GC224 Hypertension And Pregnancy
Hypertension in pregnancy encompasses a spectrum of blood pressure disorders—including chronic hypertension, gestational hypertension, preeclampsia, and eclampsia—that can lead to significant maternal and fetal morbidity if not promptly identified and managed.
Hypertension and Pregnancy – Comprehensive Exam-Ready Notes
Big idea: Hypertension in pregnancy is a heterogeneous group of conditions that are a leading cause of maternal and perinatal morbidity/mortality. The crown jewel of this lecture is pre-eclampsia – a pregnancy-specific, multi-system disorder whose definitive treatment is delivery. Understanding the classification (gestational vs. chronic, the 20-week divide), the two-stage pathophysiology (poor placentation → systemic endothelial dysfunction), and the principles of management (stabilize mother → control BP → prevent eclampsia → time delivery) is what the examiners are after. [1]
Learning objectives (directly from the lecture outline) [1]:
- Significance of hypertension in pregnancy
- Classification
- Pathophysiology of pre-eclampsia
- Diagnosis of pre-eclampsia
- Differentiation between gestational and chronic hypertension
- Management of pre-eclampsia and eclampsia
- Prevention of pre-eclampsia and eclampsia
- Chronic hypertension in pregnancy
How it fits into exams: This is one of the highest-yield O&G topics for the Fourth Summative. Past papers repeatedly examine the classification (especially the 20-week rule), diagnostic criteria, antihypertensive choices in pregnancy (and what is contraindicated – ACE inhibitors), prevention with aspirin, MgSO₄ for eclampsia, and postnatal counselling. [2][3][4]
Hypertension complicates 3–7% of pregnancies and is a leading cause of maternal mortality (eclampsia, CVA) and perinatal mortality (preterm delivery, IUGR, placental abruption). [1]
Why is it so dangerous?
- Maternal: Eclampsia (seizures → can cause cerebral haemorrhage), DIC, HELLP syndrome, acute renal failure, pulmonary oedema, liver failure, stroke, death.
- Fetal: Preterm delivery (15–67%), IUGR (10–25%), perinatal death (1–2%), hypoxia with neurological injury, placental abruption. [1]
- Long-term: Both mother and child have increased lifetime cardiovascular risk. [1]
The key dividing line is 20 weeks of gestation. [1]
| Category | Timing | Features |
|---|---|---|
| A. Gestational HT / proteinuria | After 20 weeks | New onset in previously normotensive |
| — Gestational HT (PIH) | After 20 weeks | HT alone, no proteinuria |
| — Gestational proteinuria | After 20 weeks | Proteinuria alone |
| — Gestational proteinuric HT | After 20 weeks | HT + proteinuria = Pre-eclampsia |
| B. Chronic HT / renal disease | Before 20 weeks (or pre-existing) | Known HT, renal disease, or HT presenting < 20 wk |
| — Chronic HT with superimposed PET | Chronic → worsening after 20 weeks | Sudden ↑BP, new/↑proteinuria, IUGR, multi-system features |
| C. Unclassified | Presents > 20 weeks with insufficient info | Cannot determine if chronic or gestational |
Why does 20 weeks matter? Pre-eclampsia is a disease of the second half of pregnancy – it requires a placenta that has had time to fail. Hypertension presenting before 20 weeks almost certainly reflects pre-existing (chronic) disease.
QMH local data (illustrative): total incidence ~5–7%, gestational HT ~2–3%, pre-eclampsia ~1.5–2%, eclampsia ~0.03–0.06%. [1]
3. Pathophysiology of Pre-eclampsia
Pre-eclampsia is conceptualized as having two phenotypes (which can overlap): [1]
Poor placentation → hypoxic placenta → systemic endothelial dysfunction [1]
| Stage | What Happens | Why |
|---|---|---|
| Stage 1: Poor placentation | Lack of endovascular cytotrophoblastic invasion of maternal spiral arteries in the second trimester | Normally, trophoblasts invade and remodel spiral arteries into low-resistance, high-capacity vessels. In pre-eclampsia this fails → uteroplacental circulation is too narrow |
| Stage 2: Maternal syndrome | Hypoxic placenta undergoes oxidative stress → increased release of trophoblast debris → generalized systemic inflammatory response → endothelial dysfunction | Endothelial dysfunction → vasospasm, microthrombi, capillary leak, end-organ damage |
Downstream pathophysiology [1]:
- Decreased perfusion to virtually all organs
- Endothelial dysfunction: vasospasm and microthrombi
- Reduced vasodilator prostacyclin, increased vasoconstrictive thromboxane, and platelet aggregation
- Result: hypertension, proteinuria, systemic disease
Arises from interaction between a normal placenta and a maternal constitution susceptible to microvascular disease (e.g., long-term hypertension, diabetes). [1]
- The pregnancy acts as a "metabolic and vascular stress test" that reveals a woman's future cardiovascular health.
