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
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 |
What the spiral-artery diagrams show: normal pregnancy — trophoblast remoulds the artery deep toward the myometrium; pre-eclampsia — shallow invasion near the placenta with a retained muscular arterial wall → high-resistance uteroplacental flow. [1] | 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 |
Additional severe-disease finding: The lecture’s comparison table also lists diminished fetal movement among findings associated with severe hypertensive disease. [1]
Mild vs severe hypertensive disease of pregnancy (WHO comparison table from slides) [1]:
| Finding | Mild | Severe |
|---|---|---|
| Convulsions (eclampsia) | Absent | Present |
| Diastolic BP | ≥ 90 but < 110 mmHg | ≥ 110 mmHg |
| Proteinuria | Trace or 1+ | ≥ 2+ persistently |
| Generalised oedema (face/hands) | Absent | Present |
| Headache / visual disturbance / upper abdominal pain | Absent | Present |
| Oliguria | Absent | Present (< 400 mL/24 h on this table) |
| Diminished fetal movement | Absent | Present |
Use this alongside modern organ-dysfunction definitions (severe features can exist without proteinuria).
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]
Serum magnesium levels from the lecture: [1]
| Status | Serum magnesium |
|---|---|
| Normal pregnant woman | 2 mEq/L (1 mmol/L) |
| Therapeutic level | 4–8 mEq/L (2–4 mmol/L) |
| Loss of patellar reflex | 10 mEq/L (5 mmol/L) |
| Prolonged AV conduction | 12 mEq/L (6 mmol/L) |
| Respiratory failure | 15 mEq/L (7–8 mmol/L) |
| Cardiac arrest | 24 mEq/L (12 mmol/L) |
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]
| 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) [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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