A neonate born to a mother with poorly controlled pregestational diabetes becomes jittery with capillary glucose of 28 mg/dL at 2 hours of life. The primary mechanism of this hypoglycemia is:

• A Deficient hepatic glycogen stores from intrauterine malnutrition
• B Excessive insulin degradation by immature fetal liver enzymes
• C Impaired gluconeogenesis due to congenital glucokinase deficiency
• D Beta cell hyperplasia with persistent hyperinsulinemia after abrupt loss of maternal glucose supply ✓

Explanation

Chronic maternal hyperglycemia crosses the placenta by facilitated diffusion, stimulating fetal pancreatic beta cell hyperplasia and hyperinsulinemia. After cord clamping, the glucose supply stops abruptly but insulin secretion remains high, producing hypoglycemia within hours. These infants are macrosomic, not growth restricted, ruling out depleted glycogen stores. Glucokinase deficiency is a rare monogenic disorder unrelated to maternal diabetes.

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.