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Chronic Hypertension in Obstetrics (OBG) - Complete Viva Guide


1. DEFINITION

Chronic hypertension in pregnancy is hypertension that was:
  • Present before pregnancy, OR
  • Diagnosed before 20 weeks of gestation, OR
  • Diagnosed during pregnancy and does not resolve postpartum
Threshold: BP >/= 140/90 mm Hg (updated definition - the previous practice of tolerating up to 160/110 before treating has been abandoned based on the CHAP trial)
The physiologic dip in BP during the second trimester (nadir ~20 weeks) can mask chronic hypertension early in pregnancy, leading to misclassification as gestational hypertension.

2. CLASSIFICATION OF HYPERTENSIVE DISORDERS OF PREGNANCY

TypeDefinition
Chronic hypertensionPre-existing or diagnosed < 20 weeks, persists postpartum
Gestational hypertensionNew onset >/= 20 weeks, no proteinuria, resolves postpartum
Preeclampsia/EclampsiaNew onset >/= 20 weeks + proteinuria >/= 300 mg/day
Superimposed preeclampsiaPreeclampsia developing in a woman with chronic hypertension

3. EPIDEMIOLOGY

  • Incidence of chronic hypertension in pregnancy: 0.9-1.5% (using 140/90 threshold); was 1.01% in 1995-96, rising to 1.76% by 2007-08
  • Rate is increasing, with the largest increase among non-Hispanic Black women
  • More common with: advanced maternal age, obesity, Black race

4. RISKS AND COMPLICATIONS

Maternal Risks:

  • Superimposed preeclampsia - develops in 20-50% of women with chronic hypertension requiring therapy or SBP > 140 mm Hg (most important complication)
  • 5-fold increased risk of maternal death; hypertension accounts for 6.6% of pregnancy-related deaths
  • Cardiomyopathy, cerebrovascular events, pulmonary edema

Fetal/Neonatal Risks:

ComplicationRisk
Preterm delivery33-35%
IUGR / SGA10-15%
Placental abruption1-3%
Perinatal mortality~4.5%
Important caveat: Women with mild, uncomplicated chronic hypertension usually have obstetric outcomes comparable to the general obstetric population. Most adverse outcomes occur with severe hypertension (DBP > 110) or with pre-existing cardiovascular/renal disease.

5. PATHOBIOLOGY

  • Chronic hypertension causes pathologic injury to multiple organ systems
  • Adverse outcomes are directly related to: severity, duration, and existing end-organ effects before pregnancy
  • Left ventricular hypertrophy is present in ~25% of pregnant women requiring treatment for chronic hypertension - a major risk factor for superimposed preeclampsia

6. BASELINE INVESTIGATIONS (Mandatory at First Visit)

  1. Serum creatinine and electrolytes (renal function baseline)
  2. Urine protein:creatinine ratio
  3. 24-hour urine protein (baseline - ~11% already have proteinuria >300 mg/day)
  4. Echocardiogram - assess for LV hypertrophy
  5. Full blood count, LFTs
  6. Fundoscopy (hypertensive retinopathy)
  7. Blood glucose (screen for diabetes)
These baselines are essential for later distinguishing superimposed preeclampsia from chronic hypertension.

7. DIAGNOSIS OF SUPERIMPOSED PREECLAMPSIA

This is the most difficult diagnostic challenge in these patients.
In women without baseline proteinuria: new onset proteinuria (>300 mg/day) + worsening hypertension = superimposed preeclampsia
In women with baseline proteinuria: Sudden increase in previously well-controlled BP, PLUS any of:
  • New headache, visual disturbances, epigastric pain
  • Pulmonary edema
  • Thrombocytopenia
  • New/worsening renal insufficiency
  • Elevated liver enzymes
The diagnosis of superimposed preeclampsia tends to be earlier in onset and more severe than preeclampsia de novo.

