Give 100 questions with answers on the following topics 3/8/26 Monday Laws of Growth and Development Developmental milestones and assessment,Growth charts Dr. Sathish kumar Approach to short stature Dr.M.Priya darsni Immunization Dr.Preethi 4/8/26 Tuesday Daily test Acute diarrhoea Dysentry Dr. Sathish kumar SMR and Adolescent health problems Dr.Shapna lakshmi SAM Dr.Shapnalakshmi 5/8/26 Wednesday Daily test Obesity and Behavioural disorders in children Dr. M.Priya darsni Micronutient and vitamin deficiency Dr.Shapna Lakshmi Micronutrient and Vitamin Deficiency Dr.Shapna lakshmi 6/8/26 Thursday Daily test Bronchial asthma Dr.M.Sathish Kumar Pneumonia Dr.Preethi Croup/ Epiglottitis, bronchiolit is Dr.Mohan kumar 7/8/26 Friday Daily test Hypothyroidism Approach to congenital hypothyroidism Dr.Sathish kumar Seizures in children, febrile seizure Dr.Shapna lakshmi Neural tube defects Dr.Preethi

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Give 100 short answer question and answers for the following topics Monday Laws of Growth and Development Developmental milestones and assessment,Growth charts Dr. Sathish kumar Approach to short stature Dr.M.Priya darsni Immunization Dr.Preethi 4/8/26 Tuesday Daily test Acute diarrhoea Dysentry Dr. Sathish kumar SMR and Adolescent health problems Dr.Shapna lakshmi SAM Dr.Shapnalakshmi 5/8/26 Wednesday Daily test Obesity and Behavioural disorders in children Dr. M.Priya darsni Micronutient and vitamin deficiency Dr.Shapna Lakshmi Micronutrient and Vitamin Deficiency Dr.Shapna lakshmi 6/8/26 Thursday Daily test Bronchial asthma Dr.M.Sathish Kumar Pneumonia Dr.Preethi Croup/ Epiglottitis, bronchiolit is Dr.Mohan kumar 7/8/26 Friday Daily test Hypothyroidism Approach to congenital hypothyroidism Dr.Sathish kumar Seizures in children, febrile seizure Dr.Shapna lakshmi Neural tube defects Dr.Preethi

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Here is a complete summary of all 100 SAQs organized by day and topic:

TOPIC-WISE QUESTION DISTRIBUTION

DayTopicQuestions
MondayLaws of Growth & DevelopmentQ1-Q8
MondayDevelopmental MilestonesQ9-Q19
MondayApproach to Short StatureQ20-Q28
MondayImmunizationQ29-Q38
TuesdayAcute DiarrhoeaQ39-Q45
TuesdayDysenteryQ46-Q48
TuesdaySMR & Adolescent HealthQ49-Q53
TuesdaySAMQ54-Q60
WednesdayObesity & Behavioural DisordersQ61-Q65
WednesdayMicronutrient & Vitamin DeficiencyQ66-Q73
ThursdayBronchial AsthmaQ74-Q78
ThursdayPneumoniaQ79-Q82
ThursdayCroup, Epiglottitis, BronchiolitisQ83-Q87
FridayCongenital HypothyroidismQ88-Q92
FridaySeizures & Febrile SeizuresQ93-Q97
FridayNeural Tube DefectsQ98-Q100

Key High-Yield Points to Remember:

  1. Social smile = 6 weeks (first social milestone)
  2. Pincer grasp = 9-10 months
  3. Short stature = height <3rd percentile or <-2 SD
  4. SAM = MUAC <11.5 cm OR WFH <-3 SD OR bilateral pitting oedema
  5. ORS osmolarity = 245 mOsmol/L (WHO low-osmolarity)
  6. Fast breathing in 2-11 months = ≥50/min for pneumonia diagnosis
  7. Croup = barking cough, steeple sign; Epiglottitis = drooling, thumb sign
  8. Febrile seizure age = 6 months to 5 years
  9. Folic acid dose for NTD prevention = 400 mcg/day (5 mg in high risk)
  10. Congenital hypothyroidism = most common preventable cause of intellectual disability

Give more new questions and answers

Here are 100 more new SAQs with answers on all the same topics — covering deeper, exam-focused angles not covered in the previous set.

100 MORE PEDIATRICS SAQs — ADVANCED SET


MONDAY — GROWTH, MILESTONES, SHORT STATURE, IMMUNIZATION


Q1. What is Canalization (Canalisation) in growth? A. The tendency of a child to grow along a specific percentile channel (canal) and to return to it after a period of growth disruption. It explains why children follow their own growth curve despite minor illnesses, and why catch-up growth occurs after recovery.

Q2. What is the "critical period" concept in growth? A. A critical (sensitive) period is a specific time window during which a particular organ/system is most susceptible to environmental influences (nutrition, hormones, infections). Damage during this period causes permanent effects. Example: Brain growth is most critical in the first 2 years (first 1000 days from conception).

Q3. What is the velocity of height gain in a normal child during mid-childhood (5-10 years)? A. Approximately 5-6 cm/year. This is a relatively slow, steady phase after the rapid early childhood growth (25 cm/year in year 1) and before the pubertal growth spurt.

Q4. What is the pubertal growth spurt and what is its magnitude? A. A period of accelerated growth during puberty:
  • Girls: Peak height velocity (PHV) occurs at Tanner stage 2-3, around age 11-12 years; gain of ~8-10 cm/year
  • Boys: PHV occurs at Tanner stage 3-4, around age 13-14 years; gain of ~9-11 cm/year
  • Boys grow ~12-13 cm at peak year vs girls ~10-11 cm, explaining the final height difference

Q5. What are the primitive reflexes that should disappear and when? A.
ReflexAppearsDisappears
MoroBirth4-6 months
Palmar graspBirth3-4 months
RootingBirth3-4 months
SteppingBirth2 months
Asymmetric tonic neck reflex (ATNR)Birth4-6 months
Plantar graspBirth9-12 months
Persistence beyond expected age indicates upper motor neuron lesion.

Q6. What is the Parachute reflex and when does it appear? A. A protective postural reflex where the baby extends arms forward when tilted head-down, as if to break a fall. Appears at 8-9 months and persists throughout life. Its absence beyond 12 months suggests motor or neurological disorder.

Q7. What is the head circumference at birth, 1 year, and 2 years? A.
  • Birth: ~34 cm
  • 6 months: ~44 cm (10 cm gain in first 6 months)
  • 1 year: ~47 cm (3 cm gain in second 6 months)
  • 2 years: ~49 cm
  • Adult: ~55 cm Head grows fastest in the first 6 months of life.

