GC115 I Am Pregnant Medical Problems Complicating Pregnancy
Pre-existing or newly arising medical conditions—such as hypertension, diabetes, thyroid disorders, cardiac disease, or thromboembolic disease—that complicate pregnancy and require specialized management to optimize maternal and fetal outcomes.
Medical Problems Complicating Pregnancy
This lecture (GC 115) uses a case-based framework to teach the principles of managing medical diseases that coexist with, arise from, or are worsened by pregnancy. It is not about memorizing the management of every single medical disease in detail — rather, it is about learning a systematic thinking framework that you can apply to any medical condition in a pregnant woman. [1]
The overarching theme is a four-way interaction:
- Effect of pregnancy on the disease (and its natural history)
- Effect of the disease on the pregnancy (mother and fetus)
- Effect of the disease's treatment on the pregnancy
- Effect of the pregnancy on the disease's treatment (pharmacokinetics, teratogenicity, need to change drugs)
The lecture explicitly states the concluding principle: "Treat the patient, not the disease." [1]
Learning Objectives (from Theme Case 1) [2]
- Describe the pathophysiology of a pre-existing medical disorder in pregnancy
- Describe effects of a pre-existing medical disorder on pregnancy (and vice versa)
- Describe principles of management: pre-pregnancy → antepartum → intrapartum → postpartum
- Recognize the concept of multidisciplinary approach and combined medical-obstetrics clinics
- Awareness of pre-pregnancy counselling
- Provide appropriate counselling, triage into low/high risk, and refer to tertiary centres
Three categories are explicitly listed on the lecture slide and are a very common exam stem: [1]
| Category | Examples | Why it matters |
|---|---|---|
| 1. Co-incidental / Pre-existing | DM, renal disease, pre-existing HTN, autoimmune diseases, cardiac diseases, asthma | Disease was there before pregnancy; pregnancy may worsen it or it may worsen pregnancy |
| 2. Arising as a result of pregnancy | Hyperemesis gravidarum, gestational HTN, gestational DM, acute fatty liver of pregnancy, acute renal failure or DIC secondary to obstetric complications | These conditions would not exist without the pregnancy; they resolve after delivery |
| 3. Pregnancy increases risk or aggravates | Iron deficiency anaemia, thromboembolism | Physiological changes of pregnancy (↑ plasma volume, hypercoagulability) predispose to these |
Why this classification matters
This is the lecture's scaffolding. Every case in the lecture maps onto one or more of these categories. The exam frequently asks you to classify a given condition. Understanding why each condition falls where it does requires understanding normal pregnancy physiology (↑ cardiac output ~40%, ↑ blood volume ~50%, ↑ clotting factors, relative insulin resistance from placental hormones, immune modulation).
Case 1: Hypertension in Pregnancy (Mary)
- 26-year-old domestic helper, concealed pregnancy, no antenatal care
- Presents with headache, nausea, vomiting; BP 180/100 mmHg, oedematous, urine albustix +++, fetal movement palpable [1]
This classification is directly from the lecture slides and is extremely high yield: [1]
| Type | Definition | Key Feature |
|---|---|---|
| Pre-existing hypertension | High BP before 20 weeks | Already hypertensive before pregnancy |
| Pre-existing renal disease | Proteinuria before 20 weeks (after excluding UTI) | Kidney disease causing proteinuria |
| Gestational hypertension | Normal BP before 20 weeks, high BP first detected after 20 weeks, without proteinuria | New-onset HTN of pregnancy without end-organ damage |
| Pre-eclampsia | Gestational hypertension with proteinuria (after 20 weeks) | The dangerous one: multisystem disease |
| Pre-existing + superimposed pre-eclampsia | Pre-existing HTN, develops new proteinuria after 20 weeks | Worst combination — cumulative risk |
Why 20 weeks is the cut-off: The pathophysiology of pre-eclampsia involves abnormal trophoblast invasion of spiral arteries, which occurs in the first and early second trimester. The clinical manifestations (HTN + proteinuria) typically don't appear until after 20 weeks because the placenta needs to grow large enough for its dysfunction to become clinically evident. HTN detected before 20 weeks is therefore almost certainly pre-existing.
