiesis causes increased expenditure of energy and expansion of the bone
marrow cavities of all bones, leading to osteopenia, pathologic fractures, extramedullary
erythropoiesis, and an increase in the rate of iron absorption. Patients usually are transfusion
dependent before 12 months old.

- complication?
Adolescents are subject to complications from transfusion-related iron overload
(hemochromatosis), including nonimmune diabetes mellitus, cirrhosis, heart failure, bronzing of
the skin, and multiple endocrine abnormalities (of the thyroid or gonad).
- the complications of blood transfusion?
hemochromatosis - treatment, dose? Deferoxamine
- treatment of beta type? life long transfusion and in some cases splenectomy
Treatment.
Treatment of -thalassemia major is based on a hypertransfusion program that corrects the
anemia and suppresses the patient's own ineffective erythropoiesis, limiting the stimulus for
increased iron absorption. This suppression permits the bones to heal, decreases the metabolic
expenditures, increases growth, and limits dietary iron absorption.
Splenectomy may reduce the transfusion volume, but adds to the risk of serious infection.
Chelation therapy with deferoxamine, which removes excess iron and prolongs life, should start
when laboratory evidence of iron overload is present and before there are clinical signs of iron
overload. The amount of iron the patient acquires from transfusion may be estimated by the formula
stating that each milliliter of packed RBCs contains approximately 1 mg of iron.

- definitive treatment? BM transplant

Hematopoietic stem cell transplantation in childhood, before organ dysfunction induced by iron
overload, has had a high success rate in -thalassemia major and is the treatment of choice.

.. - how long do they live? what is the main cause of death? cardiac failure
in any case, the patients died after a few years of infection or heart failure.
Survival was better for patients born in more recent years, and for females, who were less likely to
die than males (relative risk= 0.65). An article from Cyprus, which appeared in a recent issue of this
journal, confirmed the now excellent survival of thalassemia patients, due especially to a decrease in
cardiac disease.5 Similar results have been reported for UK patients.6 The first cause of death, in all
series, continues to be heart failure, followed by infection. Splenectomy, in the past performed in
the first decade of life, is now delayed for as long as possible, in order to prevent previously
unrecognized infectious and thrombotic complications.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2833059/
Nelson essential of pediatrics 5E
Discussion about cystic fibrosis (from A---Z)
Cystic Fibrosis
ETIOLOGY AND EPIDEMIOLOGY
CF, an autosomal recessive disorder, is the most common life-limiting recessive genetic disease in
whites. In the U.S., 1 in 3200 white newborns is born with CF. CF is less common in African
Americans(1: 15,000), Asians (1 : 31,000), and other populations.
The gene for CF, localized to the long arm of chromosome 7, is a large gene that encodes a
polypeptide termed cystic fibrosis transmembrane regulator (CFTR). The most common
mutation is a specific deletion of three base pairs resulting in a deletion of phenylalanine at position
F508. Hundreds of mutations of the CFTR gene have been identified. Dysfunctional epithelial
transport is associated with the CFTR mutation, leading to the clinical manifestations of CF.
The secretory and absorptive characteristics of epithelial cells are affected. The CFTR is a chloride
channel and substantially regulates epithelial chloride and possibly sodium transport. The CFTR
involvement with chloride ion conductance is responsible for the elevated sweat chloride in 99% of
CF patients. How the abnormal chloride conductance accounts for the clinical manifestations of CF
is not completely understood. It may reduce the function of airway defenses or promote bacterial
adhesion to the airway epithelium.
CLINICAL MANIFESTATIONS
page 648

page 649
Table 137-1. Complications of Cystic Fibrosis
Respiratory
Bronchiectasis, bronchitis, bronchiolitis, pneumonia
Atelectasis
Hemoptysis
Pneumothorax
Nasal polyps
Sinusitis
Reactive airway disease
Cor pulmonale
Respiratory failure
Mucoid impaction of the bronchi
Allergic bronchopulmonary aspergillosis
Gastrointestinal
Meconium ileus
Meconium peritonitis
Distal intestinal obstruction syndrome (non-neonatal obstruction)
Rectal prolapse
Intussusception
Volvulus
Fibrosing colonopathy (strictures)
Appendicitis
Intestinal atresia
Pancreatitis
 Biliary cirrhosis (portal hypertension: esophageal varices, hypersplenism)
Neonatal obstructive jaundice
Hepatic steatosis
Gastroesophageal reflux
Cholelithiasis
Inguinal hernia
Growth failure (malabsorption)
Vitamin deficiency states (vitamins A, K, E, D)
Insulin deficiency, symptomatic hyperglycemia, diabetes
Malignancy (rare)
Other
Infertility
Delayed puberty
Edema-hypoproteinemia
Dehydration-heat exhaustion
Hypertrophic osteoarthropathy-arthritis
Clubbing
Amyloidosis
CF is a chronic, insidiously progressive disease exhibiting multiple complications related to viscous
mucus, malabsorption, and infection (Table 137-1). The respiratory epithelium of patients with CF
exhibits marked impermeability to chloride and an excessive reabsorption of sodium. These
alterations in the bioelectrical properties of the epithelium lead to a relative dehydration of the
airway secretions, resulting in impaired mucociliary transport and airway obstruction. Chronic
bronchial infection then develops. Most patients are colonized with Haemophilus influenzae,
Staphylococcus aureus, or Pseudomonas aeruginosa (which predominates in older patients with
advanced disease). Chronic bronchial infection leads to cough (the most common initial pulmonary
manifestation), sputum production, hyperinflation, bronchiectasis, and eventually pulmonary
insufficiency and death. Digital clubbing is common in patients with CF, even without significant
lung disease. Chronic sinusitis is nearly universal, and nasal polyposis is common.
Most patients with CF have exocrine pancreatic insufficiency early in life (if not at birth) as a
result of inspissation of mucus in the pancreatic ducts. Maldigestion with secondary malabsorption
results in steatorrhea (large, fatty, floating, foul-smelling stools) and many secondary deficiency
states (vitamins A, D, E, and K) in untreated patients. Nutrient malabsorption also results in failure
to thrive despite a ravenous appetite. Approximately 10% of patients are born with intestinal
obstruction resulting from inspissated meconium (meconium ileus). In older patients, intestinal
obstruction may occur because of maldigestion and thick mucus in the intestinal lumen (distal
intestinal obstruction syndrome). Such events may occur after dietary indiscretions or with
inadequate pancreatic enzyme replacement. In adolescent or adult patients, relative insulin
deficiency may develop. Hyperglycemia and CF-related diabetes may become symptomatic;
ketoacidosis is rare.
Inspissation of mucus in the reproductive tract leads to dysfunction. Secondary amenorrhea is often
present as a result of chronic illness and markedly reduced body weight. Women with CF have
given birth, however. Males are almost universally azoospermic, with atrophy or absence of the vas
deferens. The failure of the sweat ducts to conserve salt may lead to heat exhaustion or to
unexplained hypochloremic alkalosis in infants.
Pulmonary infections with certain virulent strains of Burkholderia cepacia are particularly difficult
to treat and may be associated with an accelerated clinical deterioration. Allergic
bronchopulmonary aspergillosis also may complicate CF lung disease and necessitate treatment
with steroids and antifungal agents. Other potential pulmonary complications of CF include
atelectasis, progressive bronchiectasis, hemoptysis, and pneumothorax.

DIAGNOSTIC STUDIES
page 649

page 650
Table 137-2. Indications for Sweat Testing
Respiratory
Chronic or recurrent cough
Chronic or recurrent pneumonia
Recurrent bronchiolitis
Recurrent or persistant atelectasis
Hemoptysis
Staphylococcal pneumonia
Pseudomonas aeruginosa in the respiratory tract (in the absence of such circumstances as
tracheostomy or prolonged intubation)
Mucoid P. aeruginosa in the respiratory tract
Gastrointestinal
Meconium ileus
Neonatal intestinal obstruction (meconium plug, atresia)
Steatorrhea, malabsorption
Hepatic cirrhosis in childhood (including any manifestations such as esophageal varices or portal
hypertension)
Pancreatitis
Rectal prolapse
Vitamin deficiency states (A, D, E, K)
Prolonged, direct-reacting neonatal jaundice
Miscellaneous
Digital clubbing
Failure to thrive
Family history of cystic fibrosis (sibling or cousin)
Salty taste when kissed; salt crystals on skin after evaporation of sweat
Heat prostration, especially under seemingly inappropriate circumstances
Hyponatremic hypochloremic alkalosis in infants
Nasal polyps
Recurrent sinusitis
Aspermia
Absent vas deferens
The diagnosis of CF should be considered seriously in any patient with chronic or recurring
respiratory or gastrointestinal symptoms. Indications for performing a sweat test are listed in Table
137-2. The following criteria must be met for the diagnosis to be established: the presence of one or
more typical phenotypic features of CF (chronic sinopulmonary disease, characteristic
gastrointestinal and nutritional abnormalities, salt loss syndromes, and obstructive azoospermia), a
sibling with a history of CF or a positive result from a newborn screening test, a positive result
obtained from a sweat test on two or more occasions (positive if >60 mEq/L with adequate sweat
collection of at least 75 mg, borderline if 40 to 60 mEq/L, and negative if <40 mEq/L), two
mutations known to cause CF identified, or a characteristic abnormality in ion transport across nasal
epithelium shown in vivo.
Although highly specific for CF, the sweat test is subject to numerous technical problems. False-
positive and false-negative (less common) sweat test results occur in a few well-defined clinical
states (Table 137-3). Other supportive tests, such as measurement of bioelectrical potential
differences across nasal epithelium, low levels of stool elastase, and detection of a known CF
mutation by DNA analysis, may be useful. Conventional commercial CF genotyping testing for
many mutations identifies 95% of all alleles. A patient without identified alleles still can have CF.
Heterozygote detection and prenatal diagnosis of children with F508 and more than 70 other
deletions is easily accomplished. Present testing identifies greater than 90% of carriers. Prenatal
detection of a known CF genotype may be accomplished by amniotic fluid or chorionic villus
sampling.

TREATMENT.
The treatment plan should be comprehensive and linked to close monitoring and early, aggressive
intervention.
Pulmonary Therapy.
The object is to clear secretions from airways and to control infection.
Inhalation Therapy.
Aerosol therapy is used to deliver medications and hydrate the lower respiratory tract. Metered-dose
inhalers can deliver some agents such as bronchodilators and corticosteroids, with a spacer for
younger children.

Airway Clearance Therapy.

This treatment usually consists of chest percussion combined with postural drainage and derives its
rationale from the idea that cough clears mucus from large airways, but chest vibrations are required
to move secretions from small airways where expiratory flow rates are low. Chest physical therapy
(PT) can be particularly useful for patients with CF because they accumulate secretions in small
airways first, even before the onset of symptoms.
Antibiotic Therapy.
Antibiotics are the mainstay of therapy designed to control progression of lung infection. The goal is
to reduce the intensity of endobronchial infection and to delay progressive lung damage.
ORAL ANTIBIOTIC THERAPY.
AEROSOLIZED ANTIBIOTIC THERAPY.
INTRAVENOUS ANTIBIOTIC THERAPY.
Bronchodilator Therapy.
Reversible airway obstruction occurs in many children with CF, sometimes in conjunction with
frank asthma or acute bronchopulmonary aspergillosis (see Chapter 234 ). Reversible obstruction is
defined as improvement of 15% in flow rates after inhalation of a bronchodilator. Many CF
patients may improve by only 510%, however. Nevertheless, subjective benefit is claimed by many
following a -adrenergic agonist aerosol. Cromolyn sodium or ipratropium hydrochlorides are
alternative agents, but their efficacy has not been studied systematically.
Anti-Inflammatory Agents.
Corticosteroids are useful for the treatment of allergic bronchopulmonary aspergillosis and severe
reactive airway disease occasionally encountered in children with CF.
Endoscopy and Lavage.
Treatment of obstructed airways sometimes includes tracheobronchial suctioning or lavage,
especially if atelectasis or mucoid impaction is present.
Other Therapies.
Expectorants such as iodides and guaifeusin do not effectively assist with the removal of secretions
from the respiratory tract. Inspiratory muscle training can enhance maximum oxygen consumption
during exercise as well as FEV1.
TREATMENT OF PULMONARY COMPLICATIONS.
A number of pulmonary complications require extra attention or special measures.
Atelectasis.
Lobar atelectasis occurs relatively infrequently; it may be asymptomatic and noted only at the time
of a routine chest radiograph. Aggressive intravenous therapy with antibiotics and increased chest
PT directed at the affected lobe may be effective.
Hemoptysis.
Small volume hemoptysis (<20 mL) should not trigger panic and is usually viewed as a need for
intensified antimicrobial therapy and chest PT. When the hemoptysis is persistent or increases in
severity, hospital admission is indicated. .
Pneumothorax.
Chest tube placement with or without pleurodesis is often the initial therapy. An open thoracotomy
or video-assisted thoracoscopy (VATS) with plication of blebs, apical pleural stripping, and basal
pleural abrasion should be considered if the air leak persists
Allergic Aspergillosis.
Treatment is directed at controlling the inflammatory reaction with oral corticosteroids and
preventing central bronchiectasis. For refractory cases, oral itraconazole may be required.
Bone and Joint Complications.
Hypertrophic osteoarthropathy causes elevation of the periosteum over the distal portions of long
bones and bone pain, overlying edema, and joint effusions. Acetaminophen or ibuprofen may
provide relief.
Sleep-Disordered Breathing.
Prompt treatment of airway symptoms and nocturnal oxygen supplementation or bilevel positive
airway pressure (BiPAP) support in selected cases should be considered.
Acute Respiratory Failure.
In addition to aerosol, postural drainage, and intravenous antibiotic treatment, oxygen is required to
raise the arterial Pao2. An increasing Pco2 may require ventilatory assistance. Endotracheal or
bronchoscopic suction may be necessary to clear airway inspissated secretions and can be repeated
daily. Right-sided heart failure should be treated vigorously. Recovery is often slow. Intensive
intravenous antibiotic therapy and postural drainage should be continued for 12 wk after the patient
has regained baseline status.
Chronic Respiratory Failure.
Most patients improve somewhat with intensive antibiotic and pulmonary therapy measures and
can be discharged from the hospital. Low-flow oxygen therapy is needed at home
Lung transplantation is an option for end-stage lung
Heart Failure.
Furosemide (1 mg/kg administered intravenously) induced diuresis confirms the suspicion of fluid
retention. Concomitant use of spironolactone may protect against potassium depletion and facilitate
long-term diuresis. Digitalis is not effective in pure right-sided failure, but may be useful when there
is an associated left-sided dysfunction. Intensive pulmonary therapy including intravenous
antibiotics is most important.
NUTRITIONAL THERAPY.
Up to 90% of patients have loss of exocrine pancreatic function and inadequate digestion and
absorption of fats and proteins. They require dietary adjustment, pancreatic enzyme replacement,
and supplementary vitamins. In general, children with CF need to exceed the usual required daily
caloric intake to grow. The target has been set at 130 Kcal/kg of body weight. Daily supplements of
the fat-soluble vitamins are required.
Diet.
Many infants at the time of diagnosis have nutritional deficits. A low-fat, high-protein, high-calorie
diet was generally recommended in the past for older children. Some children on this diet are
deficient in essential fatty acids. With the advent of improved pancreatic enzyme products, normal
to increased amounts of fat in the diet are usually tolerated and preferred.
Pancreatic Enzyme Replacement.
Extracts of animal pancreas given with ingested food reduce but do not fully correct stool fat and
nitrogen losses. Consequently, enzyme replacement should not exceed 2,500 lipase units/kg/meal in
most circumstances. One to 3 capsules/meal is sufficient for most patients; infants need 2,0004,000
lipase units per feeding, which is most easily given mixed with applesauce. Snacks should also be
covered. The microsphere preparations usually are sufficiently effective to permit a liberal diet,
which should include homogenized milk with vitamin D. The dose of enzymes required usually
increases with age, but some teenagers and young adults may later have a decrease in their
requirement.
Vitamin and Mineral Supplements.
Because pancreatic insufficiency results in malabsorption of fat-soluble vitamins (A, D, E, K),
vitamin supplementation is recommended.
TREATMENT OF INTESTINAL COMPLICATIONS.
Meconium Ileus.
When meconium ileus is suspected, a nasogastric tube is placed for suction and the newborn is
hydrated. In many cases, diatrizoate (Gastrografin) enemas with reflux of contrast material into the
ileum not only confirm the diagnosis, but have also resulted in the passage of a meconium plug and
clearing of the obstruction. Use of this hypertonic solution requires careful correction of water
losses into the bowel. Children in whom this procedure fails require operative intervention.
Distal Intestinal Obstruction Syndrome (DIOS, Meconium Ileus Equivalent) and Other Causes of
Abdominal Symptoms.
For intermittent symptoms, pancreatic enzyme replacement should be continued or even increased
and stool softeners (polyethylene glycol [Miralax] or docusate sodium [Colace]) given. Increased
fluid intake is also recommended. Failure to relieve symptoms signals the need for large-volume
bowel lavage with a balanced salt solution containing polyethylene glycol taken by mouth or by
nasogastric tube. When there is complete obstruction, a diatrizoate enema, accompanied by large
amounts of intravenous fluids, can be therapeutic.
Gastroesophageal Reflux
Because several factors raise intra-abdominal pressure, including cough and obstructed airways,
pathologic gastroesophageal reflux is not uncommon and may exacerbate lung disease secondary to
reflex wheezing and repeated aspiration. Dietary, positional, and medication therapy should be
considered. Cholinergic agonists are contraindicated because they trigger mucus secretion and
progressive respiratory difficulty. Reduction of stomach acid secretion can help, with proton pump
inhibitors being the most effective agents. Fundoplication is a procedure of last resort.
Rectal Prolapse (see Chapter 341.5 ).
The prolapsed rectum can usually be replaced manually by continuous gentle pressure with the
patient in the knee-chest position. Sedation may be helpful. To prevent an immediate recurrence, the
buttocks can be taped closed. Adequate pancreatic enzyme replacement, decreased fat and roughage
in the diet, stool softener, and control of pulmonary infection result in improvement. Occasionally, a
patient may continue to have rectal prolapse and require sclerotherapy or surgery.
Heptobiliary Disease.
Liver function abnormalities associated with biliary cirrhosis can be improved by treatment with
ursodeoxycholic acid.
Pancreatitis.
Pancreatitis can be precipitated by fatty meals, alcohol ingestion, or tetracycline therapy. Serum
amylase and lipase levels may remain elevated for long periods. Treatment is discussed in Chapter
348 .
Hyperglycemia.
Long-term vascular complications of diabetes can occur, providing an additional rationale for good
control of blood sugar levels.
OTHER THERAPY
Nasal Polyps.
Nasal polyps (see Chapter 375 ) occur in 1520% of patients with CF and are most prevalent in the
2nd decade of life. Local corticosteroids and nasal decongestants occasionally provide some relief.
Rhinosinusitis.
.
Salt Depletion.
Sweat salt losses can be high, especially in warm arid climates. Children should have free access to
salt, and precautions against overdressing infants should be observed.
Growth and Maturation.
Delayed growth should be vigorously addressed by enhancing nutrition, treating lung disease more
vigorously, and, in selected instances, endocrine evaluation and, possibly, growth hormone therapy.
Adolescents with CF should receive specific counseling through their developing years concerning
sexual maturation and reproductive potential.
- Nelson Textbook of Pediatrics-
------------------------------------------------------------------------------------------------------------------------
---------------
1st station: Dr mn aljeesh: x-rays 1.pneumothorax
2.double bubble sign .. what causes it and presentation and what trisomy associated
Duodenal atresia appears as a double-bubble sign (gas in the stomach and enlarged proximal
duodenum),
Approximately 10% of newborns with Down syndrome have gastrointestinal tract anomalies. The
three most common defects are duodenal atresia, annular pancreas, and imperforate anus
Clinical Manifestations
Intestinal atresia presents with a history of poly-hydramnios and with abdominal distention and
bilious vomiting in the neonatal period. If intestinal perforation is present, peritonitis and sepsis are
inevitable

Nelson essential of pediatrics 5E

3.diaphragmatic hernia .. most common site and treatment
A diaphragmatic hernia is defined as a communication between the abdominal and thoracic cavities
with or without abdominal contents in the thorax ( Fig. 101-9 ). The etiology may be congenital or
traumatic. The symptoms and prognosis depend on the location of the defect and associated
anomalies. The defect may be at the esophageal hiatus (hiatal), paraesophageal (adjacent to the
hiatus), retrosternal (Morgagni), or at the posterolateral (Bochdalek) portion of the diaphragm. The
term congenital diaphragmatic hernia (CDH) typically refers to the Bochdalek form. These lesions
may cause significant respiratory distress at birth, can be associated with other congenital
anomalies, and have a significant mortality and long-term morbidity. The overall survival from the
CDH Study Group is 67%. The Bochdalek hernia accounts for up to 90% of the hernias seen in the
newborn period, with 8090% occurring on the left side. The Morgagni hernia accounts for 26% of
congenital diaphragmatic defects. The size of the defect is highly variable, ranging from a small
hole to complete agenesis of this area of the diaphragm. The management strategy for a child with a
CDH has evolved from an emergent operation to deferred repair of the defect until pulmonary
hypertension is resolved.
Specific attention is focused on monitoring the systemic and pulmonary circulation, ventilation
strategies that stabilize the infant and avoid barotraumas, and long-term management of pulmonary
function
INITIAL MANAGEMENT.
Aggressive respiratory support is often needed in children with CDH. This will include rapid
endotracheal intubation, sedation, and possibly paralysis. Arterial (pre and postductal) and central
venous (umbilical) lines are mandated, as are a urinary catheter and nasogastric tube. A preductal
Sao2 of 85% or greater should be the minimum goal. Prolonged mask ventilation, which enlarges the
stomach and small bowel thus making oxygenation more difficult, should be avoided. Barotrauma is
a significant problem; therefore, peak inspiratory pressure (PIP) must be carefully monitored and
kept below 25. Permissive hypercapnea with a Paco2 of 4560 is helpful as long the pH is above 7.3.
Gentle ventilation with permissive hypercapnea reduces lung injury and mortality. Factors that
contribute to pulmonary hypertension (hypoxia, acidosis, hypothermia) should be avoided.
Echocardiography is a critically important imaging study that guides therapeutic decisions by
measuring pulmonary and system vascular pressures and defining the presence of cardiac
dysfunction
VENTILATION STRATEGIES.
Conventional mechanical ventilation, high frequency oscillation ventilation (HFOV), and
extracorporeal membrane oxygenation (ECMO) are the three main strategies to support respiratory
failure in the newborn with CDH.
Nitric oxide is a selective pulmonary vasodilator.
ECMO.
The availability of ECMO and the utility of preoperative stabilization have improved survival.
ECMO combined with paralysis and nasogastric suction may produce a dramatic reduction of the
volume of herniated viscera.
The duration of ECMO for neonates with diaphragmatic hernia is significantly longer (714 days)
than for those with persistent fetal circulation or meconium aspiration, and may last up to 24 wk.
SURGICAL REPAIR.
The ideal time to repair the diaphragmatic defect is under debate. Most centers will wait at least 48
hr after stabilization and resolution of the pulmonary hypertension. A requirement for only
conventional ventilation, a low PIP and Fio2 below 50 are good relative indicators of stability.
- Nelson Textbook of Pediatrics-
4.air under diaphragm .. perforated viscus if 3 weeks necrotizing enterocolitis
Pneumoperitoneum is pneumatosis (abnormal presence of air or other gas) in the peritoneal cavity,
a potential space within the abdominal cavity. When present, it can often be seen on radiography,
but small amounts are often missed, [1] and CT scan is nowadays regarded as a criterion standard in the
assessment of a pneumoperitoneum. CT can visualize quantities as small as 5 cm of air or gas.
The most common cause is a perforated abdominal viscus
Causes
Perforated duodenal ulcer - The most common cause of rupture in the abdomen. Especially of
the anterior aspect of the first part of the duodenum.
Perforated peptic ulcer
Bowel obstruction
Ruptured diverticulum
Penetrating trauma
Ruptured inflammatory bowel disease (e.g.[2]megacolon)
Necrotising enterocolitis/Pneumatosis coli
Bowel cancer
Ischemic bowel
Steroids
After laparotomy
After laparoscopy
Breakdown of a surgical anastomosis
Bowel injury after endoscopy
Peritoneal dialysis [3]
Vaginal insufflation (air enters via the fallopian tubes, e.g. water-skiing, oral sex )
Colonic or peritoneal infection
From chest (e.g. bronchopleural fistula)
Non-invasive PAP (positive airway pressure) can force air down duodenum as well as down
trachea.
https://en.wikipedia.org/wiki/Pneumoperitoneum
5.foreign body .. radioopaque bal3 msare