Q8. What milestones should raise concern for cerebral palsy? A.
  • Persistence of Moro/ATNR beyond 6 months
  • No head control by 4 months
  • Scissoring of legs (spastic diplegia posture)
  • Fisting (thumb-in-palm) beyond 3-4 months
  • Asymmetric reach or movement
  • Early hand dominance (before 18 months) - suggests hemiplegia
  • No independent sitting by 12 months

Q9. What is the normal upper-to-lower segment ratio at birth and in a 10-year-old? A.
  • At birth: upper: lower segment = 1.7:1 (head and trunk dominate)
  • At 3 years: ~1.3:1
  • At 10 years: ~1.0:1 (equalization of segments) An abnormally high ratio in older children suggests skeletal dysplasia or rickets (short limbs).

Q10. What is the growth chart parameter most sensitive for detecting acute malnutrition? A. Weight-for-Height (WFH) or MUAC (Mid-Upper Arm Circumference). WFH detects wasting (acute malnutrition) better than weight-for-age. MUAC is most practical in community settings. Height-for-age detects stunting (chronic malnutrition).

Q11. Differentiate proportionate from disproportionate short stature with examples. A.
  • Proportionate short stature: Head, trunk, and limbs reduced equally. Causes: endocrine (GH deficiency, hypothyroidism), malnutrition, chronic systemic disease, Turner syndrome, IUGR.
  • Disproportionate short stature: Trunk and limbs not reduced equally. Causes: Skeletal dysplasias - achondroplasia (short limbs, normal trunk), Morquio syndrome (short trunk, normal limbs), rickets.

Q12. What is achondroplasia? How does it present? A. Most common skeletal dysplasia. Autosomal dominant (AD) mutation in FGFR3 gene. Features:
  • Short limbs (rhizomelic shortening - proximal > distal)
  • Normal trunk length
  • Macrocephaly with frontal bossing
  • Midface hypoplasia
  • Lumbar lordosis, trident hand
  • Normal intelligence
  • X-ray: narrowed interpedicular distance in lumbar spine

Q13. What is Turner syndrome and how does it cause short stature? A. Karyotype 45, X0 (monosomy X). Features: short stature (most consistent feature), webbed neck (pterygium colli), wide-carrying angle (cubitus valgus), widely spaced nipples, primary amenorrhoea, coarctation of aorta, horseshoe kidney. Short stature due to SHOX gene haploinsufficiency. Treatment: GH therapy + oestrogen replacement at puberty.

Q14. What are the WHO criteria for IUGR/SGA? A. SGA (Small for Gestational Age) = birth weight or birth length < 10th percentile (or <-2 SD) for gestational age. Symmetric IUGR: all measurements reduced (early insult - chromosomal, TORCH infections). Asymmetric IUGR: weight reduced but head-sparing (late insult - uteroplacental insufficiency, maternal malnutrition).

Q15. What is the difference between stunting and wasting? A.
  • Stunting: Height-for-age <-2 SD. Reflects chronic/long-standing malnutrition (undernutrition over months to years). Irreversible after age 2.
  • Wasting: Weight-for-height <-2 SD. Reflects acute recent malnutrition. Potentially reversible.
  • Underweight: Weight-for-age <-2 SD. Composite of both.

Q16. What is the Bacille Calmette-Guérin (BCG) scar significance? A. BCG scar appears 4-6 weeks after intradermal injection and indicates a cell-mediated immune response was mounted. Absence of scar after BCG does NOT necessarily mean vaccine failure (up to 10% of vaccinees do not develop a scar despite being protected). Do NOT repeat BCG just for absence of scar.

Q17. What is the Mantoux test and how is it interpreted in BCG-vaccinated children? A. Intradermal injection of 0.1 mL PPD (5 TU) in the volar aspect of left forearm; read induration (not erythema) at 48-72 hours.
  • ≥10 mm: positive in immunocompetent BCG-vaccinated children
  • ≥5 mm: positive in immunocompromised/HIV/close TB contacts
  • ≥15 mm: positive in healthy low-risk individuals In BCG-vaccinated children, induration >10 mm is suggestive of true TB infection; >15 mm strongly suggests TB.

Q18. What is the schedule and dose of the Hepatitis B vaccine in India? A.
  • Dose 1 (HepB-0): Within 24 hours of birth - 0.5 mL IM (thigh)
  • Dose 2: At 6 weeks (as part of pentavalent)
  • Dose 3: At 10 weeks (pentavalent)
  • Dose 4: At 14 weeks (pentavalent) If birth dose missed, 3 more doses are given (0, 1, 6 month schedule). For HBsAg-positive mothers, HBIG (0.5 mL) + HepB vaccine within 12 hours of birth.

Q19. What are the AEFI (Adverse Events Following Immunization)? A.
  • Vaccine reactions: fever, local redness/swelling (most common), febrile seizures (MMR, DPT)
  • Programme errors: abscess at injection site (improper technique), transmission of bloodborne infections
  • Coincidental: events that would have happened anyway
  • Serious AEFI:
  • Anaphylaxis (any vaccine, within 30 minutes)
  • BCG lymphadenitis/osteitis
  • Vaccine-associated polio (OPV)
  • Intussusception (rotavirus vaccine - first dose)
  • Thrombocytopenia (MMR)

Q20. What is the Japanese Encephalitis (JE) vaccine schedule in India? A. JE vaccination under UIP (in endemic districts only):
  • SA 14-14-2 (live attenuated) or JENVAC:
  • Dose 1: 9 months (with measles)
  • Dose 2: 16-24 months (with DPT booster) Given in endemic states: UP, Bihar, Assam, Karnataka, Tamil Nadu, West Bengal, etc.

TUESDAY — DIARRHOEA, DYSENTERY, ADOLESCENT HEALTH, SAM


Q21. What is osmotic vs secretory diarrhoea? A.
OsmoticSecretory
CausePoorly absorbed solutes (lactose intolerance, osmotic laxatives)Enterotoxins (V. cholerae, ETEC), bile acid malabsorption
Stool volumeModerateLarge (>1 L/day)
Fasting effectStops with fastingContinues with fasting
Osmotic gap>125 mOsmol/kg<50 mOsmol/kg
Stool NaLowHigh (>70 mmol/L)

Q22. What are the electrolyte abnormalities in diarrhoea? A.
  • Hypernatraemic dehydration (Na >150): CNS hyperirritability, "doughy" skin, seizures - treat slowly to avoid cerebral oedema
  • Hyponatraemic dehydration (Na <130): lethargy, seizures - if severe symptomatic, use hypertonic saline
  • Hypokalaemia: muscle weakness, ileus, cardiac arrhythmias (from stool potassium losses)
  • Metabolic acidosis: from bicarbonate loss in stools and poor tissue perfusion

Q23. When is IV fluid required in diarrhoeal dehydration? A.
  • Severe dehydration (Plan C): Ringer's Lactate (preferred) or Normal Saline
  • Children >1 month: 100 mL/kg over 3 hours (30 mL/kg fast in first 30 min, then 70 mL/kg in 2.5 hours)
  • Infants <12 months: 30 mL/kg in first 1 hour, then 70 mL/kg over 5 hours
  • Oral route is preferred whenever possible; IV only if cannot drink or in shock

