1.

Kawasaki disease
a) Provisional dx
Kawasaki - Diagnostic criteria:
• At least 5 days of fever PLUS 4 or 5 of the following:
• Oropharyngeal changes (cracking and fissuring of the lips; red oropharyngeal
mucosa, strawberry tongue)
• Bilateral painless, non-exudative, bulbar conjunctival injection (redness)
• Acute, unilateral, non-purulent cervical lymphadenopathy
• Maculopapular rash
• Extremity changes (erythematous palms and soles, desquamation of the fingers and
toes which begins in the periungual region)

b) Pathophysiology
 Common between 6 months to 4 years
 A non-infectious disease, systemic vasculitis affecting medium-sized arteries
 Etiology unknown but can be due to autoimmune; an infection may trigger
autoimmune process.
 Involvement of coronary artery with development of aneurysm is most dreadful
consequence because it may cause sudden death.

c) Management
 History taking and physical examination
 No specific lab investigation as it is clinically diagnosed
 Principal goal of treatment is to prevent coronary artery disease
o Intravenous immunoglobulin (IVIG) within 10 days after onset of fever to
prevent coronary artery involvement
o Aspirin

2. Henoch Scholein purpura

a) Provisional dx
HSP - Vascular purpura
between ages 3 & 10 years.
C/F:
 Palpable purpura due to inflammatory edema into the surrounding tissues along with
the extravasated blood
 Arthritis involving the ankles and knees
 Abdominal pain
 Features of acute nephritis (hematuria, hypertension, or acute renal failure)
b) Pathophysiology
 Results from an immune mediated process
 Involves the blood vessels of the skin, GI tract, the kidneys, the joints, and, rarely,
CNS.
 Presence of deposition of IgA in the walls of the affected small blood vessels that
leads to inflammation (vasculitis).
c) Management
  Complete history taking and physical examination.
 Clinically diagnosed so no specific lab investigation
 Treatment mainly supportive:
o Analgesics for arthritis.
o Corticosteroids to treat significant GI involvement or other life-threatening
symptoms.

3. VSD (Acyanotic heart disease: tachypnea, tachycardia, acyanosis)

a) Types of acyanotic congenital heart disease
VSD - Acyanotic heart disease + heart failure sign: tachypnea, tachycardia
b) Murmur grading (commonly SMALL: PSM at LLSE, LARGE: PSM at LSE/ NO MURMUR)
 Grade 1: Faint murmur, no thrill
 Grade 2: soft, no thrill (LARGE VSD)
 Grade 3: loud, no thrill (SMALL VSD)
 Grade 4: loud with thrill
 Grade 5: very loud with thrill, steto partly off the chest
 Grade 6: loudest with thrill, steto off chest
c) Management
Complete history taking and physical examination to check sign and symptoms
Investigation – CXR, ECG, ECHO
Treatment
 Small VSD:
1. No treatment: close spontaneously at 3 yrs old
2. Subacute Bacterial Endocarditis prophylaxis: dental hygiene or antibiotic
3. Yearly f/up for aortic valve prolapsed or regurgitation
4. Surgical closure indicated if prolapsed valve
 Large VSD:
1. Anti-heart failure therapy (4D)
2. If symptoms control & no Pulmonary HPT, Follow up
3. Surgical closure if complications arise

4. Asthma
a) State 4 clinical features of acute severe asthma
Severity Mild/ Moderate Severe Life-threatening
Speak In phrases In words Unable to speak
Position Prefer sitting Sits hunched
rather than lying forward
Appearance Not agitated Agitated Confused & drowsy,
hypotension
Respiratory Increased but < ≥ 30 breaths per Poor respiratory effort
rate 30 breaths per minute Silent chest
minute
Pulse rate 100 – 120 beats > 120 beats per Bradycardia
per minute minute
 SpO2 92 – 95 % < 92 % Cyanosis and < 92 %
Peak > 50 % predicted/ ≤ 50 % < 33 % predicted/
expiratory best predicted/ best best
flow rate