-some questions about direct and indirect hyperbilirubinemia

Table 62-1. Etiology of Unconjugated Hyperbilirubinemia
Hemolysis Present Hemolysis Absent
Common Blood group incompatibility: ABO, Physiologic jaundice, breast milk jaundice, internal
Rh, Kell, Duffy hemorrhage, polycythemia, infant of diabetic mother
Infection
Rare Red blood cell enzyme defects: Mutations of glucuronyl transferase enzyme
glucose-6-phosphate dehydrogenase, (Crigler-Najjar syndrome, Gilbert isease), pyloric
pyruvate kinase stenosis, hypothyroidism, immune
Red blood cell membrane disorders: thrombocytopenia
spherocytosis, ovalocytosis
Hemoglobinopathy: thalassemia

Table 62-2. Etiology of Conjugated Hyperbilirubinemia

 Common
Hyperalimentation cholestasis
CMV infection
Other perinatal congenital infections (TORCH)
Inspissated bile from prolonged hemolysis
Neonatal hepatitis
Sepsis
Uncommon
Hepatic infarction
Inborn errors of metabolism (galactosemia, tyrosinosis)
Cystic fibrosis
Biliary atresia
Choledochal cyst
1-Antitrypsin deficiency
Neonatal iron storage disease
Alagille syndrome (arteriohepatic dysplasia)
Byler disease

2nd station: Dr mahmood alshyab :

1.what do we send when we do LP and normal lab results
SPECIAL DIAGNOSTIC PROCEDURES
Cerebrospinal Fluid Analysis
Table 179-2. Analysis of Cerebrospinal Fluid
Normal Cerebrospinal Fluid Newborn >1 Month Old
Cell count 10-25/mm3 5/mm3
Protein <65-150 mg/dL <40 mg/dL
Glucose >2/3 blood glucose or >40 mg/dL >2/3 blood glucose or >60 mg/dL
Increased Polymorphonuclear and Decreased Cerebrospinal Fluid Glucose
Bacterial infection
Partially treated bacterial meningitis
Brain or parameningeal abscess
Parasitic infection
Leak of dermoid contents
 Increased Lymphocytes and Decreased Cerebrospinal Fluid Glucose
Mycobacterial infection (tuberculosis)
Fungal infection
Carcinomatous meningitis
Sarcoidosis
Increased Lymphocytes and Normal Cerebrospinal Fluid Glucose
Viral meningitis
Postinfectious disease (ADEM)
Vasculitis
Increased Cerebrospinal Fluid Protein
Infection
Venous thrombosis
Hypertension
Spinal block (Froin syndrome)
Guillain-Barr syndrome
Meningeal carcinomatosis
Mild Cerebrospinal Fluid Pleocytosis
Tumor
Infarction
Multiple sclerosis
Subacute bacterial endocarditis
Bloody Cerebrospinal Fluid
Subarachnoid hemorrhage
Subdural hemorrhage
Intraparenchymal hemorrhage
Hemorrhagic meningoencephalitis (group B streptococcus, HSV)
Trauma
Vascular malformation
Coagulopathy

Nelson essential of pediatrics 5E

2.lab called and told you its gram negative cocci what is this .. Neisseria meningitides
Neisseria meningitidis, often referred to as meningococcus, is a gram negative bacterium that can
cause meningitis and other forms of meningococcal disease such asmeningococcemia, a life-
threatening sepsis. The bacterium is referred to as a coccusbecause it is round, and more
specifically, diplococcus because of its tendency to form pairs
3.Give me the shapes of the following bacteria and if it is gram positive or negative for each
(staph, Hib, listeria)
Staphylococcus is a genus of gram-positive bacteria. Under the microscope, they appear round
(cocci), and form in grape-like clusters.[1]
Haemophilus influenzae is a Gram-negative, coccobacillary, facultatively anaerobic pathogenic
bacterium belonging to the Pasteurellaceae family.
Listeria
Listeria is a genus of bacteria that contains 10 species,[1][2] each containing two subspecies
. Listeria[3]species are gram-positive, rod-shaped, facultatively anaerobic, and non spore-
forming. The major human pathogen in the Listeria genus is L. monocytogenes. The disease
affects pregnant women, newborns, adults with weakened immune systems, and the elderly.
Listeriosis is a serious disease for humans; the overt form of the disease has acase-fatality rate of
about 20%. The two main clinical manifestations are sepsisand meningitis. Meningitis is often
complicated by encephalitis, when it is known as meningoencephalitis, a pathology that is unusual
for bacterial infections.
4. How to treat meningoccemia .. 3rd generation and vanco
Cephalosporins: Coverage and use
Third generation: less active against gram-positive organisms than the first generation
Meningitis, Sepsis, Pneumonia, UTI and many others
slide
5.why vanco .. resistance t 3rd generation
Vancomycin IV and PO, teicoplanin IV
Gram positive including MRSA and enterococcus
Meningitis
6.mechanism of action of vanco .. Vancomycin acts by inhibiting proper cell wallsynthesis in
Gram-positive bacteria. Due to the different mechanism by which Gram-negative bacteria produce
their cell walls and the various factors related to entering the outer membrane ofGram-negative
organisms, vancomycin is not active against Gram-negative bacteria (except some non-gonococcal
species of Neisseria).
7. Most common complication of miningococcemia Complications following meningococcal
disease can be divided into early and late groups. Early complications include: raised intracranial
pressure, disseminated intravascular coagulation, seizures, circulatory collapse and organ failure.
Later complications are: deafness, blindness, lasting neurological deficits, reduced IQ, and gangrene
leading to amputations 8.normal CSF results for new born
Slide abx and lecture note Meningitis

1st station ; mn el jesh ; - what are the causes of red urine? He wanted me to mention about
10...
Causes of hematuria could be either:
Causes that are not related to the urinary tract or the kidneys, or
Things related only to the urinary tract; lesions along the urinary tract and not related to the
glomrulus
itself, so outside the kidneys, [urinary tract not renal tract; you will notice the difference later
on ] or
Things inside the kidney either: glomerular or tubular [extra-glomerular], isolated or nephritis.
related to the urinary tract not to the Kidneys themselves could be:
stones,
infections, tumors,
obstructions,
traumas or
Extra-glomerular are like :
infections [pyelonephritis],
nephrocalcinosis which means calcification around the nephrons,
metabolic diseases like uric acid crystals,
stones,
hypercalciuria,
 tumors,
renal tract obstruction[renal tract not urinary tract; inside the kidney but outside the glomrulus
],
cystic kidney or
traumas and many others.
Glomerular diseases are the important ones to know and differentiate, we mention a way to
differentiate
them which is looking at the color of the urine, the shape of the RBCs, the presence of casts, clots
and
proteinuriaWe have a long list in this category but the important ones are:
Post-infectious glomerulonephritis.
IgA nephropathy.
Hereditary disorders and the most common one which is Alport Syndrome. Primary.
Benign recurrent which is also considered as hereditary.
Membrano-proliferative.
Others that are non-primary but associated with other diseases like SLE, Vasculitis
Renal hematuria could be:
Isolated Hematuria; which is mIcroscopic with no other signs or symptoms, or it could be
Nephritis; which is an inflammatory process in the glomeruli.
- how can we differentiate between them?
1- Urine color: hematuria that is related to the kidney itself or what we call glomerular hematuria
is
usually not bright in color, here the urine will be dark red or Pepsi-like color or brownish Coca-
Cola
color.
2- Blood clots: if we have glomerular hematuria its unlikely to find clots, blood clots are almost
absent in
patients urine who has glomerular hematuria, if you see clots usually its something extra-
glomerular.
3- RBCs shape: when you look at the RBCs in the glomerular disease they are dysmorphic
because they
had passed through small tubules and small capillaries.
4- RBC casts: casts are not usually present in the extra-glomerular disease, they are present in the
glomerular one.
5- Proteins: also proteins are not usually present in the patients urine having extra-glomerular
disease, they
are present in the glomerular diseases but sometimes we can find proteinuria in extra-glomerular
diseases
such as UTIs.
lecture note Hematuria
-what are the Causes of hypo- and hyper- calcemia, and what are the clinical manifestations
of each?
hypocalcemia
The clinical manifestations of hypocalcemia (ionized calcium <4.5 mg/dL; total calcium <8.5
mg/dL if serum protein is normal) result from increased neuromuscular irritability and include
muscle cramps, carpopedal spasm (tetany), weakness, paresthesia, laryngospasm, or seizure-like
activity (patient is often awake and aware during these episodes, in contrast to many episodes of
epilepsy). Latent tetany can be detected by the Chvostek sign (facial spasms are produced by lightly
tapping over the facial nerve just in front of the ear) or by the Trousseau sign (carpal spasms are
exhibited when arterial blood flow to the hand is occluded for 3 to 5 minutes with a blood pressure
cuff inflated to 15 mm Hg above systolic blood pressure). Total serum calcium concentration is
usually measured, although a determination of serum ionized calcium (approximately half the total
calcium in normal circumstances), the biologically active form, is preferable. Albumin is the major
reservoir of protein-bound calcium. Disorders that alter plasma pH or serum albumin concentration
must be considered when circulating calcium concentrations are being evaluated. The fraction of
ionized calcium is inversely related to plasma pH; alkalosis can precipitate hypocalcemia by
lowering ionized calcium without changing total serum calcium. Alkalosis may result from
hyperpnea caused by anxiety or from hyperventilation related to physical exertion. Hypoproteinemia
may lead to a false suggestion of hypocalcemia because the serum total calcium level is low even
though the ionized Ca2+ remains normal. It is best to measure serum ionized calcium if
hypocalcemia or hypercalcemia is suspected.
causes
Primary hypoparathyroidism
Pseudohypoparathyroidism
Hypomagnesemia may cause a secondary hypoparathyroidism
The etiology of hypocalcemia usually can be discerned by combining features of the clinical
presentation with determinations of serum ionized calcium, phosphate, alkaline phosphatase, PTH
(preferably at a time when the calcium is low), magnesium, and albumin. X-rays of the long bones
and hands and knees are important if the problem occurs after the neonatal period. If the PTH
concentration is not elevated appropriately relevant to a low serum calcium, hypoparathyroidism
(transient, primary, or caused by hypomagnesemia) is present. Vitamin D stores can be estimated by
measuring serum 25-hydroxyvitamin D and renal function assessed by a serum creatinine
measurement or determination of creatinine clearance

Nelson essential of pediatrics 5E

hyper- calcemia
Etiologies vary by age and other factors.
Neonates

o Neonatal primary hyperparathyroidism can begin as soon as the parathyroid glands,

functional in the first trimester of pregnancy, become hyperplastic.
Infants have malaise, constipation, and vomiting; serum calcium and parathyroid
hormone (PTH) concentrations are elevated, and serum phosphate concentration
is decreased. Aminoaciduria occurs. Rarification of bones leads to easier
fracturing.
Rehydration with isotonic sodium chloride solution and forced diuresis with
furosemide are urgently required, as well as administration of subcutaneous
calcitonin. Common side effects of subcutaneous calcitonin include facial
flushing, nausea, and vomiting.
Definitive treatment is performed by means of surgical resection, often with
reimplantation of a small amount of tissue into a more accessible ectopic site (eg,
forearm).
Neonatal primary hyperparathyroidism stems from a homozygous inactivating
mutation in a calcium-sensing receptor.
o Familial hypocalciuric hypercalcemia (FHH) is an autosomal dominant heterozygous
mutation of the same calcium receptor-sensing gene (CASR) that is abnormal in the
homozygous state in neonatal primary hyperparathyroidism.
If symptoms are observed (eg, chondrocalcinosis, pancreatitis, renal disease,
neuropsychiatric disease), they generally begin in the neonatal period; however,
patients are often asymptomatic. If the patient is asymptomatic, no treatment is
 required.
Because of the mutation, levels of calcium that are higher than usual are required
to decrease secretion of PTH. The serum PTH concentration, although within the
reference range, is inappropriately high for the degree of hypercalcemia.
Other laboratory findings include a decreased or normal serum phosphorus level,
an increased magnesium level in 50% of babies, normal levels of alkaline
phosphatase and serum 25-hydroxyvitamin D, and an appropriate level (to the
PTH) of 1,25-dihydroxyvitamin D. Serum calcium levels rarely rise above 14
mg/dL. Urine calcium excretion is decreased to less than 200 mg/d, but the level
of urine cyclic adenosine monophosphate (cAMP) is normal.
Radiographic findings are normal.

o Excessive supplementation of calcium causes hypercalcemia.

o Williams syndrome, which is associated with a deletion of elastin genes on

chromosome 7, occurs as transient[4]neonatal hypercalcemia, perhaps secondary to
increased sensitivity to vitamin D. The syndrome is associated with characteristic
elfin facies, mental retardation, andsupravalvar aortic stenosis. Generally,
hypercalcemia is symptomatic, with poor feeding and constipation, and spontaneously
remits by age 9-18 months. Treatment is a dietary restriction of calcium to 100 mg/d
and limited vitamin D intake. Hydrocortisone at 10-25 mg/kg/d or calcitonin is
sometimes helpful.
o Severe autosomal recessive hypophosphatasia is a disease of bone mineralization due
to a deficiency in tissue nonspecific alkaline phosphatase (TNSALP). Associations
vary from rachitic changes to fetal death. These children require a low-calcium high-
phosphate diet.
o Secondary hyperparathyroidism is a neonatal response to maternal hypocalcemia with
similar symptoms to primary hyperparathyroidism, except that the child undergoes a
progression from hypocalcemia to normocalcemia to hypercalcemia quickly after birth.
PTH is generally elevated. During the first few months, the parathyroid glands and
skeletal lesions normalize; therefore, only symptomatic nonsurgical treatment is
required.
o Idiopathic infantile hypercalcemia is a poorly understood disorder possibly related to
nonmalignancy-associated PTH-related protein (PTHrP), which spontaneously
resolves by age 12 months.
o Blue diaper syndrome is a selective defect in the intestinal transport of tryptophan. The
diagnosis is confirmed by analyzing urine indoles.
o Jansen metaphyseal chondrodysplasia is a rare disease of endochondral bone formation
characterized by short stature, leg bowing, short-limbed dwarfism, and a waddling gait.
Neonatally, these children appear normal but have radiographic and laboratory
abnormalities. In early childhood, the external changes become more obvious. The
condition arises from an activating mutation in the PTH/PTHrP receptor. Radiographic
findings reveal cupped and ragged metaphyses and osteitis fibrosa cystica, and
laboratory findings reveal a serum calcium level of 13-15 mg/dL, a low phosphate
level, a high level of 1,25-dihydroxyvitamin D, a high alkaline phosphatase level, and
urine hydroxyproline.
Infants: Subcutaneous fat necrosis, which manifests in neonate as violaceous plaques or
nodules overlying fatty areas, can lead to life-threatening hypercalcemia at age 1-6 months. It
is likely mediated by prostaglandin E (PGE) or due to macrophage production of 1,25-
dihydroxyvitamin D. Treatment includes corticosteroids and symptomatic support of patient.
School-aged children
o Hyperparathyroidism secondary to parathyroid adenoma or autosomal dominant
hereditary hyperparathyroidism is a rare problem in older children. Children may be
asymptomatic or symptomatic withconstipation and personality changes. Levels of
urine and serum calcium are high, whereas the serum phosphorus level is low and urine
phosphorus level is high. Unlike in most forms of hypercalcemia, which are associated
with systemic alkalosis, patients with hyperparathyroidism tend to have acidosis. This
acidosis is due to a loss of bicarbonate in the urine, giving a picture consistent with
renal tubular acidosis. Radiographic findings of osteitis fibrosa cystica may be present.
 Treatment is surgical, and corticosteroids have no role.[5]
o Multiple endocrine neoplasia (MEN) type 1 (ie, Wermer syndrome) is a rare autosomal
dominant constellation of hyperparathyroidism, pancreatic tumors, and pituitary tumors
treated by subtotal parathyroidectomy. Molecular diagnosis is now available for MEN
types 1 and 2.
General factors
o Malignancies produce hypercalcemia much less frequently in the pediatric patients than
in adults. However, pediatric malignancies that can elevate calcium include the
following:
Non-Hodgkin lymphoma or Hodgkin lymphoma

Ewing sarcoma

Neuroblastoma
[6]
Langerhans cell histiocytosis

Rhabdomyosarcoma with metastases to breast or bone marrow in adolescents

Ovarian small cell carcinoma in adolescents

Renal tumors with rhabdoid histology in infants

o Three different mechanisms are responsible, and resultant laboratory abnormalities

slightly differ.
Primarily in leukemia, PTHrP increases osteoclast resorption of bone, renal
reabsorption of calcium, and renal loss of phosphorous, leading to decreased
serum phosphate levels, increased urinary cAMP, and detectable PTHrP.
Burkitt lymphoma and multiple myeloma, as well as bony tumors or sarcomas
with bony metastases, can cause cytokine-mediated bone resorption.
Hodgkin and non-Hodgkin lymphoma may cause increased intestinal absorption
of calcium via production of 1,25-dihydroxyvitamin D by macrophages, which
contain 1-alpha-hydroxylase activity, and may maintain a normal serum
phosphorus level.
o Generally, patients with malignancy-induced hypercalcemia have decreased chloride
levels, alkalosis, increased BUN levels, increased uric acid levels, urine calcium levels
higher than 400 mg/dL, and increased urine cAMP levels. Serum alkaline phosphatase
levels may be elevated, and serum PTH levels are decreased, except in the uncommon
setting of direct stimulation of PTH production by the tumor. Serum calcium levels
greater than 14 require treatment, primarily with hydration and steroids at a dose of
1.5-2 mg prednisone equivalent/kg/d for several days.
o Thyrotoxicosis can cause sufficient bone resorption to increase serum calcium in 20%
of cases. In these patients, thyrotoxicosis can also decrease serum PTH and increase
urine excretion of cAMP and calcium. Although hypercalcemia is rarely subjectively
symptomatic to the patient, it can lead to nephrocalcinosis and renal failure. This
condition is rare in childhood, but it is possible in neonates of mothers with Graves
disease or in older children who develop Graves disease.
o Granulomatous disease, including sarcoidosis, tuberculosis (TB),Wegener disease,
berylliosis, and Pneumocystis carinii pneumonia, may cause hypercalcemia via
overproduction of 1,25-dihydroxyvitamin D by macrophages and increased extrarenal
alpha1-hydroxylase activity.
o Adrenal insufficiency can decrease the renal clearance of calcium.

o Hypercalcemia may appear in the oliguric phase of acute renal failure due to the PTH
increase stimulated by hyperphosphatemia. Also, children with renal failure treated [7]
with calcitriol for secondary hyperparathyroidism can develop a mild hypercalcemia.
o Immobilization can cause hypercalcemia.
 Medication and iatrogenic causes
o Total parenteral nutrition may cause hypercalcemia.
o Vitamin D intoxication due to ingestion of more than 50 mcg/d in infants or more than
500 mcg/d in adults can cause hypercalcemia, even in the absence of a markedly
elevated 1,25-dihydroxyvitamin D. Symptoms of hypercalcemia, including
hypertension, aortic valvular sclerosis, retinopathy, renal damage, and bony
abnormalities, can also occur 1-3 months after a large overdose of vitamin D. Serum
PTH is decreased. Levels of water-soluble preparations can drop quickly, but
hypercalcemia from an excess intake of fat-soluble preparations may persist for
months.
o Vitamin A in high doses, such as those found in retinoid therapy for acne, can directly
stimulate bone resorption by functioning as a transcription factor in osteoclast
stimulation. Trans -retinoic acid, used for treatment of some leukemias, can[8]
elevate
calcium with this mechanism, particularly when coupled with voriconazole.
o Thiazide diuretics (eg, Diuril) may cause hypercalcemia because of their action on the
distal tubule.
o Lithium causes a mild increase in serum calcium, which can occasionally increase
further in the few months after cessation of the drug secondary to parathyroid
hyperplasia or adenoma.
o Tamoxifen and oral contraceptives can exacerbate existing hypercalcemia.

o Milk-alkali syndrome (ie, Burnett syndrome) from exogenous ingestion of calcium-

containing antacids leads to renal insufficiency and metastatic calcinosis with increased
phosphorus levels, increased levels of 1,25-dihyroxyvitamin D, decreased PTH levels,
normal levels of serum alkaline phosphatase, normal urine calcium levels, and
decreased urine phosphate levels.[9] If continued over time, this may lead to
osteomalacia. This condition is particularly sensitive to the development of
hypocalcemia following treatment with bisphosphonates.
o Theophylline can cause increases in calcium via beta-adrenergic stimulation. This may
be treated with propranolol.
o Oral dietary phosphate deficiency may cause hypercalcemia.

o Vitamin-D receptor modulators (eg, paricalcitol) are newer medications used to treat
malignancy and hyperparathyroidism, which can increase serum calcium levels.

Hypercalcemia can cause symptoms at levels as low as 12 mg/dL and consistently causes symptoms
at 15 mg/dL. Hypercalcemia initially and predominantly affects the GI and nervous systems.
Symptoms include the following:
Nervous system

o Personality changes

o Malaise

o Headache

o Hallucinations
o Unsteady gait

o Proximal muscle weakness

o CNS depression

o Irritability

o Confusion

GI system

o Hypercalcemia can cause a paralytic ileus, with resultant abdominal cramping,

 constipation, anorexia, nausea, and vomiting.
o Ectopic calcification can lead to symptoms of pancreatitis, with epigastric pain and
vomiting.
o Increased gastric acid secretion may produce symptoms consistent with gastritis.
Renal symptoms

o Renal stones

o Nephrogenic diabetes insipidus (DI) with polyuria and polydipsia

o Renal failure

Musculoskeletal system - Bone pain

Ectopic calcification

o Pruritus

o Conjunctivitis

Miscellaneous symptoms

o Congenital deformity

o Other symptoms of malignancy

o Symptoms of other underlying causes of hypercalcemia

[
o Hypercalcemia-associated acute respiratory distress syndrome (rare)

Physical
See the list below:
Vital signs include the following:

o Bradycardia

o Possible hypertension

Neurologic examination findings include the following:

o Depressed sensorium

o Confusion

o Gait disturbances
o Hyporeflexia

o Proximal muscle weakness

Even at lower levels, patients can have renal failure and ectopic calcification, including renal
stones and pancreatitis.
Ectopic calcification can also manifest as conjunctivitis or band keratopathy on eye
examinations.
Neonates may be asymptomatic or may have vomiting, hypotonia, hypertension, or seizures.
At levels of 17 mg/dL, calcium phosphate precipitation through the blood and soft tissues can
lead to coma or lethal cardiac arrest.
Hypercalcemia is often asymptomatic. If hypercalcemia is symptomatic, the differential
diagnosis rests heavily on the predominating symptom.
Weakness and altered sensorium may be symptomatic of a myriad of neurologic disorders, as
well as toxins (eg, organophosphate poisoning),lupus, or thyroid dysregulation.
Weakness alone may be confused with hypokalemia, whereas ataxia is found in phenytoin
 overdoses, mass lesions, stroke syndromes, and encephalitides.
Hypertension may indicate a cardiac or renal problem.
Many manifestations of hypercalcemia (eg, pancreatitis, renal stones, gastritis, conjunctivitis)
may be caused by etiologies different from hypercalcemia.
http://emedicine.medscape.com/article/920955-clinical#b5

2nd : fesal Q ; - Take brief hx about stridor of 1 day duration ? - What's the dx . croup
Clinical manifestations:
- It starts with several days of rhinorrhea, pharyngitis, low-grade fevers and a mild cough.
- Over the next 12 to 48 hours, a progressively worsening "barky" cough, hoarseness and
inspiratory stridor are noted.
>> The onset is often rapid and typically in the early morning hours; croup symptoms
appear to subside during the day (possibly because of positioning), only to recur the
following night.
A child with significant stridor presenting during daylight, maybe more seriously affected.
Etiology:
Parainfluenza virus types I, II, III and IV are thought to be responsible for about 80%
of cases, with type I causing 5070% of severe cases
Respiratory syncytial virus
Adenovirus
Rhinovirus
Enterovirus
Measles
Influenza A & B (type A associated with severe disease)
Mycoplasma pneumoniae is thought to cause the condition very rarely

... -what's the indication of admission ?