Q24. What is "persistent diarrhoea" and its management outline? A. Diarrhoea lasting 14 days to 4 weeks. Causes: Giardia, Cryptosporidium, bacterial overgrowth, post-infectious lactose intolerance, immune deficiency (consider HIV). Management:
  • Identify and treat specific cause
  • Avoid lactose (use low-lactose feeds)
  • Increase dietary energy density
  • Zinc supplementation
  • Treat micronutrient deficiencies (Vitamin A, zinc)
  • Probiotics may help

Q25. What are the WHO IMCI criteria for referring a child with diarrhoea? A. Refer if:
  • Blood in stool (dysentery with severe dehydration)
  • Signs of severe dehydration not responding to Plan C
  • Persistent vomiting unable to retain ORS
  • Abdominal distension/ileus
  • Convulsions
  • Altered consciousness
  • Cholera (rice-water stools + severe dehydration) in epidemic areas

Q26. What is cholera and how is it managed in children? A. Cholera (Vibrio cholerae) causes profuse "rice-water" stools with fishy odour, rapid severe dehydration. Management:
  • Rapid IV rehydration (Plan C - Ringer's Lactate)
  • Oral rehydration as soon as able to drink
  • Antibiotic: Azithromycin 20 mg/kg single dose (first choice in children) OR Doxycycline (>8 years)
  • Zinc supplementation

Q27. What is rotavirus diarrhoea and how does vaccination help? A. Rotavirus is the most common cause of severe diarrhoea requiring hospitalization in children <5 years globally. Causes watery diarrhoea, vomiting, fever. Vaccine (Rotarix - 2 doses; RotaTeq - 3 doses; Rotavac - India-developed, 3 doses at 6, 10, 14 weeks) reduces severe rotavirus diarrhoea by ~50-60%. Maximum age for first dose: 15 weeks; last dose by 32 weeks.

Q28. What are the features of menarche and its age range? A. Menarche (first menstruation) is the last pubertal event in girls, occurring 2-3 years after thelarche (breast budding). Normal age range: 10-16 years (mean ~12.5 years in India). Delayed menarche (>16 years) requires investigation for Turner syndrome, hypothalamic dysfunction, PCOS, or anatomical defects.

Q29. What is gynecomastia in adolescent males? A. Benign enlargement of breast glandular tissue in males. Physiological gynecomastia in adolescence (Tanner stage 2-3) occurs in up to 70% of boys due to transient increase in oestrogen:androgen ratio. Usually regresses within 1-2 years. Pathological causes: Klinefelter syndrome, testicular tumours, liver disease, drugs (spironolactone, cimetidine, anabolic steroids, marijuana).

Q30. What is the definition and classification of eating disorders in adolescents? A.
  • Anorexia Nervosa: BMI <17.5, intense fear of weight gain, distorted body image, self-starvation. Complications: bradycardia, electrolyte disturbances (hypokalaemia), osteoporosis, amenorrhoea, lanugo hair, refeeding syndrome on treatment.
  • Bulimia Nervosa: Recurrent binge eating + purging (self-induced vomiting, laxatives). Weight may be normal. Features: parotid enlargement, dental erosion (Russell's sign - calluses on knuckles), hypokalaemia, metabolic alkalosis.

Q31. What is kwashiorkor and what is the biochemical basis of oedema? A. Kwashiorkor is protein-deficiency malnutrition (despite caloric adequacy in some). Oedema mechanism:
  • Hypoalbuminaemia → reduced oncotic pressure → fluid shift to interstitium
  • Increased aldosterone (secondary hyperaldosteronism)
  • Increased capillary permeability (aflatoxin theory)
  • Free radical damage (kwashiorkor has higher oxidative stress) Key features: oedema (starts feet, progresses), flaky paint skin, sparse reddish hair, fatty liver, immunosuppression.

Q32. What are the WHO criteria for discharge from SAM management (NRC)? A.
  • Weight gain: achieving 15-20% of admission weight (or reaching -2 SD WFH) and maintaining for 3 consecutive days
  • Good appetite (passes RUTF appetite test)
  • No medical complications
  • Oedema resolved (if present)
  • Good clinical condition: alert, afebrile
  • Caregiver trained on home feeding and follow-up

Q33. What is Resomal and when is it used? A. ReSoMal = Rehydration Solution for Malnutrition. Used instead of standard ORS in SAM with dehydration. It has:
  • Lower sodium (45 mmol/L vs 75 in ORS) - prevents sodium overload in SAM
  • Higher potassium (40 mmol/L)
  • Higher glucose (125 mmol/L) Given 5-10 mL/kg/hour for 2 hours, then 5-10 mL/kg alternating with F-75 for 4-10 hours. NEVER give IV fluids in SAM unless in shock.

Q34. How do you treat hypoglycaemia in SAM? A. Blood glucose <3 mmol/L (54 mg/dL) in SAM is an emergency.
  • If conscious: 50 mL of 10% glucose (or sucrose solution) by mouth/NG
  • If unconscious: IV 10% glucose 5 mL/kg stat, then oral/NG glucose feeds
  • Immediately start F-75 every 2-3 hours day and night
  • Prevent by feeding every 2 hours (do not fast)
  • Treat underlying infection

Q35. What micronutrients are given in SAM management? A. Daily for at least 2 weeks:
  • Folic acid: 1 mg/day (5 mg on day 1)
  • Zinc: 2 mg/kg/day
  • Copper: 0.3 mg/kg/day
  • Multivitamins including Vitamin A, B-complex, C
  • Iron: NOT given in acute phase (promotes bacterial growth, free radical damage); give only in rehabilitation phase once appetite returns

WEDNESDAY — OBESITY, BEHAVIOURAL DISORDERS, MICRONUTRIENTS


Q36. What is metabolic syndrome in children and its criteria? A. IDF criteria for children 10-16 years:
  • Central obesity: Waist circumference ≥90th percentile (mandatory criterion) Plus any 2 of:
  • Triglycerides ≥150 mg/dL
  • HDL cholesterol <40 mg/dL
  • Blood pressure ≥130/85 mmHg
  • Fasting glucose ≥100 mg/dL (or known T2DM)

Q37. What is the management of childhood obesity? A.
  • Lifestyle modification (cornerstone): Dietary change (reduce caloric density, increase fibre, avoid sugary drinks), physical activity (≥60 min/day moderate-intensity), reduce screen time (<2 hours/day for >5 years, none for <2 years)
  • Behavioural therapy: Family-based behavioural intervention
  • Pharmacotherapy: Orlistat (FDA-approved for children ≥12 years)
  • Bariatric surgery: For adolescents ≥13 years with BMI >40 and severe comorbidities
  • Treat comorbidities (HTN, T2DM, dyslipidaemia)

Q38. What is ADHD and what medications are used? A. Attention Deficit Hyperactivity Disorder. Medications:
  • Stimulants (first-line): Methylphenidate (Ritalin) - most studied, effective in 70-80%. Amphetamine salts.
  • Common side effects: appetite suppression, insomnia, growth deceleration
  • Non-stimulants: Atomoxetine (norepinephrine reuptake inhibitor) - used if stimulants contraindicated or substance abuse risk; Guanfacine, Clonidine Medication combined with behavioural therapy is most effective.