- This explains why women with pre-eclampsia have markedly increased long-term cardiovascular risk. [1]
- Combining placental and maternal contributions. [1]
Primigravida, advanced age, past obstetric history of PET, pre-existing maternal diseases (DM, HT, renal disease, antiphospholipid syndrome), obstetric conditions (multiple pregnancy, hydatidiform mole, hydrops). [1]
Why primigravida? First exposure to paternal antigens in the placenta → immunological maladaptation → poor trophoblast invasion. In subsequent pregnancies with the same partner, there is immunological "tolerance." However, recurrence still occurs (1 in 10 for PET, 1 in 4 if previous eclampsia). [1]
5. Diagnosis of Pre-eclampsia
Pre-eclampsia = new onset of hypertension after 20 weeks with one or more of the following new-onset conditions: [1]
- Proteinuria (≥ 300 mg/day)
- Other maternal organ dysfunction:
- Renal: creatinine ≥ 90 µmol/L
- Hepatic: elevated transaminases (ALT or AST) ± RUQ or epigastric pain
- Neurological: eclampsia, altered mental status, blindness, stroke, clonus, severe headache or visual disturbance
- Haematological: thrombocytopenia (platelets < 150 × 10⁹/L), DIC or haemolysis
- Uteroplacental dysfunction: e.g., IUGR, stillbirth
Key exam point: Pre-eclampsia does NOT require proteinuria if there is other organ dysfunction. [1]
BP ≥ 140/90 mmHg on two consecutive readings 4 hours apart with rest, OR one reading of DBP ≥ 110 mmHg. [1]
- Technique: Sitting, appropriate cuff size, at level of heart. [1]
- Use Korotkoff 5 (disappearance of sound) to define diastolic BP. If K5 is at or near zero (can happen in pregnancy due to high-output state), use K4 (muffling). [1]
- Mercury sphygmomanometry: prone to errors, white-coat effect. Automated devices reduce errors and measure K5. [1]
| Method | Threshold |
|---|---|
| Dipstick | 1+ or above |
| 24-hour urine protein | ≥ 300 mg/day |
| Heavy proteinuria | ≥ 1 g/day |
| Spot urine protein:creatinine ratio | Alternative to 24-hr collection |
Frontal headache, visual disturbances, epigastric pain. [1]
| Symptom | Pathophysiology |
|---|---|
| Frontal headache | Cerebral oedema and ↑ intracranial pressure |
| Visual disturbances | Impeded blood flow and ischaemic injury secondary to vasospasm of retinal arteries |
| Epigastric pain | Periportal fibrin deposition → hepatic sinusoid obstruction → stretching of liver capsule ± haemorrhage |
Exam Trap
16% of women who develop eclampsia had normal BP beforehand, and 14% had no proteinuria prior to the seizure. Pre-eclampsia has a variable presentation – do NOT rely on classic findings to rule it out. Late postpartum eclampsia can occur > 48 hours after delivery. [1]
If BP is normal and no proteinuria before 20 weeks: [1]
- HT + proteinuria afterwards → Pre-eclampsia
- HT alone afterwards → Gestational HT
If HT/proteinuria develops before 20 weeks → likely chronic HT / renal disease. Need to rule out secondary causes: renal, cardiovascular, endocrine, autoimmune disorders. [1]
Case-based approach (from lecture): A BP of 140/90 at 32 weeks at an antenatal visit → rest and recheck 4 hours later before diagnosing hypertension. [1]
| Maternal | Incidence | Fetal | Incidence |
|---|---|---|---|
| Eclampsia | < 1% | Preterm delivery | 15–67% |
| Acute renal failure | 1–5% | IUGR | 10–25% |
| Coagulopathy / DIC | Variable | Hypoxia / neurological injury | < 1% |
| Pulmonary oedema | Variable | Perinatal death | 1–2% |
| Placental abruption | 1–4% | Long-term cardiovascular morbidity (low birth weight) | Long-term |
| Liver failure / haemorrhage | < 1% | ||
| HELLP syndrome | Variable | ||
| CVA | Rare | ||
| Death | Rare | ||
