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🩺 HYPERTENSION — INTERNAL MEDICINE NOTES

Exam-Oriented | High-Yield | Made Easy

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📌 QUICK RECALL FRAMEWORK

BP = CO × TPR (Blood Pressure = Cardiac Output × Total Peripheral Resistance) All antihypertensives work by reducing CO and/or TPR.

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1. DEFINITION & CLASSIFICATION

ACC/AHA 2017 Guidelines (Most Current — Used in Exams)

Exam Pearl: If SBP and DBP fall in different categories → use the HIGHER category. (e.g., 162/92 = Stage 2, not Stage 1)

JNC 7 Classification (Older but Still Asked)

Mnemonic for JNC 7: 120/80 → 140/90 → 160/100 — each step is +20/+10

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2. EPIDEMIOLOGY — HIGH YIELD FACTS

• Affects 1/3 of adults worldwide
• Control rates in USA: < 50% (Global low/middle income: 8–14%)
• Black adults have highest prevalence and 2x higher CVD risk from HTN (REGARDS study)
• Most common cause of myocardial infarction, heart failure, AF, stroke, CKD, dementia
• After age 50 → SBP matters more than DBP (opposite of common belief - exam trap!)
• Hypertension contributes to:
  • 43% of coronary heart disease in Black adults
  • 22% of heart failure
  • 39% of strokes

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3. PATHOPHYSIOLOGY

Core Equation:

BP = CO × TPR
CO = HR × SV

Key Mechanisms of HTN:

Pressure Natriuresis - Key Concept:

• Kidneys normally respond to ↑ BP by excreting more Na⁺ (reset mechanism)
• In HTN → this curve is shifted RIGHT (more pressure needed to excrete same Na⁺)
• Reduced RAAS responsiveness makes BP salt-sensitive

Pulse Pressure = SBP − DBP

• ↑ Pulse pressure = marker of vascular stiffness
• Seen in elderly, females, diabetes
• SBP is the stronger predictor of long-term CVD mortality than DBP or pulse pressure alone

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4. ETIOLOGY

Primary (Essential) HTN — 90–95% of cases

• No identifiable cause
• Risk factors: obesity, high sodium diet, sedentary lifestyle, alcohol, family history, age, Black race

Secondary HTN — 5–10% of cases

Mnemonic: "PRCHADS" = Primary aldosteronism, Renovascular, Cushing's, Hypothyroid/Hyperthyroid, Aortic coarctation, Drugs, Sleep apnea

Exam Pearl: Suspect secondary HTN when: onset < 30 yrs, resistant HTN, hypokalemia without diuretics, abrupt BP worsening, or BP refractory to ≥ 3 drugs.

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5. DIAGNOSIS & BP MEASUREMENT

Proper Office BP Measurement (Box MUST KNOW):

1. Patient seated quietly for ≥ 5 minutes
2. Back supported, feet flat on floor
3. Arm at heart level, bare arm
4. Cuff covers 80% of arm circumference
5. Average ≥ 2 readings on ≥ 2 occasions
6. Use Korotkoff Phase V (disappearance) for diastolic

Types of BP Monitoring:

White Coat HTN = High office BP + normal ABPM → treat with lifestyle, no drugs initially Masked HTN = Normal office + high ABPM → higher CV risk, treat!

Workup for New HTN:

• Basic labs: FBS, lipid profile, serum creatinine, eGFR, urine ACR, electrolytes, CBC
• ECG: LVH (Sokolow-Lyon: S in V1 + R in V5/V6 > 35mm)
• Echo: if suspected LVH or heart failure
• Fundoscopy: Keith-Wagener-Barker grading

Keith-Wagener-Barker Retinopathy:

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6. TARGET ORGAN DAMAGE (TOD)

Mnemonic: "BRAIN-K" = Brain, Retina, Aorta (heart), In the kidney (nephropathy)

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7. TREATMENT

Step 1: Lifestyle Modifications (ALL patients)

Mnemonic: "DASH-WAS"

When to Start Drugs?

BP Targets:

ACCORD Trial: In diabetics, targeting < 120/80 vs < 140/90 - no difference in primary CV outcomes, but MORE side effects and reduced strokes only. So aggressive targets not universally recommended.