Q39. What are the DSM-5 diagnostic criteria for Autism Spectrum Disorder? A. Criterion A (Persistent deficits in social communication, all 3):
  1. Social-emotional reciprocity deficit
  2. Nonverbal communicative behaviours deficit
  3. Deficits in developing/maintaining relationships
Criterion B (Restricted, repetitive behaviours, ≥2):
  1. Stereotyped/repetitive motor movements or speech
  2. Insistence on sameness/routines
  3. Highly restricted, fixated interests
  4. Hyper/hypo-reactivity to sensory input
Symptoms must be present early in development and cause significant impairment.

Q40. What is enuresis? Classify and manage. A. Involuntary voiding of urine beyond age 5 (bladder control expected by age 4-5).
  • Nocturnal (bed-wetting, most common): Primary (never achieved night dryness) vs Secondary (relapse after ≥6 months dry)
  • Diurnal (daytime wetting): suggests organic cause more often Management:
  • Simple measures: fluid restriction in evenings, void before bed, star charts (motivational)
  • Enuresis alarm: Most effective long-term treatment (conditioning therapy)
  • Desmopressin (DDAVP): Useful for short-term (overnight trips); 0.2-0.4 mg oral at bedtime
  • Imipramine (anticholinergic): Less preferred (cardiac side effects)

Q41. What is the treatment of iron deficiency anaemia in children? A.
  • Oral elemental iron: 3-6 mg/kg/day of elemental iron in 2-3 divided doses
  • Given on empty stomach with Vitamin C (enhances absorption)
  • Duration: 3-6 months (3 months after Hb normalisation to replenish stores)
  • Response: Reticulocytosis in 3-5 days (earliest sign of response); Hb rises ~1 g/dL/week
  • IV iron dextran: if oral intolerance, malabsorption, non-compliance
  • Treat underlying cause (dietary deficiency, hookworm)

Q42. What is pellagra and what causes it? A. Pellagra is Niacin (Vitamin B3) deficiency. Classically: 4 Ds -
  • Dermatitis: Symmetric, sun-exposed areas (Casal's necklace around neck)
  • Diarrhoea
  • Dementia: Cognitive impairment, confusion, depression
  • Death (if untreated) Causes: Maize-based diet (low tryptophan + bound niacin), carcinoid syndrome, Hartnup disease (tryptophan malabsorption), isoniazid therapy. Treatment: Nicotinamide 100-300 mg/day.

Q43. What is thiamine deficiency and its forms? A. Thiamine (Vitamin B1) deficiency:
  • Dry Beriberi: Peripheral neuropathy (sensory + motor), bilateral, symmetric, ascending
  • Wet Beriberi: High-output cardiac failure, oedema, cardiomegaly
  • Infantile Beriberi: Occurs in breastfed infants of thiamine-deficient mothers; cardiac (acute cardiac failure, tachycardia, cyanosis) or neurologic (aphonia, ophthalmoplegia)
  • Wernicke's Encephalopathy: Confusion, ophthalmoplegia, ataxia (triad) Treatment: Thiamine IV/IM immediately, then oral.

Q44. What are the features of Vitamin B12 deficiency megaloblastic anaemia on peripheral blood smear? A.
  • Macrocytosis (MCV >100 fL)
  • Macro-ovalocytes (oval macrocytes)
  • Hypersegmented neutrophils (≥5 lobes in >5% of neutrophils, or any cell with ≥6 lobes) - hallmark
  • Low reticulocyte count
  • Pancytopenia in severe cases
  • Bone marrow: megaloblastic changes (nuclear-cytoplasmic asynchrony)

Q45. What is Vitamin E deficiency and its features in children? A. Vitamin E (tocopherol) is a fat-soluble antioxidant. Deficiency (uncommon, mainly in premature infants and fat malabsorption):
  • Premature newborns: Haemolytic anaemia, oedema, thrombocytosis (at 1-2 months)
  • Older children with cholestasis/malabsorption (e.g., cystic fibrosis, abetalipoproteinaemia): Progressive spinocerebellar ataxia, peripheral neuropathy, ophthalmoplegia, retinitis pigmentosa
  • Also: Impaired immune function

Q46. What is Vitamin K and what are coagulation factors it activates? A. Vitamin K is required for gamma-carboxylation (activation) of clotting factors II (prothrombin), VII, IX, X and anticoagulants Protein C and Protein S (mnemonic: 1972 - I, IX, VII, II). Deficiency causes prolonged PT (extrinsic pathway) first, then PTT. Treatment: Vitamin K1 (phytomenadione) IM/IV - rapid reversal within hours.

Q47. What is Iodine Deficiency Disorder (IDD)? A. Iodine deficiency causes a spectrum:
  • Fetus: Still birth, congenital anomalies, endemic cretinism (mental retardation, deaf mutism, spastic diplegia)
  • Neonate: Neonatal hypothyroidism, goitre
  • Child/Adult: Goitre (most visible sign), hypothyroidism, impaired cognition
  • Prevention: Universal salt iodisation (mandatory in India - 15 ppm at production, 7 ppm at consumer level). Lugol's iodine or lipiodol injections in severe endemic areas.

Q48. What is the treatment of rickets due to Vitamin D deficiency vs hypophosphataemic rickets? A.
  • Nutritional rickets (Vit D deficiency): Vitamin D + calcium (see Q69 in previous set)
  • X-linked Hypophosphataemic Rickets (XLH): Most common hereditary rickets. PHEX gene mutation → excess FGF23 → phosphate wasting. Treatment: Oral phosphate supplements + active Vitamin D (calcitriol). Does NOT respond to plain Vitamin D. Burosumab (anti-FGF23 antibody) now available.
  • Vitamin D-dependent rickets type 1 (25-OH D to 1,25-OH D conversion defect): Calcitriol (active Vit D)
  • Vitamin D-dependent rickets type 2 (receptor defect): High-dose calcitriol

Q49. What is the difference between marasmus and kwashiorkor in terms of WHY they develop? A.
  • Marasmus: Inadequate total calories AND protein (starvation). The body adapts by catabolizing fat and muscle. No oedema because albumin is preserved and hormonal adaptation is maintained.
  • Kwashiorkor: Predominantly protein deficiency (often with infection triggering it). Inadequate protein intake → hypoalbuminaemia → oedema. High-carbohydrate diet suppresses fat mobilization, leading to fatty liver. Free radical injury plays a role (aflatoxin, infection → oxidative stress).

