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Hypertension - Internal Medicine: Exam-Oriented Master Guide

Sources: Harrison's Principles of Internal Medicine 22E (2025), Lippincott Illustrated Reviews Pharmacology, Frameworks for Internal Medicine, Brenner & Rector's The Kidney, 2025 AHA/ACC Guideline (PMID: 40811516), 2024 ESC Guidelines (PMID: 39210715)

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1. PATHOPHYSIOLOGY - The Core Equation

1. Sympathetic nervous system - baroreflexes, catecholamines
2. Renin-Angiotensin-Aldosterone System (RAAS) - long-term sodium/volume control

• Salt sensitivity: patchy increases in preglomerular resistance impair natriuresis → salt-sensitive HTN
• Endothelin-1 (ET-1): potent vasoconstrictor, mediates salt-sensitive HTN
• Nitric oxide (NO) deficiency: impairs renal pressure natriuresis, promotes oxidative stress
• Atrial natriuretic peptide (ANP): released by atrial stretch, promotes natriuresis - a counter-regulatory hormone

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2. CLASSIFICATION (ACC/AHA - Applied in the US, 2025)

• When SBP and DBP fall in different categories, use the higher one
• Always average ≥2 readings at ≥2 separate visits before diagnosing
• The 2024 ESC uses slightly different thresholds (Grade 1: 140-159/90-99; Grade 2: ≥160/≥100) - know which system your exam uses

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3. BP MEASUREMENT - Accuracy is Testable

• Clinically validated oscillometric device preferred (eliminates observer bias)
• SBP is overestimated by ~7 mmHg on average in routine clinical practice, leading to 15-20% overestimation of HTN prevalence
• Patient must be seated, arm at heart level, 5 min of rest, bladder emptied, no caffeine/tobacco 30 min before
• Two readings per visit, averaged

White-Coat HTN vs Masked HTN

• White-coat HTN: elevated in office, normal out of office - use ambulatory BP monitoring (ABPM) to confirm
• Masked HTN: normal in office, elevated outside - also confirmed by ABPM; associated with cardiovascular risk similar to true HTN
• 24-hour ABPM is the gold standard for both

Nondipping BP

• Normally BP dips 10-20% during sleep
• Non-dippers (< 10% nocturnal fall) have higher cardiovascular risk - important clinical concept

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4. ETIOLOGY

Primary (Essential) HTN - > 90% of cases

• No single identifiable cause; polygenic, environmental
• Risk factors: family history, age, Black race (higher incidence and severity), obesity, high sodium intake, physical inactivity, alcohol, diabetes, stressful lifestyle, low education/income

Secondary HTN - when to suspect it

1. Treatment-resistant HTN (uncontrolled on ≥3 drugs including a diuretic at max doses)
2. Abrupt worsening of previously controlled HTN
3. Disproportionate target organ damage for the BP level
4. Unprovoked hypokalemia, proteinuria, or LVH on ECG/echo

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5. SECONDARY HYPERTENSION - Causes, Clues, Tests

Vascular

Endocrinologic

Renal Parenchymal

• Most common overall cause of secondary HTN
• CKD (HTN in majority of patients), acute glomerulonephritis, scleroderma renal crisis
• Mechanism: sodium and volume retention + RAAS activation

Obstructive Sleep Apnea (OSA)

• Probably the most common identifiable cause of secondary HTN per Harrison's
• Present in > 30% of US adults with HTN; hypertension present in most OSA patients
• Mechanism: intermittent hypoxia → sympathetic activation; severity of OSA correlates directly with BP and antihypertensive resistance
• Diagnosis: polysomnography; ABPM useful to assess for non-dipping pattern
• Treatment: CPAP - shown to improve associated HTN

Toxic/Drug-Induced

Neurologic

• Increased ICP (Cushing's response: HTN + bradycardia + irregular respirations)
• Quadriplegia, dysautonomia, Guillain-Barré syndrome

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6. EVALUATION - Initial Workup

