Preparatory Mindset
Diabetes and hypertension are the two most common medical disorders in pregnancy and together account for a large share of maternal and perinatal morbidity. The exam mindset is built around screening, criteria, and delivery timing:
- GDM: universal screening with 75 g OGTT at 24-28 weeks (CM exam tested); diagnosis on ANY ONE abnormal value (fasting ≥5.1, 1-h ≥10.0, 2-h ≥8.5 mmol/L — IADPSG/WHO criteria); first-line treatment is lifestyle, then insulin (metformin acceptable in many settings; avoid most oral agents).
- Preeclampsia: hypertension (≥140/90) + proteinuria (≥300 mg/24 h) after 20 weeks (CM exam tested); severe features (≥160/110, HELLP, eclampsia, pulmonary oedema) → deliver; the only cure is delivery; MgSO₄ prevents/treats eclampsia; antihypertensives (labetalol, nifedipine, methyldopa) control BP.
The universal theme: in pregnancy you treat the mother and the fetus together — the glucose/BP targets, the drugs, and the delivery timing all balance maternal safety against fetal maturity.
Core Concepts
1. Diabetes in pregnancy — classification
| Category | Definition |
|---|---|
| PGDM (pre-existing) | Diabetes diagnosed before pregnancy (type 1 or type 2) |
| GDM (gestational) | Glucose intolerance first recognised during pregnancy (~85% of diabetes in pregnancy) |
| GDM A1 | Diet-controlled |
| GDM A2 | Requires medication (insulin/OHAs) |
Risk factors: previous GDM (recurrence ~50%), family history of DM, BMI >30, PCOS (insulin resistance), age >35, previous macrosomic baby (>4 kg), glycosuria, high-risk ethnicity (Asian, South Asian, African-Caribbean).
2. GDM — maternal and fetal effects
Maternal: ↑ risk of preeclampsia, polyhydramnios, operative delivery, shoulder dystocia, future type 2 diabetes (~50% within 10 years).
Fetal/neonatal (driven by fetal hyperinsulinaemia from maternal hyperglycaemia):
- Macrosomia (>4 kg) → shoulder dystocia, birth injury
- Polyhydramnios → preterm labour/PROM
- Neonatal hypoglycaemia (fetal β-cells still hypersecreting after cord clamp)
- Respiratory distress syndrome (hyperinsulinaemia antagonises glucocorticoid lung maturation)
- Neonatal polycythaemia, hyperbilirubinaemia
- Long-term: offspring ↑ risk of obesity, diabetes, CVD
3 (2018CM exam tested). Screening and diagnosis of GDM
Universal screening at 24-28 weeks:
- Fasting ≥ 5.1 mmol/L - 1-h ≥ 10.0 mmol/L - 2-h ≥ 8.5 mmol/L - Any ONE abnormal → GDM
- 75 g OGTT (IADPSG/WHO):
- Alternatively: FBG ≥5.1 mmol/L → GDM (if OGTT not feasible).
Earlier screening (<24 weeks): if high risk (previous GDM, PGDM, BMI>30, glycosuria) — screen at booking with FBG/HbA1c; OGTT at 24-28 weeks regardless.
4. Management of GDM/PGDM
| Component | Detail |
|---|---|
| Blood glucose targets | Fasting <5.3 mmol/L; 1-h postprandial <7.8; 2-h <6.7 mmol/L |
| Diet + exercise | First-line — medical nutrition therapy (carbohydrate distribution), 30 min exercise |
| Pharmacotherapy | Insulin is first-line when targets not met (GDM A2); metformin increasingly used (crosses placenta, considered acceptable in many guidelines); avoid other OHAs |
| Monitoring | Self-monitoring BG 4×/day (fasting + postprandial); HbA1c (pregnancy-adjusted) |
| Fetal surveillance | USS growth 28-36 wk (macrosomia screening); antenatal CTG/NST if complicated |
| Delivery timing | Uncomplicated GDM: term (38-40 wk); PGDM or GDM A2: consider 38-39 wk; earlier if complications |
| Postpartum | 75 g OGTT at 6-12 weeks postpartum (screen for type 2 DM); lactation encouraged; long-term annual screening |
5. Hypertensive disorders of pregnancy — classification
| Category | Criteria |
|---|---|
| Gestational hypertension | BP ≥140/90 after 20 weeks, no proteinuria |
| Preeclampsia | BP ≥140/90 + proteinuria ≥300 mg/24 h (or ≥2+ dipstick) after 20 weeks; OR no proteinuria but end-organ involvement (thrombocytopenia, renal insufficiency, impaired liver, pulmonary oedema, cerebral/visual symptoms) |
| Severe preeclampsia | BP ≥160/110 (2 occasions 4 h apart) + severe features: proteinuria >5 g/24 h, oliguria, pulmonary oedema, HELLP, cerebral/visual disturbance, epigastric pain, fetal growth restriction |
| Eclampsia | Generalised tonic-clonic seizures in a preeclamptic woman (not attributable to other cause) |
| HELLP syndrome | Haemolysis, Elevated Liver enzymes, Low Platelets — a severe variant |
| Chronic hypertension | BP ≥140/90 before 20 weeks or pre-existing |
6. Pathogenesis of preeclampsia
- Placental ischaemia (abnormal trophoblast invasion → poor spiral artery remodelling) → release of anti-angiogenic factors (sFlt-1, sEndoglin) into maternal circulation → systemic endothelial dysfunction → vasoconstriction, hypertension, proteinuria (glomerular endotheliosis), coagulopathy, hepatic/neurological involvement.