Depressed sensorium
Cyanosis
Hypoxia
Pallor
Progressive stridor
Respiratory distress
Restlessness
Toxic-appearing
Wts the rx ?
Steroids
Racemic Epinephrine
Cool Mist
Antibiotics
No role
Use only recommended if bacterial complications exist
Decongestants/antihistamines
No evidence to support their use
Heliox
 Theoretical, not proven
Intubation-If needed
Slide acute upper airway obstruction

-Then another case of 6 weeks vomiting ? Take hx ? Dx?... pyloric stenosis . other ddx ?
...investigations ? lab results? Treatment ?
Laboratory and Imaging Studies
Repetitive vomiting of purely gastric contents results in loss of hydrochloric acid; the classic
laboratory finding is a hypochloremic hypokalemic metabolic alkalosis with elevated BUN
secondary to dehydration. Jaundice with unconjugated hyperbilirubinemia also occurs. Plain
abdominal x-rays typically show a huge stomach and diminished or absent gas in the intestine (Fig.
128-2). Ultrasound examination of the pylorus shows marked elongation and thickening of the
pylorus (Fig. 128-3). A barium upper GI series also may be obtained whenever doubt about the
diagnosis exists; this shows a "string sign" caused by barium moving through an elongated,
constricted pyloric channel.
Treatment
Treatment of pyloric stenosis includes IV fluid and electrolyte resuscitation followed by
surgical pyloromyotomy. Before surgery, dehydration and hypochloremic alkalosis must
be corrected, generally with an initial normal saline fluid bolus followed by infusions of
half-normal saline containing 5% dextrose and potassium chloride when urine output is
observed. For pyloromyotomy, a small incision is made, usually directly over the
pylorus or at the umbilicus, and the pyloric muscle is incised longitudinally to release the
constriction. Care is taken not to cut into the mucosa itself.

ddx
128 Esophagus and Stomach
GASTROESOPHAGEAL REFLUX
ESOPHAGEAL ATRESIA AND TRACHEOESOPHAGEAL FISTULA
ESOPHAGEAL FOREIGN BODIES
CAUSTIC INJURIES AND PILL ULCERS
PYLORIC STENOSIS
PEPTIC DISEASE
MIDGUT MALROTATION
INTESTINAL ATRESIA
OTHER CONGENITAL DISORDERS
INFLAMMATORY BOWEL DISEASE
CELIAC DISEASE
MILK AND SOY PROTEIN INTOLERANCE
INTUSSUSCEPTION
APPENDICITIS ---------------------------------------------------------------------------------------------------
------------------------------------
1st station : Dr WaeL Hayag... 6 year old male pt presented to ER with fever of 1 day duration
....take Hx PE and InVes... ( in Hx pt has vomtinig + drowsy + decrease eating and in PE
...general mild dehydrated, CNS positive kernig test other system was normal + suspected
menengitis and + Investi fundoscopy then LP then start rehydration and AB 3rd genearation
cepha and Vancomycin ) he said csf was protien 70 and glucose was decreased ... -->> bacterial
gram stain +ve diplooccicici so strep pneumonia .... the he says the pt after 2 days still has
fever -- what happen ? --- wrong dose -- he said no wrong dose --->> sub durral empyema
abcess .. Rx drainge
Subdural empyema was diagnosed in 28 of 1,034 episodes (2.7%), and was present on admission in
10 episodes and diagnosed during admission in 18. Predisposing conditions were present in 26
patients (93%), and consisted of otitis or sinusitis in 21 patients (75%). In all these patients the otitis
or sinusitis spread to the subdural space. Twenty-three patients (82%) presented with neurologic
symptoms (paresis, focal seizures, dysesthesia contralateral to the empyema). Streptococcus
pneumoniae was identified in 26 patients (93%) and Streptococcus pyogenes in 1 (3%); 1 patient
had negative CSF cultures. Clinical course was frequently complicated with seizures (50%), focal
neurologic abnormalities (54%), and hearing impairment (39%), causing an unfavorable outcome in
19 episodes (68%). Neurosurgical evacuation of the empyema was performed in 5 patients, all with
considerable midline shift.
CONCLUSIONS:
Although rare, subdural empyema must be considered in patients with community-acquired
bacterial meningitis and otitis or sinusitis, focal neurologic deficits, or epileptic seizures. S
pneumoniae is the predominant causative organism and neurosurgical intervention should be
regarded as first-choice therapy in patients with empyema causing midline shift and focal
neurologic abnormalities or a decreased level of consciousness.
http://www.ncbi.nlm.nih.gov/pubmed/23136260
BAs usually require drainage in addition to appropriate microbial therapy, so early neurosurgical
consultation is recommended.[2]
Although BA is essentially a surgical pathology, Arlotti et al.[75] recommend that choice of patients
for a medical approach must be made on an individual basis. These authors consider best candidates
for medical treatment to be those with a small abscess (<2.5 cm), in good initial clinical condition
(GCS > 12), and for whom the etiology is well-known (microorganism isolated from material other
than the abscess pus) recommendation grade C; or in the case of multiple abscesses, after surgery of
abscesses >2.5 cm or surgery of abscesses that cause a mass effect, or in patients at serious risk of
operation even if in these, the final decision must consider that the prognosis is often bad in any
case recommendation grade D.
2nd station : Dr... rola
1 year old male not compalaling from anything come for check up only with his mother ...
what u will do
about everything.. by HX : ask about FTT, reccurent infection, blood transfusion, allergy,
medical diseases, ask about what u want
PE : vital signs, Growth parameter + milestone (what appropriate for this age), general exam
,, exam for all the system ,,
------------------------------------------------------------------------------------------------------------------------
---------------
1st station : Dr. Samah :
9 Y/O presented with headache "meningitis" hx..PE..investigations..LP
contraindications..signs of increased ICP in this ptn..findings on CSF analysis..differentiate
b/w viral and bacterial.
WBC: <5 cells / mm3 normally mostly lymphocytes , in neonatal period it is
acceptable if less than 25 .
-in bacterial meningitis : 100-60,000(PMNs predominate)
- in viral meningitis : Mildly increased(Up to 1000)
*RBC : <5 normal, and in meningitis either bact.or virus =zero
*Glucose: 50-75%of Blood Glucose this is normal
-in bacterial meningitis : Decreased<40%
- in viral meningitis :normal
* Protein: 20-40 mg/dL normally
-in bacterial meningitis :increased
- in viral meningitis : Normal or Mildly Increased
*Gram stain :negative normally and in viral meningitis , only positive in bacterial
meningitis .
Gram stain (CIA-S) crystal violet iodine- alcohol-sulfer stain
Absolute contraindications to lumbar puncture are as follows:
o Unequal pressures between the supratentorial and infratentorial
compartments, usually inferred by characteristic findings on the brain CT
scan:
o Midline shift
o Loss of suprachiasmatic and basilar cisterns
o Posterior fossa mass
o Loss of the superior cerebellar cistern
o Loss of the quadrigeminal plate cistern
o Infected skin over the needle entry site
Relative contraindications to lumbar puncture are as follows:
Increased intracranial pressure (ICP)
Coagulopathy
Brain abscess
Symptoms
Infants:
Drowsiness
Separated sutures on the skull
Bulging of the soft spot on top of the head (bulging fontanelle)
Vomiting
Older children and adults:
Behavior changes
Decreased consciousness

Headache

Lethargy
Neurological symptoms, including weakness, numbness, eye movement problems, and double
vision
Seizures

Vomiting

https://www.nlm.nih.gov/medlineplus/ency/article/000793.htm

2nd station : 2 Y/O severe diarrhea and vomiting presented with drowsiness "hypovolemic
shock" .. What are you going to do "assessment and management" (hypernatremic)
volume depletion :
volume depletion occurs when you loose more than what you get
example : polyurea or diarrhea without adequate oral replacement
result : hypovolemia
conditions leading to this imbalance:
1) Decreased fluid ingestion : anorexia , coma , vomiting
2) Loosing fluids :polyurea , diarrhea , skin loss (e.g : burns)
we have to:
-determine the degree of dehydration : to asses whether the situation is
urgent or not and to calculate the amount to be given
-determine the type of fluid lost : to know the type of fluid we should
give and the duration [we know the type by measuring the level of Na
in blood.]
the type and duration of the fluid to be given to the patient is
determined by the amount of Na lost:
1) isonatremic dehydration :loss of Na + water
2) hyponatremic dehydration : more Na loss than water loss
3) hypernatremic dehydration : more water loss than Na loss
Treatment of hypernatremic dehydration :
We have to go into 3 steps :
1) give the patient his maintenance (the amount that is normally
needed)
2) replace the deficits (the already lost fluids)
3) decrease the elevated Na levels
*put in your mind that we shouldnt decrease Na levels more than 0.5-1
mEq/hour or more than 10mEq/day , otherwise the patient will
develop sever complications like cerebral edema (because fluids pass
the BBB faster than electrolytes ) . so always avoid rapid drop of Na
level and only decrease it by 10 mEq/day or a maximum of 12 mEq/day
.(put the bold sentence deep in your head)
*in sever cases we start by giving the patient normal saline boluses ( 1
or 2 bluses) until his condition becomes more stable , and here in bolus
treatment we dont look for Na concentration because normal saline
contains 154mEq/l and this will be less than his current Na level and will
not increase
------------------------------------------------------------------------------------------------------------------------
---------------
1st station: Doc from al-jeish neonate came because of seizure. what do you do. (approach to
status epilepticus)
a good history
what is the first thing that you noted
Setting, provoking factors
Responsiveness during event
Exact description of event
Sequence of events
Postictal phenomena
Paroxysmal nature
Stereotypical nature of recurrences
Seizure characteristics
With generalized movements there is altered consciousness
Stereotypical events
Cannot be provoked, suppressed or altered
Waking child from sleep
Postictal alteration in level of consciousness
Versive movements, tongue biting, incontinence
Antiepileptic Drugs (AEDs)
Broad-Spectrum Agents
Valproate
Lamotrigine
Topiramate
Levetiracetam
Narrow-Spectrum Agents
Partial onset seizures
Carbamazepine
Gabapentin
Phenytoin
Oxcarbazepine
Absence
Ethosuximide
causes of stridor. epiglottitis - clinical features. what to do. what not to do.
Do not upset the child.
 Do not examine the mouth.
Do not insert an I.V. cannula until the child is anesthetized.
Abrupt onset - usual duration of illness before hospitalization < 24 hours.
Stridor and labored respirations.
Febrile - often > 39.0 C.
Sore throat and reluctant to speak or swallow.
Aphonia, hoarseness, muffled voice
Anxious appearance.
Prefer sitting position, with jaw thrust forward
Cyanosis in later stages.
Drooling.
Tachycardia.
Tachypnea (but rarely > 40 b/min).
Retractions
INVESTIGATIONS
Labs/X-ray - may be obtained only after airway is secured!
CBC - elevated WBC with bandemia.
Blood cultures - positive 80 - 90%.
Culture of epiglottis - positive in about 50%. Caution - make sure the lab does not set this up
as a routine throat CX.
Meningitis occurs uncommonly (2-3% of cases). Consider LP in the OR in children with
signs and symptoms of meningitis
2nd station: Doc hala & another doc 2year old patient came with rapid breathing for 2hours.
take hx & what do u think the cause is: - epiglotitis (same abve)
- angioedema - she ask the clinical features & management
Cases where angioedema progresses rapidly should be treated as a medical emergency, as airway
obstruction and suffocation can occur. Epinephrine may be life-saving when the cause of
angioedema is allergic.
The skin of the face, normally around the mouth, and the mucosa of the mouth and/or throat, as well
as the tongue, swell over the period of minutes to hours. The swelling can also occur elsewhere,
typically in the hands. The swelling can be itchyor painful. There may also be slightly decreased
sensation in the affected areas due to compression of the nerves. Urticaria (hives) may develop
simultaneously.
In severe cases, stridor of the airway occurs, with gasping or wheezy inspiratory breath sounds and
decreasing oxygen levels.
Tracheal intubation is required in these situations to prevent respiratory arrest and risk of death.
Patients with HAE can also have recurrent episodes (often called "attacks") of abdominal pain,
usually accompanied by intense vomiting, weakness, and in some cases, watery diarrhea, and an
unraised, nonitchy splotchy/swirly rash. These stomach attacks can last one to five days on average,
and can require hospitalization for aggressive pain management and hydration.
HAE may also cause swelling in a variety of other locations, most commonly the limbs, genitals,
neck, throat and face. The pain associated with these swellings varies from mildly uncomfortable to
agonizing pain, depending on its location and severity. Predicting where and when the next episode
of edema will occur is impossible. Most patients have an average of one episode per month, but
there are also patients who have weekly episodes or only one or two episodes per year. The triggers
can vary and include infections, minor injuries, mechanical irritation, operations or stress. In most
cases, edema develops over a period of 1236 hours and then subsides within 25 days.
- foreign body aspiration - she ask the hx suggesting it (choking)
- heart failure - she ask the signs of heart failure in physical exam in -
Clinical findings may include hypotension, cool extremities with poor peripheral perfusion, a
thready pulse, and decreased urine output.
Chemical evidence of renal and liver dysfunction may be present, as well as a diminished level of
consciousness.
Children with uncompensated congestive heart failure, particularly older children, generally have a
lower cardiac output than that which most experienced clinicians would estimate on the basis of the
clinical signs.
Signs and symptoms of congestive heart failure include the following:
Tachycardia
Venous congestion - Right-sided (hepatomegaly, ascites, abdominal pain, pleural effusion,
edema, jugular venous distention); left-sided (tachypnea, retractions, nasal flaring or grunting,
rales, pulmonary edema)
Low cardiac output - Fatigue or low energy, pallor, sweating, cool extremities,
nausea/vomiting, poor growth, dizziness, altered consciousness, and syncope

DKA. then asked the management of DKA from top to bottom. if the patient came at
admission 500mg/dL, how many hours do we need to correct this? and the complication if we
lower the glucose too rapidly.
Phase1 Rehydration and treatment of Ketoacidosis; we start rehydration by
giving boluses of normal saline (20 cc/kg) then we calculate as 10% dehydra%on
patients, when we shift to treat Ketoacidosis we shouldn't use NAHCO3 (sodium
bicarbonate) unless the PH is less than 7.2 some people says less than 7.1 and that
because those patient already have brain edema at time of presentation so if we
administer sodium bicarbonate we will exacerbate the edema and could lead to
herniation.
Phase2 Transitional period where we try to control glucose level, we start this
phase in the 2nd hour of the management by start giving insulin to those
pa%ents, insulin dose will be 0.1 unit/kg IV and we keep monitoring glucose level
every 1/2 an hour, we need also to do blood test for Potassium, phosphorus &
Sodium, sometimes the patient will have low total body potassium even that
its level in the blood is normal so we have to added some potassium and
phosphorus to their fluid and usually we do this after they pass urine, and in
addition to that we have to check the urine of the patient weather it contain
Ketone bodies or not in order to assess the improvement of the patient, usually
negative Ketone bodies in the urine indicate that the patient is getting rid of
his Ketoacidosis, after that we will give the patient separated doses of
subcutaneous regular insulin, we divide the doses into 2/3 long ac+ng insulin &
1/3 short ac+ng insulin and an average of 3 or more shots per day because if the
patient is kept in the lower side of the normal glucose level this will help in
decreasing the incidence of small vessel affection and by this we can avoid
nephropathy, retinopathy and Ischemic heart disease in those patients.
Phase3 Continuing phase and guidance.
Note: Most of the deaths happen in DKA patient happen in those who receive
sodium bicarbonate.
Why sodium bicarbonate will cause brain edema?
NAHCO3 +H H2O+CO2 (In the brain), as you know the CO2 is freely movable so it will get out
of the
brain but water isn't freely movable so it will remain in the brain causing edema, herniation and
death.
------------------------------------------------------------------------------------------------------------------------
---------------
1st station: (it was repeated 2 times) Dr. Mohamad Khassawneh and another doctor.
Case A> 3 day old baby with sever jaundice
1) what do you think might happen> Kernictirus
2) How do you it's kernictirus> bilirubin >20, neuro signs, decreease LOC
Exams and Tests
A blood test will show a high bilirubin level (greater than 20 to 25 mg/dL). However, there is not a
direct link between bilirubin level and degree of injury..
Symptoms
The symptoms depend on the stage of BE. Not all babies with kernicterus on autopsy have had
definite symptoms.
Early stage:
Extreme jaundice
 Absent startle reflex
Poor feeding or sucking
Extreme sleepiness (lethargy) and low muscle tone (hypotonia)
Middle stage:
High-pitched cry
Irritability
May have arched back with neck hyperextended backwards, high muscle tone (hypertonia)
Poor feeding
Late stage:
Stupor or coma
No feeding
Shrill cry
Muscle rigidity, markedly arched back with neck hyperextended backwards
Seizures
Possible Complications
Complications may include:
Permanent brain damage
Hearing loss
Death
Prevention
Treating jaundice or conditions that may lead to it can help prevent this problem. Infants with the
first signs of jaundice have bilirubin level measured within 24 hours. If the level is high, the infant
should be screened for diseases that involve the destruction of red blood cells (hemolysis).
All newborns have a follow-up appointment within 2 to 3 days after leaving the hospital. This is
very important for late preterm or early term babies (born more than 2 to 3 weeks before their due
date).
3) What do you ask in hx> TORCH, blood group
Risk Factors for Development of Severe Hyperbilirubinemia in Infants of 35 or More Week's
Gestation
Jaundice observed in the first 24 h
- Blood group incompatibility with
other known hemolytic disease (G6PD deficiency)
-Gestational age 3536 wk
-Previous sibling received phototherapy
-Cephalohematoma .
- Exclusive breastfeeding, if nursing is not going well and weight loss is excessive
4) Like what group> If mom in RH -ve and baby and dad were +ve or ABO incompatibility
Causes
This condition most often develops in the first week of life, but may be seen up until the third week.
Some newborns with Rh hemolytic disease are at high risk for severe jaundice that can lead to this
condition. Rarely, BE can develop in seemingly healthy babies.

5) What do you do for treatment if bilirubin >25 > I would do exchange transfusion.
Treatment
Treatment depends on how old the baby is (in hours) and whether the baby has any risk factors
(such as prematurity). It may include:
Light therapy (phototherapy)
Exchange transfusions (removing the child's blood and replacing it with fresh donor blood or
plasma)
6) What can you do before that> Phototherapy
7) What's the mechanism of action> bilirubin is converted into a variety of photo-products
Bilirubin absorbs light in the blue range ( 420-470 nm)
Bilirubin absorbs light energy causing several photochemical reactions , most important one
is photo isomerization which helps in excretion of bilirubin in unconjugated state
Case B> 1 year old child, with decrease feeding and fatigue
1) what do you think it is , He sweats during feeding> congenital heart dx
2) Like what>VSD
ACYANOTIC shunts
Symptoms:
tachypnea, slow feeding, sweating.
Signs:
hepatosplenomegaly, possible flow murmur, failure to thrive.
CXR:
increased vascularity and large heart size.
Examples include ASD, VSD, PDA, AV Canal
3) What is the problem> left to right shunt
Increased
Pulmonary
Degree of symptoms depend on size of VSD and PVR
Vascular
Markings
Exam shows pansystolic murmur, possible diastolic rumble.

4) How
CXRdoshows
you diagnose>
cardiomegaly,clinically
ECG shows LA and LV enlargement
5) What do you find> Pansystolic murmur, loud s2
6) Other than echo, what can you do> ecg, chest x-ray
Echo
7) what do isyou
thesee instandard
gold chest xray> cardiomegaly, increased lung markings, pulmonary edema
for diagnosis
8) why pulmonary edema> heart failure is a complication
9) excellent, how do you diagnose it clinically> Hepatomegaly, pulmonary edema, tachpnea