b) 3 Risk factors for a child to get the disease

 Family history of bronchial asthma
 Presence of allergic march (starts with eczema then food allergy, then hay fever/
allergic rhinitis and asthma)
 History of severe/ prolong respiratory infection
 Exposure to environmental factors such as dust, allergens, cold air, chemical
irritants.
c) Name 4 front – line therapy for acute asthmatic attack and their mode of action
1) Gives oxygen
2) Reliever (for acute attack)
 Short-acting bronchodilators:
o Salbutamol Neb: act as selective B2 – adrenoceptor stimulant (in sympathetic
pathway) that causes the direct stimulation of β2-receptors in bronchial
smooth muscle through increase of the intracellular cyclic adenosine
monophosphate (cAMP) and hence bronchodilatation.
 Anticholinergic:
o Ipratropium Neb: it is parasympathetic action, which competitively blocking
cholinergic receptors (Acetylcholine) and decreases the production of cyclic
guanosine monophosphate (cGMP). Then lead to decreased contraction of
the smooth muscles thus bronchodilation.
 Systemic corticosteroids:
o IV hydrocortisone: Steroids can increase the expression of beta agonist
receptors and prevent their downregulation when beta agonists are
administered.
o Oral prednisolone (if severe attack)
If not improved:
 Salbutamol IV
 IV Magnesium sulphate (for severe): acts as a smooth-muscle relaxant by competing
for the calcium channel, resulting in smooth-muscle relaxation and promotion of
bronchodilation
 Others modalities:
o Nebulized Epinephrine: alpha and beta agonist & has vasoconstrictive effect,
decrease mucus production & produces bronchodilation & pulmonary
vasodilation.

Extra: management of severe acute attack of asthma

1) IV access; continuously monitor vitals and oxygen saturations
2) Oxygen (best initial step)
3) Give short-acting ß2-agonists
4) Give corticosteroids
5) Assess treatment response;
6) Consider other modalities of treatment
7) Hydration

 Controller (for chronic attack)

 Inhaled corticosteroids (budesonide, fluticasone) - decrease airway inflammation,
resulting in decreased symptoms, asthma exacerbations and bronchial hyperactivity.
 Long-acting bronchodilators (beta-agonists and anticholinergics)
 Oral theophylline – both bronchodilator effect as well as some anti-inflammatory effect
(reduce cAMP breakdown thus bronchodilation) but high incidence of side-effects
(vomiting, insomnia, headaches, poor concentration)
 Leukotriene modifiers (montelukast) – mediators of inflammation to improve lung
function and reduce exacerbations

AEBA
a) Give 4 common triggering factors
 Environmental: weather (cold), chemical irritants, allergen
 Emotional: stress
 Exercises
 Infection (URTI)
 Drugs (aspirin)

b) Define FEV1 (forced expiratory volume in first second)

The volume of air that can be forced out in one second after taking a deep breath

c) Give 2 components of Intermittent asthma

 Daytime symptoms less than once a week
 Nocturnal symptoms less than once a week
 No exercise induced symptoms
 Brief exacerbation not affecting sleep & activity
 Normal lung function
d) Outline the 3 treatment modalities acute attack of asthma
 IV access; continuously monitor vitals and oxygen saturations
 Oxygen (best initial step)
 Reliever
 Short-acting bronchodilators:
o Salbutamol Neb: act as selective B2 – adrenoceptor stimulant (in sympathetic
pathway) that causes the direct stimulation of β2-receptors in bronchial
smooth muscle through increase of the intracellular cyclic adenosine
monophosphate (cAMP) and hence bronchodilatation.
 Anticholinergic:
o Ipratropium Neb: it is parasympathetic action, which competitively
blocking cholinergic receptors (Acetylcholine) and decreases the
 production of cyclic guanosine monophosphate (cGMP). Then lead to
decreased contraction of the smooth muscles thus bronchodilation.
 Systemic corticosteroids:
o IV hydrocortisone: Steroids can increase the expression of beta agonist
receptors and prevent their downregulation when beta agonists are
administered.
o Oral prednisolone (if severe attack)