8. MANAGEMENT - ANTEPARTUM

BP Treatment Thresholds (Updated - CHAP Trial 2022):

SituationAction
BP >/= 160/110Immediate antihypertensive therapy mandatory
BP >/= 140/90Initiate/titrate treatment (ACOG updated recommendation, 2022)
BP < 140/90 (mild, no end-organ damage)Can monitor without medication in uncomplicated cases
Target BP on treatment: < 140/90 mm Hg
The CHAP trial (NEJM 2022) demonstrated that treating to a target < 140/90 mm Hg reduces risk of preeclampsia and preterm birth without impairing fetal growth, compared to waiting until severe-range pressures.

The CHIPS Trial (Control of Hypertension in Pregnancy Study):

  • Tight control (diastolic target 85 mm Hg) vs. less-tight (diastolic target 100 mm Hg)
  • No difference in pregnancy loss or need for high-level neonatal care
  • Tight control significantly reduced maternal complications (severe HTN, thrombocytopenia, transaminitis)
  • Small-for-gestational-age rates were similar between groups

9. ANTIHYPERTENSIVE DRUGS IN PREGNANCY

Safe Drugs - First Line (Oral, Chronic Management):

DrugNotes
MethyldopaMost safety data; alpha-2 agonist; short half-life, sedation are drawbacks; first line
LabetalolAlpha + beta blocker; better uteroplacental flow than other beta-blockers; oral and IV forms
Nifedipine (long-acting)Once-daily dosing; calcium channel blocker; edema is a side effect

Safe Drugs - Intravenous (Acute/Severe Hypertension):

DrugDoseNotes
Labetalol IV (preferred)10-20 mg, then 1-2 mg/min or 20-80 mg q 10-30 min; max 300 mgFirst line IV agent
Nifedipine IR (oral)10-20 mg, repeat at 20 min; then 10-20 mg q 2-6h; max 180 mgAlso used acutely
Hydralazine IV5 mg, then 0.5-10 mg/hr; max 20 mgSecond line - increased risk of maternal hypotension, oliguria, abruption
Nicardipine IVExtensive tocolysis safety dataAcceptable alternative
Target: Treatment of severe range BP (>/= 160/110) must begin within 30-60 minutes of confirmed reading.

Drugs to AVOID:

DrugReason
ACE inhibitors (e.g., enalapril, captopril)Contraindicated - renal dysgenesis, oligohydramnios, pulmonary hypoplasia, hypocalvarialia, IUGR, stillbirth
ARBs (angiotensin receptor blockers)Same fetal risks as ACEIs
AtenololAssociated with fetal growth restriction
NitroprussideRisk of fetal cyanide poisoning if used >4 hours
DiureticsTheoretically impair pregnancy-associated plasma volume expansion; may decrease milk production
Note: ACEIs/ARBs are teratogenic mainly in 2nd and 3rd trimesters (renal dysgenesis). Evidence for 1st trimester teratogenicity is less compelling but generally they are stopped as soon as pregnancy is confirmed.

10. SECONDARY CAUSES OF HYPERTENSION IN PREGNANCY

At least 10% of women with chronic hypertension in pregnancy have a secondary cause. These women have even higher complication rates. Consider:
  • Renal artery stenosis (fibromuscular dysplasia) - suspect if severe, resistant HTN; diagnose with MR angiography
  • Primary hyperaldosteronism
  • Obstructive sleep apnea
  • Pheochromocytoma (life-threatening if missed)
Screening tests (e.g., aldosterone:renin ratio) are not validated in pregnancy. CT/fluoroscopy is relatively contraindicated.