10) How do you treat the heart faiure> Diuretics, ACE inhibitors
Treat heart failure: diuretics, ACE I
Weight: concentrate formula, NG tube
Surgery
11) What's the MOA of ACE inhibitors?
ACE inhibitors work by decreasing the activity of the renin-angiotensin-aldosterone system
(RAAS). The RAAS is a complex physiological system that controls fluctuations in blood pressure.
A protein called renin is released by the juxtaglomerular apparatus in the kidneys. Renin then
produces angiotensin, the active form of which stimulates the adrenal gland to produce a hormone
called aldosterone. Aldosterone stimulates the reabsorption of water and conservation of sodium,
therefore increasing water retention and blood pressure.
ACE inhibitors block the conversion of angiotensin I to angiotensin II and the effects of angiotensin
II are therefore prevented. This competitive inhibition of ACE to prevent the formation of
angiotensin II occurs in the kidney, blood vessels, heart, brain and adrenal gland This leads to an
increase in the amount of sodium and urine excreted, reduced resistance in kidney blood vessels, an
increase in venous capacity and decreases in cardiac output, stroke work and volume.
- In severe dehydration Fluid therapy : how to calculate maintenance & deficit.
Fluid resuscitation & emergency management :
Here we should asses whether its an emergency , and calculate the
amount of fluids lost , and determine whether we should give fluids
orally or IV..
for example if a shocked person came to the emergency , we have
to intervene quickly to prevent tissue hypoxia , so we have to start
by giving IV boluses without even looking at Na levels
*a bolus contains isotonic solution whether normal saline
(0.9%saline) or ringers lactate (contains more bicarbonate) . in
children we usually give normal saline .we never add dextrose to
bolus because dextrose will increase the osmolarity and this will lead
to further fluid loss from body tissues.
*The amount of fluids in a single bolus equals 20cc/Kg and its given
over 20 to 30 minutes , but if the patient is a known case of renal
failure or his lab tests revealed that , or if he has heart problems ,
then we should give him a less and slower quantity (10cc/Kg over 30
to 60 minutes ) because if you overload him , it will be difficult to get
rid of the excess amounts.
*The number of boluses to be given depends on the patient . by
calculations you can see that every bolus decreases the percentage
of dehydration by 2% , so by giving 3 boluses you can decrease the
dehydration by 6 % and transfer a patient from sever dehydration
and shock(15%) to moderate dehydration (9% ) . so usually we give 2
to 3 boluses
*If the patient didnt urinate , we may give him the 4th bolus ,
because renal shutdown is the first thing to occur in dehydration in
order to protect other organs , and at the same time its the last
thing to be fixed after rehydration , so if he is not puffy give him the
4th and we may give him lasex to make him urinate , but if he didnt
we should stop
*If the blood pressure is normal and the extremities are warm and
the patient didnt urinate , then this may indicate a change from a
pre-renal shutdown to acute renal failure
*We should examine and asses the patient after each bolus
*K is only added when the patient urinates and we are sure that the
kidneys are working.
We have two ways to calculate the maintenance fluid :
1) The way derived from caloric losses (most commonly used) :
-the daily caloric needs of a 10 Kg person is 100 cal/ Kg , at the
same time he needs 100 cc water/Kg.
Put this box in your mind because we will need it later
Example : 7Kg patient 7 x 100 = 700 cc fluid (because 7 is from the
first 10 Kgs)
Example : 15 Kg patient 15= 10 + 5 fluid = 10x100 + 5x50 =1250 cc
(because the 5 is from the second 10Kgs of weight so we dont multiply
it by 100 like the first 10 , we multiply it by 50)
- the rule to calculate the daily water[or caloric] needs
(calculation of maintenance fluid):
The first 10 Kgs of weight needs 100 cc/Kg
The second 10 Kgs of weight needs 50cc/Kg
The third and above Kgs of weight needs 20cc
2) To calculate fluid needs (maintenance ) according to the surface
area :
They calculated total fluid losses under normal physiological
conditions and reached this formula :
Needs = 160 cc / m2 / Hour.
-Types of dehydration you know how to give fluids in hyper& hyponatremia in 24 hours
Treatment of hypernatremic dehydration :
We have to go into 3 steps :
1) give the patient his maintenance (the amount that is normally
needed)
2) replace the deficits (the already lost fluids)
3) decrease the elevated Na levels
*put in your mind that we shouldnt decrease Na levels more than 0.5-1
mEq/hour or more than 10mEq/day , otherwise the patient will
develop sever complications like cerebral edema (because fluids pass
the BBB faster than electrolytes ) . so always avoid rapid drop of Na
level and only decrease it by 10 mEq/day or a maximum of 12 mEq/day
.(put the bold sentence deep in your head)
*in sever cases we start by giving the patient normal saline boluses ( 1
or 2 bluses) until his condition becomes more stable , and here in bolus
treatment we dont look for Na concentration because normal saline
contains 154mEq/l and this will be less than his current Na level and will
not increase it .
after that we calculate the maintenance , ongoing losses , and the
deficit :
the maintenance : the daily needs (100cc/kg for the 1st 10 , 50cc/kg for
the 2nd 10 , and 20cc/kg for the rest)
the ongoing losses : how much he is loosing in diarrhea , vomiting
the deficit : and this depends on the level of dehydration : if its 10% (he
lost 10% of his body weight ) then we say :
10% = 10cc/100cc = 100cc/1000cc = 100cc/kg weight
So he lost 100cc fluid/Kg weight
The we multiply 100cc by his body weight :
Deficit = 100 x body weight
Correction of hyponatremic dehydration :
Dehydration is usually overestimated in hyponatremia , because fluids
will shift from the extra to the intracellular compartment . treatment of
hyponatremic dehydration is very similar to hypernatremic
dehydration, and the only difference is that in the Na deficit step , we
dont assume the value 3,6,9mEq/kg according to the level of
dehydration , instead we calculate it according to the formula :
Na deficit = 0.6 x body weight x (desired Na current Na)
In hypernatremic dehydration , we said that we shouldnt decrease Na
by more than 10 mEq/l , and here also in hyponatremic dehydration ,
we shouldnt increase Na by more than 10 mEq/l , otherwise the
patient will have pontine hemorrhage & demylination .
Remember these things :
D5 = 5% dextrose , and alone it doesnt contain any Na.
Normal saline = 0.9% saline , and it contains: Na : 154mEq/l
. saline = 0.45%saline , and it contains . the Na in the normal saline
2nd station: Dr Azhar
A 4 year old child keeps waking up with puffy eyes
1) What do you think it is? Nephrotic or nephritic
Complications Of Nephrotic syndrome:
Edema
1. Causes : Edema happens because of protein loss which leads to decrease in
the vascular Oncotic pressure. There is another cause of Edema which is renal
impairment that happens usually in children because of decrease osmotic pressure
that leads to kidney hypo perfusion and so fluid retention takes place as a result
of hypo perfusion, in those patients the more is the fluid retention the more severity
of the edema is. (Usually the intravascular pressure in children is good and this is
explained by the second cause -Renal Impairment-).
Why renal impairment happen? Because of:
1- Renin-Angiotensin system activation.
2- Sodium and fluid retention.
2. Character: Generalized swelling starts in the morning with puffiness around the
eyes and predictable ascites and as the day passes the edema will be more in the
dependent locations of the body e.g. lower limbs, Genitalia, Hands and sacrum
"esp. in babies", OTHER SPACES WHERE FLUID CAN ACCUMULATE are called 3rd
spaces which include scrotum, genitalia, abdomen "Ascites" and pleura "pleural
effusion"
2) How do you know which one? UA
1. Nephrotic Range proteinuria: > 40 mg /M2/hr
3) If we saw red urine, what does it mean> Nephritic
Hematuria Related to Kidneys (Renal Causes).
2 sets of causes; glomerular & extra- or non- glomerular [tubular].
2 forms; isolated hematuria & nephritis.
4) What do you see in UA in nephritic> RBC cast mostly, maybe proteinuria
Its something else and this is the most serious thing in our discussion, when we say nephrItic
syndrome this
means that you must have all of these
1) Gross mAcroscopic hematuria.
2) Abnormal kidney function.
3) Edema. H&A&G&E
4) Hypertension.
So these are the meanings of nephrItic syndrome, or these are essential to diagnose a patient with
nephritic
syndrome; they are pathologic to nephrItic syndrome.
5) What do you ask in hx> URTI maybe
Pos-Infectious Glomerulonephritis; Overview:
Post-infectious glomerulonephritis was called previously post-strep, but its now called post-
infectious
because we have other agents that can give us similar condition such as mycoplasma, staph,
influenza and many
others, but the most common one and the most well known one is the post-strep.
Usually it becomes after 10 days of pharyngitis, or 14 days after skin infection.
Pos-Infectious Glomerulonephritis; Clinical Presentation:
Most of the patients will have mild minor disease, some of them go unnoticed, they will have mild
edema,
slight impairment in kidney function, so they go unnoticed having only mIcroscopic hematuria.
Others present
with the full-blown picture.
Both of them will have a sort of nephrItic syndrome, both of them will have the 4 signs
6) If she had a skin born a few weeks ago, what might you think>Post-strep GN
7) What are you afraid of>hypertension, hyperkalemia
Pos-Infectious Glomerulonephritis; Treatment:
Is usually supportive, we do correction for the fluids, correction for the potassium K because these
patients
are in renal failure, I can give them diuretics and treat the hypertension and thats it.
.
8) What's the most imp thing in management of hyperkalemia? Ca gluconate IV
Calcium gluconate
Calcium increases the threshold potential, thus restoring the normal gradient between threshold
potential and resting membrane potential, which is abnormally elevated in hyperkalemia. Onset of
action is within 5 minutes, and duration of action is about 30-60 minutes. Doses should be titrated
with constant monitoring of ECG changes during administration; repeat the dose if ECG changes do
not normalize within 3-5 minutes.
8) What are the foods we tell the parents not to give her> bananas and orange juice
Fruits
Fruits are sources of potassium. A rich source can provide between 250 to 500 milligrams of
potassium per serving. Fruits such as apricots, avocados, orange, peaches, prunes, raisins, bananas,
figs and kiwis should be avoided because of their high potassium content.
9) When do we discharge> when the BP and potassium are under control
Only a small percentage of patients with acute glomerulonephritis require initial hospitalization, and
most of those are ready for discharge in 2-4 days. As soon as the blood pressure (BP) is under
relatively good control and diuresis has begun, most children can be discharged and monitored as
outpatients.
10) Do we give anything else> antibiotics
Some doctors give them penicillin, but penicillin will not treat this disease once it appears, they will
eradicate
the cause but they will not treat the disease
what is the first sign that is corrected after hydration >>> heart rate.
manifestation of severe ,moderate and mild dehydration. how to know if the patient is
hydrated ? is irritability or fatigue present in dehdration ?
In mild dehydration we see : thirst only , slightly dry mucous
membrane .infants will be irritable because they want to drink
In moderate dehydration we see : slight tachycardia , slightly
decreased blood pressure , dry mucous membranes , sunken eyes ,
slightly cold extremities , no loss of skin turgor , normal capillary refill
, usually they are irritable
In sever dehydration we see : decreased blood pressure , delayed
capillary refill , cold extremities , anurea , and the patient is usually
comatosed or very hypoactive.
i think the answer was both most common pathological cause of janundice in 3 day old baby ?
Breast Feeding jaundice
Occurs in the 1st week of life
Due to decreased milk intake with dehydration and/or reduced caloric intake .
Giving supplements of glucose water to breast-fed infants is associated with higher bilirubin
levels .
------------------------------------------------------------------------------------------------------------------------
---------------
1st station ( Dr.wadda7 5rees) :
what is the length of a newborn ..
when do u expect it to double? what is the weight of a newborn ..
when do u expect it to double then triple ?
Table 5-1. Rules of Thumb for Growth
Weight
1. Weight loss in first few days: 5%-10% of birth weight
2. Return to birth weight: 7-10 days of age
Double birth weight: 4-5 mo
Triple birth weight: 1 yr
Quadruple birth weight: 2 yr
3. Average weights: 3.5 kg at birth
10 kg at 1 yr
20 kg at 5 yr
30 kg at 10 yr
4. Daily weight gain:
20-30 g for first 3-4 mo
15-20 g for rest of the first yr
5. Average annual weight gain: 5 lb between 2 yr and puberty (spurts and plateaus may occur)
Height
1. Average length: 20 inches at birth, 30 inches at 1 yr
2. At age 3 yr, the average child is 3 ft tall
3. At age 4 yr, the average child is 40 in tall (double birth length)
4. Average annual height increase: 2-3 inches between age 4 yr and puberty
Head Circumference (HC)
1. Average HC: 35 cm at birth (13.5 inches)
2. HC increases: 1 cm/mo for first yr (2 cm/mo for first 3 mo, then slower); 10 cm for rest of life
when the child could draw a triangle ??
when he draw a circle then asked about square ??
when the social smile start ..
when the baby set without support??

Developmental Milestones
 Fine Motor-
Age Gross Motor Adaptive Personal-Social Language Other Cognitive
2 Moves head Regards face Alerts to bell
wk side to side
2 Lifts shoulder Tracks past Smiles Cooing
mo while prone midline responsively
Searches for sound
with eyes
4 Lifts up on Reaches for Looks at hand Laughs and squeals
mo hands object
Rolls front to Raking grasp Begins to work
back toward toy
If pulled to sit
from supine,
no head lag
6 Sits alone Transfers Feeds self Babbles
mo object hand to
hand
Holds bottle
9 Pulls to stand Starting to Waves bye-bye Says Dada and
mo pincer grasp Mama, but
nonspecific
Gets into Bangs 2 blocks Plays pat-a-cake 2-syllable sounds
sitting together
position
12 Walks Puts block in Drinks from a Says Mama and
mo cup
cup Dada, specific
Stoops and Imitates others Says 1-2 other words
stands
15 Walks Scribbles Uses spoon and Says 3-6 words
mo backward fork
Stacks 2 blocks Helps in Follows commands
housework
18 Runs Stacks four Removes Says at least 6 words
mo blocks garment
Kicks a ball "Feeds" doll
2 yr Walks up and Stacks 6 blocks Washes and dries Puts 2 words together Understands concept of
down stairs hands "today"
Throws Copies line Brushes teeth Points to pictures
overhand
Puts on clothes Knows body parts
3 yr Walks steps Stacks 8 blocks Uses spoon well, Names pictures Understands concepts of
alternating spilling little "tomorrow" and
feet "yesterday"
 Broad jump Wiggles thumb Puts on t-shirt Speech
understandable to
stranger 75%
Says 3-word
sentences
4 yr Balances well Copies O, Brushes teeth Names colors
on each foot maybe + without help
Hops on one Draws person Dresses without Understands
foot with 3 parts help adjectives
5 yr Skips Copies Counts
Heal-to-toe Understands
walks opposites
6 yr Balances on Copies Defines words Begins to understand
each foot 6 "right" and "left"
sec
Draws person
with 6 parts

when the baby usually starts to get teeths .. which one appears first ..
Upper Teeth When tooth When tooth falls
emerges out

Central 8 to 12 months 6 to 7 years

incisor

Lateral incisor 9 to 13 months 7 to 8 years

Canine 16 to 22 months 10 to 12 years

(cuspid)

First molar 13 to 19 months 9 to 11 years

Second molar 25 to 33 months 10 to 12 years

Upper Primary Teeth Development Chart

Lower Teeth When tooth When tooth falls

emerges out

Second molar 23 to 31 months 10 to 12 years

First molar 14 to 18 months 9 to 11 years

Canine 17 to 23 months 9 to 12 years

(cuspid)
Lower Teeth When tooth When tooth falls
emerges out

Lateral incisor 10 to 16 months 7 to 8 years

Central 6 to 10 months 6 to 7 years

incisor

Lower Primary Teeth Development Chart

what do u know about vaccines other than the national program ??

when to give them ??
(1)Pneumococcal polysaccharide vaccine (PPV)
23 valent vaccine (according to serotype)
Usually 2 doses (1st dose at any age >2 YO, the 2nd dose after
3-5 years)
Help prevent serious pneumococcal disease which is a serious
illness that affects children
E.g. meningitis, bacteremia, pneumonia
Anyone older than 2 years with:
Heart disease, lung disease, sickle cell disease, diabetes,
cirrhosis, lymphoma, leukemia, kidney failure, nephrotic
syndrome, asplenia, HIV infection or AIDS.
Varicella vaccine:
Can prevent chickenpox and if got chickenpox it is mild,
1.fewer number of spots 2. No fever 3. And will recover faster
Chickenpox not that severe illness within 7-10 days there
will be a complete recovery.The cause for introducing the
vaccine is the fatality cases(so severe death)
First dose: 12- 15 months of age
Second dose: 4- 6 years of age (may be given earlier if at least
3 months after the first dose)
Influenza Vaccine:
Inactivated vaccine.
Influenza viruses are always changing (shift & drift), so
influenza vaccines are updated every year, and an annual
vaccination is recommended in October or November (at the
beginning of winter).
It is recommended for
1) Children b/w 6-24 months of age & for patient 6 month
of age or older who have chronic disease (asthma, DM, HIV,
CF, sickle cell disease & cardiac condition)
2) Health care professional
Contraindications:
Influenza vaccine virus is grown in eggs. People with a severe
egg allergy & yellow fever should not get the vaccine
Meningococcal Vaccines:
1) Meningococcal polysaccharide vaccine (A/C/Y/W-135) 4
serotype. The most epidemic is A/C
Recommended to children older than 2 years AND at risk
(terminal complement component deficiency, asplenia,
military recruits ,traveling)
2)Meningococcal conjugate vaccine A/C used in Europe for
infants less than 2 YO)
Minor side effects
Rotavirus Vaccine :
An oral live vaccine
Rotavirus it is the most common cause of gastroenteritis in
children (50-60%)
In poor countries like Africa & in the area where there is a
war, children who get gastroenteritis may die from
dehydration. According to that the vaccine was introduced
and distributed by WHO to that area.
When the vaccine was introduced for the 1st time they
supposed that the vaccine increase incidence of
intussusceptions & it was withdrawn from the market until
the new one was introduced.
Children should get 3 doses :
First Dose: 2 months of age
Second Dose: 4 months of age
Third Dose: 6 months of age
what do u know about henoch -schonlein purpura ..
which IG type deposit in this disease?
what are the changes we may find if we do a biopsy for the kidney of a patient with henoch -
schonlein purpura?
IgA Nephropathy; Henoch-Schnlein Purpura HSP:
HSP Henoch-Schnlein Purpura nephritis is another variation of IgA nephropathy, so if you do a
renal
biopsy for these HSP patients you will find IgA deposits you will find the same findings of the IgA
like mesangial
IgA and IgG deposits.
But the distinguished thing in HSP is that it will present with skin rash and arthritis, so its
somehow a part
of a syndrome.
HSP is a triad of:
1) Abdominal pain. 2) Arthlargia; arthritis 3) Skin rash.
Its unnecessary for them to be all present at the same time, sometimes the patient will come with
abdominal
pain then after 2-3 weeks they will get arthritis with the skin rash, sometimes they only present with
skin rash
without the other 2 and so on...
The important thing is that the HSP nephritis doesnt always come with its syndrome [triad], so you
have to
follow the patient up to 2 years In order to say that he is not having an associated renal disease.
20-50% of children will have renal involvement at the initial presentation, some of them will have
mild
proteinuria and then it will resolve by itself, some of them will have a more sever disease, they also
may come
with nephrItic or nephrOtic syndrome.
a question about atypical kawasaki disease and its cause ??
================================
Signs and symptoms appear to parallel those in children who fulfill diagnostic criteria for typical
disease ) when clinical judgment of reliable observers is used to define incomplete Kawasaki
disease (KD). Fever for five or more days is the one common finding. However, fever may be
absent or missed in some infants. Patients with incomplete KD have less than four signs of
mucocutaneous inflammation. Some infants present only with fever and no other clinical features of
KD
The cause of Kawasaki disease is not completely known. There are a number of theories regarding
the cause, but so far, none have been proven. Some believe that the disease is caused by an infection
since outbreaks are commonly clustered and appear similar to other infectious diseases (abrupt
onset, fever, rapid resolution of symptoms within one to three weeks). It is commonly thought that a
bacterial toxin, acting as a disease trigger, initiates the disease. This toxin may come from
common bacterial infections in children, such as Staphylococcus orStreptococcus
second station (Dr.rola alsa83a) :
you are in the emergency room a mother brought her 1 month infant who cried continuously
from the early morning until 11:00 pm for the last 3 days .. in the night he slept very well with
no any problems.. what do u thing ?? I said nothing i will start with Hx .. and according to my
Hx questions she was asking many questions ... finally i reached to infantile colic as a diagnosis
.. i think she wanted this as a diagnosis
Colic often is diagnosed using Wessel's "rule of threes"-crying for more than 3 hours per day for
more than 3 days per week for more than 3 weeks. The limitations of this definition include the lack
of definition of crying (does this include fussing?) and the necessity to wait 3 weeks to make a
diagnosis in an infant who has excessive crying. The crying of colic is often described as
paroxysmal and may be characterized by facial grimacing, drawing up of the legs, and passing
flatus.

Etiology
Less than 5% of infants evaluated for excessive crying have an organic etiology. Because the
etiology of colic is unknown, this syndrome may be the extreme of the normal phenomenon of
infant crying. Nonetheless, evaluation of infants with excessive crying is warranted.
Epidemiology
Cumulative incidence rates of colic vary from 5% to 19% in different studies. Girls and boys are
affected equally. Studies vary by how colic is defined and by data collection methodology, such as
maintaining a cry diary or actual recording of infant vocalizations. Concern about infant crying also
varies by culture; this may influence what is recorded as crying or fussing.
Clinical Manifestations
The clinician who evaluates a crying infant must differentiate rare organic disease from colic, which
has no identifiable etiology. The family should be asked first to describe the crying, including
duration, frequency, intensity, and modifiability. Does the infant have associated symptoms, such as
pulling up of the legs, facial grimacing, vomiting, or back arching? When did the crying first begin?
Has the crying changed? Does anything relieve the crying? Does anything exacerbate the crying? Is
there a diurnal pattern to the crying? A review of systems is essential because crying in an infant is a
systemic symptom that can herald disease in any organ system. Past medical history also is
important because infants with perinatal problems are at increased risk for neurologic causes of
crying. Attention to the feeding history is crucial because some causes of crying are related to
feeding problems, including hunger, air swallowing (worsened by crying), gastroesophageal reflux,
and food intolerance. Questions concerning the family's ability to handle the stress of the infant's
crying and their knowledge of infant soothing strategies assist the clinician in assessing risk for
mental health comorbidities and developing an intervention plan suitable for the family.
The physical examination is an essential component of the evaluation of an infant with colic. The
diagnosis of colic is made only when the physical examination reveals no organic cause for the
infant's excessive crying. The examination begins with vital signs, weight, length, and head
circumference, looking for effects of systemic illness on growth, such as occur with infection or
malnutrition. A thorough inspection of the infant is important to identify possible sources of pain,
including skin lesions, corneal abrasions, hair tourniquets, skeletal infections, or signs of child
abuse such as fractures .Infants with common conditions such as otitis media, urinary tract
infections, mouth sores, and insect bites may present with crying. A neurologic examination may
reveal previously undiagnosed neurologic conditions, such as perinatal brain injuries, as the cause of
irritability and crying. Observation of the infant during a crying episode is invaluable to assess the
infant's potential for calming and the parent's skill in soothing the infant.
Laboratory and imaging studies are reserved for infants in whom there are history or physical
examination findings suggesting an organic cause for excessive crying. An algorithm for the
medical evaluation of an infant with excessive crying inconsistent with colic is presented in
..
------------------------------------------------------------------------------------------------------------------------
--------------- 1st station Doc Wudoh:
Newborn baby's weight.
When double.
When triple.
Stature at birth 50cm. Normal/x? When double? Develoment. When can smile? Sit without
support? Draw triangle, square
Vaccination other than the program. Which one u recommend.
At what age.
Something about egg-allergy, which vaccine you can't give.
Answered above
Anaphylaxis management. Route & dose?
epinephrine should be immediately administered as an intramuscular (IM) dose to all children with
signs and symptoms suspicious of anaphylaxis . Regardless of whether epinephrine is administered,
parents should urgently seek medical attention at the nearest ED if they are concerned about
anaphylaxis. Based on the recommended epinephrine dose of 0.01 mg/kg, these two doses are most
applicable to children weighing 15 kg or 30 kg.
2nd statio Doc Rola: 1 month old baby keep crying inconsolable, very irritable 6pm-11pm
than he's well. Sleep throughout the night. What the first thing come to your mind
(NOTHING CAME TO MY MIND). Just told her its structural problem not infection. She
said its very common.
What investigation u want to do? Let's say the baby is the same picture but throughout the
day.
Answered above
We discussed about sepsis and septic work up. She asked the normal CSF component value.
What's the first teeth to appear & when does it start to appear?
Therefore, we have what is
called septic work up. You take blood, urine and CSF (and sputum if present) samples. Then
you look for the source of infection by doing culture for them all. We aim to isolate the
microorganisms from body fluids or secretions and this is diagnostic.
The manifestations of neonatal septicemia are often vague and therefore demand a
high index of suspicion for early diagnosis (Table I). The most common and
characteristic manifestation is an alteration in the established feeding behavior in late onset
sepsis and respiratory distress in early onset sepsis. The baby, who had been active
and sucking well, gradually or suddenly, becomes lethargic, inactive or unresponsive
and refuses to suckle. Hypothermia is a common manifestation of sepsis, whilst fever
is infrequent, but the presence of fever also strongly suggests sepsis! Diarrhea,
vomiting and abdominal distension may occur. Episodes of apneic spells or gasping
may be the only manifestation of septicemia. In sick neonates, the skin may become
tight giving a hide-bound feel (sclerema) and the perfusion becomes poor (capillary
refill time of over 3 seconds). Cyanosis may appear. A critical neonate may develop
shock, bleeding and renal failure.
TABLE 1: Clinical manifestations of neonatal sepsis
Lethargy Cyanosis*
Refusal to suckle Tachypnea*
Poor cry Chest retractions*
Not arousable, comatosed Grunt*
Abdominal distension Apnea/gasping*
Diarrhea Fever
+
Vomiting Seizures
+
Hypothermia Blank look
+
Poor perfusion High pitched cry
+
Sclerema Excessive crying/irritability
+
Poor weight gain Neck retraction
+
Shock Bulging fontanel
+
Bleeding
Renal failure
* Particularly suggestive of pneumonia,
+
particularly suggestive of meningitis
The additional features of pneumonia or meningitis may be present depending upon
the localization of infection in different systems and organs of the body. The
evidence of pneumonia includes tachypnea, chest retractions, grunting, early cyanosis and
apneic spells (signs of respiratory distress) in addition to inactivity and poor feeding. Cough is
unusual. Findings on auscultation of the chest are non-specific and non- contributory (you
might hear some crepitations but as you know, the neonate may have some residual
fluids in his/her lungsthis is normal). Meningitis is often silent .
------------------------------------------------------------------------------------------------------------------------
--------------- station one : Dr Faisal child with fever and bloody diarrhea since three days.. 1-
take a history/
2- what is your diagnosis ?
3- what is the causes for bloody diarrhea ( salmonelaa , shegilla , Amoeba , intussusception
........
4-what is the treatment for each ?
what is the disease that salmonella cuz? typhiod fever
5- how can we diagnose salmonella ? what does the test called ?
6- how can we diagnosis shigella and amoeba ?
7- if he had tonic clonic seizure , what is the cuz if he have shigella
Typhoid fever is caused by Salmonella typhi and occasionally Salmonella paratyphi. These
infections are distinguished by their potential for prolonged fever, inconsistent presence of diarrhea,
and extraintestinal manifestations. . The typhoid bacillus infects humans only, and chronic carriers
are responsible for new cases.
Table 112-1. Mechanisms of Diarrhea
Primary Stool
Mechanism Defect Examination Examples Comment
Secretory Decreased Watery, normal Cholera, toxigenic Persists during
absorption, osmolality; +
Escherichia coli; fasting; bile salt
increased secretion: osmols = 2 (Na carcinoid, VIP, malabsorption also
electrolyte transport + K+) neuroblastoma, may increase
congenital chloride intestinal water
diarrhea, Clostridium secretion; no stool
difficile, leukocytes
cryptosporidiosis (AIDS)
Osmotic Maldigestion, Watery, acidic, + Lactase deficiency, Stops with fasting,
transport defects, reducing glucose-galactose increased breath
ingestion of substances; malabsorption, lactulose, hydrogen with
unabsorbable solute increased laxative abuse carbohydrate
osmolality; malabsorption, no
osmosis >2 stool leukocytes
(Na+ + K+)
Motility
Increased Decreased transit Loose to normal- Irritable bowel Infection also may
motility time appearing stool, syndrome, contribute to
stimulated by thyrotoxicosis, increased motility
gastrocolic reflex postvagotomy dumping
syndrome
Decreased Defect in Loose to normal- Pseudo-obstruction, Possible bacterial
motility neuromuscular appearing stool blind loop overgrowth
unit(s)
Stasis (bacterial
overgrowth)
Mucosal Inflammation, Blood and Celiac disease, Dysentery = blood,
inflammation decreased mucosal increased WBCs Salmonella, Shigella, mucus, and WBCs
surface area and/or in stool amebiasis, Yersinia,
colonic Campylobacter, rotavirus
reabsorption, enteritis
increased motility

VIP, vasoactive intestinal peptide; WBCs, white blood cells.