In Mary's case, she is "unclassified" because she had no antenatal care — could be any of the above. However, her symptoms are suggestive of pre-eclampsia. [1]
The lecture explicitly lists these complications: [1]
| System | Manifestations |
|---|---|
| Renal | Renal insufficiency |
| Hepatic | Liver derangement |
| Neurological | Eclampsia, altered mental status, blindness, visual scotomata, stroke, clonus, new-onset severe headaches not responsive to medication |
| Haematological | Thrombocytopenia, DIC, haemolysis (→ HELLP syndrome) |
| Uteroplacental | Fetal growth restriction, abnormal umbilical artery Doppler, stillbirth |
Why these organs are affected: Pre-eclampsia is fundamentally an endothelial disease. Abnormal placentation → release of anti-angiogenic factors (sFlt-1) → widespread maternal endothelial dysfunction → vasospasm, increased permeability, platelet activation → damage to kidneys (glomerular endotheliosis), liver (periportal necrosis), brain (vasogenic oedema), and the coagulation system.
"Should drugs be given to lower her blood pressure? Yes — irrespective of the cause of hypertension, severe hypertension should be controlled to prevent intracerebral haemorrhage." [1]
| Point | Detail |
|---|---|
| Drug choice | Most antihypertensives can be used EXCEPT ACE inhibitors |
| Dose caution | Pre-eclamptic patients are more sensitive to vasodilators — use smaller doses than in non-pregnant patients |
| Avoid rapid drops | Rapid lowering of BP may decrease uterine perfusion causing fetal hypoxia |
| Common drugs | Labetalol (IV or PO), hydralazine (IV), nifedipine (PO) |
Why ACEi are contraindicated
ACE inhibitors cross the placenta and decrease fetal renal perfusion → oligohydramnios, renal dysgenesis, skull ossification defects, IUGR, and fetal death. This is a universal contraindication in pregnancy, not just in pre-eclampsia. ARBs are equally contraindicated (same mechanism — blocking RAAS in the fetus). This is a classic exam trap.
The lecture explicitly requires these steps: [1]
- Prevention of eclampsia → Magnesium sulphate
- Investigations: CBC, renal function, liver function, coagulation tests
- Monitor fetal wellbeing when mother is stable
- Consider delivery of the baby — definitive treatment of pre-eclampsia is delivery
Why MgSO₄ and not other anticonvulsants? The MAGPIE trial showed that MgSO₄ reduces eclampsia risk by ~58% compared to placebo, and is superior to diazepam or phenytoin. It acts by stabilizing neuronal membranes (blocks NMDA receptors), causes cerebral vasodilation (reducing vasospasm), and has mild antihypertensive effects.
Case 2: Pre-existing Diabetes Mellitus in Pregnancy (Lin)
- 25-year-old clerk, insulin-dependent DM since age 16, poor compliance, recurrent DKA
- Admitted with hypoglycaemia; LMP 10 weeks ago; pregnancy test positive [1]
Three key effects are listed: [1]
| Effect | Mechanism |
|---|---|
| Blood glucose more difficult to control | Fasting hypoglycaemia (fetus siphons glucose continuously) + antagonising effect of placental hormones (hPL, progesterone, cortisol) on insulin → insulin resistance ↑ especially in 2nd/3rd trimester |
| Increased stress on cardiovascular and renal system | ↑ cardiac output, ↑ blood volume, ↑ GFR → kidneys work harder → may worsen diabetic nephropathy |
| Progression of diabetic retinopathy | Rapid improvement in glycaemic control paradoxically worsens retinopathy short-term; also haemodynamic changes in pregnancy |
Maternal aspects: [1]
- ↑ risk of pre-eclampsia
- ↑ risk of UTI (glycosuria provides substrate for bacteria)
- ↑ risk of preterm labour
- ↑ incidence of caesarean section and instrumental delivery (macrosomia, poor labour progress)
Fetal/Neonatal aspects: [1]
This comprehensive list is directly from the lecture slide:
| Complication | Mechanism |
|---|---|
| Congenital malformations (neural tube, skeletal, cardiac, renal, GI) | Hyperglycaemia is teratogenic — disrupts organogenesis in first trimester; incidence directly proportional to HbA1c |
| Preterm delivery | Associated with pre-eclampsia, polyhydramnios, infection |
| Large-for-gestational-age (macrosomia) | Fetal hyperinsulinaemia in response to maternal hyperglycaemia → anabolic hormone drives growth |
| Asphyxia and birth trauma | Macrosomic babies → shoulder dystocia, difficult delivery |
| Metabolic complications | Neonatal hypoglycaemia (baby's pancreas still producing excess insulin after cord is cut) |
| Sepsis | Immunocompromised state in DM |
| Jaundice and phototherapy | Polycythaemia (chronic fetal hypoxia → ↑ EPO) → ↑ RBC breakdown → bilirubin |
| Respiratory complications | Delayed fetal lung maturation (insulin inhibits surfactant production) |
| Long-term consequences (fetal programming) | In-utero exposure to hyperglycaemia → epigenetic changes → ↑ risk of metabolic and cardiovascular diseases in offspring |
"Management starts BEFORE pregnancy" [1]
Pre-pregnancy: [1]
- Good glycaemic control before pregnancy
- Hyperglycaemia is teratogenic
- Incidence of major congenital abnormality is directly proportional to HbA1c level
This is why pre-pregnancy counselling is critical. The critical window for teratogenicity is the first 8 weeks (organogenesis). If you only achieve tight control after discovering pregnancy (often at 6-8 weeks), you may have already missed the window.