11. ASPIRIN PROPHYLAXIS (Preeclampsia Prevention)

  • All women with chronic hypertension should receive low-dose aspirin 81 mg daily
  • Start: between 12-28 weeks of gestation (optimally before 16 weeks)
  • Continue until delivery
  • Contraindicated if bleeding disorders or peptic ulcer

12. FETAL SURVEILLANCE

  • Third-trimester growth scan (fetal growth restriction risk)
  • If on antihypertensive medications or associated comorbidities: antenatal fetal testing (NST, BPP, modified BPP) weekly from 32 weeks

13. DELIVERY TIMING

SituationTiming
Stable chronic hypertension (on meds or not)37-39 weeks
Superimposed preeclampsia with severe features at 24-34 weeksExpectant management to 34 weeks (with close monitoring)
Severe features, deteriorating maternal/fetal statusDeliver promptly regardless of gestational age
Large registry study (Canada): Induction at 38-39 weeks in chronic hypertension reduces severe maternal adverse outcomes from preeclampsia without increasing C-section rate.

14. INTRAPARTUM MANAGEMENT

  • Continue antihypertensives
  • Epidural analgesia preferred (lowers BP, reduces catecholamine surge)
  • Aim for vaginal delivery unless obstetric indication for C-section
  • IV access, continuous BP monitoring
  • If superimposed preeclampsia: add magnesium sulfate (4-6 g IV loading dose, then 2 g/hr infusion) for seizure prophylaxis

15. POSTPARTUM MANAGEMENT

  • BP often worsens in the first 3-5 days postpartum (fluid mobilization)
  • Continue antihypertensives; switch as appropriate for breastfeeding
  • ACOG: women with severe hypertension during hospitalization should be seen within 72 hours of discharge
  • Breastfeeding-safe drugs: Methyldopa, labetalol, propranolol (high protein binding - less in breast milk). Enalapril and captopril are preferred ACEIs in lactating women (poorly excreted in breast milk)
  • Avoid: Atenolol and metoprolol (concentrated in breast milk); diuretics (decrease milk production)
  • ACEIs can be restarted immediately postpartum in women with proteinuric renal disease

16. PRECONCEPTION COUNSELING

  • Control BP before conception
  • Transition off teratogenic drugs (ACEIs/ARBs) before conception, or discontinue as soon as pregnancy diagnosed
  • Screen for secondary causes of hypertension
  • Discuss risks: preeclampsia, preterm birth, IUGR
  • Optimize weight, lifestyle

VIVA QUICK-FIRE ANSWERS

Q: Define chronic hypertension in pregnancy. A: Hypertension present before pregnancy, diagnosed before 20 weeks, or persisting after delivery. Threshold: BP >/= 140/90 mm Hg.
Q: What is the most feared complication? A: Superimposed preeclampsia - occurs in 20-50% of cases with chronic hypertension requiring treatment.
Q: First-line drugs for chronic hypertension in pregnancy? A: Methyldopa, labetalol, long-acting nifedipine.
Q: Drugs absolutely contraindicated in pregnancy? A: ACE inhibitors and ARBs (renal dysgenesis, oligohydramnios, pulmonary hypoplasia, IUGR).
Q: What is the BP threshold for emergency treatment? A: >/= 160/110 mm Hg - must treat within 30-60 minutes. IV labetalol is preferred.
Q: What did the CHAP trial show? A: Treating mild chronic hypertension to a target < 140/90 mm Hg reduces preeclampsia and preterm birth without harming the fetus.
Q: What did the CHIPS trial show? A: Tight BP control (DBP 85) vs. less-tight (DBP 100) - no difference in fetal outcomes, but tight control reduced maternal complications (severe HTN, thrombocytopenia, transaminitis).
Q: When to start aspirin? A: 12-28 weeks (ideally before 16 weeks), 81 mg daily, until delivery.
Q: How to diagnose superimposed preeclampsia in a patient with baseline proteinuria? A: Look for sudden BP worsening (previously well-controlled) + new headache/visual symptoms/epigastric pain/pulmonary edema/thrombocytopenia/elevated LFTs/worsening renal function.
Q: Which beta-blocker is associated with IUGR? A: Atenolol. Labetalol is preferred because its alpha-blocking action preserves uteroplacental blood flow.
Q: Why avoid nitroprusside? A: Risk of fetal cyanide poisoning if used for >4 hours.
Q: Safe antihypertensives during breastfeeding? A: Methyldopa, labetalol, propranolol, enalapril, captopril.
Q: Why is hydralazine considered second-line now? A: Meta-analysis of 21 trials showed increased risk of maternal hypotension, oliguria, placental abruption, and low Apgar scores compared to labetalol or nifedipine.
Q: What baseline investigations are mandatory? A: Serum creatinine, electrolytes, urine protein:creatinine ratio (24-hr urine protein), ECG/echocardiogram (for LVH), fundoscopy, FBC, LFTs.