From Wyllie R: Major symptoms and signs of digestive tract disorders. In Behrman RE,
Kliegman RM, Jenson HB (eds): Nelson Textbook of Pediatrics, 17th ed. Philadelphia,
WB Saunders, 2004, p 1200.

Shigella dysenteriae may cause disease by producing Shiga toxin, either alone or combined with
tissue invasion. The incubation period is 1 to 7 days, and infected adults may shed organisms for 1
month. . The colon is selectively affected. High fever and seizures may occur, in addition to
diarrhea.
page 513

page 514
Table 112-2. Common Infectious Causes of Diarrhea and Their Virulence Mechanisms
Organisms Virulence Properties
Viruses
Rotaviruses Damage to microvilli
Caliciviruses Mucosal lesion
Astroviruses Mucosal lesion
Enteric adenoviruses (serotypes 40 and 41) Mucosal lesion
Bacteria
Campylobacter jejuni Invasion, enterotoxin
Clostridium difficile Cytotoxin, enterotoxin
Escherichia coli
Enteropathogenic (EPEC) Adherence, effacement
Enterotoxigenic (ETEC) (traveler's diarrhea) Enterotoxins (heat-stable or heat-labile)
Enteroinvasive (EIEC) Invasion of mucosa
Enterohemorrhagic (EHEC) (includes Adherence, effacement, cytotoxin
O157:H7 causing HUS)
Enteroaggregative (EAEC) Adherence, mucosal damage
Salmonella Invasion, enterotoxin
Shigella Invasion, enterotoxin, cytotoxin
Vibrio cholerae Enterotoxin
Vibrio parahaemolyticus Invasion, cytotoxin
Yersinia enterocolitica Invasion, enterotoxin
Parasites
Entamoeba histolytica Invasion, enzyme and cytotoxin production; cyst
resistant to physical destruction
Giardia lamblia Adheres to mucosa; cyst resistant to physical
destruction
Spore-forming intestinal protozoa Adherence, inflammation
Cryptosporidium parvum
Isospora belli
Cyclospora cayetanensis
Microsporida (Enterocytozoon bieneusi,
Encephalitozoon intestinalis)

Only certain strains of E. coli produce diarrhea. E. coli strains associated with enteritis are classified
by the mechanism of diarrhea: enteropathogenic (EPEC), enterotoxigenic (ETEC), enteroinvasive
(EIEC), entero-hemorrhagic (EHEC), or enteroaggregative (EAEC). EPEC is responsible for many
of the epidemics of diarrhea in newborn nurseries and in daycare centers. ETEC produce heat-labile
(cholera-like) enterotoxin, heat-stable enterotoxin, or both. ETEC causes 40% to 60% of cases of
traveler's diarrhea. EPEC and ETEC adhere to the epithelial cells in the upper small intestine and
produce disease by liberating toxins that induce intestinal secretion and limit absorption. EIEC
invades the colonic mucosa, producing widespread mucosal damage with acute inflammation,
similar to Shigella. EHEC, especially the E. coli O157:H7 strain, produce a Shiga-like toxin that is
responsible for a hemorrhagic colitis and most cases of hemolytic uremic syndrome (HUS), which
is a syndrome of microangiopathic hemolytic anemia, thrombocytopenia, and renal failure (see
Chapter 164). EHEC is associated with contaminated food, including unpasteurized fruit juices and
especially undercooked beef. EHEC is associated with a self-limited form of gastroenteritis, usually
with bloody diarrhea, but production of this toxin blocks host cell protein synthesis and affects
vascular endothelial cells and the glomeruli, resulting in the clinical manifestations of HUS.

Entamoeba histolytica (amebiasis), Giardia lamblia, and Cryptosporidium parvum are important
enteric parasites found in North America. Amebiasis occurs in warmer climates, whereas giardiasis
is endemic throughout the U.S. and is common among infants in daycare centers. E. histolytica
infects the colon; amebae may pass through the bowel wall and invade the liver, lung, and brain.
Diarrhea is of acute onset, is bloody, and contains WBCs.

LABORATORY AND IMAGING STUDIES

Initial laboratory evaluation of moderate to severe diarrhea includes a complete blood count,
electrolytes, BUN, creatinine, and urinalysis for specific gravity as an indicator of hydration. Stool
specimens should be examined for mucus, blood, and leukocytes, which indicate colitis. Fecal
leukocytes are present in response to bacteria that diffusely invade the colonic mucosa. A positive
fecal leukocyte examination indicates the presence of an invasive or cytotoxin-producing organism,
such as Shigella, Salmonella, C. jejuni, and invasive E. coli. Patients infected with Shiga toxin-
producing E. coli and E. histolytica generally have minimal fecal leukocytes.
A rapid diagnostic test for rotavirus in stool should be performed, especially during the winter. Stool
cultures are recommended for patients with fever, profuse diarrhea, and dehydration or if HUS is
suspected. If the stool test result is negative for blood and WBCs, and there is no history to suggest
contaminated food ingestion, a viral etiology is most likely. Stool evaluation for parasitic agents
should be considered for acute dysenteric illness or in protracted cases of diarrhea in which no
bacterial agent is identified.
Positive blood cultures are uncommon with bacterial enteritis except for S. typhi (typhoid fever) and
for nontyphoidal Salmonella and E. coli enteritis in very young infants. In typhoid fever, blood
cultures are positive early in the disease, whereas stool cultures become positive only after the
secondary bacteremia.
The diagnosis of E. histolytica is based on identification of the organism in the stool. Serologic tests
are useful for diagnosis of extraintestinal amebiasis, including amebic hepatic abscess.
page 515

page 516
Giardiasis can be diagnosed by identifying trophozoites or cysts in stool; less often a duodenal
aspirate or biopsy of the duodenum or upper jejunum is needed. Giardia is excreted intermittently;
three specimens are required. The Entero-Test is a nylon string affixed to a gelatin capsule, which is
swallowed. After several hours, the string is withdrawn and duodenal contents are examined for G.
lamblia trophozoites.

Table 112-3. Antibiotic Therapy for Infectious Diarrhea*

Organism Treatment
Salmonella typhi, Ampicillin, chloramphenicol,
Salmonella paratyphi TMP-SMZ, cefotaxime,
ciprofloxacin
Nontyphoidal Usually none (if 3 months old);
Salmonella ampicillin, cefotaxime,
ciprofloxacin
Shigella Children: Third-generation
cephalosporin, TMP-SMZ
Adults: fluoroquinolones
Escherichia coli
Enterotoxigenic Usually none if endemic; TMP-SMZ Prevention of traveler's diarrhea with
or ciprofloxacin for traveler's bismuth subsalicylate, doxycycline, or
diarrhea
Enteroinvasive TMP-SMZ, ampicillin if susceptible
Enteropathogenic TMP-SMZ or an aminoglycoside
Enterohemorrhagic Usually none
Enteroaggregative TMP-SMZ or an aminoglycoside
Campylobacter jejuni Mild disease needs no treatment;
erythromycin or azithromycin for
diarrhea; aminoglycoside,
ciprofloxacin, meropenem, or
imipenem for systemic illness
Yersinia enterocolitica None for uncomplicated diarrhea;
TMP-SMZ; gentamicin or
Comment
Invasive, bacteremic disease (typhoid
fever or enteric fever)
Treatment indicated if < 3 months old,
malignancy, sickle cell disease,
HIV/AIDS, or evidence of
nongastrointestinal foci of infection is
present
High prevalence of resistance to
amoxicillin
Increasing prevalence of resistance to
TMP-SMZ
Treatment reduces infectivity and
improves outcome
ciprofloxacin
No treatment if HUS is suspected
If started early (days 1-3), treatment
reduces symptoms and fecal organisms
Value of treatment of mesenteric
lymphadenitis with antibiotics is not
 cefotaxime for extraintestinal disease established
Vibrio cholerae Tetracycline, doxycycline, TMP- Fluid maintenance crucial
SMZ
Clostridium difficile Oral metronidazole, oral C. difficile is agent of antibiotic-
vancomycin associated diarrhea
(pseudomembranous colitis)
Entamoeba histolytica Metronidazole followed by Treatment determined by degree of
iodoquinol to treat luminal infection tissue invasion
Giardia lamblia Metronidazole, quinacrine, Furazolidone is only preparation
furazolidone, others available in liquid form
Cryptosporidium None; azithromycin or paromomycin A serious infection in
parvum and octreotide in persons with immunocompromised persons
HIV/AIDS

8-how can we diagnosis febrile seizure and differentiate it from other type of seizure?
Definition:
Seizures occurring in the presence of fever due to extra-cranial origin in
children ages 6 months 6 years of age.
(Firstly, you have to exclude CNS infection: meningitis & encephalitis
Types of febrile seizure:
Character Simple febrile Complex febrile
Duration < 15 minutes > 15 minutes
Body affection General : whole body focal: hands or legs
Prognosis Completely benign High risk of epilepsy
Expansion Very common Rare
Recurrence Common Rare
[pg 7]

7- if he had tonic clonic seizure , what is the cuz if he have shigella

8-how can we diagnosis febrile seizure and differentiate it from other type of seizure?

ANSWER
7) Gastroenteritis caused by Shigella.
=Certain pathogens (disease-causing organisms; e.g., viruses, bacteria) are associated with an
increased risk for febrile seizures. These pathogens include influenza A virus, which causes the flu,
human herpesvirus 6 (HHV-6), which causes roseola, and Shigella and Campylobacter bacteria,
which cause gastroenteritis (e.g., diarrhea, nausea, vomiting)

#source: http://www.healthcommunities.com/febrile-seizures/children/causes-of-febrile-
seizures.shtml

8) Febrile seizures can often be diagnosed from a description of what happened.

Further tests may be needed if the cause of the associated infection isn't clear.
It's unlikely that your doctor will see the seizure, so an account of what happened is useful.
It's useful to know:
how long the seizure lasted
what happened body stiffening, twitching of the face, arms and legs, staring and loss of
consciousness
whether your child recovered within one hour
whether they've had a seizure before
Tests to identify the source of the infection will only usually be necessary to rule out rarer
conditions which can cause similar symptoms, such as meningitis.
A blood or urine sample may be needed to test for signs of infection. It can sometimes be difficult to
obtain a urine sample from young children, so it may have to be done in hospital.
Read more about blood tests.
Further tests
Further tests may be carried out in hospital if your childs symptoms are unusual for example, if
they don't have a high temperature or their seizures don't follow the normal pattern.
Further testing and observation in hospital is also usually recommended if your child is
having complex febrile seizures.
Your child may have other tests including an electroencephalogram and lumbar puncture,
particularly if they're less than 12 months old.
These two tests are explained below.
Electroencephalogram
An electroencephalogram (EEG) measures your childs electrical brain activity through electrodes
that are placed on their scalp. Unusual patterns of brain activity can sometimes indicate epilepsy.
However, some studies have suggested that an EEG may not be useful in many cases of febrile
seizures.
Lumbar puncture
During a lumbar puncture, a small sample of cerebrospinal fluid (CSF) is removed for testing. CSF
is a clear fluid that surrounds and protects the brain and spinal cord.
A hollow needle is inserted into the base of the spine to obtain the CSF sample. During the
procedure, local anaesthetic will be used to numb your childs back so that they don't feel any pain.
A lumbar puncture can be used to determine whether your child has an infection of the brain or
nervous system.
#source: http://www.nhs.uk/Conditions/Febrile-convulsions/Pages/Diagnosis.aspx
--------------------------------------------------------------------------------------------------------------

station 2 : dr Hammori i think he is from Jordan university.

vomiting with fever since one day
1- take a history
2- if he have neck rigidity what is ur diagnosis ? what test to do ?
3- what precaution should be taken we wanna do LP ?
4- if he have 1000 RBC 1000 WBC . what is ur diagnosis ?
5- how to know if the RBC in CSF come from trauma or infection ?
6- What is the blood test to do ?
7- what is the effect in the sodium ?
they never ask u general in any subject they go deep in any question they ask u , so just study what u
can , and
finish the subject that u will answer all q , but the end it is ur chance , who is the doctor what he will
ask u ?

ANSWER

1) please refer history taking in Pediatrics Made Easy book, under topic MENINGITIS. (I'm sorry,
but it quite long to write on here)

2) Meningitis.
Investigations:
-lab studies : CBC, electrolytes (ensuing SIADH may cause severe hyponatremia) and blood
cultures.
-lumbar puncture with CSF analysis is often diagnostic
-cerebral imaging and EEG should be done in cases of atypical seizures.

#source: In A Page Pediatrics Book, 2nd edition, pg 193

3) Precaution if do LP:
-asses opening pressure , cell count, differential, glucose, protein (compare with systemic values),
bacterial culture, and PCR for viruses.
-avoid LP if signs of elevated intracranial pressure, prolonged or focal seizures, focal neurologic
signs, increased purpuric rash, Glasgow Coma Scale less than 13, or pupillary asymmetric or
dilatation are present.
-if suspect increased intracranial pressure, a head CT scan should be performed prior to LP.

#source: In A Page Pediatrics Book, pg 193

4) Bacterial meningitis (maybe, if related to result of WBC alone, no idea about RBC count, i'm
sorry)

-Normal CSF may contain up to 5 WBCs per mm3 in adults and 20 WBCs per mm3 in
newborns.6 Eighty-seven percent of patients with bacterial meningitis will have a WBC count
higher than 1,000 per mm,3 while 99 percent will have more than 100 2per mm3. Having less than
100 WBCs per mm3 is more common in patients with viral meningitis.
Elevated WBC counts also may occur after a seizure,7 in intracerebral hemorrhage, with
malignancy, and in a variety of inflammatory conditions. Table 2 lists common CSF findings in
various types of meningitis.
#source: http://www.aafp.org/afp/2003/0915/p1103.html
*I attached here the normal CSF findings, thougt it might benefit all of you.
Normal CSF findings:
-pressure = 50-180 mmH2O
-leukocytes = <4 ; 60%-70% lymphocytes, 30%-40% monocytes, 1%-3% neutrophils. ( in
/microLiter)
-protein = 20-45 mg/dL
-glucose = > 50% of serum glucose.

#source: NELSON Essentials of Pediatrics, 6th edition, pg 382

5) -Peripheral blood in the CSF after a traumatic tap will result in an artificial increase in WBCs
by one WBC for every 500 to 1,000 RBCs in the CSF. This correction factor is accurate as long as
the peripheral WBC count is not extremely high or low.
A traumatic tap occurs in approximately 20 percent of lumbar punctures. Common practice is to
measure cell counts in three consecutive tubes of CSF. If the number of RBCs is relatively constant,
then it is assumed that the blood is caused by an intracranial hemorrhage. A falling count is
attributed to a traumatic tap. The three-tube method, however, is not always reliable.8
Xanthochromia is a more reliable predictor of hemorrhage. If a traumatic tap occurs within 12 hours
of a suspected subarachnoid hemorrhage, it is reasonable to repeat the lumbar puncture one
interspace up to try and obtain clear CSF.
#source: http://www.aafp.org/afp/2003/0915/p1103.html

-RED BLOOD CELL (RBC) COUNT. While not normally found in CSF, RBCs will appear
whenever bleeding has occurred. Red cells in CSF signal subarachnoid hemorrhage, stroke, or
traumatic tap. Since white cells may enter the CSF in response to local infection, inflammation, or
bleeding, the RBC count is used to correct the WBC count so that it reflects conditions other than
hemorrhage or a traumatic tap. This is accomplished by counting RBCs and WBCs in both blood
and CSF. The ratio of RBCs in CSF to blood is multiplied by the blood WBC count. This value is
subtracted from the CSF WBC count to eliminate WBCs derived from hemorrhage or traumatic tap.

Read more: http://www.surgeryencyclopedia.com/Ce-Fi/Cerebrospinal-Fluid-CSF-

Analysis.html#ixzz42gA0ALBs

#source: http://www.surgeryencyclopedia.com/Ce-Fi/Cerebrospinal-Fluid-CSF-Analysis.html

6) blood test to do:

-CBC
-blood cultures

7) effect in sodium: increased in level of sodium, hypernatremia. (If excessive vomiting)

-Hypernatremia is almost always an indication of excessive fluid depletion. It usually occurs with
inadequate fluid intake and increased water loss. It commonly develops in elderly residents as a
result of:
Certain diseases and medical conditions
Physical or mental inability to consume sufficient fluids
Lack of thirst
Conditions that override the bodys volume control mechanisms, usually excessive diuresis or
diabetes insipidus
Fever
Vomiting
Diarrhea
Loss of excessive water through the kidneys
Receiving tube feedings with inadequate free water
#source: http://www.hcpro.com/LTC-242929-1983/Understanding-hyponatremia-and-
hypernatremia-in-dehydration.html

--------------------------------------------------------------------------------------------------------------

1st station
(Dr.Wael)
5 yrs child presented to u in the ER with limping due to pain in the left hip.
1-Dx. : Septic arthiritis.
2-DDx.
3-Rx.
4-if not responding to Antibiotics.what's next?
5-what do u think the comfortable position for his hip? Flexion. Why?? Relieve his pain.
6-how to Dx. Osteomyelitis.
7-what r the types of each of the following vaccine:RSV, BCG, Hep. B, ipv,..)

ANSWER

1) Diagnosis: Septic arthritis

2) Differential diagnosis:
Oligoarticular disease:
-infection ( Lyme disease, tuberculosis, parvovirus B19, septic arthritis, reactive arthritis, synovitis)
-psoriatic arthritis
-traumatic effusion
-malignancy

Polyarticular disease:
-gonorrhea
-SLE
-spondyloarthropathy

Systemic disease:
-malignancy
-IBD
-dermatomyositis
-SLE
-vasculitis

#source: In A Page Pediatrics Book, 2nd edition, pg 394

3) Treatment :
-Approach Considerations
Hospitalize all children presumed to have septic arthritis (SA) for empiric intravenous antibiotic
therapy. After 2-3 days of immobilization, encourage early passive range of motion.
The optimal duration of antibiotic therapy is not defined, and recommendations vary from 1-6
weeks. Thus, institutional practices will prevail. In general, 3-4 weeks of antibiotic therapy is used
to treat S aureus,H influenzae type B ,or S pneumoniae infections, while gonococcal infections are
treated for 7-10 days.
Consultations
Consultation may be indicated with an orthopedic surgeon. Septic arthritis of the hip requires
emergent irrigation and drainage to minimize risk of aseptic necrosis of the femoral head.
Consultation with an infectious diseases specialist is particularly indicated if the diagnosis is
uncertain or if the microbiology is unusual.
Splinting and Antibiotics
Splint the affected joint in a functional position for the first few days after a diagnosis of septic
arthritis (SA). Encourage early passive range of motion to stretch tendons and prevent contractures.
Once an organism is identified, an appropriate antibiotic is selected, and the child is demonstrating a
good clinical response, continue outpatient therapy with either high-dose oral antibiotics or
parenteral antibiotics. Antibiotics readily enter the joint fluid in high concentrations after oral
administration. Frequent revisits to the physician to ensure compliance and good clinical response
are essential.
Aspiration, Arthrotomy, and Drainage
No studies have compared outcomes for children with SA undergoing arthrotomy versus aspiration
alone. Traditionally, for uncomplicated septic arthritis involving joints other than the hip or
shoulder, serial needle aspirations are performed. These may be discontinued once fluid no longer
reaccumulates. Failure to reach this goal is an indication for arthrotomy and open drainage.
Urgent arthrotomy and open drainage is usually performed in septic arthritis of the hip or shoulder,
septic arthritis of other joints if no improvement occurs within 3 days of starting antimicrobial
therapy, or if a large amount of pus or debris is aspirated during diagnostic arthrocentesis. However,
in one recent study of 62 children with septic arthritis of the hip, 50 were treated successfully with
aspiration and antibiotics alone.[12]
#source: http://emedicine.medscape.com/article/970365-treatment#showall

4) Not respond to antibiotics, then?

Urgent arthrotomy and open drainage is usually performed in septic arthritis of the hip or shoulder,
septic arthritis of other joints if no improvement occurs within 3 days of starting antimicrobial
therapy, or if a large amount of pus or debris is aspirated during diagnostic arthrocentesis. However,
in one recent study of 62 children with septic arthritis of the hip, 50 were treated successfully with
aspiration and antibiotics alone.[12]
#source: http://emedicine.medscape.com/article/970365-treatment#showall

5) What do u think the comfortable position for his hip? Flexion. Why?? Relieve his pain.

6) How to diagnose Osteomyelitis

-Laboratory Studies
See the list below:
To confirm a clinical diagnosis of osteomyelitis, adequate radiologic and laboratory data are
necessary.
The WBC count is elevated in only one half of patients with or without thrombocytosis.

The C-reactive protein and erythrocyte sedimentation rate (ESR) are almost always elevated
(except in small bones infections).
There are many methods to attempt to recover the organism causing the bone infection, such
as blood, bone, or joint aspirate cultures. It is important to obtain these cultures before any
antibiotics are given.
However, at times cultures may be negative or difficult to obtain and therapy should be
guided by the most common causes.
If one is able to obtain bone and/or joint fluid aspirate for culture, a Gram stain is vital, as the
procedure itself can be bactericidal.
Consult with the microbiology laboratory prior to obtaining cultures to ensure proper culture
mediums and technique are used.
If a clinician is considering, Kingella kingae, notify the microbiology department as recovery
is improved by inoculating synovial fluid directly into blood culture bottles.
Consider performing a bone biopsy if the patient does not respond to standard therapy.

Imaging Studies
See the list below:
MRI

o This test remains the criterion standard, especially in early infections.

o On T2-weighted images, increased marrow intensity with surrounding inflammation is

suggestive of osteomyelitis. Gadolinium contrast is important to help elucidate edema
from an abscess.[10] These abnormalities need to be correlated with the clinical picture
before a diagnosis is made, as they are not specific for osteomyelitis.
Radiography
o Initial films may be normal, with or without soft tissue swelling. Bone destruction
occurs 10-15 days later and then can be appreciated on radiographs.[8, 9]
o Radiography can be useful in revealing bone tumors, fractures, and healing fractures.

o Osteopenia, lytic lesions, and periosteal changes are late radiographic signs; their
absence does not exclude a diagnosis of acute osteomyelitis.
Three-phase technetium radionuclide bone scanning

o Through enhanced uptake of the radioisotope, this procedure reveals increased

osteoblastic activity of the infected bone and distinguishes osteomyelitis from deep
cellulitis.
o Technetium bone scanning has a false-negative rate of as much as 20%, particularly in
the first few days of illness.
 o Chronic recurrent multifocal osteomyelitis, fractures, bone tumors, and surgery also
cause enhanced technetium uptake.
o It is an inexpensive test without need for sedation and with relatively quick turnaround.