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8. ANTIHYPERTENSIVE DRUG THERAPY

First-Line Drug Classes (4 pillars):

Mnemonic: "A-B-C-D" (modified) A = ACE inhibitors/ARBs C = Calcium Channel Blockers (CCBs) D = Diuretics (Thiazide type - Chlorthalidone preferred) B = Beta-blockers (NOT first line in uncomplicated HTN)

Drug Class Summary:

Best Combination Therapy:

• ACEi + CCB (Amlodipine) = Best combination per ACCOMPLISH trial
• ACEi + Thiazide = Also acceptable
• NEVER combine: ACEi + ARB, or ARB + Renin inhibitor (dual RAAS blockade = dangerous)
• If BP > 20/10 above target → start with 2-drug combination directly

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9. COMPELLING INDICATIONS (JNC 7 Table — Very High Yield)

Exam Tips:

• Black patients: CCB or Thiazide preferred first line (ACEi/ARB less effective as monotherapy)
• Pregnancy: Methyldopa (1st choice), Labetalol, Nifedipine. AVOID ACEi, ARBs, Aliskiren.
• Asthma/COPD: Avoid BB. Use CCB.
• Gout: Avoid Thiazides. Use Losartan (uricosuric property - bonus!).
• BPH + HTN: Alpha-blocker (Doxazosin).
• Raynaud's + HTN: CCB (Nifedipine).

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10. RESISTANT HYPERTENSION

Definition:

Causes to Rule Out First ("Pseudo-resistant"):

1. Poor medication adherence (MCC!)
2. White coat effect
3. Suboptimal technique
4. Volume overload (under-diuresis)
5. Drug interactions (NSAIDs, OCPs, decongestants, cocaine, licorice, erythropoietin, cyclosporine)

Truly Resistant - Look For Secondary Causes:

Mnemonic: "PRCHADS" (same as secondary HTN above)

• Primary aldosteronism (#1)
• CKD
• OSA
• Pheochromocytoma
• Cushing's syndrome
• Renal artery stenosis
• Coarctation of aorta

Management of Resistant HTN:

1. Optimize existing 3-drug regimen
2. Add Spironolactone 25–50 mg/day (evidence-based, highly effective - PATHWAY-2 trial)
3. Screen for secondary causes
4. Consider referral to HTN specialist
5. Renal denervation (investigational - modest BP reduction, not FDA approved)

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11. HYPERTENSIVE CRISIS

Definitions:

Remember: Urgency = 1% of ER visits. Emergency = 0.3% of ER visits. Most patients = exacerbation of previously diagnosed but poorly controlled HTN.

Hypertensive Emergency - Target Organ Damage Presentations:

BP Reduction Strategy (General Rule):

• First 1–2 hours: Reduce MAP by 10–15%
• Next 12–24 hours: Another 10–15% reduction
• Exception (faster reduction): Aortic dissection, cardiogenic pulmonary edema, ACS, hemorrhagic stroke

IV Drugs for Hypertensive Emergency:

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12. SPECIAL SITUATIONS

HTN in Pregnancy:

Drug of choice in pregnancy = Methyldopa AVOID: ACEi, ARBs (teratogenic - fetal renal dysgenesis)

HTN in CKD:

• Target < 130/80 mmHg
• ACEi or ARB preferred (reduce proteinuria, slow progression)
• Thiazides lose efficacy at eGFR < 30 → switch to loop diuretics
• Monitor K⁺ and creatinine after starting ACEi/ARB

HTN in Elderly:

• Isolated Systolic HTN (ISH) = most common pattern
• Treat cautiously (orthostasis risk)
• JNC 8 allows < 150/90 for age > 60 (controversial)
• Chlorthalidone, CCBs preferred

HTN in Diabetes:

• Target < 130/80 mmHg
• ACEi or ARB first line (nephroprotective)
• CCBs or thiazides as add-on

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13. EXAM MNEMONICS RAPID RECALL

"ABCD" of 1st line antihypertensives:

"5 P's" of Pheo:

Secondary HTN "PRCHADS":

Hypertensive Emergency target organs "BRAIN-K":

Cough from ACEi = bradykinin buildup → Switch to ARB (no cough)

Rebound HTN on abrupt withdrawal = Clonidine (also BB in IHD)

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14. HIGH-YIELD CLINICAL PEARLS - EXAM TRAPS ⚠️