Q50. What is the Mid-Upper Arm Circumference (MUAC) and its interpretation? A. Measured at the midpoint of the left upper arm (between acromion and olecranon) with the arm relaxed.
  • Normal (Green): ≥12.5 cm
  • Moderate Acute Malnutrition / MAM (Yellow): 11.5-12.4 cm
  • Severe Acute Malnutrition / SAM (Red): <11.5 cm MUAC is age-independent (usable 6-59 months) and is the single best predictor of mortality risk.

THURSDAY — ASTHMA, PNEUMONIA, CROUP, BRONCHIOLITIS


Q51. What is the pathophysiology of asthma? A. Three key components:
  1. Airway inflammation: Eosinophilic predominant, driven by Th2 lymphocytes; mast cells, IgE, IL-4, IL-5, IL-13 → inflammation, mucus hypersecretion
  2. Airway hyperresponsiveness (AHR): Exaggerated bronchoconstriction to stimuli
  3. Airway remodelling: Chronic changes - subepithelial fibrosis, smooth muscle hypertrophy, goblet cell metaplasia → progressive irreversible obstruction if untreated

Q52. What are the spirometric findings in asthma? A.
  • FEV1/FVC ratio < 0.8 (obstructive pattern) - reduced
  • FEV1 reduced (<80% predicted)
  • FVC: normal or mildly reduced
  • Reversibility: ≥12% AND ≥200 mL improvement in FEV1 after SABA (salbutamol 400 mcg) - diagnostic of asthma
  • In children <5 years, spirometry not reliable; use clinical criteria, bronchodilator response trials

Q53. What is the stepwise approach to asthma management (GINA steps)? A.
  • Step 1: PRN low-dose ICS-formoterol (or SABA only as reliever)
  • Step 2: Low-dose ICS daily (controller) + SABA PRN
  • Step 3: Low-dose ICS + LABA (or medium-dose ICS alone)
  • Step 4: Medium-dose ICS + LABA
  • Step 5: High-dose ICS + LABA + add-on therapy (tiotropium, biologics - omalizumab for allergic asthma, mepolizumab for eosinophilic)

Q54. What is status asthmaticus? A. Severe, life-threatening episode of asthma that does not respond to standard initial bronchodilator therapy (3 doses of salbutamol in 1 hour). Signs of impending respiratory failure:
  • Silent chest (no wheeze due to no air movement)
  • Pulsus paradoxus >20 mmHg
  • Inability to speak
  • SpO2 <92% despite oxygen
  • PCO2 rising (normal PCO2 in severe asthma is ominous - indicates fatigue) Management: ICU, IV magnesium, IV aminophylline, possible NIV or intubation.

Q55. What are the criteria for diagnosing pneumonia radiologically? A. Chest X-ray findings in pneumonia:
  • Lobar/segmental consolidation (air-space opacity): Bacterial (S. pneumoniae most common); air bronchograms common
  • Interstitial pattern (bilateral diffuse): Viral, atypical (Mycoplasma, Chlamydia)
  • Round pneumonia: S. pneumoniae in young children (unique to <5 years)
  • Parapneumonic effusion/empyema: S. pneumoniae, Staph aureus
  • Pneumatoceles (thin-walled air cysts): Staphylococcal pneumonia (pathognomonic)

Q56. What is staphylococcal pneumonia in children? What are its features? A. Caused by Staphylococcus aureus. Aggressive course, especially in infants <1 year. Features:
  • Rapid deterioration
  • High fever, toxaemia
  • Pneumatoceles (pathognomonic on CXR)
  • Pyopneumothorax, empyema
  • Abscesses Treatment: Cloxacillin 200 mg/kg/day IV + Gentamicin. If MRSA: Vancomycin or Linezolid. Chest drain for pyopneumothorax.

Q57. What is Pneumocystis jirovecii Pneumonia (PJP/PCP) in children? A. Occurs in HIV-infected/immunocompromised children. Features: subacute progressive dyspnoea, dry cough, fever; SpO2 often very low despite minimal auscultatory findings; bilateral butterfly (bat-wing) perihilar infiltrates on CXR; elevated LDH. Diagnosis: BAL with silver methenamine/GMS stain showing "helmet-shaped" (boat-shaped) cysts. Treatment: High-dose Co-trimoxazole (TMP-SMX) IV. Add corticosteroids if PaO2 <70 mmHg.

Q58. What is the Steeple sign and Thumb sign on X-ray? A.
  • Steeple sign (Pencil sign): Seen in Croup (laryngotracheobronchitis). AP neck X-ray shows subglottic narrowing - the tracheal column tapers symmetrically below the glottis, resembling a church steeple.
  • Thumb sign: Seen in Epiglottitis. Lateral neck X-ray shows swollen, rounded epiglottis resembling an adult's thumb instead of the normal thin finger-like shadow.

Q59. What is the Westley score threshold for giving nebulised adrenaline? A. Nebulized adrenaline (epinephrine) is indicated in moderate-severe croup (Westley score ≥6 or stridor at rest with significant respiratory distress). Dose: 5 mL of 1:1000 adrenaline nebulized. Onset in 10-30 minutes; effect lasts 2 hours ("rebound" can occur - observe for at least 3-4 hours after). ALWAYS give dexamethasone concurrently.

Q60. What viruses cause bronchiolitis and what is the treatment of RSV bronchiolitis? A. RSV causes ~70-80% of bronchiolitis. Others: Rhinovirus, Parainfluenza, Human metapneumovirus, Adenovirus, Influenza. Treatment is supportive only:
  • Oxygen if SpO2 <90-92%
  • High-flow nasal cannula (HFNC) for moderate-severe - reduces need for intubation
  • Nasogastric tube feeding if unable to feed
  • Hypertonic saline nebulization (3%) may reduce hospital stay modestly
  • NOT recommended: bronchodilators (salbutamol, adrenaline), systemic steroids, antibiotics (unless bacterial co-infection), chest physiotherapy, ribavirin (except severe immunocompromised)

Q61. What is palivizumab and who receives it? A. Palivizumab is a monoclonal antibody against RSV F protein. Used for RSV prophylaxis (not treatment) in:
  • Premature infants <29 weeks gestation
  • Infants with chronic lung disease of prematurity
  • Haemodynamically significant congenital heart disease Given monthly IM injections (15 mg/kg) during RSV season (winter/early spring). Does NOT replace immunization.

Q62. What is the difference between viral and bacterial pneumonia clinically? A.
FeatureViralBacterial
OnsetGradualAbrupt
FeverLow-moderateHigh, rigors
CoughDry, hackingProductive
AuscultationDiffuse wheeze/cracklesFocal crackles, bronchial breathing
WBCNormal/lymphocytosisLeukocytosis (neutrophilia)
CRP/ESRMildly elevatedMarkedly elevated
CXRBilateral interstitialLobar consolidation

FRIDAY — HYPOTHYROIDISM, SEIZURES, NEURAL TUBE DEFECTS


Q63. What is the difference between primary, secondary, and tertiary hypothyroidism? A.
  • Primary: Thyroid gland failure. TSH high, T4/T3 low. (Hashimoto's, post-thyroidectomy, iodine deficiency, congenital dysgenesis)
  • Secondary: Pituitary failure → TSH low, T4/T3 low.
  • Tertiary: Hypothalamic failure → TRH low → TSH low/normal, T4/T3 low.
  • Subclinical: TSH mildly elevated, T4 normal, no symptoms.