Indium scanning: This test, which uses indium-labeled leukocytes, is also useful, although it
has limitations in newborns, infants, and patients with neutropenia.
Gallium scanning: This study is usually not recommended because of lower specificity and
exposure to higher levels of radiation.
Ultrasonography:
o This modality is difficult to use in acute cases of osteomyelitis, with limitations based
on availability, technician-dependent results, and an inability to differentiate fluid
patterns as infectious versus traumatic.
o Clinical suspicion for deep vein thrombosis should be especially high in patients with
osteomyelitis caused by CA-MRSA who have an elevated C-reactive protein level.
Doppler venous ultrasonography is the first imaging study indicated in such cases.
However, routine screening is not yet recommended.[1, 2, 4]
Procedures
See the list below:
Bone aspiration may be necessary to identify the pathogen.

Consider bone biopsy if other diagnoses are possible (eg, tumors).

Joint aspiration is recommended if signs and symptoms suggest pathology near shoulder,
knee, or hip joints. This is critical because arthrotomy is indicated if evidence of hip or
shoulder arthritis is present.
If signs and symptoms do not begin to resolve within 48-72 hours of initiation of appropriate
antimicrobial treatment, consider bone aspiration to drain the pus, in consultation with the
orthopedic surgeon.
Staging
An osteomyelitis staging system is present in the literature for adult treatment and diagnosis of
osteomyelitis. The Cierny-Mader classification is the newest system to account for host factors to
aid with treatment. It categorizes the first part by anatomical involvement of infection, such as type
1 as medullary osteomyelitis and host type A as a normal host.[11]
#source: http://emedicine.medscape.com/article/967095-workup#showall

7) Types of following vaccine:

Vaccines of this type on U.S. Recommended
Vaccine type Childhood (ages 0-6) Immunization Schedule

Measles, mumps, rubella (MMR combined

vaccine)
Varicella (chickenpox)
Influenza (nasal spray)
Live, attenuated Rotavirus

Polio (IPV)
Inactivated/Killed Hepatitis A

Toxoid (inactivated Diphtheria, tetanus (part of DTaP combined

toxin) immunization)
Subunit/conjugate
Hepatitis B
Influenza (injection)
Haemophilus influenza type b (Hib)
Pertussis (part of DTaP combined immunization)
Pneumococcal
Meningococcal

Vaccine type Other available vaccines

Zoster (shingles)
Live, attenuated Yellow fever

Inactivated/Killed Rabies

Human papillomavirus (HPV)

Subunit/conjugate

#source: http://www.historyofvaccines.org/content/articles/different-types-vaccines

--------------------------------------------------------------------------------------------------------------

2nd station (Dr.Fareed)

13 yrs presented to the ER with yellowish discoloration of the eyes.
1-how to approach to this pateint?? Hx, PE, Inv.
-ask relevant hx. ( drug ingestion, hemolytic, family Hx...)
2-what to do in PE?
3-DDx.
4-in PE why do u think its important to evaluate her mental status?
5-what drugs u suspect this pt has taken.. If it is a suicidal attempt??
6-what Inv. u would ask for this pt.

ANSWER

1) *can refer Pediatrics Made Easy Book, in history taking, under topic Neonatal Jaundice. Maybe
not 100% related but can refer it as a guidelines. I'm sorry.

2) *same as previous question

3) DDX (*this related to neonate)

Indirect hyperbilirubinemia:
-physiologic jaundice
-ABO incompatibility
-breast milk jaundice
-Rh isoimmunization
-neonatal sepsis
-G6PD deficiency
-hereditary spherocytosis
-Gilbert disease
-Crigler-Najjar syndrome

Direct hyperbilirubinemia:
-biliary atresia
-idiopathic neonatal hepatitis
-choledochal cyst
-neonatal (TORCH) infection
-alpha-antitrypsin deficiency
-parenteral nutrition
-galactosemia

#source: In A Page Book, 2nd edition, pg 314

4) Maybe we afraid of Encephalopathy signs.

Some of the signs and symptoms of liver disease include:

Jaundice (Yellowing Of The Skin And Eye)

Pruritus (Itching)

Dark Or Tea-Colored Urine

Muscle Wasting

Skin may show liver spots , palm may be unduly bright mottled red

Retention Of Fluid: This May Take The Form Of Ascites (Swelling Of The Abdomen With
Fluid) And Or Swelling Of Ankles Or Legs With Fluid.
Easy Bruising And Bleeding (Bleeding Gums Or Frequent Nosebleeds)
Vomiting Blood

Blood In The Stool (Bright Red Blood Or Black, Tar-Like Stool)

Mental Confusion (Encephalopathy), sleep disturbance

General feeling of ill-health: These are general symptoms not necessarily indicative of liver
disease but reflect constitutional symptoms of poor health and illness in-general. These are
fatigue, weight loss, debility, weakness, malaise, and poor appetite.
 In women: Menstural irregularity, infirtilty and early menopause are not uncommon with
advanced liver disease.
In men: decreased libido, erectile dysfunction, impotence, sterility, thinning of body hair and
prominence of breast are seen with advanced liver disease.

#source: http://njms.rutgers.edu/departments/medicine/divisions/gi/liver_disease.cfm

5) Paracetamol toxicity.

Risk of severe liver damage (ie a peak ALT more than 1000 IU/L)
Based on the dose of paracetamol ingested (mg/kg body weight):
Less than 150 mg/kg - unlikely.
More than 250 mg/kg - likely.
More than 12 g total - potentially fatal.
Paracetamol can cause serious or fatal adverse effects at around 150 mg/kg for many adults. There
is considerable interpatient variability which depends on age, health and substances taken with the
paracetamol.
The level is higher for young children.
#source: http://patient.info/doctor/paracetamol-poisoning

6) Investigation:
Paracetamol level: take paracetamol level four hours post-ingestion, or as soon as the patient
arrives if:
Time of overdose is greater than four hours.
Staggered overdose (in staggered overdoses, the level is not interpretable except to
confirm ingestion).
U&E, creatinine - to look for renal failure and have a baseline.
LFTs: may be normal if the patient presents early but may rise to ALT >1000 IU/L. This is
the enzyme level taken to indicate hepatotoxicity.
Glucose: hypoglycaemia is common in hepatic necrosis and capillary blood glucose should be
checked hourly.
Clotting screen: prothrombin time is the best indicator of severity of liver failure and the INR
should be checked 12-hourly.
Arterial blood gas; acidosis can occur at a very early stage, even when the patient is
asymptomatic. It is seen in up to 10% of patients with ALF.
FBC and salicylate levels are not routinely required.

#source: http://patient.info/doctor/paracetamol-poisoning

-------------------------------------------------------------------------------------------------
first station:
dr.hala + dr mn el hashmeyye :
male with jerky movements came with his grandma, still seizuring how to deal with him ... the
patient was having hyponatremia 116
1-how to deal with him ?? .....
2-what will happen if you increased the rapidly?...
3-what is the evel of Na that we should reach to stop the seizure? ....
4-Also asked about the doses of antiepileptics ..

ANSWER

1) Management:
-keep the patient in a safe environment during the seizure to avoid injury
-avoid placing objects in the child's mouth
-if vomiting occurs, turn the patient to the side to avoid aspiration.
-treat underlying systemic causes, if possible, and avoid substances (eg, medications) that provoke
seizures.
-treat with appropriate anticonvulsant medication, as necessary:
i. Status epilepticus: Benzodiazepines, phenobarbital or phenytoin bolus, or induce pentobarbital
coma
ii. Partial seizures: carbamazepine, valproic acid, lamotrigine, phenytoin
iii. Generalized seizures: valproic acid, lamotrigine
iv. Absence seizures: Ethosuximide, valproic acid.
v. Infantile spasms: ACTH, vigabatrin, valproic acid, benzodiazepines
-a ketogenic diet (high in fat and low in carbohydrates and protein) may be of value in treating some
types of refractory seizures
-epilepsy surgery (eg, cortical resection, corpus callosotomy, vagal nerve stimulators) may be useful
in refractory cases. *might not be suitable in this case.

#source: In A Page Book, 2nd edition, pg 157

2) Hyponatremia is corrected slowly, to lessen the risk of the development of central pontine
myelinolysis (CPM), a severe neurological disease involving a breakdown of the myelinsheaths
covering parts of nerve cells. In fact, overly rapid correction of hyponatremia is the most common
cause of that potentially devastating disorder.[16] During treatment of hyponatremia, the serum
sodium (salt level in the blood) is not allowed to rise by more than 8 mmol/L over 24 hours (i.e.
0.33 mmol/L/h rate of rise). In practice, too rapid correction of hyponatremia and thence CPM is
most likely to occur during the treatment of hypovolemic hyponatremia.

#source: https://en.m.wikipedia.org/wiki/Hyponatremia#Treatment

3) Acute hyponatremia is less common, and the goal is to return the sodium levels to normal to
prevent cerebral edema and brain death. In most patients, if the source of excess water intake is
eliminated, the body's kidneys can correct the sodium abnormalities on its own. If however, coma or
seizure exists, highly concentrated intravenous sodium (3% hypertonic saline) may need to be
infused. The goal is to reverse the low sodium levels at a rate of 4-6 mEq/l every 1-2 hours.
#source: http://www.emedicinehealth.com/hyponatremia_low_sodium/page7_em.htm

4) dose of antiepileptic drugs:

#source: https://www.epilepsysociety.org.uk/sites/default/files/attachments/Chapter28Sander2015.
pdf

[pg 8]

second station:
dr mn el jaishi :
1- causes of neonatal seizure and what electrolytes causing it
2- 3 years with stridor what is yr ddx
3- who are the ones more susciptable to get epiglottitis
4- how to manage epiglottitis
5- what types of dehydration you know
6- how to differentiate between mild , mod , severe clinically
7- what is hypertension ???

ANSWER
1) the most common cause of neonatal seizures is hypoxic-ischemic encephalopathy (50-60% of
cases); other cause include:
-intracranial infections (10% of cases) : bacterial infections include group B Streptococcus, Listeria,
and E. Coli, nonbacterial causes include toxoplasmosis, cytomegalovirus,herpes simplex, and
rubella.
-intracranial hemorrhage (10% of cases) : intraventricular hemorrhage is most common, as well as
subarachnoid and subdural hemorrhages.
-metabolic disturbance (eg, hypoglycemia, hypocalcemia, hypomagnesemia, hyponatremia)
-drug withdrawal (eg, cocaine, heroin, barbiturates)
-inborn errors of metabolism are relatively rare causes.
-pyridoxine depedency is a rare condition but presents in the neonatal period.
-cerebral dysgenesis and brain malformations.

#source : In A Page book, 2nd edition, pg 310.

2) DDX of Stridor:
-Stridor is a sign of upper airway obstruction. In children, laryngomalacia is the most
common cause of chronic stridor, while croup is the most common cause of acute stridor.
Generally, an inspiratory stridor suggests airway obstruction above the glottis while an
expiratory stridor is indicative of obstruction in the lower trachea. A biphasic stridor suggests
a glottic or subglottic lesion. Laryngeal lesions often result in voice changes. A child with
extrinsic airway obstruction usually hyperextends the neck. The airway should be established
immediately in children with severe respiratory distress. Treatment of stridor should be
directed at the underlying cause.

-Causes of Stridor in Children According to Site of Obstruction

Nose and pharynx

Choanal atresia
Lingual thyroid or thyroglossal cyst
Macroglossia
Micrognathia
Hypertrophic tonsils/adenoids
Retropharyngeal or peritonsillar abscess
Larynx
Laryngomalacia
Laryngeal web, cyst or laryngocele
Laryngotracheobronchitis (viral croup)
Acute spasmodic laryngitis (spasmodic croup)
Epiglottitis
Vocal cord paralysis
Laryngotracheal stenosis
Intubation
Foreign body
Cystic hygroma
Subglottic hemangioma
Laryngeal papilloma
Angioneurotic edema
Laryngospasm (hypocalcemic tetany)
Psychogenic stridor

Trachea
Tracheomalacia
Bacterial tracheitis
External compression
#source: http://www.aafp.org/afp/1999/1115/p2289.html

3) 2-6 years old

#source: slides Management of Acute Upper Airway Obstruction

4) Management of Epiglottitis:
-keep the child quiet and avoid agitation
-call anesthetist, ENT, and consultant pediatrician.
-keep emergency trolley behind.
-do not examine throat
-oxygen may be given by mask.

Intubation:
-intubation should be performed by an anesthesiologist experienced in anesthesia of children with
severe airway obstruction.
-care of ETT including positioning, fixation, humidification, suction, and arm splinting are vital.
-an IV cannula is inserted, blood cultures taken.

Antibiotics:
-3rd generation cephalosporins (cefotaxime, ceftriaxone)
-chloramphenicol

#source: slides Management of Acute Upper Airway Obstruction

5) Types of dehydration:
-Dehydration can be categorized into isotonic, hypertonic and hypotonic, depending on how it
affects the tonicity of the extracellular fluids.

#source: http://www.ehealthstar.com/dehydration/types-pathophysiology

6) Differentiate mild, moderate, severe dehydration clinically:

#source : http://emedicine.medscape.com/article/801012-clinical#b3

7) Hypertension:
-Stage 1 hypertension = systolic and/or diastolic blood pressure between the 95th percentile and
5mmHg above the 99th percentile.
-Stage 2 hypertension = systolic and/or diastolic blood pressure greater than 99th percentile plus
5mmHg.

*blood pressure percentiles are based on gender, age, height based on measurements on three
separate occasions.

#source: In A Page book, 2nd edition, pg 112.

--------------------------------------------------------------------------------------------------------------

First station;
3 year old fever and vomiting
- hx, PE, it was meningitis
- how to manage it , I said give him antibiotics in ER then to do LP after fundoscopy. Dr asked who
do
the fundoscopy? I said the ophthalmologist
#CAN REFER ANSWER IN QUESTION BEFORE. (Meningitis)

Dr. Hala:
1- do you give the antbiotics before LP?
No.
2- when you shouldn't do LP? papilledema, if we did CT and found space occupying lession,
infection in the skin over it, abnormal anatomy of spine, but she wanted more, something to ask
parents about it but I didn't know.
3- if pt developed hyponatremia, is it real hyponatremia? what is the cause?
No, dilutional, he has SIADH
--------------------------------------------------------------------------------------------------------------

First station:
Dr. wael and a doctor from the military hospital:
Military doctor:

1. In the ER, female presents with pallor and hematurea. Her PVC was 18, bilirubin was 3.4 and
LDH was 1400.
A. Diagnosis:
-Hemolytic anemia.
B. 2 tests to confirm:
-Positive Coomb's test, CBC for high retics counts.

2. In the ER, a 7 year old patient comes with RDS.

A. Will a chest X-ray be helpful?
-Yes.
B. what can a chest X-ray tell you?
-Asthma; hyperinflation.
-Pneumothorax; collapse.
-Pneumonia; consildation.
-Cardiac causes; cardiomegaly.

3. In the ER, a 7 year-old boy presents with limping and fever.

A. Diagnosis:
-Septic arthritis.
B. treatment:
-Drain, IV antibiotics.

[pg 9]

Dr. Wael:
1-What are these vaccines made from, then he named 12 different vaccines.
2-Then he asked me to give examples of the following group of antibiotics, he named like 6.

ANSWER

1) CAN REFER ANSWER BEFORE (related to type of vaccine)

2) refer table below:

#source: http://www.orthobullets.com/basic-science/9059/antibiotic-classification-and-mechanism

--------------------------------------------------------------------------------------------------------------

Second station:
Dr. Fared Kanaan from JUH.
13 year old female with yellowish discoloration of the sclera. How will you approach:
1-History. Then you list all relevant history points.
2-Physical exam: don't forget to evaluate the neurological state of the patient.
3-DDx:
Hemolytic anemia.
Hep. A.
Gilbert.
Intoxication.
Sickle crises.
And more.
4. Tests you order:
5. If you suspect hep. A, how to confirm.
-Hepatitis A
Hepatitis A (also called infectious hepatitis) is a common form of hepatitis in children. It's caused
by the hepatitis A virus (HAV), found in the stool (feces or poop) of infected people. Infected stool
might be found in small amounts in food and on objects (such as doorknobs and diapers). Hepatitis
A can remain in the stool for several months after the initial illness, especially in younger babies and
children.
With every answer I give he went into details, tell me about Gilbert, manifestations of hemolytic
anemias, how do patients get hepatitis, intoxication with which drugs.
*CAN REFER ANSWERS BEFORE (related on jaundice)

--------------------------------------------------------------------------------------------------------------

station 1;
Dr wael and another doctor from army
6 years old male presended to the ER with fever for 1 day and liver span 30 cm.
1-DDx ???
2-whats the type of hepatitis A ???
3-whats the most likely mode of transmiision ??
4-her brother is 9 month how protect him ???
5-at which age we give tha hep A vaccine ???
el hepA sho be8rab ll polio ??!!!!
lab test within 2 hours ?? (liver enzyme )
6-AST and ALT 3000 is this confirm hepatitis ???
7-whtas the indication of admmission ??( he need 4 or 5 )
8-when to discharge ????
9-when allow him to go to school ???

ANSWER

1) DDX:
-hepatitis A
-autoimmune hepatitis
-other hepatitis virus
-adenovirus
-enterovirus
-EBV virus
-drug-induced hepatitis
-CMV virus
-hemolytic disease (eg, early stages of hemolytic uremic syndrome)
-gallstones
-Wilson disease

#source: In A Page book, 2nd edition, pg 214

2) No idea on this question

3) fecal-oral route

4) administer Immunoglobulin to children younger than 12 months.

#source: In A Page book, 2nd edition, pg 215

5) Administer Hep A vaccine to all children from 12-23 months of age.

#source: In A Page book, 2nd edition, pg 215.

6) yes, confirm hepatitis. Because ALT and AST values of 200-5000 indicates hepatitis.

#source: In A Page book,2nd edition, pg 215

7) Admit patients with hepatitis if they are showing any signs or symptoms suggestive of severe
complications. Admit and evaluate for hepatic encephalopathy any patients with altered mental
status, agitation, behavior or personality changes, or changes in sleep-wake cycle. Other admission
criteria that are suggestive of severe disease include a prothrombin time (PT) longer than 3 seconds,
a bilirubin level greater than 30 mg/dL, and hypoglycemia.
Admit any patients with intractable vomiting, significant electrolyte or fluid disturbances, or
significant comorbid illness; those who are immunocompromised; and those who are older than 50
years.
#source: http://emedicine.medscape.com/article/775507-treatment

8) When to discharge?
-not sure, but symptoms usually last less than 2 months. Disease is typically self-limited with
complete recovery (even in prolonged cases).
#notes: In A Page book, 2nd edition, pg 215
9) no idea.
-------------------------------------------------------------------------------------------------------------
2nd station Dr freed from JU
13 years old female presended to the ER with one day history of jaundice
detaild history but (Dr was happy when i asked about parcetamol as suicidal attempt , family history
about of hemolytic and malignancy and liver disease , blood transfusion and level of consciousness
to hepatic encephalopathy , drug history such as trimehtrompin , favisim )
physical examination ???

[pg 10]
DDx??
what's the dose of paracitamole lead to acute liver failure ??? 150 mg /kg
what's the antedote ?? nacytylcystine
do we do gastric lavage ??? yes if less than 2 day
------------------------------------------------------------------------------------------------------------------------
---------------
first station; Dr Samah
A 8 years old female child came to ER with generalized tonic clonic seizure.
1. Take history from her mom
(Can refer answer in Pediatric Made Easy books)

2. What investigations specific to this case you will do (patient took valproic acid, same problem
since 1 years old)
-EEG (maybe)
*can refer In A Page book, pg 157, for details.

3. How do you manage this patient

-keep the patient in a safe environment during the seizure to avoid injury
-avoid placing objects in the child's mouth
-if vomiting occurs, turn the patient to the side to avoid aspiration.
-treat underlying systemic causes, if possible, and avoid substances (eg, medications) that provoke
seizures.
-treat with appropriate anticonvulsant medication, as necessary:
i. Status epilepticus: Benzodiazepines, phenobarbital or phenytoin bolus, or induce pentobarbital
coma
ii. Partial seizures: carbamazepine, valproic acid, lamotrigine, phenytoin
iii. Generalized seizures: valproic acid, lamotrigine
iv. Absence seizures: Ethosuximide, valproic acid.
v. Infantile spasms: ACTH, vigabatrin, valproic acid, benzodiazepines
-a ketogenic diet (high in fat and low in carbohydrates and protein) may be of value in treating some
types of refractory seizures
-epilepsy surgery (eg, cortical resection, corpus callosotomy, vagal nerve stimulators) may be useful
in refractory cases..

#source: In A Page book, 2nd edition, pg 157.

--------------------------------------------------------------------------------------------------------------
Second station; Dr Mahmoud Syehab
A 8 years old child, previously healthy came with nocturnal enuresis
1. What is your differential diagnosis
2. What investigations you will do to this patient
3. What findings in urine analysis for each of your differentials
4. What kind of management you will do for this child
5. red urine, causes, how to differentiate hematuria&hemoglobinuria, investigations.

ANSWER

Question no 1, 2, 3, 4 can be found in In A Page book, 2nd edition, page 96 & 97.

5) differential diagnosis and investigation can be found in Focused History for OSCE of Pediatrics,
pg 18 & 19.

-Hematuria: The color associated with hematuria may vary from red (Figure 3) to black (Figure 4)
depending on the quantity of blood in the urine, the degree of urine acidity and the time interval that
blood has been in contact with urine. In recently formed and freshly collected acidic urine,
hematuria may be associated with urine color that is normal yellow, pink, or red. As red cells
disintegrate, they release hemoglobin, which in an acid environment, may oxidize to
methemoglobin and result in a brown or black color (Figure 4). Black urine viewed with the aid of
bright light or in a thin layer usually appears brown or deep reddish-brown.
If gross hematuria has been observed, determining when during the process of micturition its
intensity is most severe may be helpful in localizing the source of hematuria.
Hemoglobinuria and myoglobinuria: Hemoglobinuria resulting from hemoglobinemia may also
cause freshly voided urine to appear brown or black in color if hemoglobin has been oxidized to
methemoglobin. Myoglobinuria may also cause urine to appear brown. Thus, freshly collected urine
that is brown or black in color may be associated with hematuria, hemoglobinuria or myoglobinuria.
Because all three of these abnormalities may produce a positive result for occult blood detected by
reagent strips, additional investigation is required to differentiate them. A negative reagent strip test
for blood in red, black or brown urine suggests the presence of a chromogen other than hemoglobin
or myoglobin.
Differentiation of hematuria from hemoglobinuria and myoglobinuria is of obvious importance.
Centrifugation of an aliquot of a visibly discolored sample and comparison of the supernatant to an
uncentrifuged aliquot of the sample is often of value. The supernatant of samples with significant
hemoglobinuria or myoglobinuria will remain equally discolored (Figure 1). The supernatant of
samples with significant hematuria will be normal in color or less discolored, and contain significant
RBC in the sediment.
Observation of plasma may aid in differentition of myoglobinuria from hemoglobinuria. Clear
plasma in a patient with red, brown, or black urine suggests myoglobinuria or hematuria, whereas
pink plasma suggests hemoglobinuria. The ammonium sulfate solubility test may also be used to
help differentiate hemoglobinuria from myoglobinuria.
#source: http://veterinarynews.dvm360.com/discolored-urine-what-does-it-mean
--------------------------------------------------------------------------------------------------------------

Dr. Rula,
Hx. Vomiting and jaundice.
1-DDx?
2-lab tests for Hep. A?
3-Markers for liver failure vs liver inflammation?
4-Indications for admission?
5-Management of hepatic encephalopathy?
6-Infectivity period, when can he go back to school?
7-Indications for Hep A vaccine?
8-Sugar and water for jaundiced child. A myth or true? Why?

ANSWER

Question 1,2,3,4 can refer answer in question before.

5) Management of hepatic encephalopathy:

- I think this might be the answer, cause it related to hepatic encephalopathy.

