OG12.1-11,OG16.4 | Medical Disorders in Pregnancy — Graded Quiz

For acute severe hypertension in eclampsia (BP ≥160/110 mmHg), IV labetalol (starting at 20 mg IV, doubling every 10 min to a maximum of 300 mg) is a first-line antihypertensive alongside IV hydralazine and oral nifedipine. Atenolol is contraindicated in pregnancy (fetal growth restriction). Furosemide is a diuretic — not the primary treatment for hypertensive urgency in pre-eclampsia/eclampsia.

Acute severe hypertension in pregnancy (≥160/110): IV labetalol (20 mg titrated), IV hydralazine, or oral nifedipine are the three first-line agents. Atenolol is contraindicated in pregnancy. Target BP: ~140–150/90–100 mmHg — do not drop too rapidly.

The target in severe hypertension is to reduce BP to approximately 140–150/90–100 mmHg acutely. First-line IV options are labetalol and hydralazine. Oral nifedipine is also acceptable. Atenolol is avoided in pregnancy due to fetal growth restriction risk.

HELLP syndrome is defined by the triad of Haemolysis (elevated LDH, falling haematocrit, microangiopathic haemolytic anaemia), Elevated Liver enzymes (AST ≥70 IU/L), and Low Platelets (<100,000/µL). This patient fulfils all three criteria. AFLP would present with hypoglycaemia and predominantly hepatocellular failure. Pre-eclampsia alone does not account for the haemolytic triad.

HELLP triad: Haemolysis (LDH elevated, falling Hct) + Elevated Liver enzymes (AST ≥70) + Low Platelets (<100,000/µL). Distinguished from AFLP by: no hypoglycaemia; more prominent haemolysis; often occurs within the pre-eclampsia spectrum. Delivery is the definitive treatment.

HELLP = H (haemolysis: elevated LDH, schistocytes) + EL (elevated liver enzymes: AST ≥70) + LP (platelets <100,000/µL). All three criteria are met here. AFLP would show hypoglycaemia and prolonged prothrombin time disproportionate to the platelet drop.

At 37 weeks, there is insufficient time for oral iron to raise haemoglobin meaningfully before delivery (requires ~4 weeks for significant response). IV iron sucrose achieves a faster haemoglobin rise (2–4 weeks), is safe in the third trimester, and is an appropriate alternative when blood transfusion is refused. Oral iron absorption is too slow at this gestation.

At term with severe IDA and transfusion refusal: IV iron is the fastest non-transfusion option. It can raise Hb 1–2 g/dL over 2–4 weeks. Total dose IV iron (TDI) can be calculated from body weight and degree of deficiency. Oral iron is too slow at term.

Severe IDA at 37 weeks with a haemoglobin of 6.5 g/dL requires rapid haemoglobin augmentation before delivery. Oral iron will not work fast enough. IV iron sucrose achieves a faster response (1–2 g/dL rise in 2–4 weeks) and is the appropriate alternative when blood transfusion is refused.

Poor glycaemic control during the critical period of organogenesis (weeks 3–8) is associated with a 2–3 fold increased risk of congenital malformations, predominantly cardiac defects (ventricular septal defect, transposition of great arteries) and neural tube defects. This risk is proportional to HbA1c at conception. Macrosomia, neonatal hypoglycaemia, and RDS are complications of hyperglycaemia later in pregnancy, not organogenesis.

Pre-gestational diabetes: congenital malformations (cardiac, NTD) from poor glycaemic control during organogenesis (weeks 3–8). Later hyperglycaemia causes macrosomia, neonatal hypoglycaemia, polycythaemia, RDS, shoulder dystocia. Preconception HbA1c target <6.5% reduces malformation risk.

Organogenesis occurs during weeks 3–8. Hyperglycaemia during this window drives structural malformations (cardiac and NTDs). The risk is proportional to HbA1c at conception — this is why preconception counselling and achieving HbA1c <6.5% before conception is critical for women with pre-gestational diabetes.

Acute decompensation in mitral stenosis (pulmonary oedema) during pregnancy is managed medically first: rate control (beta-blocker or digoxin) to allow adequate diastolic filling time, and diuresis (furosemide) to reduce preload. Beta-blockade also reduces tachycardia, which is the most common precipitant of decompensation in MS. Percutaneous balloon mitral valvotomy (PBMV) under fluoroscopy can be performed if medical management fails. Delivery at 24 weeks would produce an extremely premature infant and is not indicated unless the mother's life cannot otherwise be saved.