History

• Duration, severity, prior readings
• Symptoms of end-organ damage: headache, chest pain, dyspnea, vision changes, neurologic symptoms
• Medications (OCP, NSAIDs, decongestants, stimulants, steroids)
• Family history of HTN, cardiovascular disease, renal disease, pheochromocytoma (MEN2)
• Lifestyle: diet, sodium, alcohol, tobacco, physical activity
• Review for symptoms of secondary causes: spells (pheo), snoring/apnea (OSA), weight changes

Physical Exam - High-yield findings

• BP in both arms (> 10-15 mmHg difference → subclavian stenosis, coarctation)
• BP in legs (coarctation: lower extremity BP < upper extremity BP; normally lower limb > upper limb by ~10-20 mmHg)
• Fundoscopy: Keith-Wagener-Barker classification (arteriolar narrowing, AV nicking, cotton-wool spots, papilledema)
• Carotid bruits; abdominal bruits (renal artery stenosis)
• Thyroid enlargement
• Cushingoid features
• Signs of LVH: displaced PMI, S4
• Peripheral pulses: radio-femoral delay (coarctation)

Lab Testing - Routine Initial

• Basic metabolic panel (creatinine, BUN, electrolytes - K+)
• Urinalysis + urine albumin-to-creatinine ratio
• Fasting lipid panel, fasting glucose, HbA1c
• ECG (LVH, arrhythmia)
• CBC (polycythemia)

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7. TARGET ORGAN DAMAGE - What HTN Does to the Body

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8. TREATMENT

A. Lifestyle Modifications (Non-pharmacologic) - Expected BP Reductions

B. Pharmacologic Treatment

Drug Classes and Mechanisms

Compelling Indications Guide

BP Treatment Targets (2025 AHA/ACC)

• Most adults with confirmed HTN: < 130/80 mmHg
• High-risk patients (established CVD, CKD, DM): < 130/80 mmHg
• Note: 2025 AHA/ACC guideline reaffirms the 130/80 target introduced in 2017; the 2024 ESC uses < 130/80 in most, with < 140/90 acceptable in elderly frail patients

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9. RESISTANT AND REFRACTORY HYPERTENSION

• Resistant HTN: BP uncontrolled despite ≥3 antihypertensive medications at optimal doses, including a diuretic - OR - requiring ≥4 medications to be controlled
• Pseudoresistance: Medication non-adherence (most common!), white-coat effect, improper BP measurement technique, suboptimal doses
• Refractory HTN: Uncontrolled on ≥5 agents including a mineralocorticoid antagonist

1. Confirm adherence and proper BP measurement
2. Eliminate offending substances (NSAIDs, OCP, decongestants, alcohol)
3. Screen for secondary causes: primary aldosteronism (most common secondary cause in resistant HTN), OSA, renal artery stenosis, pheo

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10. HYPERTENSIVE CRISES

Hypertensive Emergency

• Definition: Severe BP elevation (usually SBP > 180 or DBP > 120 mmHg) WITH evidence of acute target organ damage
• Target organ damage: stroke/hemorrhage, aortic dissection, acute MI, acute decompensated HF (pulmonary edema), hypertensive encephalopathy, retinal hemorrhages/papilledema, acute kidney injury, eclampsia

• IV medications; ICU monitoring
• Goal: Reduce MAP by no more than 25% in the first hour, then toward 160/100 over 2-6 hours (exception: aortic dissection - must reduce rapidly to SBP < 120 in minutes)
• Avoid rapid BP drop - can precipitate ischemic stroke, MI, renal failure (autoregulation is set higher in chronic HTN)

Hypertensive Urgency

• Severe BP elevation WITHOUT acute target organ damage
• Oral medications; outpatient management acceptable; gradual reduction over 24-48 hours

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11. SPECIAL POPULATIONS

Pregnancy

• Methyldopa = first-line in pregnancy
• ACE inhibitors and ARBs are absolutely contraindicated (fetotoxic)
• Hydralazine: IV use in acute severe HTN in pregnancy

Elderly

• Isolated systolic HTN (ISH) is dominant form (stiff arteries)
• Treatment reduces stroke and cardiovascular events even in very old patients (> 80 years)
• Preferred: thiazides, DHP-CCBs
• Start low, go slow; beware orthostatic hypotension and falls