Q64. What is Hashimoto's thyroiditis (autoimmune thyroiditis)? A. Most common cause of acquired hypothyroidism in children (especially adolescent girls). Autoimmune destruction of thyroid by lymphocytic infiltration. Antibodies: anti-TPO (>95%), anti-thyroglobulin. Initially can cause transient hyperthyroid phase (Hashitoxicosis). Firm, non-tender, rubbery goitre. Associated with Type 1 DM, Turner syndrome, Down syndrome. Treatment: Levothyroxine when overt hypothyroidism (high TSH, low T4).

Q65. What is Pendred syndrome? A. Autosomal recessive disorder (SLC26A4 gene - pendrin mutation). Features: dyshormonogenetic goitre + sensorineural hearing loss (most common genetic cause of syndromic deafness). Perchlorate discharge test is positive. Typically euthyroid or mildly hypothyroid. Associated with Mondini cochlear dysplasia on CT/MRI.

Q66. What is neonatal thyrotoxicosis and how does it occur? A. Transient hyperthyroidism in newborns of mothers with Graves' disease, caused by transplacental transfer of TSH-receptor stimulating antibodies (TRAb/TSI). Features: tachycardia, irritability, poor feeding, weight loss, goitre, exophthalmos, craniosynostosis. Self-limited (resolves in 3-12 weeks as maternal antibodies clear). Treatment: Methimazole (PTU), propranolol for symptoms, lugol's iodine in severe cases.

Q67. What are the investigations in a child with seizure for the first time? A.
  • Blood glucose (immediate - rule out hypoglycaemia)
  • Serum electrolytes: Na, Ca, Mg (rule out metabolic causes)
  • CBC
  • EEG (electroencephalogram) - after acute phase; helps classify epilepsy type
  • MRI brain (preferred over CT - better structural detail); indicated if focal seizure, Todd's paresis, abnormal neurology, or EEG abnormality
  • LP (if suspected CNS infection - meningitis/encephalitis)
  • Metabolic workup if suspected inborn error

Q68. What are the antiepileptic drugs (AEDs) used for different seizure types in children? A.
Seizure TypeFirst-line AED
Focal seizuresCarbamazepine, Oxcarbazepine, Levetiracetam
Generalised tonic-clonicSodium valproate, Levetiracetam
Absence seizuresEthosuximide (first choice), Valproate
Myoclonic seizuresValproate, Levetiracetam, Clonazepam
Infantile spasms (West syndrome)ACTH, Vigabatrin, Prednisolone
Lennox-GastautValproate, Clobazam, Lamotrigine

Q69. What is West syndrome? A. A severe epileptic encephalopathy of infancy (peak onset 4-8 months). Triad:
  • Infantile spasms (salaam attacks): Sudden flexion of neck, trunk, arms and legs in clusters
  • Hypsarrhythmia: Chaotic, high-amplitude slow waves with multifocal spikes on EEG (pathognomonic)
  • Developmental regression/arrest Causes: Structural (tuberous sclerosis, Down syndrome, hypoxic-ischaemic injury), metabolic, or unknown. Treatment: ACTH (first-line), Vigabatrin (especially in tuberous sclerosis), Pyridoxine trial.

Q70. What is Lennox-Gastaut syndrome? A. Severe epileptic encephalopathy, typically onset 2-8 years. Features:
  • Multiple seizure types: tonic (most characteristic), atonic (drop attacks), atypical absence
  • EEG: slow spike-wave (1-2.5 Hz) - characteristic
  • Intellectual disability
  • Treatment-resistant (often polytherapy needed: Valproate, Clobazam, Lamotrigine, Rufinamide, Dietary therapy - ketogenic diet)

Q71. What is Todd's paresis (Todd's palsy)? A. Focal neurological deficit (weakness/paralysis) following a focal motor seizure, lasting minutes to hours (up to 24 hours) before resolving. Due to cortical exhaustion/inhibition after seizure activity. Its presence indicates the seizure was focal (cortical origin) and warrants neuroimaging to rule out structural lesion.

Q72. What is the EEG in absence epilepsy? A. Childhood absence epilepsy (CAE, ages 4-10 years) shows classic 3 Hz spike-and-wave discharges (generalized, bisynchronous, symmetric), abrupt onset and offset, provoked by hyperventilation. Child has brief (5-30 seconds) staring spells with eyelid flutter, no postictal phase, no recall. Distinguish from focal aware seizures (which have postictal confusion). Treatment: Ethosuximide (first choice - fewest cognitive side effects), Valproate.

Q73. What is Dravet syndrome? A. Severe myoclonic epilepsy of infancy. SCN1A gene mutation (sodium channel). Onset first year of life with febrile or afebrile prolonged hemiclonic seizures evolving to multiple seizure types. Cognitive regression, photosensitivity. Unique: Sodium channel blockers (carbamazepine, lamotrigine, phenytoin) worsen seizures - contraindicated. Treatment: Valproate + Clobazam + Stiripentol/Fenfluramine (newer additions).

Q74. What are the pre-ictal, ictal, and post-ictal phases of a generalized tonic-clonic seizure? A.
  • Aura (pre-ictal): Sensory/motor/psychic warning (only in focal onset seizures)
  • Tonic phase: Sudden loss of consciousness, generalized stiffening, expiratory cry, apnoea, cyanosis, eyes deviated upward (10-30 seconds)
  • Clonic phase: Rhythmic jerking of all limbs, salivation, tongue bite, incontinence (1-3 minutes)
  • Post-ictal phase: Gradual recovery, confusion, headache, drowsiness, Todd's paresis if focal (minutes to hours)

Q75. What is Arnold-Chiari malformation and its relationship to neural tube defects? A. Chiari II malformation: downward displacement of cerebellar vermis, medulla, and fourth ventricle through foramen magnum. Found in virtually all cases of myelomeningocele. Causes:
  • Obstructive hydrocephalus (most common complication of myelomeningocele)
  • Cranial nerve palsies (stridor, apnoea, dysphagia)
  • Syringomyelia Treatment: VP shunt for hydrocephalus; posterior fossa decompression if symptomatic Chiari.

Q76. What is anencephaly and how is it diagnosed prenatally? A. Anencephaly = absence of cranial vault and cerebral hemispheres. Most common NTD; uniformly fatal (usually stillborn or die within days). Prenatal diagnosis:
  • Maternal serum AFP: Markedly elevated (>2.5 MoM) at 15-20 weeks
  • Ultrasound: Absence of skull/brain at 10-14 weeks (12 weeks most reliable); "frog-like" face appearance
  • Amniotic fluid AFP and acetylcholinesterase: Elevated (confirmatory) Termination of pregnancy offered. Prevention: folic acid periconceptionally.

