1. CASE 3

2. نرگس حجازی 5ساله با شرح حال تشنج فوکال که از 7روز قبل فنوباربیتال مصرف کرده است. Cc:تب از 2روز قبل و راش ماکولو پاپولر اریتماتوز T=39

3. LAB:
WBC:
HB:
PLT:
EOS: 3% %
ESR:
CRP:3+
UC(-)
BC(-)
AST:
ALT:
ALP:

4. PLAN
قطع فنوباربیتال و شروع کلونازپام
قطع تب پس از 4روز
بهبود راشها پس از 2روز

5. DX
DRESS S.

6. FOLLOW UP
عدم ادامه تب
WBC:6.9
HB:12.8
PLT:376
EOS:3.4
ESR”23 CRP:NEG
ALT:14
AST:45
ALP:374

8. Case 4
5 month girl
Cc:FTT
History of 2 hospitalization for pneuminia and FTT
Bw:2700
Nw:4.5

9. LAB:
Wbc ph:7.5
Hb: co2:29
Plt: Hco3:24.6
Ur: SE:NL
Cr: AST: ALT54 ALP590
Na:134
K:3.4

10. CXR: infiltration
Other lab NL
PLAN:
Ab therapy
Sweat test:
cl=65
na=55

11. DX
CYSTIC FIBROSIS
PLAN:SWEAT TEST

13. In the name of GOD

14. CASE 1

15. ID: AmirHossein Rahmani
CC: Weakness
PI: A 10yrs old male presented with nausea and headache from 1 days ago followed by walking disability and weakness. He had a history of paresthesia in distal parts of the limbs from 1 month later.

16. PMH
Without a significant abnormality

17. Physical Examination Normal vital sign Normal general examination
Normal cranial nerves
Normal sensory system
Normal DTR
Force of lower limbs
Flexor plantar reflex

18. Laboratory Data BS: 141 Urea: 36 Cr: 0.7 Na: 137 K: 4.5 Ca: 10.1
WBC: Neut: 80/ Lym: 12
RBC: 4.4 Hb: Hct: 36.4
Plt:
CPK: 248

19. EEG
Showed sharp waves at occipitotemboral lobe
Brain CT Scan:
Normal

20. Psychiatric consult: Conversion Disorder

21. Final diagnosis
Conversion disorder

22. CASE: 2

23. ID: Saleheh Golmakani
CC: Weakness and gait disorder
PI: A 8 yrs old female presented with flue- like syndrome from 4 days ago followed by low back pain and walking disability.

24. PMH
No significant abnormality

25. Physical Examination Normal vital sign Normal general examination
Normal cranial nerves
Sensory level at thoracolumbar area
Decrease muscular force at lower limbs
DTR of lower limbs
Plantar reflex: Babinski

26. Laboratory Data BS: 81 Urea: 40 Cr: 0.5 K: 4.2 Ca: 10.1 Mg: 2.3
U/A: Nl
RBC: 4.5/ Hb:13.5/ Hct: 39.4/ MCV: 85.8
WBC: 7700 (neut: 72, lym: 20)
CSF:
sugar: 79/ pr: 19/ LDH: 26/ chol: 0
WBC: 47 (neut:80, lym: 20)/ RBC: 0

27. others Anti- HIV: neg Anti- HTLV1: neg Anti ds DNA: 21 C3: 175 C4: 35
ANA: 9
RF: neg
B/C: neg
U/C: neg
CSF/C: neg

28. SSEPS: Nl
MRI:
hyperintensity of right temporoparietal lobe and medula at T2

29. Demyelinating disorder probably MS
Final diagnosis
Demyelinating disorder probably MS

32. Case Report

33. An 6 m old infant came with CC of FTT + Cough
CASE 1
An 6 m old infant came with
CC of FTT + Cough

34. Lab Results VBG: Ph =7.30 PCO2 = 13.7 HCO3 = 7.7 Urea : 19 _ Cr : 0.5
U/A : Ph = 6
U/C : Neg
B/C : Neg

35. Radiology
Plenty of stones with the size of 0.5 _ 1.5mm in calises in both kidneys and nephrocalcinosis

36. Diagnosis
Renal Tubular Acidosis type I (RTA I)

38. Primary Familial Secondary Idiopathic , sporadic Autosomal dominant
Autosomal rersessive
Secondary
Sjogren syndrome
Hypercalciuria
Hyperglobulinemia
Ifosfamide
Cirrhosis
Systemic lupus erythematosus (may be hypercalemic)
Sickle cell anemia ( may be hypercalemic)
Lithium carbonate
Rheumatioid arthritis
Obstructive uopathy
Renal transplantation

39. Diagnosis
Type I RTA is presented with normal AG(hyperchloremic metabolic acidosis) metabolic compensation for respiratory alkalosis produces an electrolyte pattern that is identical to that seen in a normal AG acidosis thus the first step in the diagnosis of the patient with the reduced serum bicarbonate and elevated chloride concentration is to confirm that metabolic acidosis is present by measuring the blood Ph

40. Urine Ph
Patient with normal renal function and normal renal acidification mechanism would develop metabolic acidosis usually have a urine Ph of 5.3 or less as ammonia (NH3) defuses into the tubular lumen it mostly combines with hydrogen ions to form ammonium (NH4+) the reduction in the free hydrogen ion concentration elevates the urine Ph depending upon the chronicity of the acidosis and the degree of hypokalemia the urine Ph may be 5.5 or higher .

41. In most cases of distal RTA the urine Ph is persistently 5.5 or higher

42. Treatment
The correction of the metabolic acidosis results is restoration of normal growth rates in children and also has the following benefits:
Minimizing new stone formation and nephrocalcinosis .
Demolishing calcium losses induced by bone buffering of some of the return acid .

43. The aim of alkali therapy is to achieve a relatively normal serum bicarbonate concentration (22 to 24 meq/lit)
Children may require as much as 4_8 meq/kg/day in divided doses because they often have a higher fix urine Ph as a result fixed bicarbonate losses are frequently higher than in adults .
Potassium citrate alone or with sodium citrate (polycitrate) is indicated in patient with persistent hypokalemia or calcium stone disease but not in patients with the hyperKalemic form of distal RTA

45. CASE 2
A 3.5 year old boy with the history of 2 times complex seizure in the last month and under the treatment with Phenobarbital which happened to appear with fever , rash and conjuctivitis and didn’t respond to antibiotic therapy

46. Lab Results
WBC=
Hb =
Plt =
ESR =
CRP =

47. U/A : NL
U/C : Neg
B/C : Neg
AST =
ALT =
ALP = 649
Echocardiography : NL

49. Diagnostic criterias of Kawasaki disease

50. Laboratory criterias

51. Algorithm