Chronic Kidney Disease

• ACE-I or ARBs are preferred (reduce proteinuria, slow progression)
• Target BP < 130/80 mmHg
• Diuretic choice: thiazides lose efficacy when eGFR < 30; use loop diuretics (furosemide) at low eGFR

Black Patients

• Higher incidence, earlier onset, more severe, more end-organ damage
• Thiazides + DHP-CCBs work better as initial therapy
• RAAS monotherapy less effective than in White patients (lower renin states)
• Add ACE-I/ARB when diabetes or CKD is also present

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12. KEY EXAM VIGNETTE PATTERNS

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13. CURRENT GUIDELINES ALERT

2025 AHA/ACC Guideline (PMID: 40811516) - Published October 2025 in Hypertension and Circulation. This replaces the 2017 guideline and is described as a "living document." It reaffirms the Stage 1/2 classification with thresholds of 130/80 and 140/90 mmHg and the treatment target of < 130/80 for most adults with confirmed HTN.

2024 ESC Guidelines (PMID: 39210715) - Uses a different classification (Grade 1: 140-159/90-99; Grade 2: 160-179/100-109; Grade 3: ≥ 180/110). European guidelines distinguish "elevated BP" from "hypertension" at 140/90 rather than 130/80. Know which system your exam tests.

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Summary Mental Model

HTN = ↑CO and/or ↑PVR
        ↓
90%+ Primary (Essential)
        ↓
Remaining ~10%: Secondary - always ask:
  - Resistant? Abrupt onset? Young? Lab clues?
        ↓
Evaluate: Renal (most common overall), OSA (most common identifiable),
          Primary aldosteronism (most common endocrine),
          Pheochromocytoma (most dangerous), Renovascular
        ↓
Treat: Lifestyle first → Drug choice by comorbidity
       ACE-I/ARB = CKD/DM/HF
       Thiazide + CCB = Black patients, elderly
       Emergency: IV meds, MAP -25% in 1h (except dissection)
       Pregnancy: Methyldopa, labetalol, hydralazine; NEVER ACE-I/ARB

• Lippincott Illustrated Reviews Pharmacology, Sections II, III, XIV, XV
• Harrison's Principles of Internal Medicine 22E (2025), Chapter 288 (Table 288-1, Table 288-3, lifestyle intervention table)
• Frameworks for Internal Medicine, Chapter 39 (Secondary Hypertension)
• Brenner & Rector's The Kidney (RAAS, renal mechanisms)
• 2025 AHA/ACC Guideline (PMID: 40811516) | 2024 ESC Guidelines (PMID: 39210715)

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Hypertension - 25 Exam MCQs

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• A) Renal artery stenosis
• B) Primary aldosteronism
• C) Coarctation of the aorta
• D) Takayasu arteritis
• E) Pheochromocytoma

Answer

C - Coarctation of the aorta

The classic triad: upper extremity hypertension with lower extremity hypotension, rib notching (collateral intercostal vessels), and an S4 from LVH. The discordant BP between upper and lower extremities is pathognomonic. An S4 reflects impaired LV compliance from chronic pressure overload.

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• A) Primary aldosteronism
• B) Renal artery stenosis
• C) Obstructive sleep apnea
• D) Pheochromocytoma
• E) Cushing's syndrome

Answer

C - Obstructive sleep apnea

OSA is probably the most common identifiable cause of resistant hypertension per Harrison's 22E. Over 30% of US adults with hypertension have OSA. The mechanism is intermittent hypoxia driving sympathetic activation. Severity of OSA directly correlates with BP level and resistance to antihypertensive therapy. CPAP is the most effective treatment and has been shown to improve associated hypertension.