During pregnancy: [1]
- Strict glycaemic control
- Oral hypoglycaemics are not contraindicated (though strict control is more difficult to achieve with them)
- Insulin usually needed
- Monitor for maternal and fetal complications
Multidisciplinary team: [1]
- Endocrinologist — readjust insulin dosage
- Dietitian — review diet, advise extra caloric intake for the baby
- DM nurse — instruct on day-to-day insulin adjustment, hotline contact
- Detailed fetal ultrasound — exclude congenital abnormalities
Antenatal care: [1]
- Regular follow-up by obstetrician and endocrinologist
- Regular ultrasound for fetal growth
Delivery: [1]
- Labour induced at 39 weeks
- Tight blood glucose control using insulin-dextrose drip and potassium replacement during labour
- Baby: early feeding, regular dextrostix monitoring
Why induce at 39 weeks? Continuing pregnancy beyond 39 weeks in diabetic mothers increases the risk of stillbirth (placental insufficiency) and further macrosomia. Induction before 39 weeks increases neonatal respiratory morbidity unless there are other indications.
A woman who is not diabetic may become diabetic during pregnancy or diabetes may be first detected during pregnancy = gestational diabetes. She and her baby face similar problems but usually to a milder degree. Management is similar — good glycaemic control is the cornerstone, by diet ± insulin. [1]
Case 3: Thyroid Disease in Pregnancy (Tina)
- 35-year-old with Grave's disease, had RAI at 30, on thyroxine 100mcg daily, poorly compliant
- Pregnant at 12 weeks: TSH 6.8 mU/L, normal FT4, clinically euthyroid [1]
Transient biochemical hyperthyroidism can occur in early pregnancy, especially in women with hyperemesis gravidarum — no clinical features of thyrotoxicosis [1]
Why? hCG shares structural homology with TSH (both are glycoprotein hormones with a common alpha subunit). In early pregnancy, hCG peaks at 10-12 weeks and can weakly stimulate the TSH receptor → ↑ FT4, ↓ TSH. This is physiological and does NOT require treatment. In hyperemesis, hCG levels are even higher, so this effect is more pronounced.
Thyroid disease, especially autoimmune thyroiditis, occurs more frequently in the postpartum period [1]
Why? Pregnancy causes relative immune suppression (to tolerate the semi-allogeneic fetus). Postpartum, the immune system "rebounds" → flare of autoimmune conditions including Hashimoto's thyroiditis and postpartum thyroiditis.
Thyroxine has no known adverse effect on the pregnancy unless clinically hyperthyroid [1]
Subclinical hypothyroidism (high TSH, normal FT4) is associated with preterm labour and increased incidence of delayed neurological development in offspring — but this is observational data only; effectiveness of routine screening and treatment not known yet [1]
Why does maternal hypothyroidism affect the fetus? Before ~20 weeks, the fetus relies entirely on maternal T4 (which crosses the placenta and is converted to T3 in fetal tissues) for brain development. After 20 weeks, the fetal thyroid starts functioning, but maternal T4 remains important throughout.