1. SBP > DBP as predictor after age 50 - examiners love to flip this.
2. Chlorthalidone > HCTZ (longer acting, better outcomes in ALLHAT) - use chlorthalidone when they say "best thiazide."
3. ACEi + ARB combination = CONTRAINDICATED (dual RAAS blockade - worsens renal outcomes).
4. Never give BB alone in pheo - causes paradoxical hypertension from unopposed α stimulation.
5. Aortic dissection = most aggressive BP reduction of all emergencies (SBP < 120 within minutes).
6. Ischemic stroke: Do NOT aggressively lower BP (lose autoregulation in penumbra). Only lower if > 220/120 (no thrombolytics) or > 185/110 (with thrombolytics).
7. ACCOMPLISH trial = ACEi + CCB superior to ACEi + Thiazide in reducing CV events.
8. ALLHAT trial = Chlorthalidone as effective as CCB or ACEi; reduced HF more.
9. Losartan has a uricosuric effect - best ARB in patient with HTN + gout.
10. Methyldopa = DOC in pregnancy; causes Coombs positive hemolytic anemia (side effect).
11. Spironolactone for resistant HTN = highly effective (PATHWAY-2 trial).
12. Hydralazine = DOC for HTN in pregnancy emergencies (IV), also causes lupus-like syndrome at high doses.

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15. QUICK REVISION FLOWCHART

NEW HTN DIAGNOSED
       ↓
Measure BP properly (avg ≥2 readings on ≥2 visits)
       ↓
Rule out White Coat HTN (ABPM if needed)
       ↓
Lifestyle modifications for ALL
       ↓
Drug therapy?
→ Stage 1 + 10-yr ASCVD < 10% → Lifestyle only
→ Stage 1 + 10-yr ASCVD ≥ 10% → Add drug
→ Stage 2 (≥ 140/90) → Drug + Lifestyle
       ↓
Choose drug based on compelling indication
(ACEi/ARB + CCB/Thiazide as first combo)
       ↓
Target < 130/80 (most patients)
       ↓
Not at goal after 4–6 weeks?
→ Increase dose OR Add second drug
       ↓
Resistant? (≥ 3 drugs, including diuretic)
→ Add Spironolactone
→ Screen for secondary causes
→ Refer to specialist

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🩺 HYPERTENSION — PRACTICE QUESTIONS

Internal Medicine | Exam-Oriented | Priyanka Sachdev Style

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SECTION A: CLASSIFICATION & DIAGNOSIS

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• A. Normal
• B. Elevated
• C. Stage 1 Hypertension
• D. Stage 2 Hypertension

✅ Answer: C — Stage 1 Hypertension

ACC/AHA 2017: Stage 1 = SBP 130–139 OR DBP 80–89 mmHg. His SBP 134–136 falls in Stage 1 range. The DBP 84–85 also falls in Stage 1. The higher category is used — Stage 1 HTN. Note: JNC 7 would have called this "pre-hypertension" — know which guideline is being asked!

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• A. Stage 1 HTN based on DBP
• B. Stage 2 HTN based on SBP
• C. Stage 1 HTN because both values are used
• D. Hypertensive urgency

✅ Answer: B — Stage 2 HTN based on SBP

SBP 162 = Stage 2 (≥ 140). DBP 92 = Stage 1 (80–89). Rule: when SBP and DBP fall in different categories, use the higher category. So Stage 2 applies. This is a classic exam trap.

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• A. Masked hypertension
• B. White coat hypertension
• C. Stage 1 hypertension
• D. Stage 2 hypertension

✅ Answer: B — White coat hypertension

High office BP + normal home BP + normal ABPM = White coat HTN. Management: lifestyle modifications, no immediate drug therapy, repeat ABPM in 6–12 months. Contrast with masked HTN = normal office + high ABPM → higher CV risk, treat!

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• A. Normal
• B. Elevated
• C. Stage 1 Hypertension
• D. Stage 2 Hypertension

✅ Answer: C — Stage 1 Hypertension

SBP 128 = Elevated (120–129 AND < 80). BUT DBP 82 = Stage 1 (80–89). Use the higher category → Stage 1 HTN. The AND vs OR rule catches many students here.

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SECTION B: PATHOPHYSIOLOGY & SECONDARY HTN

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• A. Renovascular hypertension
• B. Pheochromocytoma
• C. Primary aldosteronism
• D. Cushing's syndrome

✅ Answer: C — Primary aldosteronism

The triad of resistant HTN + hypokalemia + no diuretic use strongly points to primary aldosteronism (Conn's syndrome). It is the most common cause of secondary hypertension (5–15% of all HTN). Screening test = Aldosterone-to-Renin Ratio (ARR). ARR > 30 is highly suggestive.