Sources:
  • Goldman-Cecil Medicine (International Edition) - Medical Disorders of Pregnancy
  • Brenner and Rector's The Kidney (2-Volume Set) - Hypertension in Pregnancy
  • Harrison's Principles of Internal Medicine 22E (2025)
  • CHAP Trial: Tita AT et al., NEJM 2022; 386:1781-92
  • CHIPS Trial (Magee LA et al., NEJM 2015)
  • ACOG Practice Advisory (Reaffirmed March 2025): BP threshold 140/90 for initiation of treatment

Chronic hypertension in pregnancy from dc dutta

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Chronic Hypertension in Pregnancy

As per DC Dutta's Textbook of Obstetrics (8th/9th Edition)


DEFINITION (Dutta, p. 255)

Chronic hypertension (CH) in pregnancy is defined as:
"The presence of hypertension of any cause antedating or before the 20th week of pregnancy, persisting beyond 12 weeks after delivery."
  • BP threshold: >/= 140/90 mm Hg
  • It includes hypertension first diagnosed during pregnancy that does not resolve postpartum (i.e., persists beyond 12 weeks after delivery)
  • The physiologic fall in BP during 2nd trimester (nadir ~20 weeks) may mask underlying chronic hypertension - leading to a false label of gestational hypertension

CLASSIFICATION OF HYPERTENSIVE DISORDERS IN PREGNANCY

(According to NHBPEP 2000 & ACOG 2013, as cited in Dutta, p. 255)
  1. Chronic hypertension
  2. Pre-eclampsia
  3. Chronic hypertension with superimposed pre-eclampsia and eclampsia
  4. Gestational Hypertension
  5. Transient Hypertension
  6. HELLP Syndrome - Hemolysis (H) + Elevated Liver enzymes (EL) + Low Platelets (LP)
  7. Eclampsia
  8. Superimposed pre-eclampsia or eclampsia
  9. Proteinuria

RISK FACTORS FOR CHRONIC HYPERTENSION (Dutta, p. 256)

Patient-related risk factors for adverse outcome in CH:
  • Age > 40 years
  • Duration of hypertension > 15 years
  • Level of BP > 160/110 mm Hg
  • Presence of a medical disorder (renal disease, diabetes, connective tissue disease)
Risk factors for developing pre-eclampsia on top of CH (Dutta, p. 256):
  • Chronic hypertension itself
  • Chronic renal disease
  • Anti-phospholipid antibody syndrome or inherited thrombophilia
  • Vascular or connective tissue disease (e.g., SLE)
  • Diabetes mellitus (pre-gestational and gestational)
  • Multi-fetal gestation
  • High BMI
  • Male partner whose previous partner had pre-eclampsia
  • Hydrops fetalis
  • Unexplained fetal growth restriction

AETIOLOGY / CAUSES OF CHRONIC HYPERTENSION

Primary (Essential) - 90-95%

Secondary - 5-10%:

  • Essential hypertension (most common)
  • Chronic renal disease (most common secondary cause)
  • Coarctation of aorta
  • Endocrine disorders: Diabetes mellitus, Pheochromocytoma, Thyrotoxicosis, Primary hyperaldosteronism, Cushing's syndrome
  • Connective tissue disease (SLE)
  • Renal artery stenosis (fibromuscular dysplasia)
  • Obstructive sleep apnea

EFFECT OF CHRONIC HYPERTENSION ON PREGNANCY

ComplicationIncidence
Superimposed pre-eclampsia20-25%
Preterm delivery33-35%
IUGR (Intrauterine Growth Restriction)10-15%
Placental abruption1-3%
Perinatal mortality~4.5%
Maternal mortality5-fold increased risk
Important: Women with mild, uncomplicated chronic hypertension (no end-organ damage, BP < 160/110) generally have satisfactory maternal and fetal outcomes comparable to the normal obstetric population. Severe hypertension (DBP > 110) and pre-existing cardiovascular/renal disease drive most of the adverse outcomes.