Decompensated mitral stenosis in pregnancy: rate control (beta-blocker or digoxin) + diuresis (furosemide). Precipitants = tachycardia and fluid overload. If refractory: PBMV preferred over open surgery (30% fetal mortality on cardiopulmonary bypass). Avoid ergometrine at all times.

Medical management comes first: rate control (metoprolol/digoxin) and diuresis. PBMV is indicated if severe MS is refractory to medical management. Caesarean delivery at 24 weeks risks extreme prematurity and is not the first step. Cardiac surgery on bypass carries a 30% fetal mortality and is a last resort.

This is acute pyelonephritis — upper UTI with systemic features (fever, rigors, loin pain). In pregnancy, pyelonephritis requires hospital admission and IV antibiotics (cephalosporins such as cefazolin or ceftriaxone are preferred; gentamicin may be added if gram-negative sepsis is suspected). Oral nitrofurantoin is appropriate for uncomplicated lower UTI and ASB, not pyelonephritis. Nitrofurantoin should also be avoided near term (>36 weeks).

Pyelonephritis in pregnancy = hospital admission + IV antibiotics (cephalosporins first-line; aminoglycosides for severe sepsis, with monitoring). Oral nitrofurantoin is for ASB/uncomplicated cystitis, NOT pyelonephritis. Nitrofurantoin is also avoided after 36 weeks (risk of neonatal haemolysis).

Pyelonephritis = upper UTI with systemic features. It requires IV antibiotics and hospitalisation in pregnancy due to the risk of preterm labour, sepsis, and maternal deterioration. Oral agents are inappropriate for pyelonephritis with rigors and systemic illness.

This is intrahepatic cholestasis of pregnancy (ICP), characterised by pruritus (palms/soles, worse at night), elevated serum bile acids (≥10 µmol/L, severe ≥40 µmol/L), and normal or mildly elevated transaminases without jaundice. The primary fetal risk is sudden intrauterine fetal death, likely from bile acid-induced cardiac arrhythmia in the fetus. Ursodeoxycholic acid reduces symptoms and bile acids; delivery by 37–38 weeks is recommended for severe ICP.

ICP: T3 pruritus (palms/soles, nocturnal), elevated bile acids ≥10 µmol/L, normal bilirubin, mildly elevated transaminases. Primary fetal risk = sudden intrauterine death (especially severe ICP with bile acids ≥40 µmol/L). Management: ursodeoxycholic acid, delivery ≤37–38 weeks for severe cases.

ICP is characterised by pruritus + raised serum bile acids. The fetus is at risk of sudden stillbirth (mechanism likely bile acid-induced cardiac arrhythmia), meconium staining, and preterm labour. ICP does NOT cause fetal hepatic failure or hydrops.

MCA PSV >1.5 MoM indicates significant fetal anaemia (sensitivity >80% for moderate-severe anaemia) because anaemic fetal blood has lower viscosity and flows faster. An MCA PSV of 1.4 MoM is near the threshold, and in the context of a positive ICT with a significant titre (critical titre ≥1:16 in most centres), this warrants fetal blood sampling (cordocentesis) and intrauterine transfusion if fetal Hb is <10 g/dL. This has replaced amniocentesis for Delta OD450 as the primary monitoring tool.

In Rh-sensitised pregnancies: MCA PSV >1.5 MoM = fetal anaemia → cordocentesis ± IUT. MCA Doppler has replaced amniocentesis/Delta OD450. Critical titre (varies by lab, often ≥1:16) triggers close surveillance. Sensitised mothers require fortnightly MCA Doppler surveillance.

MCA PSV >1.5 MoM = fetal anaemia. This near-threshold value (1.4 MoM) in the context of a significant anti-D titre warrants proceeding to fetal blood sampling. MCA Doppler detects fetal anaemia non-invasively — it has largely replaced amniocentesis for OD450 measurement.

