NEET-PG Pediatrics Previous Year Questions (2017–2026)

Correct answer: C. Elective device closure.

Any PDA that remains audible beyond infancy will not close spontaneously and carries a lifelong risk of infective endarteritis, and (with larger shunts) of volume overload. The standard of care for a persistent PDA in a child is therefore elective closure, most often by a transcatheter device (occluder), reserving surgical ligation for anatomy unsuitable for a device.

Incorrect Options:

• A. Close only if symptomatic: waiting for symptoms leaves the endarteritis risk unaddressed.
  Awaiting symptoms is not the preferred strategy.
• B. Watch until adolescence: a duct patent at 4 years will not spontaneously close.
  Continued observation alone does not remove the risk.
• D. Trial of indomethacin: prostaglandin inhibitors close the duct only in preterm neonates and are ineffective in a term child.
  Indomethacin works only during early neonatal life.

High-Yield Facts:

• Ductal patency in the fetus depends on prostaglandin E2; it normally closes functionally within 1-3 days of birth.
• Classic sign of a PDA is a continuous machinery murmur in the left infraclavicular area with bounding pulses.
• Indomethacin or ibuprofen close a PDA in preterm infants; a term child needs device or surgical closure.
• Prostaglandin E1 is used to keep the duct OPEN in duct-dependent congenital heart lesions.

Correct answer: A. Maternal uncle (the mother's brother).

Haemophilia A is X-linked recessive. An affected boy inherits his single X chromosome carrying the mutation from his mother, who is an obligate (usually unaffected) carrier. Because the mother received one of her X chromosomes from her own mother (the grandmother, also a carrier), her brothers each had a 50% chance of inheriting the affected X. Therefore the maternal uncle is the relative most likely to be affected.

Incorrect Options:

• B. Paternal uncle: the paternal line does not carry the affected X that reached this boy.
  Paternal relatives are not the source in X-linked recessive disease.
• C. The father: he is unaffected and cannot transmit the X to his son (he gives the Y).
  No male-to-male (father-to-son) transmission.
• D. The mother: she is a carrier and typically unaffected, not diseased.
  The mother is an obligate carrier, usually asymptomatic.

High-Yield Facts:

• Haemophilia A (factor VIII deficiency) and haemophilia B (factor IX) are both X-linked recessive.
• Affected males inherit the mutant X from a carrier mother; maternal uncles are the classic affected relatives.
• There is no father-to-son transmission in X-linked disease.
• Lab: prolonged aPTT with normal PT and platelet count; confirm with factor VIII assay.

Correct answer: C. Hypophosphataemic rickets.

The combination of low phosphate, normal calcium, high alkaline phosphatase and renal phosphate wasting with normal renal function points to X-linked hypophosphataemic rickets. A PHEX gene mutation leads to excess FGF23, which drives renal phosphate loss and suppresses calcitriol. Treatment is oral phosphate plus calcitriol, or the anti-FGF23 antibody burosumab.

Incorrect Options:

• A. Nutritional rickets: caused by vitamin D deficiency, with low calcium and low phosphate, not isolated phosphate wasting.
  Dietary vitamin D deficiency, not renal phosphate wasting.
• B. Renal osteodystrophy: occurs in chronic kidney disease, with high phosphate and abnormal renal function.
  Renal osteodystrophy accompanies CKD, not normal kidneys.
• D. Vitamin D-dependent rickets: due to a defect in calcitriol production or action, with low calcium; treated with calcitriol.
  Vitamin D-dependent rickets is a calcitriol pathway defect.

High-Yield Facts:

• X-linked hypophosphataemic rickets: PHEX mutation → high FGF23 → renal phosphate wasting.
• Biochemistry: low phosphate, normal calcium, high ALP, high FGF23, normal/low calcitriol.
• Treatment: oral phosphate + calcitriol, or burosumab (anti-FGF23 antibody).
• Nutritional rickets differs by showing low calcium and low phosphate from vitamin D lack.