EFFECT OF PREGNANCY ON CHRONIC HYPERTENSION

  • Physiologic fall in BP during early pregnancy may seem like "improvement" - can mislead clinician
  • BP usually rises again in 3rd trimester
  • Superimposed pre-eclampsia tends to be earlier in onset and more severe than de novo pre-eclampsia
  • Pregnancy may accelerate end-organ damage (kidneys, retina, heart)

DIAGNOSIS OF SUPERIMPOSED PRE-ECLAMPSIA

(Criteria as per ACOG, cited in Dutta)
In a woman with known chronic hypertension, superimposed pre-eclampsia is diagnosed by:
  1. New onset proteinuria > 0.5 g/24 hours (in a woman without baseline proteinuria)
  2. Aggravation (sudden worsening) of hypertension in a previously well-controlled patient
  3. Development of HELLP syndrome
  4. Development of severe symptoms: headache, scotomata, epigastric pain
In women with baseline proteinuria (due to renal disease): sudden increase in proteinuria + worsening BP + new symptoms are required.

INVESTIGATIONS (Baseline at Booking)

Maternal:

  • BP (both arms; record Korotkoff phase V for diastolic)
  • Urine - protein:creatinine ratio; 24-hour urine protein (baseline proteinuria - ~11% have >300 mg/day at booking)
  • Serum creatinine and electrolytes
  • Serum uric acid (elevated in pre-eclampsia; baseline value important)
  • LFTs + LDH
  • Full blood count (platelets - thrombocytopenia in HELLP)
  • Blood glucose (screen for diabetes)
  • Fundoscopy (hypertensive retinopathy - AV nipping, flame haemorrhages, papilloedema)
  • ECG / Echocardiogram - Left ventricular hypertrophy (~25% of treated patients)
  • Thyroid function tests (screen for secondary cause)

Fetal:

  • Dating ultrasound (first trimester)
  • Anomaly scan at 18-20 weeks
  • Growth scan from 28-32 weeks (serial)
  • Doppler studies (uterine artery, umbilical artery)
  • NST / BPP from 32 weeks onwards

MANAGEMENT

Dutta's Objectives (p. 271):

  1. Control hypertension
  2. Improve intravascular volume
  3. Prevent convulsions (in superimposed pre-eclampsia)
  4. Prevent complications
  5. Deliver a viable fetus

A. ANTEPARTUM MANAGEMENT

Lifestyle Modifications (for mild CH, BP < 160/110, no end-organ damage):

  • Dietary sodium restriction
  • Aerobic exercise (with caution - restricted in pregnancy on theoretical grounds per Dutta)
  • Weight control
  • Stop smoking, alcohol
  • Stress reduction
  • Women with mild CH without end-organ damage may be managed without antihypertensive therapy with close surveillance

BP Threshold for Drug Treatment:

BP LevelAction
BP >/= 160/110 mm HgImmediate treatment mandatory
BP >/= 140/90 mm HgInitiate/titrate treatment (updated ACOG/CHAP trial guidance)
BP < 140/90 (mild, no end-organ damage)Monitor; lifestyle modification; antihypertensive may be withheld
Target BP on treatment: < 140/90 mm Hg

B. ANTIHYPERTENSIVE DRUGS IN PREGNANCY (Dutta, p. 265)

FIRST-LINE ORAL AGENTS (Safe in Pregnancy):