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• A. 24-hr urinary cortisol
• B. Aldosterone-renin ratio
• C. 24-hr urinary metanephrines
• D. Renal artery Doppler

✅ Answer: C — 24-hr urinary metanephrines

Classic "5 P's" of pheochromocytoma: Pressure (episodic HTN), Palpitations, Perspiration, Pain (headache), Pallor. Best initial test = 24-hr urine metanephrines and catecholamines (sensitivity ~98%). Plasma free metanephrines also acceptable. Once biochemically confirmed → imaging (CT abdomen).

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• A. Renovascular hypertension
• B. Coarctation of the aorta
• C. Primary aldosteronism
• D. Takayasu's arteritis

✅ Answer: B — Coarctation of the aorta

Classic triad: radio-femoral pulse delay + upper limb BP > lower limb BP + rib notching (due to collateral intercostal arteries eroding rib undersurfaces). Occurs in young patients. Confirmatory test = CT aortogram / MRI aorta. Associated with bicuspid aortic valve and Turner syndrome.

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• A. Diastolic blood pressure
• B. Pulse pressure
• C. Systolic blood pressure
• D. Mean arterial pressure

✅ Answer: C — Systolic blood pressure

Classic exam trap! Many think DBP is more important, but after age 50, SBP is the stronger predictor of CVD mortality. DBP actually falls after 50 (due to vascular stiffness), widening pulse pressure. The Chicago Heart Association study confirmed long-term risk should be assessed mainly on SBP.

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• A. White coat hypertension
• B. Obstructive sleep apnea
• C. Primary aldosteronism
• D. Anxiety disorder

✅ Answer: B — Obstructive sleep apnea

OSA is a major cause of resistant HTN and is strongly associated with a non-dipping pattern on ABPM (nocturnal BP fails to fall ≥ 10%). Other non-dipping causes: CKD, diabetes, autonomic dysfunction. OSA screening = Epworth sleepiness scale + polysomnography.

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SECTION C: TREATMENT — LIFESTYLE & DRUGS

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• A. Start ACE inhibitor immediately
• B. Lifestyle modifications only
• C. Start thiazide diuretic + lifestyle modifications
• D. Refer to cardiologist

✅ Answer: B — Lifestyle modifications only

ACC/AHA 2017: For Stage 1 HTN, drugs are started only if 10-yr ASCVD ≥ 10%. His risk is only 7% → lifestyle modifications alone (DASH diet, sodium restriction, weight loss, exercise, alcohol reduction). Reassess in 3–6 months.

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• A. Sodium restriction (< 2.4 g/day)
• B. DASH diet
• C. Aerobic exercise (30 min, most days)
• D. Weight loss

✅ Answer: B — DASH diet

DASH diet reduces BP by 8–14 mmHg — the largest single lifestyle intervention effect. Aerobic exercise reduces by 4–9 mmHg, sodium restriction by 2–8 mmHg, and weight loss by ~1 mmHg/kg.

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• A. Amlodipine
• B. Chlorthalidone
• C. Lisinopril
• D. Hydrochlorothiazide

✅ Answer: C — Lisinopril (ACE inhibitor)

In Black patients, ACEi and ARBs are less effective as monotherapy due to lower renin activity. Preferred agents = CCBs (amlodipine) and Thiazide diuretics (chlorthalidone). Chlorthalidone is preferred over HCTZ (longer-acting, better outcomes in ALLHAT trial). Note: ACEi/ARBs ARE still used in Black patients with compelling indications (DM, CKD, HF).

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• A. Add a cough suppressant and continue lisinopril
• B. Switch to a calcium channel blocker
• C. Switch to losartan (ARB)
• D. Add a thiazide diuretic

✅ Answer: C — Switch to losartan (ARB)

ACEi-induced cough is caused by bradykinin accumulation (ACE normally degrades bradykinin). Incidence: 10–15% (higher in Asian patients). ARBs block AT1 receptor directly, do not increase bradykinin → no cough. ARBs have same therapeutic efficacy as ACEi.