| Long-term cardiovascular morbidity | Significant |
The magnitude of risk depends on gestational age at diagnosis, delivery timing, severity, and presence of associated medical disorders. [1]
8. Management of Pre-eclampsia
The definitive treatment of pre-eclampsia is delivery. [1] Timing is a balance between severity of pre-eclampsia and risk of prematurity. [1]
Four pillars of management: [1]
- Stabilize the mother – BP control, fluid balance, prevent eclampsia
- Screen for and manage complications – HELLP, DIC, pulmonary oedema, renal failure, stroke, fetal growth
- Plan for delivery – the only cure
- Monitor fetus – CTG, USG (growth, liquor volume, Doppler)
Criteria for severe PET: [1]
| Category | Features |
|---|---|
| Symptoms | Headache, visual disturbance, epigastric or RUQ pain, nausea and vomiting |
| Signs | BP ≥ 160/110, proteinuria 3+ or 4+ or > 3 g/day, gross and rapidly progressive oedema, brisk jerks or clonus, oliguria (< 30 mL/h) |
| Lab | Thrombocytopenia, impaired LFT, impaired RFT, abnormal clotting profile |
BP Control: [1]
Decrease risk of cerebral haemorrhage (≥ 160/110 mmHg), but avoid sudden lowering of BP → fetal distress. Keep DBP between 90 and 100.
- IV labetalol or hydralazine [1]
Why Not Drop BP Too Fast?
The uteroplacental circulation has no autoregulation – it depends entirely on maternal BP driving blood through the (already narrowed) spiral arteries. A sudden BP drop → acute fetal distress. Pre-eclamptic patients are also more sensitive to vasodilators, so use smaller doses. [6]
Monitor maternal well-being: BP, blood tests (CBP, L/RFT, urate, coagulation profile), urine protein:creatinine ratio or 24-hr urine protein, symptoms [1]
Monitor fetal well-being: Cardiotocogram, USG for growth/liquor volume/Doppler studies, fetal movement [1]
Steroid prophylaxis if < 34 weeks gestation [1]
Control BP [1]
Thromboprophylaxis: Pressure stockings ± LMWH [1]
MgSO₄ for severe pre-eclampsia [1]
Timing of delivery: Depends on gestation and severity [1]
Vaginal or Caesarean section – Caesarean is NOT always needed (exam trap!) [1] Epidural anaesthesia is preferred if no coagulopathy [1]
Monitoring during delivery: [1]
- Fetus: continuous fetal heart monitoring
- Maternal: BP, symptoms
- If on MgSO₄: monitor jerks, respiratory rate, urine output (watch for Mg toxicity)
- Avoid fluid overload
- Postpartum: Watch for convulsion, pulmonary oedema
9. Eclampsia
Eclampsia = occurrence of convulsion in pregnancy unless known epilepsy or other cause. [1]
- High index of suspicion – eclampsia until proven otherwise
- Can occur up to 10 days post delivery
- 1.8% mortality
- Generalized tonic-clonic type [1]
ABC → Prevention of injury and aspiration → Stabilize maternal condition [1]
- Magnesium Sulphate (10% risk of second seizure) [1]
- Fluid balance
- BP control (uteroplacental, cerebral perfusion)
- Screen for secondary/associated complications: HELLP, coagulopathy, pulmonary oedema, renal failure, stroke
- Planning for delivery – mode depends on clinical assessment (non-reassuring fetal heart rate → emergency CS)
Low therapeutic-toxic range. Excreted in urine. [1] Toxicity: respiratory depression and cardiac arrest. [1]
Monitoring (must know for exam):
- Patellar reflex (loss = early sign of toxicity)
- Urine output > 30 mL/h (renal excretion – if oliguric, Mg accumulates)
- Respiratory rate > 12/min
- ± Checking blood magnesium level
- Continue MgSO₄ infusion until 24 hours after delivery [1]
MgSO₄ Monitoring Mnemonic
"PUR": Patellar reflex, Urine output, Respiratory rate. Loss of patellar reflex is the earliest sign of Mg toxicity – check before each dose. Antidote for MgSO₄ toxicity = IV calcium gluconate 10%.