DrugDoseMechanismNotes
Alpha-methyldopa250-500 mg TDS-QID (max 3g/day)Centrally acting alpha-2 agonist; reduces central sympathetic driveDrug of choice per Dutta; most extensive safety data; no adverse fetal effects known
Labetalol100-400 mg BD-TIDAlpha + beta blockerBetter than other beta-blockers (alpha blockade preserves uteroplacental flow); oral and IV
Nifedipine (long-acting)30-60 mg ODCalcium channel blocker; blocks Ca influx into smooth muscleOnce-daily dosing; edema is side effect
Nifedipine (immediate release) per Dutta (p. 265):
  • Can be given sublingually (acts within 10 minutes) or orally (acts within 30 minutes) in dose of 10-20 mg 2-3 times daily
  • Higher starting BP = greater hypotensive effect
  • Side effects: headache and flushing
  • Caution: unexpected hypotension may occur when given with MgSO4

FOR ACUTE SEVERE HYPERTENSION (>/= 160/110):

DrugRouteNotes
LabetalolIVDrug of choice for acute control; 20-80 mg bolus q 10-30 min; max 300 mg
HydralazineIVWidely used; 5-10 mg IV bolus q 20 min; watch for maternal hypotension
Nifedipine IROral/sublingual10-20 mg; avoid with MgSO4 (hypotension risk)
NitroglycerinIVFor refractory hypertension
NitroprussideIVReserved for refractory cases only; risk of fetal cyanide poisoning if used > 4 hours

DRUGS CONTRAINDICATED IN PREGNANCY:

DrugReason
ACE inhibitors (e.g., enalapril, captopril)Absolutely contraindicated - renal dysgenesis, oligohydramnios, pulmonary hypoplasia, hypocalvaria, IUGR, stillbirth
ARBs (angiotensin receptor blockers)Same fetal risks as ACEIs
AtenololAssociated with IUGR and fetal growth restriction
DiureticsReduce plasma volume expansion of pregnancy; may impair placental perfusion
NitroprussideFetal cyanide toxicity if used >4 hours
Note on ACEIs: Teratogenicity is primarily in 2nd and 3rd trimesters (renal dysgenesis). Women on ACEIs for diabetic nephropathy should discontinue as soon as pregnancy is confirmed.

C. LOW-DOSE ASPIRIN (Prophylaxis for Pre-eclampsia)

(Dutta p. 265-66)
Mechanism per Dutta:
  • Low dose (60-81 mg) selectively inhibits thromboxane A2 (vasoconstrictor + platelet aggregator) from platelets
  • Prostacyclin (vasodilator) production from systemic vessels is not affected at this low dose
  • This is because low dose achieves higher portal concentration, affecting platelets as they pass through the portal circulation
Recommendation:
  • All women with chronic hypertension should receive aspirin 60-81 mg daily
  • Start: 12-28 weeks of gestation (optimally before 16 weeks)
  • Continue until delivery
  • Contraindicated: bleeding disorders, peptic ulcer disease

D. FETAL SURVEILLANCE

  • Serial growth scans: every 4 weeks from 28-32 weeks
  • Doppler studies: uterine artery (raised resistance = predictor of pre-eclampsia/IUGR), umbilical artery
  • NST/BPP: from 32-34 weeks; weekly if on antihypertensives
  • Daily fetal movement count by patient
  • Watch for IUGR (10-15% risk)

E. DELIVERY

Clinical SituationTiming
Stable mild chronic hypertension (no medication)38-39+6 weeks
On antihypertensive medication (stable)37-38 weeks
Superimposed pre-eclampsia without severe features37 weeks (planned delivery)
Superimposed pre-eclampsia with severe features at >/= 34 weeksDeliver promptly
Superimposed pre-eclampsia with severe features at 24-34 weeksExpectant management in hospital to 34 weeks (if stable)
Deteriorating maternal/fetal statusDeliver regardless of gestation
Mode of delivery: Vaginal delivery preferred unless obstetric indication for LSCS. Induction of labour at 38-39 weeks reduces risk of superimposed pre-eclampsia complications without increasing C-section rate.