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• A. Hydrochlorothiazide
• B. Amlodipine
• C. Losartan
• D. Metoprolol

✅ Answer: C — Losartan

Losartan is the only ARB with a uricosuric effect - it inhibits URAT1 transporter in the proximal tubule, increasing uric acid excretion. Hydrochlorothiazide should be AVOIDED in gout (raises uric acid). Losartan = best antihypertensive in HTN + gout.

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• A. Beta-blocker
• B. ACE inhibitor alone
• C. Calcium channel blocker (long-acting nifedipine or amlodipine)
• D. Thiazide diuretic

✅ Answer: C — Calcium channel blocker

Beta-blockers are contraindicated in asthma (bronchospasm). For HTN + angina in an asthmatic: use long-acting dihydropyridine CCBs (amlodipine, nifedipine) — excellent for both HTN and angina. Non-DHP CCBs (verapamil, diltiazem) are also anti-anginal but can cause AV block and are avoided in HFrEF.

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• A. ACEi + Thiazide diuretic
• B. ACEi + Beta-blocker
• C. ACEi + CCB (Amlodipine)
• D. ARB + CCB

✅ Answer: C — ACEi + CCB (Amlodipine)

The ACCOMPLISH trial showed that Benazepril (ACEi) + Amlodipine (CCB) was superior to Benazepril + HCTZ in reducing cardiovascular events, despite similar BP reduction. This made ACEi + CCB the preferred 2-drug combination in HTN management.

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• A. Reflex tachycardia
• B. Rebound hypertension
• C. First-dose orthostatic hypotension
• D. Hyperkalemia

✅ Answer: C — First-dose orthostatic hypotension

Alpha-1 blockers (prazosin, doxazosin) classically cause first-dose orthostatic (postural) hypotension — sudden BP drop on standing. Patients should be counseled to take the first dose at bedtime and rise slowly. This is why alpha-blockers are NOT first-line for HTN (despite dual benefit in BPH + HTN).

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• A. Methyldopa
• B. Nifedipine
• C. Labetalol
• D. Enalapril

✅ Answer: D — Enalapril (ACE inhibitor)

ACEi and ARBs are absolutely contraindicated in pregnancy (especially 2nd and 3rd trimester) → cause fetal renal tubular dysplasia, oligohydramnios, neonatal renal failure, skull hypoplasia (VACTERL-like effects). Safe drugs in pregnancy: Methyldopa (DOC), Labetalol, Nifedipine (slow-release), Hydralazine.

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SECTION D: COMPELLING INDICATIONS

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• A. Amlodipine
• B. Chlorthalidone
• C. Lisinopril
• D. Metoprolol

✅ Answer: C — Lisinopril (ACE inhibitor)

In diabetes + proteinuria/microalbuminuria, ACEi (or ARB) is the drug of choice. They reduce intraglomerular pressure, decrease proteinuria, and slow progression of diabetic nephropathy — independent of BP-lowering effect. This is a compelling indication backed by multiple RCTs (RENAAL, IDNT, HOPE trials).

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• A. Amlodipine + Thiazide
• B. ACEi + Beta-blocker + Spironolactone
• C. CCB + ARB
• D. Alpha-blocker + Thiazide

✅ Answer: B — ACEi + Beta-blocker + Spironolactone

Post-MI with reduced EF (HFrEF): compelling indications are ACEi + BB + MRA (spironolactone). This combination reduces mortality (proven in RALES, EMPHASIS-HF trials). Amlodipine can be added for additional BP control but is not the priority here. Note: Verapamil and diltiazem are avoided in HFrEF.

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• A. Hydrochlorothiazide
• B. Chlorthalidone
• C. Furosemide (loop diuretic)
• D. Spironolactone

✅ Answer: C — Furosemide (loop diuretic)

Thiazide diuretics lose efficacy at eGFR < 30 mL/min (they require secretion into the tubular lumen to work). With advanced CKD (eGFR 24), loop diuretics (furosemide, torsemide) are preferred. Spironolactone is risky in advanced CKD due to hyperkalemia risk.

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SECTION E: RESISTANT HTN & EMERGENCIES

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• A. Add metoprolol
• B. Add spironolactone 25–50 mg/day
• C. Add doxazosin
• D. Refer for renal denervation

✅ Answer: B — Add spironolactone 25–50 mg/day

This patient has resistant HTN (BP above goal on 3 max-dose drugs including a diuretic). The PATHWAY-2 trial demonstrated spironolactone is the most effective add-on agent for resistant HTN, outperforming bisoprolol and doxazosin. Mechanism: suppresses aldosterone excess, which is often subclinical in resistant HTN. Monitor K⁺ and renal function.