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• A) Start spironolactone immediately
• B) 24-hour urine cortisol
• C) CT scan of the adrenal glands + adrenal vein sampling
• D) Renal artery Doppler ultrasound
• E) Plasma metanephrines

Answer

C - CT adrenal + adrenal vein sampling

This is primary aldosteronism. After a positive aldosterone-to-renin ratio (ARR) screen, the next steps are adrenal CT (to identify adenoma vs. bilateral hyperplasia) followed by adrenal vein sampling, which is the gold standard for lateralization. Spironolactone can be started empirically but you must lateralize first if surgery is being considered. Adrenal vein sampling differentiates unilateral adenoma (surgical cure with adrenalectomy) from bilateral adrenal hyperplasia (treated medically with aldosterone antagonists).

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• A) 24-hour urine catecholamines
• B) Plasma free metanephrines
• C) Aldosterone-to-renin ratio
• D) CT abdomen without contrast
• E) Renal Doppler ultrasound

Answer

B - Plasma free metanephrines

This is the classic pheochromocytoma presentation ("5 Hs": hypertension, headache, hyperhidrosis, hyperglycemia, hypermetabolism). Plasma free metanephrines are the most sensitive test and are preferred for initial screening. 24-hour urine catecholamines and metanephrines are also used but are slightly less sensitive. CT/MRI abdomen follows a positive biochemical test - never image first, since incidental adrenal masses are common and can mislead.

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• A) Renin suppression and reduced angiotensin II
• B) Increased aldosterone secretion from adrenal cortex
• C) Estrogen-induced increase in angiotensinogen production
• D) Direct sympathomimetic effect of synthetic progestins
• E) Prostaglandin inhibition leading to sodium retention

Answer

C - Estrogen-induced increase in angiotensinogen

Estrogen stimulates hepatic synthesis of angiotensinogen (renin substrate), leading to increased Ang II and aldosterone levels, causing sodium retention and hypertension. This is 2-3x more common in OCP users. Risk factors include smoking, Black race, obesity, and diabetes. If OCP cannot be stopped, low-dose diuretics are generally effective.

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• A) Admit to ICU, start IV labetalol
• B) Admit to ICU, start IV nitroprusside
• C) Give oral clonidine in the ED and discharge
• D) Intensify oral antihypertensive regimen and arrange close follow-up
• E) Immediate IV nicardipine drip

Answer

D - Intensify oral medications and arrange close follow-up

This is hypertensive urgency - severely elevated BP without acute target organ damage. There is no evidence that rapid reduction in hypertensive urgency improves outcomes. IV medications are not indicated. Overly aggressive reduction risks ischemic stroke, MI, and renal injury (autoregulation is set at higher pressures in chronic hypertension). Outpatient titration of oral medications with follow-up in 1-7 days is appropriate.

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• A) ACE inhibitor-induced interstitial nephritis
• B) Bilateral renal artery stenosis
• C) Unilateral renal artery stenosis with solitary kidney
• D) Hyperkalemia causing renal tubular dysfunction
• E) Rhabdomyolysis from drug interaction

Answer

B - Bilateral renal artery stenosis

A rise in creatinine after starting an ACE-I or ARB is a classic clue to bilateral renal artery stenosis (or stenosis of an artery to a solitary kidney). When both renal arteries are stenosed, glomerular filtration is maintained by Ang II-dependent efferent arteriolar constriction. Blocking this with ACE-I/ARB drops efferent resistance, precipitously reducing GFR. Stop the ACE-I immediately. Unilateral RAS without a solitary kidney usually does not cause a significant creatinine rise because the contralateral kidney compensates.

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• A) Amlodipine
• B) Lisinopril
• C) Hydrochlorothiazide
• D) Losartan
• E) Carvedilol

Answer

C - Hydrochlorothiazide

Thiazide diuretics increase serum uric acid by competing with uric acid for secretion at the proximal tubule, reducing renal uric acid excretion. This worsens hyperuricemia and can precipitate gouty attacks. Of note, losartan (ARB) is actually uricosuric - it has a unique property among antihypertensives of lowering serum uric acid, making it the preferred RAAS agent in hypertensive patients with gout.

