MCQs: Hypertension & Diabetes in Pregnancy (Obstetrics)

SECTION A: HYPERTENSION IN PREGNANCY

• A) Gestational hypertension
• B) Chronic hypertension with superimposed preeclampsia
• C) Preeclampsia with severe features
• D) Eclampsia
• E) HELLP syndrome

Answer: C - Preeclampsia with severe features. New hypertension after 20 weeks with maternal organ dysfunction (elevated transaminases, proteinuria) meets criteria for preeclampsia. Eclampsia requires seizure activity. HELLP requires hemolysis + thrombocytopenia + elevated liver enzymes as a triad.

(Comprehensive Clinical Nephrology 7e; Creasy & Resnik's MFM)

• A) BP ≥140/90 mmHg before 20 weeks gestation
• B) New hypertension after 20 weeks without features of preeclampsia, resolving by 12 weeks postpartum
• C) BP ≥160/110 mmHg after 20 weeks with proteinuria
• D) Hypertension diagnosed in the first trimester
• E) White-coat hypertension confirmed by 24-hour ABPM

Answer: B - Gestational hypertension is new hypertension after 20 weeks in the absence of features of preeclampsia. Approximately 25% progress to preeclampsia. It normally resolves by 12 weeks postpartum; persistence beyond that suggests chronic hypertension.

(Comprehensive Clinical Nephrology 7e)

• A) New hypertension after 20 weeks
• B) Proteinuria
• C) Maternal organ dysfunction
• D) Uteroplacental dysfunction
• E) Either B, C, or D alongside new hypertension

Answer: B - Proteinuria is NOT essential if other organ dysfunction criteria are present. Preeclampsia = new hypertension after 20 weeks + maternal organ dysfunction OR uteroplacental dysfunction. Proteinuria (uPCR >30 mg/mmol) is one possible criterion but not mandatory.

(Comprehensive Clinical Nephrology 7e)

• A) Renal glomerulosclerosis
• B) Failure of spiral artery remodeling by trophoblasts
• C) Excessive production of placental growth factor (PlGF)
• D) Autoimmune destruction of endothelial cells
• E) Ventricular hypertrophy from chronic hypertension

Answer: B - Deficient spiral artery remodeling by trophoblasts leads to uteroplacental ischemia, oxidative stress, and an imbalance between proangiogenic (PlGF) and antiangiogenic (sFlt-1) factors, producing systemic endothelial dysfunction.

(Comprehensive Clinical Nephrology 7e)

• A) Labetalol
• B) Nifedipine
• C) Methyldopa
• D) ACE inhibitors
• E) Hydralazine

Answer: D - ACE inhibitors (and ARBs) are contraindicated in pregnancy due to fetotoxicity - they cause oligohydramnios, renal tubular dysplasia, and neonatal renal failure. The three most commonly used antihypertensives in pregnancy are labetalol, nifedipine, and hydralazine.

(Harrison's Principles of Internal Medicine 22e; Fuster & Hurst's The Heart 15e)

• A) Oral amlodipine, IV enalapril
• B) IV labetalol, IV hydralazine, oral nifedipine
• C) Oral metoprolol, IV furosemide
• D) IV sodium nitroprusside, oral atenolol
• E) Sublingual nifedipine, IV methyldopa

Answer: B - IV labetalol, IV hydralazine, and oral nifedipine (when IV access is unavailable) are the drugs of choice for acute severe hypertension in pregnancy. Sodium nitroprusside is potentially fetotoxic. Sublingual nifedipine is not recommended.

(Rosen's Emergency Medicine; Fuster & Hurst's The Heart 15e)

• A) Lowering blood pressure acutely
• B) Prevention and treatment of seizures (eclampsia prophylaxis)
• C) Treating thrombocytopenia
• D) Reducing proteinuria
• E) Improving fetal lung maturity

Answer: B - Magnesium sulfate is superior to all other agents for seizure prevention and treatment in preeclampsia/eclampsia. It does NOT lower blood pressure directly. Routine IV magnesium sulfate is recommended in preeclampsia with severe features. It should not be delayed when indicated.