10. Prevention
Low-dose aspirin (75 mg) is recommended for prevention of pre-eclampsia in women at high risk. Start before 16 weeks. [1]
Why aspirin? Pre-eclampsia involves an imbalance of prostacyclin (vasodilator, anti-aggregatory) and thromboxane A₂ (vasoconstrictor, pro-aggregatory). Low-dose aspirin selectively inhibits platelet COX-1 → reduces thromboxane A₂ more than prostacyclin → restores balance → reduces risk of PET, preterm birth < 34 weeks, and serious adverse outcomes. [1]
| Level | Strategy |
|---|---|
| Primary | Early detection and control of gestational HT or pre-eclampsia |
| Secondary | Prophylactic MgSO₄ in severe PET |
| Tertiary | Prevent subsequent convulsions with MgSO₄ |
MgSO₄ is recommended for prevention of eclampsia in women with severe pre-eclampsia in preference to other anticonvulsants. [1]
Vitamin C, D, E supplements and diuretics are NOT recommended for prevention. [1]
- Weak evidence for bed rest
- Weak evidence for corticosteroids for HELLP syndrome [1]
11. Antihypertensive Therapy in Pregnancy
| Drug | Class | Key Points | Side Effects |
|---|---|---|---|
| Methyldopa | Alpha₂-agonist | Widely used, safe, well tolerated. Slow onset (3–6 h). 1st line historically. | Dizziness, postural hypotension, nightmare, depression, abnormal LFT |
| Labetalol | Combined α + β blocker | Vasodilation. More rapid onset (2 h). Preserves uteroplacental blood flow better than pure β-blockers. Can be given IV for acute control. | Flushing, light-headedness, palpitations, scalp tingling |
| Nifedipine MR | CCB (dihydropyridine) | Modified release only – NOT immediate release (would cause acute BP drop → fetal distress + headache) | Headache, tachycardia, flushing, N+V |
| Hydralazine | Vasodilator | ↑HR and CO. Used extensively IV for acute severe HT in PET. | Tachyphylaxis, headache, flushing, light-headedness, nausea, palpitations |
Avoid propranolol (IUGR, neonatal depression) and ACE inhibitors (fetal death, neonatal renal failure). [1]
| Contraindicated Drug | Why |
|---|---|
| ACEI / ARB | Crosses placenta → fetal renal abnormalities, renal failure, oligohydramnios, neonatal death [1][6][7] |
| Propranolol (pure β-blocker) | IUGR, neonatal depression [1] |
| Sodium nitroprusside | Contraindicated in pregnancy (cyanide toxicity risk to fetus) [8] |
| Diuretics | Intravascular volume contraction → reduced placental perfusion; reduced milk production [7] |
Exam Discriminator
Methyldopa vs. Labetalol vs. Aspirin vs. MgSO₄: The lecture MCQ tests this directly. Aspirin prevents pre-eclampsia. Methyldopa and labetalol treat hypertension. MgSO₄ prevents/treats eclampsia (seizures), not PET itself. [1]
Assessment: Are the antihypertensive agents she has been taking safe in pregnancy? [1]
Key points: [1]
- BP may fall slightly in the second trimester (normal physiological change – don't be fooled into stopping medication)
- Prognosis depends on whether there is superimposed pre-eclampsia (occurs in ~17%), deterioration of renal function, or progression of underlying disorder (e.g., SLE)
- If on ACEI/ARB → must switch to methyldopa, labetalol, or nifedipine MR before conception or as soon as pregnancy confirmed [1][7]
Chronic HT with Superimposed PET
Suspect when: [1]
- Sudden raised BP
- Increased or new development of proteinuria
- IUGR
- Features of multi-system disorders
Recurrence of PET: 1 in 10; 1 in 4 if previous eclampsia. [1]
Long-term cardiovascular risk after PET (BMJ 2007): [1]
- HT: relative risk 3.70 after 14.1 years
- Ischaemic heart disease: RR 2.16 after 11.7 years
- Stroke: RR 1.81 after 10.4 years
Contraception: If BP normal postpartum, no contraindication to combined oral contraceptive pills. [1]
Resolution: Hypertension and proteinuria should resolve by 6 weeks after delivery. If not → suspect chronic HT / renal disease and investigate. [1]