Management of Cerebral Edema

Cerebral edema occurs in as many as 80% of patients. It increases intracranial pressure (ICP),
resulting in impaired cerebral effusion. This can result in irreversible neurologic damage, and death.
Cytotoxic and vasogenic edema are present, presumably caused by release of neurotoxins in the
circulation.
Insertion of an ICP monitor in patients with grade 3 encephalopathy is advisable to detect cerebral
edema early in its course.
Preventive measures include positioning the patient with the head elevated and avoidance of any
manipulations that increase ICP. Other preventive measures are the avoidance of hypothermia and
hypercapnia, controlling agitation, and instituting moderate hyperventilation.
Continuously monitoring ICP in severe illness is of vital importance, especially in stage 3 or 4 of
hepatic encephalopathy. Mannitol is used in patients with documented ICP greater than 30 mm Hg
and is considered in patients with progressive edema.
#source: http://emedicine.medscape.com/article/929028-treatment#d13

6)
How soon do symptoms appear?
The symptoms commonly appear within 28 days of exposure, with a range of 15-50 days.
For how long is an infected person able to spread the virus?
The contagious period begins one to two weeks before symptoms appear, and is minimal about one
week after the onset of jaundice. Food workers should be excluded from work for at least two
weeks after the onset of clinical symptoms of hepatitis A. If jaundiced, food workers should
not return to work for at least one week after onset of jaundice
#source: https://www.health.ny.gov/diseases/communicable/hepatitis/hepatitis_a/food_service_wo
rkers_fact_sheet.htm

7)
Who should obtain the hepatitis A vaccine?
Hepatitis A vaccine is recommended for the following persons:
Travelers to areas with increased rates of hepatitis A
Men who have sex with men
Injecting and non-injecting drug users
Persons with clotting-factor disorders (e.g., hemophilia)
Persons with chronic liver disease (including persons with chronic hepatitis B or chronic
hepatitis C virus infection)
All children aged 12-23 months; children not fully vaccinated by age two
The hepatitis A vaccine may also be used in certain outbreak situations where ongoing transmission
is occurring. Although studies of certain occupational groups (for example, food service workers,
health care workers, child care workers, sewerage workers) have not shown an increased risk, such
people may consider vaccination if they wish to further reduce their risk or are in communities
where ongoing outbreaks are occurring.
#source: https://www.health.ny.gov/diseases/communicable/hepatitis/hepatitis_a/food_service_wo
rkers_fact_sheet.htm

8)
Treatments Not Recommended For Decreasing Jaundice In The Breastfeeding Infant:
Supplementing with sugar waterIn fact, this can worsen jaundice by interfering with breast
milk intake and breast milk production. It can also delay the reduction of bilirubin levels.
Discontinuing breastfeedingThis can ultimately make jaundice worse and can sabotage a
mothers effort to provide her child with the best nutrition possible. Frequent and efficient
feedings of breast milk are the best way to decrease jaundice.

#source: http://americanpregnancy.org/breastfeeding/breastfeeding-and-jaundice/

--------------------------------------------------------------------------------------------------------------

Dr. Waddah,
1-Doubling of weight at what age?
2-Tripling of height?
3-Drawing a triangle? Circle? Square?
4- Sitting without support? Social smile?
5- Mention vaccines not in the Jordanian program? And there respective age of administration?
6- Egg yolk allergy, what vaccine should be given with caution?
7-Drug of choice for anaphylaxis? Route?
--------------------------------------------------------------------------------------------------------------

Dr.Khader From JU
13 year old female presented to the ER with jaundice of 1 day duration.
approach HX,physical,examination, Investigation.
He wanted a detailed HX. in each section why did u ask this question. like contact with jaundiced
patients, eating outside, vaccines, Drug hx, associated symptoms like fever,abdominal pale,pale
stool, dark urine, family hx. of similar cases..etc.

*p/s- answer can refer to previous question.

[pg 11]
DDX?
if your patient has deterioration of level of consciousness what do u suspect?
(Fulminant hepatic failure as a complication).
Drug that can give u such picture?
What investigations do you order?
*can refer answer for the previous same question
=======================================================================
Dr.Wael Hayajneh and another doctor from the army
1-how is the x-ray helpful for an emergency doctor?
2-if your patient suddenly deteriorated what do u suspect?
3-what do u see in foreign body?
4-You have a male patient with Jaundice, LDH 1000 and billirubin 3.
what do u suspect?
5-simplest exam to confirm(Friday and no labs)?
6-next step?
7-how to classify anemia according to coomb's?
8-is coomb's positive or negative in G6PD?
Dr Wael
9-(5 most common causes of fever in a child aged 2 months)
- what is the commonest cause of fever in general among this age group?
ANSWER
1) consolidation,pneumothorax, foreign body
2) blocked airways, metabolic acidosis (maybe)
-Complications include metabolic disorders (acidosis, low blood sugar), patent ductus
arteriosus, low blood pressure, chronic lung changes, and bleeding in the brain. (Complications of
RDS in neonate)
#source: https://en.m.wikipedia.org/wiki/Infant_respiratory_distress_syndrome
3) atelectasis, hyperinflation
4) hemolytic anemia
5) retics
6) coomb's test.
7) *anti-globulin test = Coombs test
Autoimmune hemolytic anemia
Conditions in this category include warm autoimmune hemolytic anemia, cold agglutinin syndrome,
mixed- or combined-type autoimmune hemolytic anemia, and paroxysmal cold hemoglobinuria.[4]
Warm autoimmune hemolytic anemia is the most common type of autoimmune hemolytic anemia
and is generally associated with warm-reactive IgG autoantibodies. Three patterns of reactivity may
be found on a direct antiglobulin test: IgG alone, complement alone, or both.
Cold agglutinin syndrome is associated with cold-reactive autoantibodies, most frequently
immunoglobulin M (IgM). In areas of low temperature in the peripheral circulation, IgM binds to
the RBCs and causes complement to also adhere to the RBCs. As the RBCs circulate to areas of
higher temperature, the IgM may dissociate, but the complement remains. Additionally, the standard
direct antiglobulin test will not detect IgM coating of RBCs. As such, complement alone is
commonly detected on the direct antiglobulin test.
In a patient with mixed-type autoimmune hemolytic anemia, the direct antiglobulin test commonly
detects both IgG and C3.
Paroxysmal cold hemoglobinuria is caused by a biphasic hemolysin, known as the Donath-
Landsteiner hemolysin. This autoantibody is an IgG complement-fixing antibody that reacts with
RBCs in the colder areas of the circulation. The IgG causes C3 to bind irreversibly to RBCs;
subsequently, the IgG dissociates from RBCs in warmer parts of the body. Thus, the direct
antiglobulin test is typically positive only for complement.
Drug-induced hemolysis
Drugs may cause a positive direct antiglobulin test result and/or immune-mediated hemolysis, with
an incidence of approximately 1 in 1 million.[4]
Drugs can induce the formation of antibodies, either against the drug itself or against intrinsic RBC
antigens or the RBC membrane. This may result in a positive direct antiglobulin test result, immune
hemolysis, or both.
Drugs commonly implicated in this include penicillin, second- and third-generation cephalosporins,
alpha-methyldopa, and procainamide, among others.
#source: http://emedicine.medscape.com/article/1731264-overview
8) negative
9) Acute fevers in infants and children are usually caused by an infection. Teething does not
typically cause fever over 101 F.
The most common causes are
 Respiratory infections due to a virus, such as colds or flu
Gastroenteritis (infection of the digestive tract) due to a virus
Certain bacterial infections, particularly ear infections (otitis media), sinus infections,
pneumonia, and urinary tract infections
Newborns and young infants are at higher risk of certain serious infections because their immune
system is not fully developed. Such infections may be acquired before birth or during birth and
include sepsis (a serious bodywide infection), pneumonia, and meningitis.
Children under 3 years old who develop a fever (particularly if their temperature is 102.2 F [39 C]
or higher) sometimes have bacteria in their bloodstream (bacteremia). Unlike older children, they
sometimes have bacteremia with no symptoms besides fever (called occult bacteremiasee Occult
Bacteremia). Vaccines against the bacteria that usually cause occult bacteremia ( Streptococcus
pneumoniae and Haemophilus influenzae type B [HiB]) are now widely used in the United States
and Europe. As a result, occult bacteremia is less common. However, pneumococcal strains that are
not a part of the current pneumococcal vaccine or other bacteria can sometimes cause it.
#source: https://www.msdmanuals.com/home/children's-health-issues/symptoms-in-infants-and-
children/fever-in-infants-and-children
--------------------------------------------------------------------------------------------------------------
1st station>>> dr wael w kman wa7d mn el jaish:
1- acute resp. distress>>> give 3 findings on xray with the DDx
2- 5 yrs baby with jaundice, pallor and hematuria>>>G6PD
3- what invs u will ask for if it was friday and there's no labs opened... -retics
4- what are the main types of hemolytic anemias
5- how to differentiate b/n congenital and acquired hemolytic anemias
ANSWER
*Question 1, 2, 3 can refer answer in previous question.
4) Main types of hemolytic anemia:
-Types of Hemolytic Anemia
There are many types of hemolytic anemia. The condition can be inherited or acquired. "Inherited"
means your parents passed the gene for the condition on to you. "Acquired" means you aren't born
with the condition, but you develop it.
Inherited Hemolytic Anemias
With inherited hemolytic anemias, one or more of the genes that control red blood cell production
are faulty. This can lead to problems with the hemoglobin, cell membrane, or enzymes that maintain
healthy red blood cells.
The abnormal cells may be fragile and break down while moving through the bloodstream. If this
happens, an organ called the spleen may remove the cell debris from the bloodstream.
Sickle Cell Anemia
Sickle cell anemia is a serious, inherited disease. In this disease, the body makes abnormal
hemoglobin. This causes the red blood cells to have a sickle, or crescent, shape.
Sickle cells don't last as long as healthy red blood cells. They usually die after only about 10 to 20
days. The bone marrow can't make new red blood cells fast enough to replace the dying ones.
In the United States, sickle cell anemia mainly affects African Americans.
Thalassemias
Thalassemias (thal-a-SE-me-ahs) are inherited blood disorders in which the body doesn't make
enough of certain types of hemoglobin. This causes the body to make fewer healthy red blood cells
than normal.
Thalassemias most often affect people of Southeast Asian, Indian, Chinese, Filipino, Mediterranean,
or African origin or descent.
Hereditary Spherocytosis
In this condition, a defect in the surface membrane (the outer covering) of red blood cells causes
them to have a sphere, or ball-like, shape. These blood cells have a lifespan that's shorter than
normal.
Hereditary spherocytosis (SFER-o-si-to-sis) is the most common cause of hemolytic anemia among
people of Northern European descent.
Hereditary Elliptocytosis (Ovalocytosis)
Like hereditary spherocytosis, this condition also involves a problem with the cell membrane. In this
condition, the red blood cells are elliptic (oval) in shape. They aren't as flexible as normal red blood
cells, and they have a shorter lifespan.
Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency
In G6PD deficiency, the red blood cells are missing an important enzyme called G6PD. G6PD is
part of the normal chemistry inside red blood cells.
In G6PD deficiency, if red blood cells come into contact with certain substances in the bloodstream,
the missing enzyme causes the cells to rupture (burst) and die.
Many factors can trigger the breakdown of the red blood cells. Examples include taking sulfa or
antimalarial medicines; being exposed to naphthalene, a substance found in some moth balls; eating
fava beans; or having an infection.
G6PD deficiency mostly affects males of African or Mediterranean descent. In the United States,
the condition is more common among African Americans than Caucasians.
Pyruvate Kinase Deficiency
In this condition, the body is missing an enzyme called pyruvate (PI-ru-vate) kinase. Not having
enough of this enzyme causes red blood cells to break down easily.
This disorder is more common among the Amish than other groups.
Acquired Hemolytic Anemias
With acquired hemolytic anemias, your red blood cells may be normal. However, some other
disease or factor causes the body to destroy red blood cells and remove them from the bloodstream.
The destruction of the red blood cells occurs in the bloodstream or, more commonly, in the spleen.
Immune Hemolytic Anemia
In immune hemolytic anemia, your immune system destroys your red blood cells. The three main
types of immune hemolytic anemia are autoimmune, alloimmune, and drug-induced.
Autoimmune hemolytic anemia (AIHA). In this condition, your immune system makes antibodies
(proteins) that attack your red blood cells. Why this happens isn't known.
AIHA accounts for half of all cases of hemolytic anemia. AIHA may come on very quickly and
become serious.
Having certain diseases or infections can raise your risk for AIHA. Examples include:
Autoimmune diseases, such as lupus
Chronic lymphocytic leukemia
Non-Hodgkin's lymphoma and other blood cancers
Epstein-Barr virus
Cytomegalovirus
Mycoplasma pneumonia
Hepatitis
HIV
AIHA also can develop after you have a blood and marrow stem cell transplant.
In some types of AIHA, the antibodies made by the body are called warm antibodies. This means
they're active (that is, they destroy red blood cells) at warm temperatures, such as body temperature.
In other types of AIHA, the body makes cold-reactive antibodies. These antibodies are active at cold
temperatures.
Cold-reactive antibodies can become active when parts of the body, such as the hands or feet, are
exposed to temperatures lower than 32 to 50 degrees Fahrenheit (0 to 10 degrees Celsius).
Warm antibody AIHA is more common than cold antibody AIHA.
Alloimmune hemolytic anemia. This type of hemolytic anemia occurs if your body makes
antibodies against red blood cells that you get from a blood transfusion. This can happen if the
transfused blood is a different blood type than your blood.
This type of hemolytic anemia also can occur during pregnancy if a woman has
Rh-negative blood and her baby has Rh-positive blood. "Rh-negative" and "Rh-positive" refer to
whether your blood has Rh factor. Rh factor is a protein on red blood cells.
For more information, go to the Health Topic Rh Incompatibility article.
Drug-induced hemolytic anemia. Certain medicines can cause a reaction that develops into
hemolytic anemia. Some medicines, such as penicillin, bind to red blood cell surfaces and can cause
antibodies to develop.
Other medicines cause hemolytic anemia in other ways. Examples of these medicines include
chemotherapy, acetaminophen, quinine and antimalarial medicines, anti-inflammatory medicines,
and levodopa.
Mechanical Hemolytic Anemias
Physical damage to red blood cell membranes can cause them to break down faster than normal.
Damage may be due to:
Changes in the small blood vessels.
An artificial heart valve or other device used in blood vessels.
Hemodialysis (HE-mo-di-AL-ih-sis). This treatment for kidney failure removes waste
products from the blood.
A heart-lung bypass machine, which may be used during open-heart surgery.

Preeclampsia (pre-e-KLAMP-se-ah) or eclampsia. Preeclampsia is high blood pressure during

pregnancy. Eclampsia, which follows preeclampsia, is a serious condition that causes seizures
in pregnant women.
Malignant hypertension (hi-per-TEN-shun). This is a condition in which your blood pressure
suddenly and rapidly rises.
Thrombotic thrombocytopenic purpura (throm-BOT-ik throm-bo-cy-toe-PEE-nick PURR-
purr-ah). This rare blood disorder causes blood clots to form in small blood vessels
throughout the body.
Blood cell damage also may occur in the limbs as a result of doing strenuous activities, such as
taking part in marathons.
Paroxysmal Nocturnal Hemoglobinuria
Paroxysmal nocturnal hemoglobinuria (HE-mo-GLO-bih-NYU-re-ah), or PNH, is a disorder in
which the red blood cells are faulty due to a lack of certain proteins. The body destroys these cells
more quickly than normal.
People who have PNH are at increased risk for blood clots in the veins and low levels of white
blood cells and platelets.
Other Causes of Damage to Red Blood Cells
Certain infections and substances also can damage red blood cells and lead to hemolytic anemia.
Examples include malaria and blackwater fever, tick-borne diseases, snake venom, and toxic
chemicals.
#source: https://www.nhlbi.nih.gov/health/health-topics/topics/ha/types
5) *answer can be found in the previous question.
--------------------------------------------------------------------------------------------------------------
2nd satation>>> dr khader from JU:
a man came to ER holding his 5 years old son... saying his child drank a drug bottle
1-take Hx... PE....
2-then if it was paracetamol toxicity what is ur management...
3-anti dote and dose...
4-how to do gastric lavage and its contraindications
ANSWER
*Question 2, 3, 4 included in this source. (refer In A Page book, 2nd edition, pg 413)
--------------------------------------------------------------------------------------------------------------
1st station dr faisal
5 year old patient presented to the clinic with fever and 1 week duration of bloody diarrhea ..
1- take history (can refer Focused Hx for OSCE of Pediatrics, pg 6, and pg 16)
2- 5 DDx
3- then he asked about each one of them ( e-coli , shigella , salmonella and ameba )
4- what is the appropriate antibiotic for each one
5- what is typhoid fever , clinical presentation , how to confirm it
6- if patient had seizure what do u think the cause ( shigella ) what is the patho-physiology for this (
i talked about shiga toxin!!)
ANSWER
2) DDX:
-GE
-anal fissure
-milk @ soy protein intolerance
-IBD
-infectious diarrhea
-juvenile polyps
-Meckel's diverticulum
#source: http://www.uptodate.com/contents/bloody-stools-in-children-beyond-the-
basics?source=outline_link&view=text&anchor=H4#H4
*Question 3, 4 can refer In A Page book ,2nd edition, pg 73.
5)
Typhoid fever, also known as enteric fever, is a potentially fatal multisystemic illness caused
primarily by Salmonella enterica, subspecies enterica serovar typhiand, to a lesser extent, related
serovars paratyphi A, B, and C.
The protean manifestations of typhoid fever make this disease a true diagnostic challenge. The
classic presentation includes fever, malaise, diffuse abdominal pain, and constipation. Untreated,
typhoid fever is a grueling illness that may progress to delirium, obtundation, intestinal hemorrhage,
bowel perforation, and death within 1 month of onset. Survivors may be left with long-term or
permanent neuropsychiatric complications.
S typhi has been a major human pathogen for thousands of years, thriving in conditions of poor
sanitation, crowding, and social[1]chaos. It may have responsible for the Great Plague of Athens at the
end of the Pelopennesian War. The name S typhi is derived from the ancient Greek typhos, an
ethereal smoke or cloud that was believed to cause disease and madness. In the advanced stages of
typhoid fever, the patient's level of consciousness is truly clouded. Although antibiotics have
markedly reduced the[2]frequency of typhoid fever in the developed world, it remains endemic in
developing countries.
S paratyphi causes the same syndrome but appears to be a relative newcomer. It may be taking over
the typhi niche, in part, because of immunological naivete among the population and incomplete
coverage by vaccines that target typhi.
Note that some writers refer to the typhoid and paratyphoid fever as distinct syndromes caused by
the typhi versus paratyphi serovars, while others use the term typhoid fever for a disease caused by
either one. We use the latter terminology. We refer to these serovars collectively as typhoidal
salmonella.
#source: http://emedicine.medscape.com/article/231135-overview
[pg 12]

-what is the criteria for fibril seizure !

- what are the causes of hyperkalemia and then asked about each single answer i gave .. were it is
more common in acute or chronic renal failure !
give me management of hyperkalemia ( i started by making sure that it's true hyperkalemia , and
gave him all the medication but still the pt is not responding .. MOOOOVE .. send the pt to dialysis
..

2nd station ,,
Dr Eyad Amawi from JU
3 year old pt with history of vomiting and diarrhea of one day duration
- take history in details
- what u look for in physical examination
- what investigation u order . and asked in details about them
- fluid resuscitation !
- asked about HUS , pre-renal failure , hyper and hypo k & na
- what do u see in stool analysis !
- asked how to diagnose bacterial overgrowth , rotazym test for rotavirus ..
and many others !!

--------------------------------------------------------------------------------------------------------------

First station;
Dr. Jomana from Jordan University Hospital.
First, she told me that I will ask you about three cases.
1. Patient assessed to have dehydration due to GE:
Physical Examination and Vital signs.
Why may have tachypnea.
Management wise. Fluids amount and electrolytes.
What you will do if the patient didn't respond to hydration.

2. Patient with generalised Oedema give differential.

Nephrotic syndrome definition
Test you will do.
Most common cause. (Minimal Change Disease)
Treatment of the cause.
Then council the mother about what may he present( infections , increased risk of thrombosis) and
why those happen.
What GI disease may cause same picture. ( protein Intolerance)
Pathophysiology of nephrotic causing oedema.

#source: refer In A Page book, 2nd edition, pg 102 & 103

3. ABG for a patient with metabolic acidosis.

Next test or thing you will look at ( anion Gap)
Patient with metabolic acidosis and hypokalemia diagnosis ( RTA) a little questions about types.
Hypocholermic metabolic alkalosis ( Barter Syndrome)

second station ;
Dr. Faisal Qtaish
- about a patient with fever and cough. Pneumonia
PE
Investigations
Treatment and complications like pleural effusion

#source: refer In A Page book, 2nd edition, pg 40 & 41

[pg 13]

--------------------------------------------------------------------------------------------------------------

First station;

Neonate 1st day of life; nurse calling you couse he is not feeding well!!
how you council the mother for the right way in feeding her baby!!
What will you think about if baby is not feeding at all!?!
-:the problem was with the mother,this is her 1st child, and she dosent know how to feed him, wut
should she do ???
Would you think of sepsis?! How would you confirm dx in a hospital with no facilities?!
- pt took milk from external source; ... And the problem appeared to be from the mother!!
also he asked about colostrum (the first milk that's produced in the first 2 days, 2-5 days, yellow in
color, it is high in proteins, immunoglobulin, minerals and low in lactose and fat.)
- how would you know the child is feeding enough? (Sleep after feeding, 1.5-2 hours after feeds)
- how do u differentiate between breast feeding jaundice; and breast milk jaundice!!
- what are the benefits of breast feeding for the mother and the baby??

For baby:
-get secretory IgA, immunoglobulin and nonspecific immune factors.
-reduce incidence of food allergies and eczema.
-some studies state that breastfeed infant is associated with higher intelligence later in life.

For mom:
-decrease incidence of certain disease like postmortem hemorrhage (because of oxytocin) ,
amenorrhea, ovarian and premenopausal breast cancer and possibly osteoporosis.
-helps in weight loss (help regain the pre-pregnancy weight)
#source: lecture notes Neonatal Nutrition

-Symptoms of otitis media????!!

-what will you see in ear examination !!

--------------------------------------------------------------------------------------------------------------

Second station
Pt 6 yrs old; deteriorated level of consiousness!!!
What would you do!!
What to ask in hx ; wt to look for in examination !!
-in the 2nd case (Dr.Sama7 =D)>> if the pt has unilateral dilated Pupil > wuts ur Dx ??
'Mortality and morbidity rates associated with anisocoria depend entirely upon the specific
pathophysiology.
Several causes of anisocoria are life threatening, including Horner syndrome due to carotid
dissection or third nerve palsy due to an aneurysm or uncal herniation.
Other causes of anisocoria are completely benign (eg, simple or physiologic anisocoria), although
the unnecessary evaluation of these disorders may produce morbidity inadvertently.'
#source: http://emedicine.medscape.com/article/1158571-overview#a6

- pt with fever and rash!! What you think about!!?!

What would you do?!

Important to rule out meningococcemia!!!

The differential diagnosis for febrile patients with a rash is extensive. Diseases that present
with fever and rash are usually classified according to the morphology of the primary lesion.
Rashes can be categorized as maculopapular (centrally and peripherally distributed),
petechial, diffusely erythematous with desquamation, vesiculobullouspustular and nodular.
Potential causes include viruses, bacteria, spirochetes, rickettsiae, medications and
rheumatologic diseases. A thorough history and a careful physical examination are essential to
making a correct diagnosis. Although laboratory studies can be useful in confirming the
diagnosis, test results often are not available immediately. Because the severity of these
illnesses can vary from minor (roseola) to life-threatening (meningococcemia), the family
physician must make prompt management decisions regarding empiric therapy.
Hospitalization, isolation and antimicrobial therapy often must be considered when a patient
presents with fever and a rash.