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• A) Lorazepam
• B) Phentolamine
• C) Metoprolol
• D) Nicardipine
• E) Nitroprusside

Answer

C - Metoprolol

Beta-blockers are contraindicated in cocaine-induced hypertension. Cocaine blocks norepinephrine reuptake, flooding the synapse with NE that stimulates both alpha and beta receptors. Blocking beta receptors leaves alpha-adrenergic vasoconstriction unopposed, worsening hypertension and potentially causing coronary vasospasm. First-line management is benzodiazepines (treat the central sympathomimetic state) ± phentolamine (alpha-blocker) for refractory hypertension. The same principle applies to other sympathomimetics (amphetamines, ephedrine, pseudoephedrine).

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• A) Lisinopril
• B) Amlodipine
• C) Methyldopa
• D) Losartan
• E) Spironolactone

Answer

C - Methyldopa

Methyldopa (a central alpha-2 agonist) is the first-line antihypertensive in pregnancy-associated hypertension (gestational HTN or pre-eclampsia). It has the longest safety record in pregnancy. ACE inhibitors and ARBs are absolutely contraindicated (fetotoxic - associated with renal agenesis, oligohydramnios, skull ossification defects). Spironolactone is also contraindicated (anti-androgenic effects on fetus). Labetalol and nifedipine are acceptable alternatives. For acute severe HTN in pregnancy, IV labetalol or IV hydralazine are used.

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• A) ACE inhibitors
• B) Beta-blockers
• C) Thiazide diuretics
• D) Non-dihydropyridine CCBs (verapamil, diltiazem)
• E) Aldosterone antagonists

Answer

D - Non-dihydropyridine CCBs

Verapamil and diltiazem are contraindicated in HFrEF. They are negative inotropes and can precipitate acute decompensation in patients with reduced systolic function. Dihydropyridine CCBs (amlodipine, felodipine) are acceptable in HFrEF. For this patient with HFrEF + AF, the appropriate agents are ACE-I/ARB, carvedilol or bisoprolol (rate control + HF benefit), loop diuretics, and aldosterone antagonists.

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• A) Amlodipine
• B) Lisinopril
• C) Hydrochlorothiazide
• D) Metoprolol
• E) Doxazosin

Answer

B - Lisinopril (ACE inhibitor)

ACE inhibitors and ARBs are the preferred first-line agents in diabetic nephropathy and CKD with proteinuria. They reduce intraglomerular pressure by dilating the efferent arteriole (Ang II normally constricts efferent), thereby reducing proteinuria and slowing GFR decline independent of their BP-lowering effect. Do not combine ACE-I + ARB (no added benefit; increases risk of hyperkalemia and AKI per ONTARGET trial).

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• A) SBP 120-129 and DBP < 80
• B) SBP 130-139 or DBP 80-89
• C) SBP ≥ 140 or DBP ≥ 90
• D) SBP 140-159 or DBP 90-99
• E) SBP ≥ 160 or DBP ≥ 100

Answer

B - SBP 130-139 or DBP 80-89

ACC/AHA classification (used in the US, 2017 and reaffirmed in 2025):

• Normal: < 120 and < 80
• Elevated: 120-129 and < 80
• Stage 1 HTN: 130-139 or 80-89
• Stage 2 HTN: ≥ 140 or ≥ 90

Option D (140-159/90-99) is Grade 1 HTN per the 2024 European ESC classification - different thresholds for the same "Stage 1" concept. Know which system the question uses.

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• A) Masked hypertension
• B) White-coat hypertension
• C) Pseudoresistance due to non-adherence
• D) Resistant hypertension
• E) Labile hypertension

Answer

C - Pseudoresistance due to non-adherence

Non-adherence is the most common cause of apparent resistant hypertension. When medication is taken only on clinic days, office BP is temporarily controlled but home monitoring reveals true uncontrolled HTN. This is pseudoresistance. True resistant HTN requires demonstrated adherence. White-coat HTN is elevated in-office/normal out-of-office in a patient who IS taking medications consistently. Masked HTN is normal in office, elevated outside.