Not a separate slide-set in this lecture but repeatedly mentioned. HELLP = Hemolysis, Elevated Liver enzymes, Low Platelets. It is a severe variant/complication of pre-eclampsia. [1]
- Hemolysis: Microangiopathic haemolytic anaemia (schistocytes on blood film, ↑LDH, ↑indirect bilirubin)
- Elevated liver enzymes: Hepatic ischaemia from sinusoidal fibrin deposition → transaminitis
- Low platelets: Consumption via microthrombi
- Management: Deliver. Weak evidence for corticosteroids for HELLP. [1]
Understanding normal cardiovascular changes in pregnancy helps you understand why pre-eclampsia is so dangerous and why management decisions are made the way they are:
- Blood volume: ↑ 40–50% (plasma volume ↑ > RBC mass → physiological anaemia of pregnancy)
- Cardiac output: ↑ 30–50%
- Peripheral vascular resistance: ↓ (vasodilation, progesterone effect)
- BP: Normally falls in mid-pregnancy (trough at ~24 weeks), returns to baseline by term
- Hypercoagulable state: ↑ clotting factors, ↓ natural anticoagulants → protects against postpartum haemorrhage but ↑ VTE risk [9]
In pre-eclampsia, the normal vasodilation fails → instead you get vasoconstriction, endothelial dysfunction, and reduced organ perfusion. The increased blood volume of pregnancy worsens hypertension and increases pulmonary oedema risk.
These are the lecturer's own MCQs – extremely high yield as they show the exact framing of exam questions: [1]
MCQ 1: Pregnant woman at 38 weeks, BP persistently > 140/90, urine albumin negative. Diagnosis?
- Answer: B. Gestational hypertension (HT after 20 weeks, no proteinuria, no prior HT) [1]
MCQ 2: Which medication should be used to prevent pre-eclampsia?
- Answer: C. Low-dose aspirin (Methyldopa and labetalol treat HT; MgSO₄ prevents eclampsia, not PET; hydralazine treats acute severe HT) [1]
MCQ 3: Which statement about pre-eclampsia is CORRECT?
- Answer: D. Corticosteroid is needed for fetal lung maturation if PET diagnosed before 34 weeks
- A is wrong (PET affects both mother and fetus), B is wrong (vaginal delivery is possible), C is wrong (risk is higher in subsequent pregnancies if had PET, though overall risk is 1 in 10), E is wrong (aspirin can prevent it) [1]
Exam Intelligence
| Trap | Correct Understanding |
|---|---|
| "Oedema is part of the diagnostic triad of PET" | Oedema is omitted from all modern definitions – too common in normal pregnancy [1] |
| "Eclampsia only happens before delivery" | Can occur up to 10 days postpartum [1] |
| "Caesarean section is always needed" | Vaginal delivery is possible and sometimes preferred [1] |
| "MgSO₄ prevents pre-eclampsia" | MgSO₄ prevents/treats eclampsia (seizures). Aspirin prevents pre-eclampsia [1] |
| "ACE inhibitors are safe in pregnancy" | Absolutely contraindicated – fetal renal failure, death [1][7] |
| "Normal BP excludes pre-eclampsia" | 16% of women with eclampsia had normal BP beforehand [1] |
| "Antihypertensives prevent superimposed PET" | They reduce severe HT but NOT PET risk [1] |
| "Sodium nitroprusside for HT emergency in pregnancy" | Contraindicated in pregnancy [8] |
| "Pre-eclampsia requires proteinuria" | Not anymore – organ dysfunction alone qualifies [1] |
| "Nifedipine immediate release is fine" | Only modified release – immediate release causes precipitous BP drop → fetal distress [1][7] |
- Keep DBP between 90 and 100 – not too low (fetal distress from uteroplacental hypoperfusion), not too high (cerebral haemorrhage risk ≥ 160/110) [1]
- Target BP < 140 in first hour for pre-eclampsia/eclampsia [8]
Past Paper Questions
Stem: "A 40-year-old woman was attending her first antenatal visit at 13 weeks of gestation. She had good past health and no significant family history of disease. Her blood pressure measured 150/98 mmHg and her pulse was 90 beats per minute. The urine dipstix test was negative for both sugar and albumin. What is the LIKELY diagnosis?"