- "Disease of theories" — cause unknown; risk: primiparity, previous preeclampsia, family history, multiple pregnancy, chronic hypertension, renal disease, APS, high BMI.
7. Management of preeclampsia/eclampsia
Principles: the only definitive treatment is DELIVERY. BP control prevents maternal complications; MgSO₄ prevents/treats seizures.
| Component | Detail |
|---|---|
| Antihypertensives | Labetalol (oral/IV), nifedipine (oral), methyldopa (oral, safe but slower) — target SBP <160 / DBP <110 (severe); <140/90 ideally. Avoid ACE-I/ARB (fetotoxic). |
| Seizure prophylaxis/treatment | MgSO₄ (4-6 g IV loading then 1-2 g/h infusion) for severe preeclampsia/eclampsia; monitor reflexes, respiratory rate, urine output; antidote = calcium gluconate 10% 10 mL IV for toxicity (loss of DTRs, respiratory depression) |
| Delivery | Severe preeclampsia: deliver after stabilisation (≥34 wk: deliver; <34 wk: steroids + deliver after 48 h if safe, or earlier if uncontrolled) |
| Mild/gestational HTN | Outpatient surveillance; BP + urine protein weekly; serial USS growth |
| Eclampsia management | ABC + MgSO₄ + control BP + deliver (usually within hours of stabilisation); consider ICU; MgSO₄ continued 24 h post-partum |
| Steroids | Betamethasone/dexamethasone for fetal lung maturity if <34 wk and delivery expected |
| Postpartum | BP may spike postpartum — continue monitoring 3-5 days; antihypertensives as needed |
Complications to monitor: eclampsia (cerebral oedema, haemorrhage), HELLP, pulmonary oedema, renal failure, placental abruption, IUGR, DIC.
High-Yield Points
| Topic | Must-remember |
|---|---|
| GDM screening | 75 g OGTT at 24-28 wk — any ONE abnormal = GDM |
| GDM criteria | Fasting ≥5.1 / 1-h ≥10.0 / 2-h ≥8.5 mmol/L |
| GDM treatment | Diet first; insulin when needed (GDM A2); metformin acceptable |
| GDM targets | Fasting <5.3; 1-h <7.8; 2-h <6.7 mmol/L |
| Neonatal hypoglycaemia | From fetal hyperinsulinaemia — screen babies of diabetic mothers |
| Postpartum screen | OGTT at 6-12 weeks — GDM → future T2DM risk |
| Preeclampsia | BP ≥140/90 + proteinuria ≥300 mg/24 h after 20 wk |
| Severe preeclampsia | BP ≥160/110 + severe features (HELLP, eclampsia, pulmonary oedema, oliguria) |
| Definitive cure | Delivery |
| Seizure prevention | MgSO₄; toxicity antidote calcium gluconate |
| Antihypertensives | Labetalol, nifedipine, methyldopa; avoid ACE-I/ARB |
| HELLP | Haemolysis + ↑LFT + ↓platelets — severe variant |
Topic Summary
GDM (85% of diabetes in pregnancy) is screened by 75 g OGTT at 24-28 weeks and treated with lifestyle then insulin (target fasting <5.3 mmol/L), with delivery at term and postpartum OGTT. Preeclampsia = HTN + proteinuria after 20 weeks, severe if ≥160/110 or end-organ involvement; the only cure is delivery, seizures are prevented by MgSO₄, BP by labetalol/nifedipine/methyldopa. Both disorders increase maternal and fetal risk (macrosomia, IUGR, preterm delivery, long-term disease) — screening and timely delivery are the interventions that matter.
LMCHK OSCE Practice — Gestational Diabetes Counselling
Station setup: A 32-year-old woman (G2P1, previous macrosomic baby 4.2 kg) attends her 26-week antenatal visit. Her 75 g OGTT: fasting 5.6, 1-h 10.8, 2-h 9.2 mmol/L.
Candidate tasks (8 min):
- Interpret the OGTT — fasting ≥5.1 confirms GDM (any one abnormal value).
- Explain GDM to the patient in plain language (pregnancy-related glucose intolerance, usually resolves after delivery).
- Outline the management plan — glucose monitoring (fasting + postprandial), diet/exercise, targets (fasting <5.3, 1-h <7.8), insulin if not met; USS growth surveillance; delivery at term.
- Discuss fetal effects honestly (macrosomia, shoulder dystocia, neonatal hypoglycaemia) and how treatment reduces them.
- Arrange postpartum OGTT at 6-12 weeks and explain long-term type 2 diabetes risk (~50%).
Key marking cues:
- Correctly identifies GDM from the fasting value (no need to wait for all values).
- Gives a structured management plan (monitoring, targets, insulin escalation).
- Counsels on neonatal hypoglycaemia and macrosomia risks.
- Schedules postpartum OGTT and long-term follow-up.
Companion station — Severe preeclampsia:
A 30-year-old primigravida at 33 weeks presents with BP 170/112, headache, epigastric pain, proteinuria 2+, platelets 95.
- Diagnose severe preeclampsia (≥160/110 + symptoms + proteinuria + thrombocytopenia).
- Immediate actions: IV labetalol/nifedipine to control BP; MgSO₄ loading dose; betamethasone for fetal lung maturity; bloods (platelets, LFT, creatinine); plan delivery after stabilisation (or sooner if deteriorating); ICU-ready.
- MgSO₄ toxicity monitoring: absent DTRs, respiratory rate <12, oliguria → stop infusion, calcium gluconate.
- Explain to patient: delivery is the only cure; preeclampsia may persist/peak postpartum.