(Brenner & Rector's The Kidney; Swanson's Family Medicine Review; Creasy & Resnik's MFM)

• A) Hypertension, Edema, Leukocytosis
• B) Hemolysis, Elevated Liver enzymes, Low Platelets
• C) Hyperreflexia, Elevated Creatinine, Low Protein
• D) Hemoglobinuria, Elevated Lipids, Low Platelet
• E) Hepatomegaly, Elevated Bilirubin, Leukopenia

Answer: B - HELLP = Hemolysis + Elevated Liver enzymes + Low Platelets (< 100,000/μL). It is a severe form of preeclampsia, can occur without proteinuria. Elevated liver enzymes distinguish it from TTP/HUS.

(Brenner & Rector's The Kidney; Goldman-Cecil Medicine)

• A) No increased risk compared to normotensives
• B) An approximately doubled risk (~8%) of developing preeclampsia
• C) A 50% risk of progression to eclampsia
• D) Normal home BP readings of ≥135/85 mmHg
• E) Chronic hypertension requiring lifelong treatment

Answer: B - White-coat hypertension (office BP ≥140/90 but home BP <135/85 mmHg) is not benign in pregnancy - it carries approximately 8% risk of preeclampsia, roughly double the background risk.

(Comprehensive Clinical Nephrology 7e)

• A) Gestational hypertension
• B) Preeclampsia
• C) Chronic hypertension
• D) White-coat hypertension
• E) Transient hypertension of pregnancy

Answer: C - Chronic hypertension is defined as BP ≥140/90 mmHg that predates pregnancy OR is detected before 20 weeks' gestation and persists beyond 12 weeks postpartum. Gestational hypertension resolves by 12 weeks postpartum.

(Comprehensive Clinical Nephrology 7e)

SECTION B: DIABETES IN PREGNANCY

• A) Autoimmune destruction of beta cells
• B) Pregravid insulin resistance amplified by placental hormones in late gestation
• C) Excess placental glucagon production
• D) Decreased renal glucose threshold
• E) Type 1 diabetes unmasked by pregnancy

Answer: B - Pregnancy causes a 50-60% decrease in total insulin sensitivity, amplified in women with underlying metabolic risk. GDM reflects reduced beta-cell function relative to insulin resistance, not meeting the demand. Insulin sensitivity decreases most between 16 and 37 weeks.

(Creasy & Resnik's MFM)

• A) Fasting glucose at first antenatal visit, then HbA1c at 28 weeks
• B) 50g GCT (glucose challenge test) at 24-28 weeks; if positive, a 100g 3-hour OGTT
• C) 75g OGTT at booking for all women
• D) Random blood glucose at every antenatal visit
• E) Urine glucose dipstick as primary screen

Answer: B - The 2-step approach (Carpenter-Coustan or NDDG criteria) involves a 50g non-fasting glucose challenge test at 24-28 weeks; women who fail proceed to a 100g 3-hour OGTT for diagnosis. The 1-step approach uses a 75g 2-hour OGTT.

(Textbook of Family Medicine 9e; Quick Compendium of Clinical Pathology 5e)

• A) Oligohydramnios
• B) Fetal growth restriction and microcephaly
• C) Macrosomia, polyhydramnios, and neonatal hypoglycemia
• D) Placental abruption exclusively
• E) Anencephaly in Type 2 diabetes only

Answer: C - Poorly controlled maternal diabetes leads to fetal hyperinsulinism in response to maternal hyperglycemia, causing macrosomia, polyhydramnios (excess fetal urination), and neonatal hypoglycemia (after cord clamping removes maternal glucose supply). Neural tube defects (not microcephaly) are associated with early first-trimester hyperglycemia.