5. Leukemia
a) Dx
a. Definition : malignant neoplasm of haematopoetic stem cell characterised by
diffuse replacement of bone marrow with neoplastic cells and leukemic cells
infiltrate liver, spleen , lymph node and other tissues.
b) 2 relevant lab ix
a. Peripheral blood film –
i. Anaemia : normochromic normocytic
ii. Blasts cells present >20%
iii. Thrombocytopenia
iv. Pancytopenia
v. WCC  or normal
b. Bone marrow aspiration - presence of blasts cells >20% & hypercellularity
i. AML (Auer rods may be present)
c) Give 4 phases of treatment for this condition.
a. Induction of remission – aim to kill rapidly to enter remission phase
i. combination therapy for 4 weeks ( vincristine, danorubicin,
asparaginase, steroid (pred/dexa) intrathecal methothrexate)
b. Consolidation of remission – to bring down tumour burden to very low levels
i. blocks of intensive chemotherapy (cyclophosphamide )
ii. CNS treatment/prophylaxis with IT methothrexate
c. Intensification – to clear minimal residual disease
i. 2-3 blocks of multiagent chemotherapy (monthly vincristine,steroid
(dexa for 5 days) , weekly oral methothrexate/
d. Maintenance – 2/3 years of chemotherapy
i. oral methothrexate, cincristine and prednisolone or dexa.
ii. Co-trimoxazole as prophylaxis against pneumoxytic carinni infection.
CML – phase

Chronic anorexia, night sweats

huge splenomegaly
LN enlargement
accelerated phase bleeding manifestions (epistaxis,
menorrhagia)
blast crisis Ix – blast >20% in BM or PBF,
extramedullary infiltration by blasts
 marked splenomegaly
refractoriness to treatment which previously
was effective

3 years old child with fever and epitaxis, pallor, generalised lymphadenopathy,
purpuric rash and hepatosplenomegaly.
a) 3 differential diagnosis [1.5m]
ALL, AML, Lymphoma
b) Provisional diagnosis and justify [1.5m]
c) 2 investigation to confirm diagnosis [2m]
FBC – pancytopenia
Bone marrow aspiration – ALL or AML
PBF: presence of lymphblasts
BMA: >20% of blasts cells in bone marrow, hypercellular marrow fragments and
cell traits

6. Viral croup
Fever, coryza, noisy breathing. Father had cold last week. Physical examination:
respiratory rate increase, substernal and subcostal recession, loud stridor. On
auscultation, no crepitus or wheeze
a) Provisional dx (1M)
Croup
b) 3 differential dx (1.5M)
Bacterial tracheitis
Acute epiglottitis
Foreign body
Acute laryngitis
c) Management (2.5M)
 Mild
o Inhalation of warm moist air
o Oral dexamethasone
o Or Nebulised steroids - budesonide (if vomiting)
 Moderate
o Oral dexa and/or nebulised budesonide
o nebulised adrenaline if no improvement
 Severe
o nebulised adrenaline + parenteral dexa + nebulised budesonide +
oxygen.
o If not improved : intubate

7. Septic arthritis
5 years old child fever with right knee joint pain, refuse to move the joint and stay in fix
position
 a) Differential diagnosis
a. Septic arthritis / acute suppurative arthritis
b. Acute osteomyelitis
c. Trauma of the knee
d. Juvenile rheumatoid arthritis
b) Investigations
a. Aspiration of joint space under ultrasound guidance and culture to identify
the organism
b. X ray – to exclude trauma or bony lesions
c. FBC -  wcc in acute phase
d. Blood culture and sensitivity
c) If the joint infected, what is commonest organism
a. Staphylococcus aureus (>2 years old)
b. H. Inflyenzae (<2 years or if prior to Hib vaccination)

