Page 31 of 33
PE12.1-8,PE13.1-4 | Micronutrients — Graded Quiz
Click any question card to reveal the correct answer.
A 4-year-old from Bihar presents to the ophthalmology OPD with corneal ulceration in the left eye and a history of night blindness. His right eye shows triangular white foamy patches at 3 o'clock and 9 o'clock on the bulbar conjunctiva. Under the WHO/Bitot classification this child is at which stage of xerophthalmia, and what is the MOST urgent intervention?
Correct. Corneal ulceration is WHO xerophthalmia stage X3A (ulceration <1/3 of corneal surface) or X3B (>1/3) — both are sight-threatening emergencies. Treatment is 2 lakh IU Vitamin A on day 1, day 2, and 2 weeks, PLUS local eye care and antibiotics.
WHO xerophthalmia stages: XN (night blindness), X1A (conjunctival xerosis), X1B (Bitot's spots), X2 (corneal xerosis), X3A/X3B (ulceration), XS (scarring). Stages X2 and above are corneal and sight-threatening; treat as an emergency with 2 lakh IU × 3 doses.
Incorrect. Corneal ulceration is xerophthalmia stage X3, a sight-threatening emergency. The therapeutic schedule is 2 lakh IU Vitamin A orally on day 1, day 2, and at 2 weeks. Night blindness is XN; Bitot's spots are X1B; corneal xerosis is X2.
Click to reveal answer
A physician wants to prescribe stoss therapy for a 3-year-old with florid nutritional rickets (confirmed low 25-OH Vitamin D). Which regimen is CORRECT for stoss therapy and what radiological sign is used to assess healing?
Correct. Stoss therapy for rickets is a single oral dose of 600,000 IU (6 lakh IU) of Vitamin D. Radiological healing — appearance of a 'zone of provisional calcification' (dense line across the metaphysis) — is assessed at 4–6 weeks, not on day 2.
Stoss therapy = 600,000 IU (6 lakh IU) Vitamin D in a single dose (oral or IM for malabsorption). Prophylaxis: 400 IU/day from birth. Healing is radiological: dense zone of provisional calcification at metaphysis at 4–6 weeks. Also supplement calcium 500–1000 mg/day when dietary intake is low.
Incorrect. Stoss (shock) dose for nutritional rickets is a single oral dose of 600,000 IU. Healing is assessed radiologically by the appearance of a 'zone of provisional calcification' at 4–6 weeks.
Click to reveal answer
A term neonate born at home in a rural area develops bleeding from the umbilicus on day 4 of life. Mother reports no antenatal care and no injections given at birth. Platelet count is normal; PT is markedly prolonged; APTT is prolonged; fibrinogen is normal. Vitamin K prophylaxis was not given. What is this condition called and what is the treatment?
Correct. Classic VKDB presents on days 2–7. The pattern of prolonged PT + prolonged APTT + normal platelet count + normal fibrinogen in a neonate not given Vitamin K at birth is diagnostic. Treatment: Vitamin K 1 mg IV (slowly); severe or life-threatening bleeding also requires FFP for immediate correction.
VKDB types: early (<24 h, maternal drugs), classic (2–7 days), late (2–8 weeks — breastfed infants, cholestasis). Coagulation profile: prolonged PT + APTT, normal fibrinogen, normal platelets. Prevention: Vit K 1 mg IM at birth (0.5 mg if <1.5 kg).
Incorrect. Normal fibrinogen and platelets with isolated prolongation of PT and APTT in a neonate without Vitamin K prophylaxis = classic VKDB (days 2–7). DIC has low fibrinogen; haemophilia has only APTT prolonged; ITP has thrombocytopenia.
Click to reveal answer
A 9-month-old girl is brought with irritability and pallor. Her mother, a strict vegetarian, reports exclusively breastfeeding with no complementary foods. CBC: Hb 8 g/dL, MCV 110 fL, blood smear shows macro-ovalocytes and hypersegmented neutrophils. Serum B12 is very low. Which BEST explains the neural risk in this infant if untreated?
Correct. Vitamin B12 (cobalamin) is essential for myelin synthesis. Deficiency in infants causes progressive demyelination, presenting as hypotonia, developmental regression, and seizures. This is subacute combined degeneration adapted to the infantile context (affecting posterior and lateral columns).