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• A. Hypertensive urgency
• B. Acute ischemic stroke
• C. Hypertensive encephalopathy
• D. Subarachnoid hemorrhage

✅ Answer: C — Hypertensive encephalopathy

Key features: severe HTN + encephalopathy (confusion, headache, visual disturbance) + papilledema + absence of focal neurological signs + normal CT. MRI may show PRES (Posterior Reversible Encephalopathy Syndrome) — symmetrical vasogenic edema in posterior occipital regions. Treatment: IV labetalol or nicardipine; reduce MAP by 20–25% in first hour.

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• A. < 160/100 mmHg within 6 hours
• B. MAP reduction of 25% over 24 hours
• C. SBP < 120 mmHg within minutes
• D. SBP < 140 mmHg within 1–2 hours

✅ Answer: C — SBP < 120 mmHg within minutes

This is Type A aortic dissection — the most aggressive BP emergency. Target: SBP < 120 mmHg + HR < 60 bpm as fast as possible. Use IV Labetalol (controls both HR and BP) or IV Esmolol + Nitroprusside. Beta-blocker FIRST to prevent reflex tachycardia from nitroprusside. This is the ONLY HTN emergency where near-normalization is the immediate goal.

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• A. IV Metoprolol first, then phenoxybenzamine
• B. IV Phentolamine first, then IV Propranolol if tachycardia persists
• C. IV Labetalol only (covers both alpha and beta)
• D. IV Nitroprusside alone

✅ Answer: B — Phentolamine first, then propranolol if needed

In pheo crisis: ALWAYS alpha-block FIRST, then beta-block. If beta-blocker given first → paradoxical severe hypertension (blocks vasodilatory β2 receptors, leaving α1-mediated vasoconstriction unopposed). Phentolamine or phenoxybenzamine first → then propranolol for tachycardia. Note: Labetalol has mixed α/β activity but its β-blocking effect predominates, so it's not ideal for acute pheo crisis.

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• A. IV Labetalol + oral nifedipine
• B. IV MgSO₄ + IV Hydralazine or Labetalol
• C. Emergency cesarean without medications
• D. IV Furosemide + oral methyldopa

✅ Answer: B — IV MgSO₄ + IV Hydralazine or Labetalol

This is eclampsia (pre-eclampsia + seizures). Two immediate priorities: (1) MgSO₄ for seizure control/prevention — NOT a standard anticonvulsant, it works by reducing CNS excitability and promoting vasodilation. (2) IV Hydralazine or Labetalol for acute BP control. Definitive treatment = delivery. MgSO₄ toxicity: loss of deep tendon reflexes → respiratory depression → cardiac arrest. Antidote = IV Calcium gluconate.

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• A. Aggressively lower BP to < 130/80 mmHg immediately
• B. Lower BP only if > 220/120 mmHg; target 15% reduction over 24 hrs
• C. Give IV labetalol immediately to reach < 140/90 mmHg
• D. No treatment; BP will self-correct

✅ Answer: B — Only treat if > 220/120; reduce by 15% over 24 hrs

In acute ischemic stroke without thrombolytics: DO NOT aggressively lower BP. The ischemic penumbra loses cerebral autoregulation and depends on systemic BP for perfusion. Only treat if BP > 220/120 mmHg, and reduce by only 15% over 24 hours. If thrombolytics are planned → treat if BP > 185/110 mmHg before and during thrombolysis.

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SECTION F: SIDE EFFECTS & DRUG INTERACTIONS

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• A. Add antihistamine and continue lisinopril
• B. Switch to ARB immediately; give IV corticosteroids
• C. Stop lisinopril; administer epinephrine if severe; switch to ARB for future BP control
• D. Stop lisinopril and start amlodipine only; ARBs also cause angioedema

✅ Answer: C — Stop lisinopril; give epinephrine if severe; switch to ARB

ACEi-induced angioedema is bradykinin-mediated (NOT IgE-mediated) → antihistamines and corticosteroids are less effective. Can occur months to years after starting. Stop ACEi immediately. Severe cases → IV epinephrine, airway management. ARBs do NOT cause angioedema through bradykinin; they can be used (with caution - rare cross-reactivity ~ 5–10%). DO NOT rechallenge with any ACEi.