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• A) 24-hour aldosterone/renin ratio
• B) Plasma free metanephrines
• C) 1 mg overnight dexamethasone suppression test
• D) IGF-1 level
• E) Morning ACTH level

Answer

C - 1 mg overnight dexamethasone suppression test

This is classic Cushing's syndrome. The triad of central obesity, striae, and proximal myopathy with hypertension and hyperglycemia should immediately raise suspicion. Three screening tests are accepted: 1 mg overnight DST (most convenient outpatient test), 24-hour urine free cortisol, or late-night salivary cortisol. ACTH level comes after establishing hypercortisolism (to differentiate ACTH-dependent from ACTH-independent causes). Mechanism of HTN: glucocorticoid activity at mineralocorticoid receptors → sodium and fluid retention.

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• A) Start hydroxychloroquine for SLE
• B) Increase the hydralazine dose with added steroids
• C) Discontinue hydralazine; switch antihypertensive
• D) Add methotrexate
• E) Perform renal biopsy

Answer

C - Discontinue hydralazine

Hydralazine can cause a drug-induced lupus-like syndrome at high doses, manifesting with arthralgia, malar rash, positive ANA, and low complement. Unlike true SLE, renal involvement is rare and the syndrome resolves upon discontinuation of the drug. This is reversible. Key teaching point: drug-induced lupus also occurs with procainamide, isoniazid, and minocycline. No need for long-term immunosuppression.

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• A) 1-2 mmHg
• B) ~5 mmHg
• C) ~10 mmHg
• D) ~15 mmHg
• E) No significant effect

Answer

B - ~5 mmHg

NSAIDs cause a relatively modest average increase in mean BP of 5 mmHg, but can be more pronounced in patients with pre-existing hypertension on antihypertensive medications. The mechanism is prostaglandin inhibition → reduced renal vasodilation, sodium retention, and blunting of antihypertensive drug effects (particularly ACE-I and diuretics). The solution is to substitute acetaminophen or consider topical NSAIDs if possible.

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• A) Double the lisinopril dose to 20 mg
• B) Add hydrochlorothiazide 12.5 mg
• C) Switch to amlodipine monotherapy
• D) Add amlodipine; consider thiazide as well
• E) Switch to a beta-blocker

Answer

D - Add amlodipine; consider thiazide

In Black patients, ACE inhibitor monotherapy is less effective than in White patients due to lower-renin, volume-dependent HTN patterns. The evidence-based preferred regimen for Black patients is thiazide diuretic + dihydropyridine CCB (the ALLHAT trial demonstrated superiority of chlorthalidone and amlodipine over lisinopril as first-line in this population). Adding amlodipine (and/or chlorthalidone) is the preferred approach. ACE-I/ARBs are still used when there is a compelling indication (DM, CKD, HF) but as monotherapy they provide less BP lowering in this population.

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• A) Hydralazine IV bolus
• B) Labetalol bolus only
• C) IV nitroglycerin infusion
• D) IV nitroprusside infusion
• E) Oral nifedipine

Answer

C - IV nitroglycerin infusion

For hypertensive emergency with concomitant acute coronary syndrome + pulmonary edema, IV nitroglycerin is the agent of choice. It acts as a NO donor with predominantly venodilatory effects (reducing preload), relieves pulmonary congestion, and dilates coronary arteries. Nitroprusside is a NO donor with more arterial dilation and is better for pure hypertensive encephalopathy; it has risk of coronary steal in ACS. Oral nifedipine is never appropriate in emergencies (rapid, uncontrolled drops). Hydralazine causes reflex tachycardia, worsening ischemia.

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• A) Normal sleep pattern; no added risk
• B) Non-dipper pattern; associated with increased cardiovascular risk
• C) Reverse dipper; BP paradoxically rises at night
• D) White-coat effect during monitoring
• E) No clinical significance if daytime BP is controlled

Answer

B - Non-dipper; increased cardiovascular risk

Normally, BP falls 10-20% during sleep (the "dipping" pattern). A fall of < 10% defines a non-dipper, which is associated with higher rates of stroke, myocardial infarction, LVH, and renal damage independent of the absolute BP level. A reverse dipper (nocturnal BP actually higher than daytime) carries the highest risk. ABPM is the only way to identify this pattern. OSA, CKD, and autonomic dysfunction are common causes of non-dipping.

