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Clinical Specialties · OB/GYN

Gestational Diabetes

A Step 2 CK–focused walkthrough of gestational diabetes: hPL-driven insulin resistance, the two-step vs one-step screening/diagnosis pathway, diet-then-insulin management with glucose targets, and delivery/postpartum decisions — anchored by the classic board discriminator that GDM (unlike pregestational DM) causes no congenital anomalies. Every cutoff and next-best-step verified against ACOG standards.

12 min readHigh yield

The concept in one arc

Gestational diabetes mellitus (GDM) is glucose intolerance first recognized during pregnancy. Placental hormones — chiefly human placental lactogen (hPL), plus progesterone, cortisol, and prolactin — drive insulin resistance that rises across the 2nd trimester and peaks in the 3rd, which is exactly why screening is timed to 24–28 weeks. A patient whose β-cells cannot out-secrete this resistance becomes hyperglycemic.

The single highest-yield discriminator: because GDM emerges after the first trimester (after organogenesis), it does not cause congenital malformations — unlike pregestational diabetes. Instead the fetus faces problems of excess growth and hyperinsulinemia: macrosomia, birth trauma, and neonatal hypoglycemia.

Expect a predictable chain of decisions: universal screening at 24–28 weeks → confirmatory OGTTdiet first, insulin if uncontrolled → fetal surveillance and delivery timing → postpartum reclassification.

Blue circle, the international symbol for diabetes
The blue circle, the global symbol for diabetes. GDM is glucose intolerance first recognized during pregnancy. · Wikimedia Commons — IntDiabetesFed — Public domain, via Wikimedia Commons
Screening & diagnosis
  • Universal screen at 24–28 weeks: non-fasting 50 g 1-hour glucose challenge test (GCT)
  • Early screen at the first prenatal visit if high risk: obesity (BMI ≥30), prior GDM, prior macrosomic infant, strong family history, PCOS, glucosuria
  • GCT ≥140 mg/dL (some centers use 130–135 for higher sensitivity) → proceed to the diagnostic OGTT; a 1-h ≥200 is often treated as GDM outright
  • Two-step (Carpenter-Coustan) — US standard: fasting 100 g 3-hour OGTT; need ≥2 abnormal values → FPG ≥95, 1h ≥180, 2h ≥155, 3h ≥140
  • One-step (IADPSG): fasting 75 g 2-hour OGTT; only ≥1 abnormal → FPG ≥92, 1h ≥180, 2h ≥153
  • Classify: A1GDM = diet-controlled; A2GDM = requires medication

Two-step vs one-step diagnosis

FeatureTwo-step (US standard)One-step (IADPSG)
Screening step50 g 1-h GCT (≥140) firstNone — go straight to OGTT
Diagnostic test100 g 3-h OGTT (fasting)75 g 2-h OGTT (fasting)
Abnormal values needed≥2≥1
Cutoffs, mg/dL (F/1h/2h/3h)95 / 180 / 155 / 14092 / 180 / 153
Net effectFewer diagnosesMore diagnoses
Diagram summarizing oral glucose tolerance test and fasting glucose thresholds
The OGTT confirms the diagnosis after a positive 50 g screen. · Wikimedia Commons — Aydintay — Public domain, via Wikimedia Commons
Vignette — the diagnostic pathway

Stem: A 29-year-old at 26 weeks has a routine non-fasting 50 g GCT of 168 mg/dL. She feels well.

Next best step: This is a screen, not a diagnosis → order the 100 g 3-hour OGTT (do not start treatment yet).

Follow-up: Fasting 98, 1h 190, 2h 150, 3h 120 → two abnormal values (fasting ≥95 + 1-h ≥180) meet Carpenter-CoustanGDM confirmed.

Management now: Begin nutritional therapy + moderate exercise and self-monitored blood glucose (fasting and 1–2 h postprandial). Do not start a drug reflexively — most patients meet targets on diet alone (A1GDM).

Vignette — escalation & the newborn

Case 1: After 1–2 weeks of diet, her log shows fasting values 105–115 and 1-h postprandial in the 150s — above the targets of <95 and <140. Next step: Add pharmacotherapy — insulin is first-line (does not cross the placenta); metformin/glyburide are alternatives that do cross. She is now A2GDM → begin antenatal fetal surveillance and monitor growth.

Case 2: A term infant of a mother with GDM becomes jittery and tremulous ~1 hour after birth. Dx / next step: Neonatal hypoglycemia from fetal hyperinsulinemiacheck a glucose, feed early, and give IV dextrose if severe or symptomatic.

Management, delivery & postpartum
  • First-line: medical nutrition therapy + exercise + glucose self-monitoring
  • Glucose targets: fasting <95, 1-h postprandial <140, 2-h postprandial <120 mg/dL
  • Uncontrolled → insulin (preferred/first-line); metformin and glyburide cross the placenta and are alternatives
  • A2GDM / poorly controlled: antenatal testing (NST, AFI) plus growth ultrasounds
  • Delivery timing: well-controlled A1GDM at 39–40+6 wks; well-controlled A2GDM ~39–39+6 wks; poorly controlled → individualize earlier (37–38+6)
  • Macrosomia: offer cesarean if estimated fetal weight ≥4500 g in diabetics (shoulder-dystocia risk)
  • Postpartum: 75 g 2-hour OGTT at 4–12 weeks to reclassify; ~50% develop type 2 diabetes over the following 10–20 years
Numbers & the classic discriminator

Diagnostic cutoffs — the ladder peaks then falls:

  • Two-step 3-h (100 g): 95 → 180 → 155 → 140. Fasting climbs to a 1-h peak, then declines. Need 2 to diagnose.
  • One-step 2-h (75 g): 92 → 180 → 153. Need just 1.
  • Treatment targets are lower/rounder: 95 / 140 / 120 (fasting / 1-h / 2-h postprandial).

Board discriminator (a true classic): GDM = NO congenital anomalies (arises after organogenesis). If the stem shows caudal regression syndrome, transposition of the great vessels, or NTDs → think pregestational diabetes, not GDM.

Pregestational vs gestational diabetes

FeaturePregestational DMGestational DM
Hyperglycemia timingPresent at conception/organogenesisOnset after 1st trimester
Congenital anomaliesYes — caudal regression (classic), cardiac (TGA, VSD), NTDsNo
Spontaneous abortionIncreasedBaseline
Shared neonatal risksMacrosomia, hypoglycemia, RDS, polycythemia, hypocalcemiaSame — macrosomia, hypoglycemia, RDS, polycythemia, hypocalcemia
Key workup pointPreconception HbA1c optimizationScreen at 24–28 wks; postpartum OGTT

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