The lecture explicitly states: [1]
| Point | Detail |
|---|---|
| RAI contraindicated | Radioactive iodine crosses the placenta → destroys fetal thyroid |
| PTU and carbimazole commonly used | No known teratogenicity (note: some guidelines cite CMZ with aplasia cutis, but the lecture says "no known teratogenicity") |
| PTU preference in first trimester | Crosses placenta less; however, risk of maternal liver failure |
| Both can cause neonatal hypothyroidism | Usually reversible |
| Grave's disease autoantibodies | TSH receptor antibodies (TRAb) can cross the placenta → neonatal thyrotoxicosis (rare but important) |
Clinical pearl from Block A Endocrine: [3]
- First trimester: use PTU (less teratogenic risk of CMZ, though lecture downplays this)
- Second trimester onwards: switch to CMZ (PTU has hepatotoxicity risk)
- Always stabilize thyroid function before conception — uncontrolled hyperthyroidism is worse for pregnancy than the drugs
Two explanations for her high TSH: [1]
- Poor compliance to thyroxine replacement
- True subclinical hypothyroidism
Action: Check compliance, reinforce importance of compliance; increase dosage if compliant but TSH still elevated
Case 4: SLE in Pregnancy (Tung)
- 30-year-old with SLE (lupus nephritis at 24), unplanned pregnancy at 27 during flare → rapid renal deterioration → pregnancy terminated
- Now on prednisolone 5mg/day, normal renal function, mild proteinuria 600mg/day, wants to try again [1]
Three fundamental principles from the lecture: [1]
-
Pregnancy is associated with changes in the immune system — some autoimmune diseases may worsen, some may improve during pregnancy
- SLE tends to flare (especially lupus nephritis)
- Rheumatoid arthritis often improves (Th2 shift in pregnancy)
-
Pregnancy may further stress the end-organ/system affected by the autoimmune disease (e.g., kidney)
-
Pregnancy is contraindicated during an acute flare and is safest during remission
The lecture explicitly lists these transplacental antibody effects: [1]
| Antibody | Effect on Baby |
|---|---|
| Anti-platelet antibodies (ITP) | Fetal thrombocytopenia |
| Anti-Ro (SSA) antibodies | Congenital heart block (irreversible) |
| Anti-La (SSB) antibodies | Neonatal lupus (skin rash, usually self-limiting) |
| Lupus anticoagulant / Anticardiolipin | IUGR and pregnancy loss (antiphospholipid syndrome mechanism — thrombosis of placental vessels) |
2025 Past Paper Alert
The 2025 Fourth Summative MCQ Q76 directly asks: "A fetus has complete heart block on anomaly scan at 20 weeks. What maternal blood test should be performed?" Answer: Anti-Ro antibody [4]. This is a direct application of this lecture slide.
Listed explicitly: [1]
- Autoimmune thyroiditis → hypothyroidism → affects fetal neurological development
- Renal disease + hypertension → IUGR, ↑ superimposed pre-eclampsia
- ITP → excessive bleeding during delivery
From the lecture slides: [1]
| Drug | Risk |
|---|---|
| Steroids | IUGR, fetal cleft lip (small risk) |
| Azathioprine | Relatively safe |
| Methotrexate | Contraindicated in pregnancy (potent teratogen — folate antagonist → neural tube defects, limb defects, craniofacial abnormalities) |
| Cytotoxic drugs | Potentially teratogenic |
Yes — her disease is well controlled on low-dose steroids. But need to: [1]
- Check antibodies: anti-Ro, lupus anticoagulant, anticardiolipin
- Prepare for small to moderate increased risk of pre-eclampsia, IUGR, pregnancy loss
- Joint management by rheumatologist and obstetrician
Case 5: Cardiac Disease in Pregnancy (Lian)
- 17-year-old student, TOF diagnosed at birth, corrective surgery in childhood
- Good RV function on digoxin, but has pulmonary regurgitation, awaiting pulmonary valve replacement
- On frusemide; unplanned, unwanted pregnancy at 26 weeks [1]
Heart failure can occur during pregnancy in a woman with well-compensated cardiac disease: [1]
| Mechanism | Explanation |
|---|---|
| Physiological ↑ cardiac output | CO increases ~40% by 28-32 weeks — a diseased heart may not cope |
| Antenatal anaemia | Dilutional anaemia → heart needs to work harder |
| Tocolytic drugs | Beta-adrenergics (e.g., ritodrine) for arresting preterm labour → ↑ HR, ↑ CO |
| Stress and physical demand of labour | Each contraction autotransfuses ~500mL blood into circulation |
| Excessive IV fluids | Iatrogenic volume overload |
Postpartum period: decrease in uterine blood volume → increases effective circulatory volume → volume overload → can precipitate heart failure (often RIGHT heart failure) → increase R-to-L shunting especially with pulmonary hypertension [1]
Why the postpartum period is dangerous: When the uterus contracts after delivery, it essentially autotransfuses 500-1000mL of blood back into the maternal circulation. In a heart that's already struggling, this sudden volume load can tip it into failure. This is the same reason why the 6-week postpartum period has the highest VTE risk.
