An infant born at 29 weeks of gestation develops tachypnea, expiratory grunting, and cyanosis shortly after birth. Chest radiograph shows diffuse ground-glass opacities with air bronchograms. The mother had poorly controlled gestational diabetes. The primary biochemical basis of this infant's disease is:

• A Excess fetal insulin suppressing cortisol-induced surfactant synthesis ✓
• B Meconium obstruction of terminal bronchioles
• C Congenital absence of type I pneumocytes
• D Maternal transfer of anti-Ro antibodies damaging fetal lungs

Explanation

Neonatal respiratory distress syndrome results from deficient pulmonary surfactant due to immaturity of type II pneumocytes. Maternal diabetes increases risk because fetal hyperinsulinemia counteracts the corticosteroid induction of surfactant protein and phospholipid synthesis, delaying lung maturation even in a heavier-than-expected baby. Meconium aspiration, absent type I pneumocytes, and anti-Ro associated congenital heart block are unrelated mechanisms.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.