NPS NPS Neonatal Physiology and Pathophysiology 2 — Questions and Answers
Question 1: Why are preterm neonates at increased risk for hypoglycemia compared to term infants?
- Higher insulin secretion
- Limited glycogen stores and immature gluconeogenesis (Correct answer)
- Increased glucose uptake by brown fat
- Maternal diabetes causing beta-cell hyperplasia
Correct answer: Limited glycogen stores and immature gluconeogenesis
Preterm neonates have limited hepatic glycogen stores, immature gluconeogenic enzymes, and high glucose utilization by the rapidly growing brain.
Question 2: Patent ductus arteriosus (PDA) in a preterm neonate creates a left-to-right shunt. Which organ is MOST at risk from increased blood flow?
- Kidney
- Brain
- Lungs (Correct answer)
- Liver
Correct answer: Lungs
Left-to-right PDA shunting increases pulmonary blood flow, causing pulmonary edema, worsening respiratory failure, and increased risk of BPD.
Question 3: Retinopathy of prematurity (ROP) development is primarily driven by which pathophysiological mechanism?
- Hyperoxia causing cessation of retinal vascularization followed by hypoxia-driven neovascularization (Correct answer)
- Direct light toxicity to the retina
- Systemic hypertension causing retinal artery damage
- Vitamin A deficiency impairing photoreceptor development
Correct answer: Hyperoxia causing cessation of retinal vascularization followed by hypoxia-driven neovascularization
Hyperoxia stops normal retinal vessel growth; when oxygen is reduced, VEGF-driven pathological neovascularization occurs, which can cause retinal detachment.
Question 4: A neonate has persistent metabolic acidosis with an elevated anion gap. Which condition should be suspected?
- Respiratory alkalosis from hyperventilation
- Inborn error of metabolism (Correct answer)
- Normal anion gap acidosis from diarrhea
- Hypoalbuminemia
Correct answer: Inborn error of metabolism
An elevated anion gap metabolic acidosis in a neonate raises concern for inborn errors of metabolism (e.g., organic acidemias, maple syrup urine disease, or congenital lactic acidosis).
Question 5: Which physiological change explains the normal 'physiological jaundice' seen in healthy term newborns at 2–5 days of life?
- Liver immaturity causing conjugated hyperbilirubinemia
- Breakdown of fetal RBCs releasing unconjugated bilirubin exceeding immature hepatic conjugation capacity (Correct answer)
- Breastfeeding causing increased enterohepatic circulation only
- Hemolysis from ABO incompatibility
Correct answer: Breakdown of fetal RBCs releasing unconjugated bilirubin exceeding immature hepatic conjugation capacity
Physiological jaundice results from increased breakdown of short-lived fetal RBCs combined with immature hepatic UDP-glucuronosyltransferase activity and increased enterohepatic recirculation.
Question 6: A newborn with trisomy 21 (Down syndrome) is found to have a large atrioventricular septal defect (AVSD). What is the most likely reason this lesion is particularly associated with trisomy 21?
- Gene on chromosome 21 directly causes cardiac malformation
- Defects in endocardial cushion formation are common in trisomy 21 (Correct answer)
- Pulmonary hypertension prevents normal cardiac development
- Thyroid dysfunction from trisomy 21 impairs heart formation
Correct answer: Defects in endocardial cushion formation are common in trisomy 21
Trisomy 21 is associated with defective endocardial cushion development, leading to AVSD (affecting the AV valves and septal tissue) in up to 40% of affected individuals.
NPS NPS Neonatal Physiology and Pathophysiology 2
Why are preterm neonates at increased risk for hypoglycemia compared to term infants?