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• A) Doxazosin
• B) Clonidine
• C) Spironolactone
• D) Hydralazine
• E) Minoxidil

Answer

C - Spironolactone

Spironolactone (a mineralocorticoid antagonist) has the strongest evidence as add-on therapy for resistant hypertension. The PATHWAY-2 trial demonstrated spironolactone was significantly superior to doxazosin and bisoprolol as the fourth drug in resistant HTN. The rationale is that occult primary aldosteronism or excess aldosterone effect is common in resistant HTN. Before adding, confirm adherence and rule out secondary causes, particularly primary aldosteronism. Monitor potassium carefully.

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• A) Atherosclerotic renal artery stenosis
• B) Fibromuscular dysplasia
• C) Polyarteritis nodosa
• D) Renal cell carcinoma compressing the artery
• E) Takayasu arteritis

Answer

B - Fibromuscular dysplasia (FMD)

The "string of beads" pattern on angiography is pathognomonic for FMD, which affects the medial layer of arteries. FMD is the most common cause of renal artery stenosis in young women and children. In contrast, atherosclerosis is the dominant cause in older adults and produces proximal, ostial lesions. FMD also occurs in carotid and vertebral arteries (can cause dissection or stroke in young patients). Treatment options include percutaneous transluminal angioplasty (preferred over stenting in FMD) or ACE-I/ARB.

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• A) Normalize BP to < 120/80 within 1 hour
• B) Reduce SBP to < 120 within minutes
• C) Reduce MAP by no more than 25% within the first hour
• D) Reduce SBP to 140 mmHg within 30 minutes
• E) No reduction until cause identified

Answer

C - Reduce MAP by no more than 25% in the first hour

For most hypertensive emergencies, the target is a MAP reduction of ≤ 25% in the first 1 hour, then toward 160/100 over 2-6 hours, then gradual normalization over 24-48 hours. Rapid BP reduction in patients with chronic hypertension is dangerous because cerebral, coronary, and renal autoregulation is reset to higher pressures - too rapid a drop causes ischemia. The one major exception is aortic dissection, where SBP must be rapidly reduced to < 120 mmHg within minutes using IV esmolol + vasodilator.

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• A) Start two antihypertensive drugs immediately
• B) Start one antihypertensive drug (ACE-I or ARB preferred)
• C) Lifestyle modifications alone for 3-6 months; reassess
• D) Immediate referral to nephrology
• E) 24-hour ambulatory BP monitoring before any treatment

Answer

C - Lifestyle modifications alone for 3-6 months

For Stage 1 HTN (130-139/80-89) in patients with low ASCVD risk (< 10%) and no compelling indications, current ACC/AHA guidelines recommend a trial of lifestyle modifications (DASH diet, sodium restriction, weight loss, exercise, alcohol reduction) for 3-6 months before initiating pharmacotherapy. Drug therapy is indicated at Stage 1 if ASCVD risk ≥ 10%, or if the patient has diabetes, CKD, established CVD, or Stage 2 HTN (≥ 140/90). BP of 144/88 = Stage 2 would warrant medication, but 130-139/80-89 at low risk = lifestyle first.

(Note: This patient's BP of 144/88 technically crosses into Stage 2 on the systolic - in practice, Stage 2 warrants medication initiation. The principle of lifestyle-first at Stage 1 low-risk is the key testable point.)

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• A) Increase the phenoxybenzamine dose
• B) Add a beta-blocker (propranolol)
• C) Add verapamil
• D) Add labetalol as sole agent first
• E) Nothing; tachycardia is expected and benign

Answer

B - Add a beta-blocker AFTER alpha-blockade is established

The critical rule in pheochromocytoma preoperative preparation: always establish alpha-blockade first, then add beta-blockade if needed for tachycardia. If a beta-blocker is given first (or alone), it blocks the vasodilatory beta-2 receptors in peripheral vessels, leaving alpha-mediated vasoconstriction unopposed - precipitating a hypertensive crisis. Once adequate alpha-blockade is in place (typically 7-14 days), a beta-blocker can be safely added to control the reflex tachycardia. Phenoxybenzamine is the preferred preoperative alpha-blocker (irreversible, long-acting).

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