#source: http://www.aafp.org/afp/2000/0815/p804.html
--------------------------------------------------------------------------------------------------------------
1) a case of skin rash
- history, types of rash, examination,...
- differentiate by exam between ITP and Meningeicoccal rash...
2) Also gasoline ingestion..
-In cases of hydrocarbon aspiration, the patient's temperature may be elevated due to the body's
reaction to the foreign substance. Respiratory, central nervous system (CNS), and gastrointestinal
(GI) findings may be present, as well as cardiac arrhythmias, mucosal irritation, and chemical burns
of the skin.
Respiratory findings may include the following:
Coughing

Choking
Tachypnea

Grunting

Cyanosis
Rales

Wheezing

CNS findings may include the following:

Headache

Dizziness

Lethargy

Ataxia

Seizures

Coma

GI findings may include the following:

Nausea

Vomiting

Abdominal pain

#source: http://emedicine.medscape.com/article/1010734-clinical#b4
3) Also ABG values and Qs about it..
4) ddx diagnosis of stridor , (dif between croup and epiglottitis )
-croup
-epiglottitis
-pharyngitis
-mastoiditis
#source: Pediatrics Made Easy book, under topic Croup & Epiglottitis

-foreign body
-angioedema
-bacterial tracheitis
-retropharyngeal abcess
-diptheria
#source: Management of Acute Upper Respiratory Tract Infection slide.
5) ddx of loss of consciousness
6) rheumatic fever, thalasemia and blood transfusion ( complications) , dif between IDA and
thalasemia minor.

--------------------------------------------------------------------------------------------------------------
Dr.Faisal Qtesh:
- 2yr old presented with fever cough (hx, exam, inv )
- antibiotic complications..
*this answer refer to infants
Is it safe to give antibiotics to infants?
Like all medications, antibiotics can cause side effects or other problems such as:
Allergic reactions. Only about five out of 100 children are truly allergic to antibiotics. Most
develop hives or red, swollen, itchy welts. "Compared with hives, a rash is much less severe and is
more likely related to a viral infection, not a medication response," says Dr. Munjal. Still, you
should let your doctor know if your baby develops a rash while taking antibiotics. "Treating the rash
with an allergy medication like Benadryl usually isn't necessary," says Dr. Munjal.
Side effects. About one in 10 children experience side effects from taking antibiotics. The most
common are diarrhea, nausea, and stomach pain. "In addition to targeting bad bacteria, antibiotics
kill off healthy bacteria in the gut. This can lead to stomach upset or diarrhea," says Dr. Munjal.
Antibiotic resistance. As more antibiotics are used through the years, certain medications may
become less effective at killing certain bacteria. This is known as antibiotic resistance, and it's a key
reason that doctors are more cautious these days about prescribing antibiotics only when absolutely
necessary.
#source: http://www.parents.com/baby/health/antibiotics/babies-and-antibiotics/

[pg 14]

Dr. jumana:
- 2 yr presented with stidor Hx DDx how to differentiate
- case FTT 2yrs old with hx of constipation and hypokalemia (inv and diagnosis) types of RTA.. a
case metabolic alkalosis hyperchloremia hypokalemia diagnosis!!!! then a case of hematuria DDx
invX wt
do u expect to see under microscope how do u manage cystitis post strep
--------------------------------------------------------------------------------------------------------------

Dr; rula saq3an :

--> a scenario of UTI for the first time : what would you ask in history ? what would you see in P/E ,
what investigation you want to order and why ? phrophylactic antibiotics and duration? would you
order MCUG ,
? how will you explain the procedure for the mother ? if MCUG is not indicated and the mother ask
you to do it how to tell her this test is not useful ? if the child complains of recurrent UTI ; would
you odered for DMSA
? when to wait the infection to resolve or do it immediately
Dr, Mahmoud al-sheyyab
- 6 year old child, his mom tried to awake him up in the morning and he seemed to be unconscious;

what are the possible causes? if hypoglycemia what was the possible mechanism ? what to ask in
history ?
what to do in P/E ? management
this child has ingested the oral hypoglycemic agents of his father.
- What is physiologycal anemia? Why it occure and when

--------------------------------------------------------------------------------------------------------------
Dr Faisal:
A case of pneumonia how to diagnose and manage? 5 days later the child came with fever though
the AB was sensitive what do you expect? Pleural effusion. Management? Drainage.
Dr from JU:
1- A case of stridor, what's your ddx?
2- A child with gastroenteritis, what signs do you look for on examination? How much fluid will
you give him?
#source: In A Page book, 2nd edition, pg 72 & 73.
3- Generalized edema, ddx? Investigations and management for nephrotic syndrome?
#source: refer In A Page book, 2nd edition,pg 102, 103.
4- DDX of metabolic alkalosis?
------------------------------------------------------------------------------------------------------------------------
---------------
Dr Mahmoud Shyab :
1. ABG calculations ( hx : hyperventilation )
2. comatose child , DDx ?

Dr Roula :
1. give Invx for Nephrotic Syndrome
2. If the results were : hypoalbuminemia + normal urine ...DDx ?
-liver disease
-heart disease (CHF)
-chronic malnutrition
-protein losing enteropathy

3. Do we give Albumin ? and What should we do before that ?

-we give, but we give fluid resuscitation (colloid) before that.
[pg 15]

Case 1 : Dr from AlJaish:

1) 2 yr-old child with loss of consciousness give ur DDx.
2) iron deficiency anemia what do u see on blood film
3) thalassemia what do u see on blood film and how do diagnose it and what do u see on Hg
electrophoresis.
4) give the major criteria of rheumatic fever.
Jones criteria: CASES
-Carditis
-Arthritis
-Subcutaneous nodule
-Erythema marginatum
-Sydenham chorea

Case 2: Dr from AlOrdonieh:

- 6 yr-old child with loss of consciousness give all the DDx: postictal state, head trauma
-what does it cause:
brain concussion+hemorrhage), status epilipticus, metabolic (hypoglycemia) and electrolyte
distrabances(name them), DKA, hypertensive encephalopathy,shock, stroke(how: due to emboli
from for ex AF & SBE), brain tumors, what else???
- stridor: give the DDx u know.
- How to differentiate between croup and epiglottitis.
- how to treat croup... I said: mist, nebulized epinephrine, IM steroids(and she wants u to say that
dexamethozone is the prefered one and why it is prefered).
- regarding acute epiglottitis:
- what is the most caustive agents. (Hemophilus influenza B)
- how to treat. (Refer answer from question before)
- what things u should avoid while dealing with him, I said: I avoid putting canula and oral exam till
I call the anesthetist.
- where do the anesthetis intubate the patient, I said: in the ER.
- what drug to give.
- how to avoid resistance against the antibiotic u give, here I became confused and didn't know what
the Dr wants.
------------------------------------------------------------------------------------------------------------------------
---------------
my exam was about septic shock and it's management,what are other ways if Iv line is not possible,
and what drugs we give in Interosseus route and what does gram+ and gram - means and what is the
color in each stain!! all in one station.
-Gram staining, also called Gram's method, is a method of staining used to
differentiate bacterial species into two large groups (Gram-positive and Gram-negative). The name
comes from the Danish bacteriologist Hans Christian Gram, who developed the technique.
Gram staining differentiates bacteria by the chemical and physical properties of their cell walls by
detecting peptidoglycan, which is present in a thick layer in Gram-positive
bacteria.[1][page needed] In a Gram stain test, Gram-positive bacteria retain the crystal violet dye,
while a counterstain (commonly safranin or fuchsine) added after the crystal violet gives all Gram-
negative bacteria a red or pink coloring.
#source: https://en.m.wikipedia.org/wiki/Gram_staining
--------------------------------------------------------------------------------------------------------------

2nd station with Dr.Hala about anapylactic because of eggs!! and what is my aprouch to this pt she
wanted details
Like ABC all in detailes and the dose of adrenaline and counselling she also asked about allergies in
general and vaccination.
and in the first station he also asked about what drugs do you give if Iv fluid including crystaloids
and plasma expanders didn't work

------------------------------------------------------------------------------------------------------------------------
--------------

[pg 16]

Station 1:

dr. Ma7mood shyyab..

4 years old... last night he was hypoactive.. today he is having fever and skin rash.. what do you
think doctor!! (
ba3d majhood 3atheem, zattait meningococcemia)
What cause with meningococcemia? What is the type of rash? Where do u see this rash? How is the
mechanism of the rash in general!!! ( ana mn lamma 7akali el case golt rawwa7at.. bs lamma sa2alni
3n el rash.. hooon golt
wallah la nkayyef..rawwa7at!!!) And he asked for other dx... then he asked what do u want to do for
him in the ER? How can u be sure this is meningococcemia? What is ur management? (Every
answer and every word u say,
he will ask u about it!!! So do not make my mistake and only answer things u know!!!)

Station 2: dr rola..
My case was nephrotic.... what do u know about nephrotic syndrome? If the pt is having
hypoalbuminemia and edema but there was no albumin in the urine, what is the cause?(decrease
production, decrease intake(what is
this disease called...!!), increase excretion by stool)...
Is hypoalbuminemia a danger thing? How does the albumin affect ur body if it was
low(mechanism)? Tayeb on the lungs?!
acute otitis media dose ?duration ? 90 mg/kg/day amoxicillin for 10 days

--------------------------------------------------------------------------------------------------------------
Q1 : regarding the dose of Iron I give the patient...In the past years Qs Once he talks about
elemental iron and how much iron sulphate contains elemental iron , and in another time he says it's
5 mg/Kg ferrous sulphate, so which one to answer with?

Q2 : the increase in Hg level after giving iron , is it 2 g/week or 1g/week?

dose recommended for children is 3 to 6 mg/kg/day of elemental iron ( in dr hala's lecture ) ,each
325 mg ferrous sulfate contains 65 mg elemental iron , therapeutic doses of iron should increase
hemoglobin levels by 0.7-1.0 g/dL per week.
What is the cause of improved symptoms shortly after Iron supplementation of IDA patient?
according to the lecture appetite improved by 24 hours due to replacement of intracellular iron
enzymes

.
( (
[]


! :
! .
! : !


! : .

55. Meningitis

Q1: Causes?
Aseptic: non bacterial meningitis in a previously untreated patient with antibiotic
Viral: 90% due to enterovirus
Bacterial: [<3m; GBS (agalactiae)]
[>3m; S. pneumonia, N. meningitidis, H. influenza]
[10y; N. meningitidis]
Q2: Physical examination?
Vital signs, Head circumference, diplopia, rash
Sign of increase ICP: Bradycarida / HTN / irregular breathing / bulging
fontanelle / sunset eyes / papilladema / cranial nerve palsy 3-4-6
Meningeal signs: Kernig / Brudzinski / Nuchal ridgidity
(in >2y) Q3: Investigations?
Lumbar Puncture [L3-
L4] 5 samples;
5. Microbiology lab; culture and stain
6. Chemistry lab; glucose and protein
7. Cell differentials; cell counts, WBC, RBC
8. Cytology; neoplasm, tumor
9. PCR; for HSV [according to Dr.
Dawood] Q4: Treatment?
Emperical antibiotic [Ceftriaxone +
Vancomycin] After cx result:
10.Strep. Pneumonia [Pencillin 10-14 d, Vancomycin if resistant]
11.HiB [Augmentin 7 - 10 days]
12.N. Meningitids [Augmentin 5-7 d]
13.If partially treated [Ceftriaxone 7-10 d]
14.Gram ve [Ceftriaxone 3 wks]
15.Dexamethasone especially with H. Influenza (1h before 1 st dose of
antibiotic) Q5: What is Cushings triad of increased ICP?
Hypertension, Bradycardia, Chyene strokes breathing (irregular
breathing) Q6: How to treat?
Treat by Mannitol and hyperventilation
Q7: What happen if lumbar puncture was done in patient with increase ICP?
Brain herniation 1
 56. Pneumonia

Q1: Presentations?
Fever (more with bacterial), cough, wheeze, chest pain, epigastric pain
(lower lobe)
Tachypnea is a must presentation for LRTI
11.<2m: 60bpm
12.2-12m: 50bpm
13.1-5y: 40bpm
14.>5y: 20bpm
Q2: On physical examinations?
Inspection: Sign of respiratory distress
Palpitation: Increased TVF, asymmetrical chest expansion
Percussion: Dullness
Auscultation: Localized crackles, bronchial breathing, decrease breath sound
+
wheeze
Q3: Which patient should be admitted?
- Children with severe pneumonia (respiratory distress and hypoxemia)
- Infants <6m with suspected bacterial CAP
- Suspicious of resistant pathogen such as MRSA
- Lack of optimum care at home
- Previous failure of oral antibiotics
- Poor oral intake and vomiting
Q4: Patient was given IV ceftriaxone but was not improved despite
positive culture for S. pneumonia, which antibiotic should we add and
why?
We add Vancomycin due to resistant S. pneumonia
Q5: If the patient is 9 y/o, which microorganism could be the cause other
than s. pneumonia and how to treat them?
Atypical bacteria [M. pneumonia, C.
pneumonia] We treat with Macrolides;
Azithromycin.
(Macrolides are used in Gram +ve, atypical bacterial, Bordetella petussis;
whooping cough, also in patients who are allergic to penicillin)
2
 57. Congenital heart disease

Q1: What are the three communications presented in fetal circulation that
close after birth?
PDA / PFO / Ductus
Venosus Q2: What to ask
in history?
- Antenatal scan (cardiac malformation / fetal arrythmias / hydrops)
- Family history of CHD
- Prenatal history; DM / Rubella infx / Teratogenic drugs
- Perinatal history; premature / meconium aspiration / neonatal asphyxia
Q3: Physical
examinations? Sign of
Acute HF:
[Left] sign of respiratory distress
[Right] hepatomegaly / edema
/ascites
FTT: weight, height, head
circumference CVS: Heaves,
murmur
Others: dysmorphic features (associated with other genetic
syndromes) Q4: Investigations?
Hyperoxia test; to differentiate cause of cyanosis due to cardiac or
pulmonary problem
CXRay; cardiomegaly
Echocardiogram
[DIAGNOSTIC] EKG
Q5:
Treatment?
ABC
Correct metabolic acidosis, electrolytes, hypoglycemia, prevent
hypothermia IV Protaglandin E if duct dependent
Consult the cardiologist
(No treatment; we wait for it to close spontaneously unless indicated)

3
 58: ITP

Q1: What is thrombocytopenia and the symptoms of ITP?

Thrombocytopenia is platelet count below 50k per microlitre (ITP
due to destruction of platelets)
Visible symptoms of ITP:
Spontaneous formation of bruises and petechiae (especially on the
extremities), Superficial bleeding; from the nostrils / gums / hematuria /
GI bleed
Malaise, fatigue, general weakness (with or without blood loss)
Hx of URTI is important in history (2/3 of the cases following previous
infectious illness especially EBV)
Q2: What are the complications if there is an extremely low count
(<5k)? Subarachnoid or intracerebral hemorrhage + internal
bleeding
Q3: Pathogenesis?
Autoantibodies, usually IgG, are against the platelet membrane
glycoproteins IIb IIIa or Ib IX, inappropriately signaling them for
destruction by macrophage and monocytes in the spleen and liver.
Q4: How to diagnose ITP?
By exclusion; Leukemia, medications (Quinine, LMWH), Lupus
erythematous, Cirrhosis, HIV, Hepatitis C
Q5: Treatment and when to
start? Children with platelet
<30k
- Corticosteroids; reduce the production of antiplatelet antibodies
[emergency: Dexamethasone, mild; oral perdnisone]
- IVIG; block receptors on membrane thus decrease destruction
- Platelet transfusion (only in emergency and usually unsuccessful in
producing long term platelet because the underlying autoimmune
mechanism will also destroy donor platelets
Q6: Other use of IVIG other than ITP?
GBS, Kawasaki disease
4
 59: Acute otitis media (AOM)

Q1: What to ask in history?

- Symptoms: Ear pain, discharge, fever, sleep disturbance
- Risk factor: Recent URTI, day care, bottle feeding, previous episode of
OM, passive smoke exposure, family history of concurrent otitis media in
children, any immunodeficiency, vaccine (the vaccine did not protect
against non typable HiB)
Q2: Physical examination?
By otoscope; Red, bulging and thickened tympanic membrane, with loss of
light reflex, purulent discharge, perforated membrane with drainage,
decrease mobility with pneumatic otoscope.
Q3: What are the organisms that cause AOM?
Bacterial: S. Pneumonia, non typable HiB, Moraxhella
Catarrhalis Virus: RSV, Influenza

60: UGIB in a patient with liver disease

Q1: A child presented at the ED as a case of UGIB, known case of liver

disease, what comes to your mind?
Coagulation disorder
Q2: What is your first
management? ABC (if air is
patent)
Q3: He is breathing fine, what do you want to exam in
circulation? BP, Pulse, capillary refill if BP was low
Q4: Pulse was high and capillary refill was 4 sec, your next step?
IV access, blood sample and resuscitation with 20mL/kg of normal
saline bolus Q5: What other fluid you can use?
Ringer lactate (?)
Q6: What investigations will you request?
CBC; Hb, platelet / coagulation profile / blood cross match
Q7: If Hb was 9, platelets normal, PT and PTT are prolonged, what is your
next step? Fresh frozen plasma and may consider for blood transfusion
5
 61: Fluid therapy

Start with bolus 20mL/kg Normal saline over 20mins during resuscitation
(repeat as needed)
Rapid volume depletion
20mL/kg Normal saline over
2h Maintenance
Maintenance fluid: 1st 10kg = 100
mL/kg 2nd 10kg =
50 mL/kg The rest
= 20 mL/kg
Maintenance Na+ =
3mEq/100mL Isonatremia
Deficit
Fluid Deficit = dehydration % x
weight Na+ Deficit =
8mEq/100mL
(Other notes: Mild = 3mEq x wt / Moderate = 6mEq x wt / Severe =
9mEq x wt) Hypernatremia
Deficit
Extra fluid = 4 x weight x (Na measured 145)
Fluid deficit = (dehydration % x weight) +
extra fluid Na+ deficit = 8mEq/100cc (Extra
fluid not included)
[Do not correct more than 12mEq/day to avoid cerebral
edema] Hyponatremia
Deficit
Fluid deficit = dehydration % x wt
Na+ deficit = 0.6 x weight x (135 Na measured)
[Do not correct more than 12mEq/day to avoid pontine hemorrhage]
[If Na+ correction needs more than 1 day dont forget to multiply the
maintenance]

6
 62: DKA

Q1: What to ask in history?

Symptoms of hyperglycemia: Polyuria, Polydipsia, Polyphagia, Nocturnal
enuresis Symptoms of DKA: Abdominal pain, vomiting, Kussmaul breathing
(rapid and deep), ketone breath (fruity breath)
Triggering factors: History of infections, steroids,
stress Q2: Physical examinations?
Sign of dehydration, Sign of RDS, sign of
infections Conscious level + orientation (altered
mental status) Q3: DDx for DKA?
Gastroenteritis / acute appendicitis / pneumonia / salicylate toxicity / lactic
acidosis Q4: What to order?
CBC; WBC / Electrolytes (Na / K) - hyperkalemia / KFT / Blood
glucose / ABG (metabolic acidosis) / Urinalysis (ketonuria) / Blood
ketone (ketonemia) Q5: Definition of DKA?
Hyperglycemia usually greater than 300 mg/dL with ketonuria and a
serum bicarbonate level <15 mmol/L or serum pH <7.30 (metabolic
acidosis)
Q6: Treatment?
1. ABC + 2 IV lines
2. Bolus Normal saline 20cc/kg; then access degree of dehydration + IV
fluid
3. Within 2nd hour start IV insulin 0.1 U/kg/hr slowly (to avoid cerebral
edema)
4. No NaHCO3 only if pH <7.2 and severe enough to compromise
cardiac contractility
5. If K<5 and the patient passed urine, replace with KCl
6. Regular insulin with subcutaneous insulin
7. If concomitant infections manage accordingly
Q7: If patient developed cerebral oedema, how to manage?
Intubation, hyperventilation, mannitol, monitor glucose hourly,
monitor electrolytes and vital signs
Q8: When to say ketoacidosis is relieved?
Once ketones are negative in urine, usually within 36
hours Q9: Causes of mortality in DKA?
Cerebral oedema, severe hypokalemia, hypocalcemia (due to excess use of
Potassium phosphate or osmotic losses)
7
 63: Hyperkalemia in renal failure patient

Q1: Clinical presentation of hyperkalemia?

Nausea, fatigue, muscle weakness or tingling
sensations Q2: Causes?
Acute and chronic renal failure / glomerulonephritis / Drugs [ACEI,
NSAIDs, Angiotensin II receptor blocker and potassium-sparing diuretics
(spironolactone)] / early DKA / Trauma / Burn / Surgery / Chemotherapy
Q3: Investigations
K+ level (Normal 3.5
5.3) ECG
KFT
Q4: Treatment?
1. IV calcium gluconate 10% 2cc/kg over 5mins (to temporarily protect
the heart and muscles from the effects of hyperkalemia)
2. Sodium bicarbonate 1-2mg/kg over 5 to 30 mins (to counteract acidosis
and to promote movement of potassium from the extracellular space
back into the cells)
3. IV glucose and insulin
4. Diuretics (to decrease the total potassium stores)
5. Beta 2 adrenergic receptors; albuterol / epinephrine
6. Dialysis (if other measures have failed or if RF present again)

64: Anaphylaxis

Q1: A boy with a history of eating fish 30 minutes ago, presented with
stridor and facial oedema, what is your diagnosis?
Anaphylaxis (food
allergy) Q2: What is
your next step? ABC +
IV access and IV fluid
Q3: What is the
treatment? Epinephrine
With antihistamine and steroids (in-hospital observation for between 2
and 24 hours is recommended once they return to normal due to concern
of biphasic
anaphylaxis) 8
Q4: What is the mechanism of action for each?
Epinephrine: maintains blood pressure, antagonize the effects of
released mediators and inhibits further release of mediators
Antihistamines has a slower onset than epinephrine
Corticosteroids given to prevent a potential late-phase reaction
(biphasic anaphylaxis)
Q5: What do you want to advice the mother?
Strict avoidance of the food, education on label reading and food
preparation. Epinephrine should be available at all time.

65: Hypertensive encephalopathy

13 y/o female presented to the ED with a history of 3 days fever,

headache and seizure, you gave diazepam and she is now
doing well

Q1: What to focus in history? [positive for VURD]

Past medical history of VURD (recurrent pyelonephritis may result renal
scarring) Prematurity /FTT
Bronchopulmonary dysplasia
History of umbilical artery
catheterization History of head and
abdominal trauma
FHx of heritable diseases (neurofibromatosis / HTN)
Medications (steroids, TCA, cold remedies, medication for
ADHD) Dietary history including caffeine and salt
consumption
Q2: What to focus in exam? [positive for BP:
210/110] Blood pressure
Q3: Investigations to
order? CBC, electrolytes,
KFT, LFT
Q4: What do you think the cause of
seizure? Hypertensive encephalopathy
Q5: What is the pathophysiology behind it?
Vasoconstriction, increased permeability, loss of coordination
between vasodilation and vasoconstriction, causing oedema
Q6: How to treat?
Antihypertensive ACEI / ARB / CCB
Q7: What is the cause for her hypertensive9 encephalopathy?
Due to VURD
Q8: What to order for VURD?
DMSA scan (to look for renal scarring)

66: IDA

1 y/o girl was transferred to haematology clinic due to pallor that is noticed
by her general practitioner

Q1: What to focus in history?

(Positive for exclusively breast feeding, negative for all other causes of
anaemia) Q2: What investigations to order?
CBC; Hb (5.1), MCV, MCHC, WBC (7000), Platelets
(650,000) Blood film, TIBC (elevated), Serum ferritin
(low)
Q3: What do you
think? Iron deficiency
anaemia
Q4: How you treat her? And dosage?
Iron supplement (3 for mild 6 for mod to severe
mg/kg/d) Use iron-fortified formula and infant cereal
Q5: When do you expect her to improve after
treatment? 2 months
Q6: Will you stop the treatment after 2
months? No, we continue for another 2
months
Q7: What other nutritional deficiencies she may
have? Vitamin D deficiency
Q8: What is the complication for
this? Rickets
Q9: What to order?
X-ray of wrist and lower limbs
Q10: What are you going to see in lab
investigations? Decrease calcium / decrease
phosphate
Q11: What is
treatment? Vitamin D
supplement

10
List of the cases that were asked:

1. DKA
2. Hereditary spherocytosis
3. ITP
4. HSP
5. Meningitis / meningococcemia
6. Acute otitis media
7. Gastroenteritis and fluid therapy
8. Status asthmaticus
9. Pneumonia
10. Febrile seizure
11. Acute Heart failure
12. UGIB (patient with liver disease)
13. Hyperkalemia (patient with renal failure)
14. Anaphylaxis