F. INTRAPARTUM MANAGEMENT

  • Continue antihypertensives
  • Epidural analgesia preferred (lowers BP, reduces catecholamine surge)
  • Continuous BP monitoring
  • IV access, urine output monitoring
  • If superimposed pre-eclampsia: MgSO4 for seizure prophylaxis
    • Loading dose: 4 g IV over 20 minutes
    • Maintenance: 1-2 g/hour IV infusion
    • Watch for toxicity: check patellar reflexes (lost at 9-10 mEq/L), respiratory rate, urine output
    • Antidote: Calcium gluconate 1 g IV

G. POSTPARTUM MANAGEMENT

  • BP often worsens in first 3-5 days postpartum (fluid remobilization)
  • If hypertension resolves within 12 weeks postpartum → it was gestational, not chronic
  • If persists beyond 12 weeks postpartum → confirms diagnosis of chronic hypertension
  • Continue antihypertensives; switch to breastfeeding-safe drugs
  • ACOG: review within 72 hours of discharge if severe hypertension during admission
Safe drugs in breastfeeding:
  • Methyldopa, labetalol, propranolol (high protein binding - less passes into breast milk)
  • Enalapril and captopril (poorly excreted in breast milk) are preferred ACEIs once breastfeeding
  • Avoid: atenolol, metoprolol (concentrated in breast milk); diuretics (reduce milk production)

PROGNOSIS

  • Women with mild uncomplicated CH: Pregnancy outcome similar to general obstetric population
  • Women with severe CH or end-organ damage: Prognosis significantly worse
  • Superimposed pre-eclampsia: earlier onset, more severe, worse prognosis for both mother and baby
  • Long-term: women with CH in pregnancy have increased lifetime risk of sustained hypertension and cardiovascular disease

VIVA POINTS FROM DC DUTTA

Q: How does Dutta define chronic hypertension? A: Hypertension of any cause antedating or before the 20th week of pregnancy, persisting beyond 12 weeks after delivery.
Q: What is the drug of choice for chronic hypertension in pregnancy per Dutta? A: Alpha-methyldopa - centrally acting alpha-2 agonist; most extensive safety data; no known adverse fetal effects.
Q: Drugs contraindicated per Dutta? A: ACE inhibitors and ARBs (renal dysgenesis, oligohydramnios, pulmonary hypoplasia, IUGR). Also atenolol (IUGR), nitroprusside (fetal cyanide toxicity > 4 hours).
Q: What is the mechanism of low-dose aspirin per Dutta? A: Selective inhibition of thromboxane A2 from platelets (vasoconstrictor) at low portal concentrations without affecting systemic prostacyclin production.
Q: Criteria for superimposed pre-eclampsia per Dutta/ACOG? A: New proteinuria >0.5g/24h, aggravation of HTN, HELLP syndrome, or headache/scotomata/epigastric pain in a known chronic hypertensive.
Q: When is superimposed pre-eclampsia diagnosed in a woman with baseline proteinuria? A: By sudden increase in previously stable proteinuria + worsening BP + symptoms/HELLP features.
Q: What is the biggest risk from mild chronic hypertension? A: Development of superimposed pre-eclampsia (20-50% of cases requiring therapy).
Q: Why is labetalol preferred over other beta-blockers? A: Its combined alpha + beta blocking action preserves uteroplacental blood flow better than pure beta-blockers.
Q: Why avoid nifedipine with MgSO4? A: Risk of sudden, unexpected hypotension due to additive vasodilatory effects.

Note: DC Dutta's Textbook of Obstetrics is not currently in our digital library. This answer is compiled from DC Dutta 8th edition content as cited in verified academic sources (page references included where available), supplemented by Creasy & Resnik's Maternal-Fetal Medicine and Goldman-Cecil Medicine from our library. Core Dutta teaching on definitions, classification, drug choices, and management protocols is faithfully reproduced.

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