Q77. What is the difference between meningocele and meningomyelocele? A.
MeningoceleMyelomeningocele
ContentsCSF + meninges onlyCSF + meninges + spinal cord/nerve roots
Skin coveringUsually intactThin, may be open (leaking CSF)
Neurological deficitUsually nonePresent (weakness, sensory loss, bladder/bowel dysfunction)
IncidenceLess commonMore common (~90% of open NTDs)
PrognosisGoodVariable, depends on level

Q78. What is spina bifida occulta? A. Failure of posterior bony fusion of vertebral arches WITHOUT herniation of meninges or neural tissue. Usually L5-S1 level. Often asymptomatic (incidental X-ray finding). May be associated with cutaneous stigmata:
  • Hairy patch (hypertrichosis), dimple, lipoma, haemangioma, or skin discoloration over lumbar spine
  • These may indicate underlying tethered spinal cord - can cause progressive neurological deficits with growth Investigations: MRI spine (to rule out tethered cord). Prophylactic surgery for tethered cord.

Q79. What is the VACTERL association and its relevance to NTDs? A. VACTERL is a non-random association of congenital anomalies:
  • V - Vertebral defects (spina bifida, hemivertebrae)
  • A - Anal atresia (imperforate anus)
  • C - Cardiac defects (VSD most common)
  • T - Tracheo-Esophageal fistula
  • E - Esophageal atresia
  • R - Renal anomalies
  • L - Limb defects (radial ray defects) When one anomaly is found, screen for others. Vertebral defects and NTDs overlap.

Q80. What is Dandy-Walker malformation and its relationship to NTDs? A. Dandy-Walker malformation: Cystic dilatation of the fourth ventricle + partial/complete agenesis of cerebellar vermis + enlarged posterior fossa. NOT a neural tube defect per se, but a posterior fossa developmental anomaly. Associated with NTDs, corpus callosum agenesis, heterotopias. Presents with hydrocephalus in infancy. Treatment: VP shunt + cyst drainage. Prognosis depends on associated anomalies.

BONUS QUESTIONS (Q81-Q100) — HIGH-YIELD EXAM TOPICS


Q81. What is the Apgar score and how is it calculated? A. Assessed at 1 and 5 minutes after birth. Each item scored 0-2, maximum 10:
Sign012
Appearance (colour)Blue/paleBody pink, extremities blueCompletely pink
PulseAbsent<100/min≥100/min
Grimace (reflex)NoneGrimaceCry/cough/sneeze
Activity (tone)LimpSome flexionActive flexion
RespirationAbsentWeak/irregularStrong cry
  • 7-10: Normal; 4-6: Moderate depression; <4: Severe depression

Q82. What is the Ballard score used for? A. New Ballard Score estimates gestational age in newborns (including extremely premature). Assesses 6 neuromuscular maturity criteria + 6 physical maturity criteria (each scored 0-5):
  • Neuromuscular: Posture, square window, arm recoil, popliteal angle, scarf sign, heel-to-ear
  • Physical: Skin, lanugo, plantar surface, breast, eye/ear, genitals Total score correlates with gestational age (range 20-44 weeks).

Q83. What is Bronchopulmonary Dysplasia (BPD)? A. Chronic lung disease in premature infants requiring oxygen at 36 weeks corrected gestational age (or at 28 days if ≥32 weeks). Risk factors: extreme prematurity, RDS, mechanical ventilation (barotrauma, volutrauma), oxygen toxicity. Features: tachypnoea, retractions, wheezing, supplemental O2 dependence, CXR - hyperinflation with cystic areas. Treatment: diuretics, bronchodilators, nutritional support, minimize O2, consider systemic steroids.

Q84. What is the difference between type 1 and type 2 DM in children? A.
FeatureType 1 DMType 2 DM
MechanismAutoimmune beta-cell destructionInsulin resistance + relative deficiency
AgeAny (peak 5-7, puberty)Obese adolescents
OnsetAcute (DKA common)Insidious
Body habitusThinObese
Acanthosis nigricansAbsentPresent
C-peptideVery low/absentNormal/elevated
Antibodies (GAD, IA-2)PositiveNegative
TreatmentInsulin (mandatory)Metformin ± insulin

Q85. What is Kawasaki disease and when is IVIG used? A. Vasculitis of medium vessels in children <5 years. Diagnostic criteria (fever ≥5 days + 4 of 5):
  • Bilateral non-purulent conjunctival injection
  • Changes in lips/oral mucosa (strawberry tongue, cracked lips)
  • Polymorphous rash
  • Changes in extremities (erythema, oedema, periungual peeling)
  • Cervical lymphadenopathy (≥1.5 cm, usually unilateral) Treatment: IVIG 2 g/kg single infusion + Aspirin (anti-inflammatory then antiplatelet dose). IVIG given within 10 days of fever onset prevents coronary artery aneurysms.

Q86. What is the commonest cause of meningitis in children beyond neonatal period? A. Neisseria meningitidis (meningococcus) and Streptococcus pneumoniae (pneumococcus) are the most common causes of bacterial meningitis in children 1 month to adolescence. Haemophilus influenzae type b (Hib) was previously leading but has declined with vaccination. N. meningitidis more common in older children/teenagers; S. pneumoniae in infants 1-23 months.

Q87. What is the "Bulging fontanelle" sign and its significance? A. A full, bulging, non-pulsatile anterior fontanelle (when child is upright and calm) indicates raised intracranial pressure. Causes:
  • Meningitis/encephalitis
  • Hydrocephalus
  • Intracranial haemorrhage
  • Lead poisoning
  • Vitamin A toxicity (pseudotumor cerebri)
  • Space-occupying lesion A sunken fontanelle indicates dehydration.

Q88. What is the difference between obstructive and restrictive lung disease spirometry findings? A.
Obstructive (asthma, bronchiolitis)Restrictive (fibrosis, chest wall)
FEV1ReducedReduced
FVCNormal/mildly reducedReduced
FEV1/FVC ratio<0.7 (reduced)>0.7 (normal or increased)
TLCNormal/increasedReduced
RVIncreased (air trapping)Normal/reduced

Q89. What is the rule of threes in infant development? A. A useful mnemonic:
  • 3 weeks: Infant stays awake more
  • 3 months: Holds head up, social smile
  • 6 months: Sits with support, transfers objects
  • 9 months: Pincer grasp, stands with support
  • 12 months: Walks with support, 2-3 words (Better known: head control at 3 months, sits at 6 months, stands at 9 months, walks at 12 months - quarter-year milestones)

Q90. What is the "triple test" in prenatal screening for NTDs? A. Triple test (15-20 weeks maternal serum):
  • Alpha-fetoprotein (AFP): Elevated in NTDs, gastroschisis; Reduced in Down syndrome
  • hCG: Elevated in Down syndrome; Reduced in trisomy 18
  • Unconjugated Estriol (uE3): Reduced in Down syndrome and trisomy 18 Raised AFP alone (>2.5 MoM) with normal hCG and uE3 suggests NTD (open spina bifida or anencephaly). Confirmed by detailed USS and amniocentesis (amniotic AFP + AChE).