Options: A. Chronic hypertension, B. Gestational hypertension, C. Normal physiological change in pregnancy, D. Pre-eclampsia
Answer: A. Chronic hypertension
Rationale: Hypertension presenting at 13 weeks (before 20 weeks) in a woman with no prior records = chronic hypertension. Gestational HT by definition develops after 20 weeks. Pre-eclampsia requires proteinuria or organ dysfunction AND presentation after 20 weeks. The BP of 150/98 is NOT a normal physiological change. [1][3]
Stem: "A 40-year-old G1P0 woman was seen in the antenatal ward for regular uterine contraction every 10 minutes at 39 weeks of gestation. Her antenatal course was so far uneventful. Her blood pressure was persistently elevated at 160/95 mmHg and the dipstick test for urine protein was 3+. She was otherwise well."
(a) What is the MOST LIKELY diagnosis? (1 mark) Answer: Pre-eclampsia (new hypertension ≥ 140/90 + proteinuria 3+ after 20 weeks in a previously normotensive woman)
(b) List initial investigations. (5 marks) Answer: CBC (platelet count), LFT (AST/ALT), RFT (creatinine, urate), coagulation profile (PT/aPTT), 24-hr urine protein or spot protein:creatinine ratio, ± blood group and hold
(c) List antihypertensive drugs commonly used to control high blood pressure during pregnancy. (2 marks) Answer: Labetalol, methyldopa (also accept nifedipine MR, hydralazine)
(d) If she develops a generalised seizure, what is the MOST LIKELY diagnosis (1 mark) and what medication would you give to stop the seizure? (1 mark) Answer: Eclampsia; Magnesium sulphate (MgSO₄)
Stem: "A 40-year-old, BMI 35 kg/m², Gravida 1 Para 1 woman, just delivered 2 days ago by emergency lower segment Caesarean section for pre-eclampsia. She was noted to have fever 38.0°C. The operation was uncomplicated. Urinary catheter was inserted before the operation with clear urine. Lochia was not heavy, the uterus was well contracted and non-tender. Chest was clear. Left calf tenderness and swelling were noted."
Question: What is the MOST IMPORTANT subsequent investigation to confirm the cause of her fever?
Options: A. CT Pulmonary Angiography, B. D-dimer blood test, C. Ultrasound Doppler of venous system of lower limb, D. Ventilation-perfusion scan
Answer: C. Ultrasound Doppler of venous system of lower limb
Rationale: Left calf tenderness + swelling post-CS for pre-eclampsia → deep vein thrombosis is the most likely diagnosis (multiple risk factors: pre-eclampsia, obesity, CS, postpartum). DVT is confirmed by compression/Doppler USS of lower limb veins. D-dimer is elevated in pregnancy and postpartum (useless). CTPA and V/Q scan are for PE, not DVT diagnosis. [10][9]
Stem: "A 36-year-old pregnant woman at 28 weeks of gestation complained of dizziness in supine position..."
This question is about supine hypotension syndrome (aortocaval compression), not pre-eclampsia directly, but tests understanding of cardiovascular physiology in pregnancy. The underlying changes include ↑ blood volume, ↑ cardiac output, ↓ peripheral vascular resistance, and compression of the IVC by the gravid uterus in supine position. Routine antenatal investigation at 28 weeks = OGTT (to rule out gestational diabetes). [11]
Stem: "A 35-year-old, G1P0, woman was at 20 weeks of pregnancy. The foetus was found to have complete heart block on anomaly scan. What maternal blood test should be performed to look for the underlying cause?"
