MBBS Paediatrics Syllabus

What oxygen concentration is recommended to initiate resuscitation in term versus preterm neonates?

Term ($\geq 35$ weeks): start with 21% (room air). Preterm ($< 35$ weeks): start with 21–30% oxygen, titrating to preductal $\text{SpO}_2$ targets.

What is the dose and route of epinephrine in neonatal resuscitation?

Epinephrine $0.01$–$0.03$ mg/kg ($0.1$–$0.3$ mL/kg of 1:10,000) IV/IO; if endotracheal, $0.05$–$0.1$ mg/kg. Given if HR remains $< 60$ bpm after adequate ventilation and compressions.

Differentiate physiological from pathological neonatal jaundice by timing.

Physiological jaundice appears after 24 h, peaks at days 3–5 (term), and resolves within 1–2 weeks. Pathological jaundice appears within the first 24 h, rises rapidly ($> 5$ mg/dL/day), or is prolonged ($> 14$ days).

What type of bilirubin causes kernicterus, and what is the danger?

Unconjugated (indirect) hyperbilirubinaemia; lipid-soluble unconjugated bilirubin crosses the blood–brain barrier and deposits in basal ganglia, causing kernicterus (bilirubin encephalopathy).

List common causes of conjugated (direct) hyperbilirubinaemia in a neonate.

Biliary atresia, neonatal hepatitis, choledochal cyst, TORCH infections, metabolic disorders (galactosaemia, $\alpha_1$-antitrypsin deficiency), and total parenteral nutrition cholestasis. Direct bilirubin $> 2$ mg/dL or $> 20\%$ of total is significant.

What are the two main treatment modalities for neonatal unconjugated hyperbilirubinaemia?

Phototherapy (converts bilirubin to water-soluble lumirubin via photoisomerisation) and exchange transfusion (for severe levels or signs of acute bilirubin encephalopathy).

Differentiate early-onset from late-onset neonatal sepsis.

Early-onset: $\leq 72$ h (often $< 24$ h) of life, acquired vertically; commonly Group B Streptococcus and E. coli. Late-onset: $> 72$ h, often nosocomial/community; commonly coagulase-negative staphylococci, S. aureus, Klebsiella.

What is the classic clinical triad/features suggesting neonatal sepsis?

Nonspecific: temperature instability, poor feeding, lethargy, respiratory distress/apnoea, and may progress to shock. 'Not doing well' is the hallmark. Sepsis screen + blood culture confirm diagnosis.

Name the TORCH infections.

Toxoplasmosis, Other (syphilis, varicella, parvovirus B19, HIV), Rubella, Cytomegalovirus, and Herpes simplex virus.

What is the most common cause of viral pneumonia and of bacterial pneumonia in children?

Most common viral cause: Respiratory Syncytial Virus (RSV). Most common bacterial cause: Streptococcus pneumoniae (pneumococcus).

What WHO clinical signs define pneumonia and severe pneumonia in children?

Pneumonia: fast breathing (RR $\geq 50$/min for 2–11 months, $\geq 40$/min for 1–5 years) and/or chest indrawing. Severe/very severe pneumonia: any general danger sign (inability to drink, persistent vomiting, convulsions, lethargy, central cyanosis).

What organism causes acute epiglottitis, and what is its classic presentation?

Haemophilus influenzae type b (Hib). Presents with the 'tripod/sniffing' position, drooling, dysphagia, muffled voice, and high fever with toxic appearance — a medical emergency (do not examine throat).

Differentiate viral croup from epiglottitis by causative agent and X-ray sign.

Croup (laryngotracheobronchitis): parainfluenza virus; barking cough, inspiratory stridor; 'steeple sign' on AP neck X-ray. Epiglottitis: Hib; 'thumb sign' on lateral neck X-ray.

What are the most common causes of acute viral and bacterial gastroenteritis in children?

Most common viral cause: Rotavirus (and norovirus). Common bacterial causes: Shigella, Salmonella, Campylobacter, and enterotoxigenic E. coli.

