Gestational Diabetes MCQ — NEET PG Practice Question | NEETPGAI
Gestational Diabetes
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baby OBG
A 32-year-old multiparous woman with GDM diagnosed at 26 weeks is counselled on maternal and fetal complications. Regarding the complications and long-term sequelae of GDM, all of the following are associated with GDM EXCEPT:
A. Neonatal hypocalcaemia and hypomagnesaemia due to maternal hyperglycaemia-induced fetal hyperinsulinaemia
B. Increased risk of maternal type 2 diabetes mellitus within 5–10 years postpartum
C. Neonatal respiratory distress syndrome due to delayed fetal lung maturity
D. Intrauterine growth restriction as the primary fetal complication in poorly controlled GDM
IUGR is NOT a typical complication of GDM. In fact, GDM is associated with fetal macrosomia (excessive fetal growth), not growth restriction. IUGR is seen in pre-eclampsia, placental insufficiency, and maternal vascular disease — not hyperglycaemia.
Why Other Options Are True Complications
Table
Complication
Mechanism
Clinical Significance
Neonatal hypocalcaemia & hypomagnesaemia
Maternal hyperglycaemia → fetal hyperinsulinaemia → suppression of parathyroid hormone (PTH) and magnesium reabsorption
Presents as jitteriness, seizures, tetany in first 24–72 hours of life
Maternal type 2 DM
GDM indicates underlying insulin resistance; 50–60% develop type 2 DM within 5–10 years
Requires postpartum glucose tolerance testing and lifestyle counselling
Neonatal RDS
Fetal hyperinsulinaemia inhibits surfactant synthesis and delays lung maturity; also associated with preterm delivery
Risk increases with poor glycaemic control; antenatal corticosteroids recommended if preterm delivery anticipated
The hallmark of GDM is fetal macrosomia with hyperinsulinaemia, not growth restriction. Poorly controlled GDM leads to large-for-gestational-age (LGA) infants at risk of birth trauma and metabolic derangements.
Warning
Do not confuse GDM (hyperglycaemia → macrosomia) with pre-eclampsia or placental insufficiency (which cause IUGR). This is a classic exam trap.
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