Fetal size is smaller and preterm labour is more frequent because: [1]
- Normal physiological increase in cardiac output may be limited by the cardiac condition → reduced uteroplacental perfusion
- Hypoxia in cyanotic heart disease → fetal growth restriction
This is a critical slide: [1]
| Drug | Effect on Pregnancy |
|---|---|
| Diuretics | May limit normal physiological volume expansion → IUGR |
| Warfarin | ↑ risk of congenital abnormalities (warfarin embryopathy), fetal loss |
| ACE inhibitors | Fetal loss, oligohydramnios, ↓ fetal renal perfusion |
Warfarin embryopathy: Warfarin crosses the placenta (unlike heparin). It inhibits vitamin K-dependent proteins needed for fetal bone/cartilage development → nasal hypoplasia, stippled epiphyses, chondrodysplasia punctata. Most dangerous in weeks 6-12. After first trimester, the main risk is fetal intracranial haemorrhage (due to anticoagulation of the fetus).
Listed from the lecture: [1]
- Teratogenic drugs may need to be substituted before pregnancy and in the first trimester
- Pharmacokinetic changes in pregnancy affect serum levels of drugs (e.g., digoxin, warfarin — ↑ plasma volume → ↓ drug levels → need dose adjustments)
- Careful readjustment of dosage during pregnancy
- Cardiac catheterization (X-ray exposure), open heart surgery (hypotension, hypothermia, hypoxia) carry high risks during pregnancy
From the lecture: [1]
| Consideration | Detail |
|---|---|
| Antibiotic prophylaxis for endocarditis | Needed for mechanical heart valves or grossly damaged valves but NOT for most other cases |
| Thromboembolism prevention | Essential in patients with mechanical valves or those at high risk |
| Mode & timing of delivery | Availability of multidisciplinary specialists; in general, spontaneous onset of labour, vaginal delivery ± epidural analgesia carries lowest risks but must be individualized |
The lecture walks through the actual management: [1]
- Joint case conference: obstetricians, paediatric + adult cardiologists, anaesthesiologists
- Continued digoxin and frusemide
- Paediatric cardiologist assessed every 4 weeks → every 2 weeks from 32 weeks
- Frusemide increased at 32 weeks for progressive SOB
- Fetal growth monitored every 4 weeks → along 10th centile
- Labour induced at 38 weeks with epidural analgesia
- No antibiotics cover needed (no mechanical valve, no grossly damaged valve)
- Normal vaginal delivery, baby boy 2.7kg, healthy
- Barrier contraception advised (hormonal methods may increase thromboembolism risk in cardiac patients)
- Pulmonary valve replacement to be scheduled after delivery
Case 6: Epilepsy in Pregnancy (Hong)
- 28-year-old, grand mal epilepsy on phenytoin since age 16
- Stopped phenytoin when she found out she was pregnant (worried about teratogenicity)
- Had 3 attacks in one month after stopping [1]
"Many antiepileptic drugs are teratogenic" — cleft lip and palate, neural tube defects [1]
"Should antiepileptic drugs be stopped? If epilepsy cannot be controlled without drugs, DO NOT stop the drugs. Consider monotherapy if possible." [1]
Why not stop? Uncontrolled seizures pose a greater risk to both mother and fetus than the teratogenic risk of the drugs. Grand mal seizures cause maternal hypoxia, which causes fetal hypoxia → potential fetal brain injury or death. Status epilepticus can be fatal. The teratogenic risk of AEDs is ~4-8% (vs. 2-3% baseline), but the risk of seizure-related harm from stopping medication is higher.