What organism classically causes bloody diarrhoea (dysentery) and may precipitate haemolytic-uraemic syndrome?

Shigella dysenteriae (Shiga toxin) and enterohaemorrhagic E. coli O157:H7. HUS = triad of microangiopathic haemolytic anaemia, thrombocytopenia, and acute kidney injury.

List the most common bacterial causes of meningitis in neonates versus children 3 months–5 years.

Neonates: Group B Streptococcus, E. coli, Listeria monocytogenes. Children (3 mo–5 yr): Streptococcus pneumoniae, Neisseria meningitidis, and Hib (where unvaccinated).

What are the typical CSF findings in bacterial meningitis?

Raised opening pressure, turbid appearance, neutrophilic pleocytosis (high WBC), high protein, and low glucose (CSF:serum glucose ratio $< 0.4$).

Compare CSF findings in viral versus tuberculous meningitis.

Viral: clear, lymphocytic pleocytosis, mildly raised protein, normal glucose. Tuberculous: clear/cobweb, lymphocytic, markedly raised protein, low glucose, with very high opening pressure.

Which diseases are targeted by the pentavalent (DPT-HepB-Hib) vaccine?

Diphtheria, Pertussis (whooping cough), Tetanus, Hepatitis B, and Haemophilus influenzae type b.

What are the classic clinical features (3 C's) of measles, and what pathognomonic sign precedes the rash?

The 3 C's: Cough, Coryza, Conjunctivitis. Koplik spots (white spots on buccal mucosa) are pathognomonic and appear before the maculopapular rash that spreads cephalocaudally.

What are the cardinal features of pertussis, and which organism causes it?

Bordetella pertussis. Paroxysmal coughing fits followed by an inspiratory 'whoop', post-tussive vomiting; marked lymphocytosis on blood count. Catarrhal $\to$ paroxysmal $\to$ convalescent stages.

Define asthma and its underlying pathophysiology.

A chronic inflammatory airway disorder with reversible airflow obstruction, bronchial hyperresponsiveness, and airway inflammation — causing recurrent wheeze, cough, breathlessness, and chest tightness.

What is the first-line reliever and first-line controller medication in childhood asthma?

Reliever: short-acting $\beta_2$-agonist (SABA, e.g., salbutamol). Controller: inhaled corticosteroid (ICS), the mainstay of long-term control.

How does PEFR variability help in diagnosing/monitoring asthma?

Peak expiratory flow rate (PEFR) shows diurnal variability; reversibility is confirmed by a $\geq 12\%$ increase in $\text{FEV}_1$ after bronchodilator. Diurnal variability $> 13\%$ supports asthma.

Define bronchiolitis: cause, age group, and key clinical findings.

Lower respiratory tract infection, usually by RSV, in infants $< 2$ years (peak 2–6 months). Features: coryza followed by wheeze, fine crepitations, tachypnoea, chest retractions, and hyperinflation. Management is mainly supportive.

What is the inheritance pattern and genetic defect in cystic fibrosis?

Autosomal recessive mutation in the CFTR gene (chromosome 7); the commonest mutation is $\Delta F508$. CFTR is a chloride channel; defect causes thick viscous secretions.

What diagnostic test confirms cystic fibrosis and what is the threshold?

The sweat chloride test; sweat chloride $\geq 60$ mmol/L is diagnostic (60 is the cutoff; 30–59 intermediate). CF causes elevated sweat chloride due to defective $\ce{Cl-}$ reabsorption.

What are the main clinical manifestations of cystic fibrosis?

Recurrent respiratory infections (Pseudomonas, S. aureus), pancreatic exocrine insufficiency with malabsorption/steatorrhoea, meconium ileus in neonates, failure to thrive, and male infertility.

How is dehydration from diarrhoea classified (WHO) by clinical signs?