A TSH of 4.8 mIU/L exceeds the first-trimester upper limit of 2.5 mIU/L (trimester-specific range T1: 0.1–2.5 mIU/L), confirming hypothyroidism. Levothyroxine is initiated or dose-adjusted. Monitoring every 4 weeks in the first trimester (when maternal thyroid hormone is the sole source for fetal neurodevelopment) and every 4–6 weeks thereafter is standard. Using non-pregnant ranges (upper limit ~5 mIU/L) would falsely reassure.

Trimester-specific TSH ranges: T1 0.1–2.5, T2 0.2–3.0, T3 0.3–3.0 mIU/L. Applying non-pregnant ranges risks missing hypothyroidism. Levothyroxine dose often increases 25–30% in pregnancy. Monitor TSH every 4 weeks in T1, then 4–6 weekly. Untreated hypothyroidism = fetal neurodevelopmental impairment.

The non-pregnant upper limit for TSH (~5 mIU/L) does NOT apply in pregnancy. The trimester-specific T1 upper limit is 2.5 mIU/L. A TSH of 4.8 mIU/L in T1 requires levothyroxine therapy. Carbimazole treats hyperthyroidism, not hypothyroidism.

The gravid uterus progressively displaces the caecum and appendix superiorly and laterally as pregnancy advances. By 20–22 weeks, the appendix may be at the level of the right flank or even the right hypochondrium, so tenderness shifts away from the classical McBurney's point (one-third of the way from ASIS to umbilicus). Leukocytosis up to 15,000–20,000/µL is physiological in pregnancy, making WBC unreliable for diagnosing appendicitis. MRI (preferred) or ultrasound are the investigations of choice; delay in surgery worsens maternal and fetal outcome.

Appendix position in pregnancy: pelvic in T1 → McBurney's level → right flank at 20 weeks → right hypochondrium at 36 weeks. Do not rely on McBurney's point or WBC for diagnosis. Use MRI or USS. Principle: surgical delay = greatest fetal risk (not the operation itself).

The key caveat is that the appendix migrates superolaterally in pregnancy, so classical McBurney's point tenderness is NOT reliable after the first trimester. Physiological leukocytosis in pregnancy (up to 15,000–20,000/µL) also confounds interpretation. Peritoneal signs are attenuated by the stretched abdominal wall.

Low-dose aspirin (75–150 mg daily), started before 16 weeks (ideally before 12 weeks), inhibits platelet aggregation and thromboxane A2 synthesis, improving uteroplacental perfusion in women at risk of placenta-mediated IUGR and pre-eclampsia. This is the only evidence-based pharmacological intervention for preventing recurrent IUGR and pre-eclampsia. It should be continued until 36–37 weeks. Bed rest has no benefit in IUGR prevention. LMWH is reserved for thrombophilia-associated IUGR.

Prevention of recurrent IUGR: low-dose aspirin 75–150 mg/day started before 16 weeks (preferably before 12 weeks), continued until 36–37 weeks. Also: smoking cessation, nutritional optimisation, calcium supplementation if deficient. LMWH for thrombophilia-associated cases only.

Low-dose aspirin (75–150 mg/day) commenced before 16 weeks is the only intervention with robust RCT evidence for reducing recurrent placenta-mediated IUGR and pre-eclampsia. Folic acid prevents NTDs (continue beyond 12 weeks for other benefits) but does not prevent IUGR. LMWH is indicated only in inherited thrombophilias with prior placental vascular complications.

With a viral load of 22,000 copies/mL at 36 weeks (well above the 1,000 copies/mL threshold), intrapartum MTCT risk is significantly elevated. Elective caesarean section at 38 weeks reduces intrapartum transmission by approximately 50–80% in women with high viral loads. Adding a second ART regimen does not achieve viral suppression quickly enough before delivery. The plan is: LSCS at 38 weeks + continuation of maternal ART + infant nevirapine prophylaxis.

NACO PPTCT: viral load <1000 copies/mL = vaginal delivery acceptable. Viral load ≥1000 copies/mL = elective LSCS at 38 weeks to minimise intrapartum MTCT. Infant prophylaxis (nevirapine) given regardless of delivery mode. Investigate cause of virological failure (adherence, resistance).

Under NACO guidelines, viral load ≥1000 copies/mL at 36 weeks is an indication for elective caesarean section to reduce intrapartum MTCT. Vaginal delivery is permitted for viral load <1000 copies/mL. A viral load of 22,000 copies/mL (likely due to poor adherence or virological failure) requires delivery by LSCS.