"Folic acid supplement decreases the incidence of congenital abnormalities associated with antiepileptic drugs" [1]
Why folic acid? Many AEDs (especially phenytoin, carbamazepine, valproate) interfere with folate metabolism. Folate is essential for neural tube closure (occurs at day 28). High-dose folic acid (5mg/day, not the standard 0.4-0.5mg) is recommended for women on AEDs — ideally started before conception.
"Detailed prenatal ultrasound examination to assess fetal anatomy" [1]
Case 7: Thromboembolism in Pregnancy (Jane)
- 39-year-old smoker, 80kg, threatened miscarriage at 12 weeks, advised bed rest
- Developed mild SOB after one week in bed → given cough remedy
- Collapsed and died at home
- Postmortem: massive pulmonary embolism [1]
Critical Teaching Point
This case illustrates a catastrophic outcome from inappropriately prescribing bed rest. The lecture explicitly teaches: "Do not prescribe bed rest for conditions where this is not proven to be effective — do not prescribe bed rest for threatened miscarriage, IUGR." Bed rest increases VTE risk without proven benefit for these conditions. This is an exam favourite.
Virchow's triad — all three components are present during pregnancy: [1]
| Component | Pregnancy Mechanism |
|---|---|
| Immobility | Relatively less mobile during pregnancy |
| Hypercoagulability | ↑ clotting factors (fibrinogen, VII, VIII, X, vWF), ↓ protein S; further increases postpartum; viscosity may increase in hyperemesis |
| Obstruction to blood flow | Gravid uterus compresses IVC and iliac veins |
Why is postpartum period highest risk? [5] The hypercoagulable state is most pronounced immediately postpartum (nature's mechanism to prevent haemorrhage after placental separation). Combined with immobility after delivery (especially post-caesarean) and the sudden release of uterine venous obstruction → highest VTE risk at 6 weeks postpartum.
The lecture divides risk factors into pre-existing and current: [1]
Pre-existing:
- Advanced age, obesity, ethnicity
- Smoking
- Congenital or acquired thrombophilia
- Personal/family history of thromboembolism
Current (pregnancy and treatment related):
- Pre-eclampsia, hyperemesis, bed rest, caesarean delivery, postpartum genital tract infection
- Concurrent: infection, immobilization due to injury, long-haul flights
Key prevention strategies from the lecture: [1]
| Strategy | Detail |
|---|---|
| Minimize immobility | Do NOT prescribe bed rest for threatened miscarriage, IUGR |
| Adequate hydration | Prevents haemoconcentration |
| Compression stockings | Graduated compression |
| Prophylactic anticoagulation | For women at increased risk during pregnancy and postpartum |
Anticoagulation choices in pregnancy: [1]
| Drug | Notes |
|---|---|
| LMWH / Unfractionated heparin | Drug of choice — does NOT cross placenta [5] |
| Warfarin | Crosses the placenta and has long half-life — can be used in second trimester and early third trimester when organogenesis is complete, and postpartum |
From Block A Haematology: [5]
- Warfarin crosses placenta → risk of fetal ICH and teratogenicity
- Regimen: Switch to LMWH in first trimester (↓ teratogenicity) and > 36 weeks (avoid PPH — warfarin's long half-life makes epidural and delivery dangerous)
- Cover up to 6 weeks postpartum (highest risk period)
- Use pre-pregnancy weight for dose calculation
This is the systematic thinking approach the lecture teaches: [1]
For ANY medical condition in pregnancy, ask four questions:
The final summary slide lists the overarching principles: [1]
- Obstetric conditions can mimic medical conditions (e.g., pre-eclampsia mimicking hypertensive encephalopathy)
- Women with chronic medical diseases can get pregnant → pre-pregnancy counselling, contraceptive advice, careful drug use
- Effects of pregnancy on pre-existing medical disease AND its treatment
- Effects of medical disease AND its treatment on pregnancy
- Consider BOTH mother and baby
- Prevalence of some medical diseases increases during pregnancy or postpartum (e.g., VTE)