Answer: D. Anti-Ro antibody (Neonatal lupus → congenital complete heart block is associated with maternal anti-Ro/SSA antibodies crossing the placenta)
This integrates with SLE in pregnancy, which is itself a risk factor for pre-eclampsia. [10]
| Related Topic | Connection to HT in Pregnancy |
|---|---|
| DM in pregnancy (GDM) | Both are metabolic stress tests; GDM is a risk factor for PET; both have long-term metabolic consequences [12] |
| VTE in pregnancy | PET + CS + immobility = high VTE risk; use LMWH (the only antenatal anticoagulant that can be used); warfarin and NOACs cross placenta [9] |
| SLE in pregnancy | SLE flares in pregnancy; antiphospholipid syndrome → PET risk; anti-Ro → neonatal lupus [13] |
| Thyroid disease in pregnancy | Switch carbimazole/MMZ to PTU in first trimester (teratogenicity); uncontrolled hyperthyroidism worsens pregnancy outcomes [14] |
| General HT (GC 058) | Secondary causes of HT, BP measurement technique, antihypertensive classes [15] |
| Biochemical investigation of HT | Aldosterone:renin ratio, catecholamines – relevant if investigating chronic HT before 20 weeks [16] |
High Yield Summary
Classification: 20-week dividing line. Before = chronic HT. After + proteinuria/organ dysfunction = pre-eclampsia. After + HT alone = gestational HT.
Pathophysiology: Failed trophoblast invasion of spiral arteries → placental hypoxia → oxidative stress → trophoblast debris → systemic endothelial dysfunction → vasospasm, microthrombi, organ damage.
Diagnosis: BP ≥ 140/90 (×2, 4 hrs apart) + proteinuria ≥ 300 mg/day OR organ dysfunction (renal, hepatic, neurological, haematological, uteroplacental). Oedema no longer diagnostic.
3 Classic Symptoms: Frontal headache (cerebral oedema), visual disturbance (retinal artery vasospasm), epigastric pain (liver capsule stretching).
Definitive treatment = DELIVERY. Balance severity vs. prematurity.
Antihypertensives: Methyldopa (1st line), labetalol (IV for severe), nifedipine MR, hydralazine. AVOID ACEI/ARB (fetal renal failure), propranolol (IUGR).
Target DBP in severe PET: 90–100 mmHg.
MgSO₄: Prevents/treats eclampsia. Monitor patellar reflex, urine output > 30 mL/h, RR > 12/min. Continue 24h post-delivery.
Prevention: Low-dose aspirin 75 mg before 16 weeks for high-risk women. NOT vitamins C/D/E, NOT diuretics.
Postnatal: PET recurrence 1 in 10 (1 in 4 after eclampsia). ↑ Long-term CVD risk. HT/proteinuria should resolve by 6 weeks; if not → chronic HT/renal disease. OCP fine if BP normal.
Active Recall - Hypertension and Pregnancy
[1] Lecture slides: GC 224. Hypertension and Pregnancy.pdf [2] Past papers: 2024 Fourth Summative SAQ.pdf [3] Past papers: 2020 Fourth Summative Assessment MCQ paper.pdf (Q10) [4] Past papers: 2021 Fourth Summative SAQ.pdf (Q1) [5] Lecture slides: Block C - Hypertension and Pregnancy (CFB WCS in 2023_24).pdf [6] Lecture slides: Block C - I am pregnant_ medical problems complicating pregnancy.pdf [7] Senior notes: MBBS Final MB (Medicine) (Felix PY Lai).pdf (p.334–336) [8] Senior notes: Ryan Ho Cardiology.pdf (p.182–183); Maksim Medicine Notes.pdf (p.78) [9] Senior notes: Block A - Leg swelling and chest pain_ deep vein thrombosis; pulmonary embolism; Thrombophilia.pdf (p.19) [10] Past papers: 2025 Fourth Summative MCQ.pdf (Q10, Q76) [11] Past papers: 2023 Fourth Summative SAQ.pdf (Q2) [12] Senior notes: Block A - Polyuria and polydipsia_ glucose metabolism; diabetes mellitus; diabetic ketoacidosis.pdf (p.6) [13] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf (p.724) [14] Senior notes: Block A - I am losing weight and sweating all the time.pdf (p.19) [15] Senior notes: Block A - High blood pressure_ hypertension.pdf [16] Lecture slides: GC 153. Biochemical Investigation of Hypertension.pdf
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