8. Dysentery
2 years child with abdominal pain,...having stool mixed with blood sometimes

a) possible organisms
a. shigella dysenteriae
b. shigella sonnei
c. salmonella
d. campylobacter jujeni
e. Enteroinvasive E.coli
b) DDx
a. Ulcerative colitis
b. Crohn’s colitis
c) what are 3 findings in stool microscopic examination (NOT SURE)
i. increased in leucocyte count
ii. presence of occult blood
iii. presence of cysts, ova or parasite
d) Outline management
a. Fluid resuscitation (Treatment A/B/C)
b. Antibiotic/antimicrobial/antiprotozoal therapy according to culture and
sensitivity
c. Symptomatic treatment
d. Education
i. Hand hygiene
ii. Good sanitation
iii. Drink purified water

1. Acute gastroenteritis
a. What is the most common organism
i. Rotavirus
 ii. Vibrio cholerae
iii. Escherichia coli
b. Management in severe dehydration
Plan C
i. IV fluid + ORS
ii. Fluid for resuscitation 20ml/kg until out of shock with NS0.9% or Hartmann
solution
iii. Fluid for rehydration (percentage of fluid loss times weight in g) +
maintenance for next 24 hours
iv. Reassess hydration every 1-2 hourly
c. 4 complications of acute gastroenteritis
i. Malnutrition
ii. Dehydration and shock
iii. Seizure
iv. Metabolic acidosis
v. Septicemia
vi. Secondary lactose intolerance
vii. Hemolytic uremic syndrome
viii. Septicemia
ix. Secondary lactose intolerance
x. Hemolytic uremic syndrome

MEQ 9-12

9. A mother come to you, ask for advices regarding breastfeeding

a) Is there any situation that the mother cannot give breastfeeding?

Absolute contraindication:
(a) Inborn errors of metabolism: Galactosemia, phenylketonuria
(b) Mother on certain medications
i. anti-cancer drug
ii. anti-thyroid drugs
iii. radioisotopes
Not contraindications:

(a) Mother with active TB

a. Just immunized baby at birth and
b. Be on INH for 6 weeks or longer
(b) HBsAg positive mother
a. Just give immunoprophylaxis and active immunization to newborn

b) Suggestions for breastfeeding in working mother

(a) Working mother can successfully breastfeed as many working places have
creche (nursery)
(b) Mother can breastfeed during breaks in work
 (c) If unable to breastfeed, collect and store expressed breastmilk in a sterile
container and kept in refrigerator to be given later (warm it before feeding
the baby)
(d) To avoid “nipple confusion”, do not use commercial feeder (feeding bottle)
use spoon to feed expressed milk
c) What is calorie intake for her?
In general, a nursing mom needs about 500 calories more than her own daily calorie
requirment

10.Anemia

a) Define nutritional anemia and what causes it. (cant find the exact definition or
causes from books or lecture notes; based on what I understand, internet and bit of
lecture notes hehe)
a) Nutritional anemia is defined as a reduction of the hemoglobin concentration
below the range of values for age and sex due to nutritional disorders
b) Commonly due to iron deficiency, vit b12/folic acid deficiency, or other
vitamins and mineral needed for hb formation
 Insufficient intake
 Rapid growth
 Low birth weight
 Excessive intake of cow’s milk
 Occult or over blood loss: hookworm infection, cow’s milk
 Malabsorption

b) Name 2 causes of microcytic, hypochromic anemia.

a) IDA
b) Thalassaemia
c) Lead toxicity
d) Pyridine deficiency
c) What is the most common of nutritional anemia and the management?
Iron deficiency anemia
a) Therapeutic iron – minimum 3-4 months
b) Encourage iron rich diet especially animal source of iron: red meat, liver
c) Correction of underlying cause (eg. dewormation)