No dehydration ($< 5\%$): alert, normal eyes/thirst. Some dehydration (5–10%): restless/irritable, sunken eyes, thirsty, skin pinch goes back slowly. Severe ($> 10\%$): lethargic, very sunken eyes, unable to drink, skin pinch goes back very slowly ($> 2$ s).

What is the WHO low-osmolarity ORS composition and the role of zinc in diarrhoea?

Low-osmolarity ORS: $\approx 75$ mEq/L sodium, 75 mmol/L glucose, total osmolarity $\approx 245$ mOsm/L. Zinc (10–20 mg/day for 10–14 days) reduces duration and severity of diarrhoea.

What is Plan C of WHO diarrhoea management (severe dehydration) for a child $>12$ months?

IV Ringer's lactate 100 mL/kg: give 30 mL/kg in the first 30 min, then 70 mL/kg over the next 2.5 h. (Infants $<12$ months: 30 mL/kg over 1 h, then 70 mL/kg over 5 h.) Reassess and give ORS once able to drink.

Define GERD in children and distinguish it from physiological gastro-oesophageal reflux.

Physiological reflux (regurgitation) is common in infants and self-resolving by ~12–18 months. GERD is reflux causing troublesome symptoms or complications: failure to thrive, oesophagitis, feeding refusal, recurrent aspiration, or Sandifer syndrome.

What is the first-line management approach for infant GERD, and what pharmacological options exist?

First-line: conservative — smaller frequent feeds, thickened feeds, upright positioning after feeds, and trial of cow-milk-protein elimination. Pharmacological: proton pump inhibitors or $\ce{H2}$-receptor antagonists for confirmed GERD/oesophagitis.

Classify Protein-Energy Malnutrition: marasmus versus kwashiorkor.

Marasmus: severe wasting, weight $< 60\%$ expected, no oedema, marked muscle/fat loss ('old man' face). Kwashiorkor: bilateral pitting oedema, weight 60–80% expected, hypoalbuminaemia, hair/skin changes, hepatomegaly (fatty liver).

What are the WHO criteria for diagnosing severe acute malnutrition (SAM)?

Weight-for-height/length $< -3$ SD (z-score), and/or mid-upper arm circumference (MUAC) $< 11.5$ cm (in children 6–59 months), and/or presence of bilateral pitting oedema.

List the 10 steps of WHO inpatient management of severe acute malnutrition (overview).

Treat/prevent: (1) hypoglycaemia, (2) hypothermia, (3) dehydration (use ReSoMal), (4) electrolyte imbalance, (5) infection; correct (6) micronutrient deficiencies; achieve (7) cautious feeding, (8) catch-up growth, (9) sensory stimulation, and (10) prepare for follow-up.

Why is iron withheld initially in severe malnutrition management?

Iron is delayed until the stabilisation phase is complete (usually after ~1 week, in the rehabilitation phase) because free iron promotes bacterial growth and oxidative stress (free-radical injury), worsening infection.

Describe the haemodynamics and murmur of a Ventricular Septal Defect (VSD).

Left-to-right shunt (high to low pressure). Produces a harsh pansystolic (holosystolic) murmur at the left lower sternal border; smaller defects often give louder murmurs. Large VSDs cause heart failure and pulmonary hypertension.

What is the most common congenital heart defect, and what is the natural history of small VSDs?

VSD is the most common congenital heart defect. Small (muscular) VSDs frequently close spontaneously in the first 1–2 years of life and may need no intervention.

Describe the typical murmur and ECG/chest findings of an Atrial Septal Defect (ASD).

Left-to-right shunt giving a wide, fixed split $\text{S}_2$ and an ejection systolic murmur at the upper left sternal border (pulmonary area) from increased flow. ECG: right axis deviation with RBBB (ostium secundum); right atrial/ventricular enlargement.

What is Eisenmenger syndrome and how does it relate to VSD/ASD?

Long-standing large left-to-right shunt $\to$ pulmonary hypertension $\to$ reversal to a right-to-left shunt, producing cyanosis. It is an irreversible complication that contraindicates surgical defect closure.