B12-deficient infants (vegan-mother-breastfed): megaloblastic anaemia + irreversible neurological damage if untreated. B12 is required for myelin synthesis. Early treatment with hydroxocobalamin/cyanocobalamin IM is critical to prevent permanent regression. B12 found only in animal products.
Incorrect. B12 deficiency affects myelin synthesis, causing irreversible neurological damage (developmental regression, hypotonia, subacute combined degeneration) if untreated. Neural tube defects are a folate-in-utero risk, not infant B12 deficiency.
Click to reveal answer
A 15-month-old child on a maize-predominant diet in a tribal district presents with a symmetrical scaly hyperpigmented rash on the dorsum of both hands and feet, angular stomatitis, and diarrhoea. He is also irritable. What is the most likely diagnosis and its pathophysiology?
Correct. Pellagra (4 Ds: Diarrhoea, Dermatitis — photosensitive, symmetrical on sun-exposed skin, Dementia/irritability, Death) results from niacin/tryptophan deficiency. Maize is deficient in niacin and tryptophan. Niacin is needed to synthesise NAD/NADP — essential coenzymes in energy metabolism.
Pellagra: 4 Ds (Diarrhoea, Dermatitis — Casal's necklace on photosensitive areas, Dementia/irritability, Death if untreated). Maize is deficient in niacin and tryptophan. Treatment: nicotinamide 50–300 mg/day. High-maize diet in tribal/subsistence communities is the classic Indian setting.
Incorrect. The classic triad of symmetrical photosensitive dermatitis, diarrhoea, and irritability/dementia on a maize diet = pellagra (Niacin/B3 deficiency). Maize is low in both niacin and tryptophan (precursor for niacin). Zinc deficiency causes acrodermatitis enteropathica (periorificial distribution); riboflavin deficiency causes glossitis/corneal vascularisation.
Click to reveal answer
A 2-year-old presents with painful, swollen gums that bleed easily, perifollicular haemorrhages on the lower limbs, and a 'frog-leg' posture with refusal to move. X-ray of the knee shows a dense line at the metaphysis with a translucent zone below it and corner fractures. Which X-ray sign and Vitamin C dose combination is CORRECT?
Correct. Scurvy radiological signs: Frankel's line (dense line at metaphysis = zone of provisional calcification), Trümmerfeld zone (translucent band below Frankel's), Pelkan spurs (lateral margin fractures), and Wimberger's ring (bone-in-bone ring of density in epiphysis). Treatment: Vitamin C 100–300 mg/day orally for 2–4 weeks.
Scurvy X-ray signs: Frankel's line (dense metaphyseal line), Trümmerfeld zone (translucent zone), Pelkan spurs (corner fractures), Wimberger's sign (epiphyseal ring), periosteal elevation. Treatment: Vitamin C 100–300 mg/day for 2–4 weeks. RDA for Vitamin C: 40 mg/day for children.
Incorrect. Looser's zones and Erlenmeyer flask deformity are signs of rickets/storage disease, not scurvy. Scurvy shows Frankel's line + Trümmerfeld zone + Pelkan spurs. Treatment is Vitamin C 100–300 mg/day, not Vitamin D or Vitamin K.
Click to reveal answer
A 6-week-old infant born to a mother who took high-dose phenobarbitone throughout pregnancy presents with generalised seizures not responsive to anticonvulsants. Blood glucose is normal. Seizures stop within minutes of giving a parenteral injection. What deficiency is MOST likely, and what is the mechanism of action of its replacement?
Correct. Pyridoxine-dependent seizures occur in neonates/infants whose mothers took anticonvulsants (phenobarbitone, phenytoin) which deplete B6, or in neonates with a genetic GABA metabolism defect. Pyridoxal phosphate (active B6) is an essential cofactor for GAD (glutamate decarboxylase) which converts glutamate → GABA. Low GABA → seizures.
Pyridoxine-dependent seizures: respond dramatically to IV/IM pyridoxine. Mechanism: B6 (pyridoxal phosphate) is coenzyme for GAD → GABA synthesis. Causes: maternal anticonvulsants, isoniazid, genetic ALDH7A1 mutations. Treat with pyridoxine 50–100 mg IV during seizure, then 5–10 mg/day maintenance.
Incorrect. Seizures in a neonate of a phenobarbitone-treated mother that stop with parenteral pyridoxine = pyridoxine-dependent seizures. B6 (pyridoxal phosphate) is the cofactor for GAD which synthesises GABA from glutamate.