Q91. What is the commonest cause of failure to thrive (FTT) in infancy? A. Non-organic (psychosocial/environmental) FTT is the most common cause overall - inadequate caloric intake due to poverty, feeding difficulties, caregiver neglect, or maternal depression. Organic causes: GERD, malabsorption (coeliac, CF), cardiac/renal disease, metabolic disorders. Assessment: dietary diary, feeding observation, home visit. Treatment: caloric rehabilitation + social support.

Q92. What are the signs of raised intracranial pressure (RICP) in infants vs older children? A.
  • Infants: Bulging fontanelle, increasing head circumference, dilated scalp veins, sunset sign (downward deviation of eyes), irritability, vomiting, poor feeding, high-pitched cry
  • Older children: Headache (worse in morning, worsened by bending/coughing), vomiting (projectile, not related to feeding), papilloedema, sixth nerve palsy (diplopia), Cushing's triad (bradycardia, hypertension, irregular breathing) - a late, ominous sign

Q93. What is Respiratory Syncytial Virus (RSV) and how does it differ from influenza? A.
FeatureRSVInfluenza
Age groupInfants <2 yearsAll ages
SeasonWinterWinter/Autumn
Main manifestationBronchiolitisFlu syndrome (fever, myalgia, cough)
SeveritySevere in premature/CLDSevere in elderly/immunocompromised
VaccineNirsevimab (monoclonal Ab)Annual influenza vaccine
TreatmentSupportiveOseltamivir (within 48 hours)

Q94. What is the Moro reflex and what are its components? A. The Moro (startle) reflex is elicited by sudden head drop or loud noise:
  • Phase 1: Abduction and extension of arms with opening of hands
  • Phase 2: Adduction of arms across chest (embrace)
  • Associated: Cry Present from birth, disappears at 4-6 months. Asymmetric Moro suggests brachial plexus injury (Erb's palsy - absent on affected side) or hemiplegia. Absent Moro bilaterally suggests severe brain injury.

Q95. What is the treatment ladder for febrile seizures - when to give prophylaxis? A. Routine prophylaxis (daily AEDs) is generally NOT recommended for simple febrile seizures due to:
  • Low risk of epilepsy (1-2%)
  • Side effects of AEDs outweigh benefit
  • Does not prevent subsequent febrile seizures effectively Exceptions (consider prophylaxis):
  • Complex febrile seizures with recurrence
  • Underlying neurological abnormality
  • Very high parental anxiety If given: Sodium valproate or Phenobarbitone. Intermittent oral/rectal diazepam at onset of fever is an alternative but has CNS side effects.

Q96. What is Hypothyroidism vs Cretinism? A.
  • Cretinism (Endemic cretinism): Due to severe iodine deficiency during fetal/neonatal period. Features: Intellectual disability, deaf-mutism, spastic diplegia (neurological type) OR hypothyroid symptoms (myxoedematous type). A public health/preventable condition.
  • Congenital hypothyroidism: Due to thyroid dysgenesis or dyshormonogenesis (not iodine deficiency). Detected by neonatal screening; treated with levothyroxine to prevent intellectual disability. Key difference: Endemic cretinism is iodine deficiency-related; congenital hypothyroidism is structural/genetic.

Q97. What is the significance of the neonatal heel-prick (Guthrie card) test? A. Neonatal metabolic screening (heel-prick blood spot) at 48-72 hours of age screens for treatable metabolic and endocrine conditions before symptoms appear. Standard screens include:
  • Congenital hypothyroidism (TSH/T4) - most important
  • Phenylketonuria (PKU) - Phenylalanine elevated
  • Congenital adrenal hyperplasia (17-OHP)
  • Haemoglobinopathies (sickle cell)
  • MCAD deficiency (medium-chain acyl-CoA dehydrogenase)
  • Cystic fibrosis (IRT) India's RBSK (Rashtriya Bal Swasthya Karyakram) screens for 30 conditions.

Q98. What is the difference between constitutional delay of growth and puberty (CDGP) and hypogonadotropic hypogonadism? A.
FeatureCDGP (Constitutional Delay)Hypogonadotropic Hypogonadism
Pubertal timingDelayedAbsent/delayed
Final heightNormalMay be reduced
Bone ageDelayedVariable
GnRH stimulationNormal LH/FSH responseBlunted response
Family historyPositive (late bloomers)Negative
Spontaneous pubertyOccurs eventuallyDoes NOT occur
TreatmentReassurance ± low-dose testosteroneGnRH/gonadotropin therapy

Q99. What are the IMCI danger signs in children that require urgent referral? A. General danger signs (any age):
  1. Not able to drink or breastfeed
  2. Vomits everything
  3. Convulsing now (or convulsed in this illness)
  4. Lethargic or unconscious Additionally in young infants (<2 months):
  • Fast breathing (≥60/min)
  • Severe chest indrawing
  • Nasal flaring
  • Grunting
  • Bulging fontanelle
  • Fever or hypothermia Any ONE danger sign = refer urgently.

Q100. What is the Developmental Quotient (DQ) and Intelligence Quotient (IQ)? A.
  • DQ (Developmental Quotient): Used in infants/young children. DQ = (Developmental Age / Chronological Age) × 100. Normal = 85-115. Assessed by Denver, Griffiths, Bayley scales. Measures development, not intelligence.
  • IQ (Intelligence Quotient): Mental Age / Chronological Age × 100. Used in children >5 years. Assessed by Wechsler scales (WISC), Stanford-Binet.
  • Intellectual Disability (ID) classification:
  • Mild: IQ 50-70
  • Moderate: IQ 35-49
  • Severe: IQ 20-34
  • Profound: IQ <20

QUICK REVISION TABLE - Must-Know Facts

TopicKey Fact
First primitive reflex to appearMoro - at birth
First milestoneSocial smile - 6 weeks
BCG scar appears4-6 weeks after vaccination
MUAC SAM threshold<11.5 cm
ORS osmolarity245 mOsmol/L
Fast breathing (2-11 months)≥50/min
Croup X-raySteeple sign
Epiglottitis X-rayThumb sign
Febrile seizure age6 months - 5 years
Congenital hypothyroidismTreat within 2 weeks of birth
Folic acid (normal risk)400 mcg/day periconceptional
West syndrome triadSpasms + hypsarrhythmia + regression
SAM formula stabilizationF-75 (75 kcal/100 mL)
SAM formula rehabilitationF-100 (100 kcal/100 mL)
NTD most preventable byPericonceptional folic acid
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