11.Bilirubin
(a) Briefly explain bilirubin metabolism.
i. Bilirubin metabolism take place in the liver
ii. Bilirubin is produced by the breakdown of erythrocytes
iii. Unconjugated bilirubin formed from non-iron portion of heme and
transported to liver by bounding to albumin
iv. In the liver it is conjugated into conjugated bilirubin by glucuronic
acid this process is catalyzed by uridine glucoronyl transferase
 v. This conjugated bilirubin secreted into bile then into intestine where it is
converted into urobilinogen by the bacteria in the gut and
eliminated in stools as stercobilin
vi. The urobilinogen is also reabsorb and re-enter liver to be secreted as
urobilin in urine or enter the enterohepatic urobilinogen cycle

(b) What are the investigations to be done when there is liver damage?
Lab investigations:
Evidence of liver damage:
Liver function test
i. Total bilirubin level
ii. Liver enzymes -Elevated
a. Alanine aminotransferase
b. Aspartate aminotransferase
c. Alkaline phosphatase
d. Serum albumin – Deranged
iii. Coagulation profile – PT/INR

Underlying cause and complication:

 FBC – Hb, WBC, Plt

 Serum electrolytes
 Infective screening – Hep B, TORCHES etc

Imaging:

 Abdominal ultrasound

(c) What are the type of viral hepatitis that are transmitted by parenteral route?
i. Hepatitis B
ii. Hepatitis C

12.A boy presented with oedema and massive proteinuria. Nitrite and
leukocyte esterase were negative.

a) State the diagnosis.

i. Nephrotic syndrome
b) Pathophysiology.
i. Derangement in the capillary walls of the glomeruli due to structural or
physiochemical alterations in GBM
ii. This results in increased permeability to plasma proteins allowing protein to
escape into glomerular filtrate
iii. Long standing or extremely heavy proteinuria cause serum albumin
decreased
iv. Resulting in hypoalbuminemia and drop in plasma colloid oncotic pressure
causing extravasation of fluid into extravascular space hence oedema
v. Intravascular volume will also drop and reduced the renal blood flow. This
triggers released of Renin from renal juxtaglomerular cells and stimulate RAA
 axis (angiotensin-aldosterone axis), which promotes the retention of salt and
water by kidney  further aggravate existing oedema
vi. Other than oedema, massive proteinuria and hypoalbuminemia can cause
hyperlipidemia as hypoalbuminemia triggers increased synthesis of lipoprotein
and massive proteinuria cause loss of an inhibitor of lipid synthesis.
vii. Net result is hyperlipidemia
viii. Lipiduria - due to the increased permeability of GBM to lipoproteins and
hence presence of lipid in urine
c) Important complications.

 Prone to infection especially staphylococcal and pneumococcal (loss of

immunoglobulin in urine)
 Thrombotic and thromboembolic complications ( loss of endogenous
anticoagulants & antiplasmins in urine)
 Renal vein thrombosis (hypercoagulable state particularly in patient with
membranous nephropathy)

The 9 years old boy presented with Haematuria , edema, hypertension ， no

skin rash other PE were normal

a) Give the pdx

 Acute glomerulonephritis
b) Give 4 ix
 Lab ix
 Urinalysis: RBC cast and dysmorphic RBC
 FBC: dilutional anemia
 Serum creatinine and BUSE – Elevated due to reduced GFR
 C3 level - Low
 ASO titre – positive/elevated if post-streptococcal onfection
 Imaging
 Renal ultrasound (echogenic kidneys)
c) What is the Pathophysiology
 Immune-mediated inflammation affecting glomerular structure either by
 Deposition of circulating antigen–antibody complexes to the
glomerulus; or
 Formation of the immune complexes in situ (within the
glomerulus), as in glomerulus exposed to polysaccharides and
endotoxin