| Drug | Safe in Pregnancy? | Notes |
|---|---|---|
| Labetalol | ✅ Yes | First-line antihypertensive in pregnancy |
| Nifedipine | ✅ Yes | Second-line; calcium channel blocker |
| Hydralazine | ✅ Yes | IV for acute severe HTN |
| MgSO₄ | ✅ Yes | Eclampsia prevention/treatment |
| Insulin | ✅ Yes | Mainstay for DM control in pregnancy |
| Oral hypoglycaemics | ✅ Not contraindicated | Lecture explicitly states "not contraindicated" |
| Thyroxine | ✅ Yes | No adverse effects unless clinically hyperthyroid |
| PTU | ✅ Yes (1st trimester) | Less placental transfer; risk of liver failure |
| Carbimazole | ✅ Yes (2nd/3rd trimester) | Risk of aplasia cutis (debated); lecture says "no known teratogenicity" |
| Prednisolone | ✅ Yes (low dose) | Small risk of IUGR, cleft lip |
| Azathioprine | ✅ Relatively safe | Can continue if needed |
| LMWH / Heparin | ✅ Yes | Does not cross placenta |
| Folic acid | ✅ Yes | Essential; high dose (5mg) with AEDs |
| Digoxin | ✅ Yes | May need dose adjustment |
| ACE inhibitors | ❌ Contraindicated | Oligohydramnios, renal dysgenesis, fetal death |
| ARBs | ❌ Contraindicated | Same mechanism as ACEi |
| Warfarin | ⚠️ Conditional | Teratogenic 6-12 weeks; can use 2nd trimester, postpartum |
| Methotrexate | ❌ Contraindicated | Potent teratogen |
| Radioactive iodine | ❌ Contraindicated | Destroys fetal thyroid |
| Valproate | ⚠️ Avoid if possible | Highest teratogenic risk among AEDs (NTD ~10%) |
Exam Intelligence
- Classification questions: "Classify hypertensive disorders of pregnancy" — know the 20-week cut-off
- Drug safety: "Which drugs are contraindicated?" — ACEi, warfarin (1st trimester), MTX, RAI
- Clinical scenarios: Case vignette → identify the four-way interaction
- Investigation interpretation: Pre-eclampsia workup (CBC, RFT, LFT, coagulation)
- Antibody-related fetal effects: Anti-Ro → congenital heart block (2025 MCQ Q76)
- VTE risk: Why pregnancy is a hypercoagulable state; why bed rest is dangerous
| Year | Question | Theme |
|---|---|---|
| 2021 SAQ Q1 | Pre-eclampsia at 39 weeks | Diagnosis, investigations, antihypertensives, eclampsia management [6] |
| 2022 MCQ Q13 | Post-LSCS DVT | VTE risk factors post-delivery [7] |
| 2025 MCQ Q76 | Fetal complete heart block | Anti-Ro antibody [4] |
| 2023 SAQ Q2 | Supine hypotension at 28 weeks | IVC compression by gravid uterus [8] |
Exam Traps to Avoid
- Confusing gestational HTN with pre-eclampsia: Gestational HTN has NO proteinuria; pre-eclampsia = gestational HTN + proteinuria (or other end-organ involvement)
- Thinking all AEDs should be stopped in pregnancy: Uncontrolled seizures are MORE dangerous than drug teratogenicity
- Prescribing bed rest for threatened miscarriage: No proven benefit; increases VTE risk
- Using ACEi in pregnancy: Never — even if the mother has diabetic nephropathy or heart failure
- Forgetting the postpartum period: Many conditions flare or present postpartum (thyroiditis, VTE, heart failure)
- Thinking oral hypoglycaemics are contraindicated: The lecture explicitly says they are NOT contraindicated (though insulin is usually needed for tight control)
-
Classify hypertensive disorders of pregnancy. (SAQ, 4-5 marks)
- Pre-existing HTN, pre-existing renal disease, gestational HTN (without proteinuria), pre-eclampsia (with proteinuria), pre-existing + superimposed pre-eclampsia
-
A 26-year-old presents at 34 weeks with BP 170/110, proteinuria +++, headache. What are your initial investigations?
- CBC (thrombocytopenia/haemolysis), RFT (renal insufficiency), LFT (liver derangement), coagulation (DIC), fetal CTG
-
Why is ACEi contraindicated in pregnancy?
- Crosses placenta → ↓ fetal renal perfusion → oligohydramnios, renal dysgenesis, skull ossification defects, fetal death
-
How does pre-existing DM affect the fetus? List 5 complications.
- Congenital malformations, macrosomia, neonatal hypoglycaemia, RDS, NNJ, preterm delivery
-
A woman on warfarin for mechanical mitral valve becomes pregnant. How do you manage anticoagulation?
