## Pathophysiology of Gestational Diabetes **Key Point:** Gestational diabetes is fundamentally a disorder of **insulin resistance**, not absolute insulin deficiency. The pregnant state itself induces progressive insulin resistance due to placental hormones (human placental lactogen, progesterone, cortisol). ### Mechanism of GDM Development **High-Yield:** In normal pregnancy, insulin secretion increases to compensate for pregnancy-induced insulin resistance. When the pancreatic β-cell reserve is insufficient to maintain euglycemia despite increased insulin output, gestational diabetes develops. 1. Placental hormones (especially hPL) antagonize insulin action 2. Insulin resistance increases progressively from 2nd to 3rd trimester 3. β-cells attempt to compensate with increased secretion (hyperinsulinemia) 4. If compensation fails → fasting and postprandial hyperglycemia ### Why Other Options Are Incorrect | Metabolic Complication | Frequency in GDM | Reason | |---|---|---| | **Insulin resistance + hyperinsulinemia** | **Most common** | **Fundamental pathophysiology** | | Diabetic ketoacidosis | Rare | Requires absolute insulin deficiency; GDM patients retain β-cell function | | Hypoglycemic episodes | Uncommon | Occurs only if insulin/sulfonylureas overdosed; not the natural metabolic state | | Lactic acidosis | Rare | Associated with metformin in renal impairment; not a primary GDM consequence | **Clinical Pearl:** The **fasting insulin level is elevated** in GDM even when fasting glucose is normal—this is the hallmark of insulin resistance. This distinguishes GDM from Type 1 diabetes, where insulin levels are low. **Warning:** Do not confuse GDM with Type 1 diabetes. Type 1 presents with **insulin deficiency** (low C-peptide, positive autoantibodies); GDM presents with **insulin resistance** (high C-peptide, negative autoantibodies).
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