(Creasy & Resnik's MFM; Rosen's Emergency Medicine)

• A) Conceive immediately as dialysis protects the fetus
• B) Avoid pregnancy entirely - success rates are near zero
• C) Undergo prepregnancy renal transplantation for significantly better outcomes
• D) Switch to peritoneal dialysis which eliminates fetal risk
• E) Proceed with IVF; dialysis does not affect fetal outcomes

Answer: C - Pregnancy on dialysis for diabetic ESRD carries a live birth rate of ~54%, with 87% preterm delivery. A prepregnancy renal transplant is the recommended strategy, as transplant outcomes are substantially better (74% live birth rate).

(Creasy & Resnik's MFM)

• A) Insulin requirements are stable throughout pregnancy
• B) Requirements increase progressively from conception onwards
• C) Requirements may decrease in early pregnancy (9-16 weeks) then increase most between 16-37 weeks, plateau near term
• D) Requirements decrease throughout and return to normal at delivery
• E) Requirements double in the first trimester, then halve in the third trimester

Answer: C - In well-controlled T1DM, insulin requirements show variable changes in early gestation with decreases between 9-16 weeks, the greatest increase between 16-37 weeks (reflecting peak insulin resistance), and a plateau or small decline near term.

(Creasy & Resnik's MFM)

• A) Sulfonylureas (glipizide)
• B) Insulin
• C) Metformin alone as first-line
• D) Thiazolidinediones
• E) SGLT-2 inhibitors

Answer: B - Insulin is the gold-standard pharmacologic treatment for GDM when lifestyle measures fail. Metformin and glibenclamide have been studied but insulin remains preferred, especially as metformin crosses the placenta. The Cochrane evidence compares all three (glibenclamide, metformin, insulin) but insulin is most recommended.

(Creasy & Resnik's MFM references)

• A) Neonatal hypertension
• B) Neonatal hypoglycemia after delivery
• C) Neonatal renal failure
• D) Neonatal polycythemia exclusively
• E) Neonatal hypothyroidism

Answer: B - Fetal beta cells hypertrophy in response to chronic maternal hyperglycemia. After delivery and separation from maternal glucose supply, continued fetal insulin secretion causes neonatal hypoglycemia. This is a direct and immediate postnatal risk.

(Creasy & Resnik's MFM; Rosen's Emergency Medicine)

• A) HbA1c only, at 5 years postpartum
• B) A 75g OGTT at 6-12 weeks postpartum, then periodically
• C) Fasting glucose only, at 1 year
• D) No follow-up is needed once GDM resolves
• E) Insulin tolerance testing

Answer: B - Women with GDM have a significantly elevated lifetime risk of Type 2 diabetes. Guidelines recommend a 75g 2-hour OGTT (not just fasting glucose or HbA1c) at 6-12 weeks postpartum, followed by periodic rescreening (every 1-3 years).

(Tietz Textbook of Laboratory Medicine 7e)

SECTION C: COMBINED / HIGH-YIELD SCENARIOS

• A) Oral atenolol
• B) Oral captopril
• C) IV labetalol or oral nifedipine
• D) Oral furosemide
• E) IM dexamethasone

Answer: C - This is preeclampsia with severe features in a diabetic pregnancy. Acute BP control uses IV labetalol or oral nifedipine. ACE inhibitors (captopril) are absolutely contraindicated. Atenolol has adverse fetal effects. Furosemide reduces placental perfusion. Steroids aid fetal lung maturity but do not treat BP.

(Harrison's 22e; Fuster & Hurst's The Heart 15e; Rosen's Emergency Medicine)

• A) BP rises above 160/110 mmHg at any gestational age
• B) New organ dysfunction features (as per preeclampsia criteria) develop after 20 weeks in a woman with known chronic hypertension
• C) Proteinuria first appears in the first trimester
• D) The woman requires more than two antihypertensives
• E) Platelet count falls below 200,000/μL

Answer: B - Superimposed preeclampsia = new development of preeclampsia features (organ dysfunction, uteroplacental dysfunction) after 20 weeks in a woman with pre-existing chronic hypertension. A rise in BP alone is not sufficient; new end-organ criteria must be met.

(Comprehensive Clinical Nephrology 7e)

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