- Switch to LMWH in first trimester (teratogenicity risk); can resume warfarin in second trimester; switch back to LMWH at 36 weeks (avoid PPH); continue anticoagulation for 6 weeks postpartum
-
What fetal complication is associated with maternal anti-Ro antibodies?
- Congenital heart block
-
List 3 reasons why VTE risk is increased in pregnancy.
- Immobility, hypercoagulability (↑ clotting factors, ↓ protein S), venous obstruction by gravid uterus
-
A patient with epilepsy discovers she is pregnant. Should she stop her AEDs?
- No — uncontrolled seizures pose greater risk. Consider monotherapy. Give high-dose folic acid. Perform detailed anomaly ultrasound.
High Yield Summary
Core Framework: For any medical condition in pregnancy, systematically consider: (1) Effect of pregnancy on disease, (2) Effect of disease on pregnancy, (3) Effect of treatment on pregnancy, (4) Effect of pregnancy on treatment. Always consider BOTH mother and fetus.
Hypertension: Classify by 20-week cut-off. Pre-eclampsia = HTN + proteinuria after 20 weeks. Treat severe HTN to prevent ICH. Use MgSO₄ for eclampsia prevention. ACEi contraindicated. Definitive treatment = delivery.
DM: Hyperglycaemia is teratogenic (risk ∝ HbA1c). Start good control BEFORE pregnancy. Fetal risks: malformations, macrosomia, neonatal hypoglycaemia, RDS, NNJ. Manage with insulin + multidisciplinary team. Induce at 39 weeks.
Thyroid: Transient biochemical hyperthyroidism in early pregnancy is physiological (hCG effect). RAI contraindicated. PTU for 1st trimester, CMZ for 2nd/3rd. Subclinical hypothyroidism may affect fetal neurodevelopment.
Autoimmune/SLE: Safest in remission. Autoantibodies cross placenta (anti-Ro → congenital heart block, LA → pregnancy loss). Azathioprine relatively safe; methotrexate absolutely contraindicated.
Cardiac: Pregnancy ↑ CO by 40% → may precipitate heart failure. Postpartum autotransfusion is dangerous. Warfarin teratogenic in 1st trimester. Spontaneous vaginal delivery with epidural is generally safest.
Epilepsy: Do NOT stop AEDs — uncontrolled seizures are more dangerous. Use monotherapy. High-dose folic acid. Anomaly scan.
VTE: All components of Virchow's triad present in pregnancy. Do NOT prescribe bed rest for threatened miscarriage. LMWH is anticoagulant of choice (does not cross placenta). Highest risk = 6 weeks postpartum.
Active Recall - Medical Problems Complicating Pregnancy
[1] Lecture slides: GC 115. I am pregnant medical problems complicating pregnancy.pdf [2] Lecture slides: Block C - O&G Theme Case 1.docx.pdf (Learning Objectives) [3] Senior notes: Block A - I am losing weight and sweating all the time_ causes of severe, weight loss; thyrotoxicosis; hypothyroidism.pdf (PTU/CMZ in pregnancy) [4] Past papers: 2025 Fourth Summative MCQ.pdf (Q76 — anti-Ro antibody and congenital heart block) [5] Senior notes: Block A - Leg swelling and chest pain_ deep vein thrombosis; pulmonary embolism; Thrombophilia.pdf (Pregnancy-related VTE management) [6] Past papers: 2021 Fourth Summative SAQ.pdf (Q1 — pre-eclampsia management) [7] Past papers: 2022 Fourth Summative MCQ.pdf (Q13 — post-LSCS DVT) [8] Past papers: 2023 Fourth Summative SAQ.pdf (Q2 — supine hypotension in pregnancy)
GC114 Climacteric Symptoms Menopause And Related Illness; Amenorrhoea
Climacteric symptoms encompass the vasomotor, psychological, and urogenital manifestations arising from ovarian hormone decline during the menopausal transition, while amenorrhoea refers to the absence of menstruation due to physiological, pathological, or iatrogenic causes.
GC117 I Want To Have A Baby Male And Female Infertility
Male and female infertility refers to the inability of a couple to achieve pregnancy after 12 months of regular unprotected intercourse, resulting from disorders of sperm production or function, ovulatory dysfunction, tubal damage, uterine abnormalities, or unexplained factors in either partner.