Click to reveal answer
A paediatrician in Manipur notices a cluster of schoolchildren with goitre. Survey data show 20% of children aged 6–12 years have visible goitre. The district is mountainous. Salt testing shows median iodine of 8 ppm at consumer level. Which of the following CORRECTLY describes the public health classification and intervention?
Correct. WHO/UNICEF classifies IDD burden by goitre prevalence: mild 5–19.9%, moderate 20–29.9%, severe ≥30%. 20% goitre prevalence = moderate IDD. The primary population-level intervention is enforcement of Universal Salt Iodisation (≥15 ppm at consumer, ≥30 ppm at production). The 8 ppm consumer level is below the 15 ppm minimum, confirming USI is failing.
IDD burden classification (WHO/UNICEF): mild 5–19.9% TGR, moderate 20–29.9%, severe ≥30%. USI standard: ≥30 ppm at production, ≥15 ppm at consumer. Spectrum: subclinical iodine deficiency → goitre → hypothyroidism → cretinism (irreversible, congenital). Neonatal TSH screening for hypothyroidism.
Incorrect. 20% total goitre prevalence (TGR) = moderate IDD. The inadequate iodine in salt (8 ppm vs required 15 ppm) confirms a USI enforcement failure. The intervention is enforcing USI standards, not just dietary diversification or daily potassium iodide tablets.
Click to reveal answer
A 14-month-old presents with failure to thrive, irritability, and three-day history of tetany. Mother says the child has been on a dairy-free diet due to allergy and receives no supplements. Biochemistry: calcium 6.8 mg/dL (low), phosphate 3.0 mg/dL (low-normal), alkaline phosphatase 650 IU/L (high), PTH 280 pg/mL (high). Vitamin D 25-OH is undetectable. What SINGLE blood test would BEST distinguish between nutritional Vitamin D deficiency rickets and primary hypoparathyroidism?
Correct. PTH is the single best differentiator: in nutritional rickets (Vit D deficiency), PTH is ELEVATED (secondary hyperparathyroidism — body trying to maintain calcium). In primary hypoparathyroidism, PTH is LOW or absent. This child already has elevated PTH (280 pg/mL), confirming nutritional Vit D rickets, not hypoparathyroidism.
Hypocalcaemia differential: nutritional rickets (low Ca, elevated ALP, HIGH PTH, low/undetectable Vit D) vs hypoparathyroidism (low Ca, normal ALP, LOW PTH). Calcium and Vitamin D supplementation: calcium 500–1000 mg/day + Vitamin D 400–2000 IU/day (or stoss 600,000 IU). Always treat the underlying cause.
Incorrect. The key distinguishing test between Vitamin D deficiency rickets and hypoparathyroidism is PTH: elevated in Vit D rickets (secondary HPT); low/absent in hypoparathyroidism. Alkaline phosphatase is elevated in both; urine Ca:Cr and magnesium are secondary investigations.
Click to reveal answer
A researcher is reviewing the National Iron Plus Initiative (NIPI) and the Weekly Iron and Folic Acid Supplementation (WIFS) programme. Which of the following CORRECTLY pairs the age group with the elemental iron + folic acid dose?
Correct. NIPI for 5–10 years: 30 mg elemental iron + 250 mcg folic acid WEEKLY. The scheme is: 6–59 mo = 1 mg/kg/day + 100 mcg FA for 100 days/year; 5–10 yr = 30 mg + 250 mcg FA weekly; 10–19 yr = 45 mg + 400 mcg FA weekly (WIFS); pregnant women = 60 mg + 400 mcg FA daily.
NIPI age-group matrix: (1) 6–59 mo: 1 mg/kg/day Fe + 100 mcg FA × 100 days/year; (2) 5–10 yr: 30 mg Fe + 250 mcg FA weekly; (3) 10–19 yr (WIFS): 45 mg Fe + 400 mcg FA weekly; (4) pregnant: 60 mg Fe + 400 mcg FA daily. This programme targets anaemia reduction across the lifecycle.
Incorrect. The correct NIPI schedule for 5–10 years is 30 mg elemental iron + 250 mcg FA WEEKLY. 45 mg + 400 mcg weekly is the adolescent WIFS dose; 6–59 months gets 1 mg/kg/day + 100 mcg FA for 100 days/year.
Click to reveal answer