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• A. Amlodipine + HCTZ
• B. Lisinopril + spironolactone
• C. Metoprolol + amlodipine
• D. Furosemide + nifedipine

✅ Answer: B — Lisinopril + spironolactone

Dual RAAS blockade (ACEi + MRA) causes additive hyperkalemia. ACEi reduces angiotensin II → less aldosterone → less K⁺ excretion. Spironolactone blocks aldosterone receptor → further K⁺ retention. Combination significantly increases risk of dangerous hyperkalemia and worsening renal function. Monitor K⁺ closely if this combination is used.

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• A. Hypertensive urgency; start oral amlodipine
• B. Clonidine rebound hypertension; restart clonidine, then taper slowly
• C. Pheo crisis; start phentolamine
• D. Malignant hypertension; start IV nitroprusside

✅ Answer: B — Clonidine rebound hypertension; restart and taper

Abrupt clonidine withdrawal causes rebound hypertension due to sudden loss of central α2 agonism → sympathetic surge. Treatment: restart clonidine and taper gradually. Also seen with beta-blockers in IHD patients (can precipitate MI). Always taper these drugs — never stop abruptly.

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BONUS — VIVA / SPOT DIAGNOSIS QUESTIONS

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• a) Dry cough
• b) Lupus-like syndrome
• c) Hypertrichosis
• d) Gynecomastia
• e) Gingival hyperplasia
• f) Rebound HTN on withdrawal

✅ Answers:

• a) ACE inhibitors (bradykinin accumulation)
• b) Hydralazine (at high doses → drug-induced lupus)
• c) Minoxidil (used topically for alopecia!)
• d) Spironolactone (anti-androgen effect)
• e) Amlodipine (CCBs — also nifedipine)
• f) Clonidine (also beta-blockers in IHD)

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✅ Answer:

• Grade I: Arteriolar narrowing, increased light reflex
• Grade II: AV nipping (nicking), copper/silver wiring
• Grade III: Flame hemorrhages, cotton-wool spots, hard exudates
• Grade IV: Grade III + Papilledema

Grade IV = Malignant (accelerated) hypertension — a hypertensive emergency requiring IV treatment.

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✅ Answer: No — rapid BP reduction in hypertensive urgency is NOT beneficial and is potentially harmful. Aggressive IV/oral BP lowering can precipitate target organ ischemia (cerebral, coronary, renal). Management: restart any stopped medications, add/adjust oral therapy, and arrange prompt outpatient follow-up within 24–72 hours. Most patients do NOT need ER admission.

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📊 SCORING GUIDE

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🩺 HYPERTENSION — PRACTICE Q&A

Exam Accurate | Ultra Easy | Instant Recall Style

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📦 SECTION A: CLASSIFICATION

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• A. Normal
• B. Elevated
• C. Stage 1 HTN ✅
• D. Stage 2 HTN

🧠 WHY?

Stage 1 = SBP 130–139  OR  DBP 80–89
          ↑ 134 fits        ↑ 85 fits
→ Stage 1 HTN ✓

Trap: JNC 7 calls this "Pre-hypertension" — know WHICH guideline is being asked!

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• A. Stage 1 based on DBP
• B. Stage 2 based on SBP ✅
• C. Stage 1 combined
• D. Hypertensive urgency

🧠 WHY?

SBP 162 → Stage 2  (≥140)
DBP 92  → Stage 1  (80–89)

RULE: When they differ → use the HIGHER one
              ↓
          Stage 2 ✓

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• A. Masked hypertension
• B. White coat hypertension ✅
• C. Stage 1 HTN
• D. Stage 2 HTN

🧠 WHY?

High OFFICE BP
  + Normal HOME BP      → White Coat HTN ✓
  + Normal ABPM

━━━━━━━━━━━━━━━━━━━━━━━━━━
Flip it = MASKED HTN:
  Normal OFFICE BP
  + High HOME/ABPM      → Higher CV risk!
                           TREAT!
━━━━━━━━━━━━━━━━━━━━━━━━━━

White coat = lifestyle only, no drugs. Masked = treat like real HTN.

---

• A. Normal
• B. Elevated
• C. Stage 1 HTN ✅
• D. Stage 2 HTN

🧠 WHY?

SBP 128 = "Elevated" (120–129 AND <80)
DBP 82  = Stage 1    (80–89)

Use the HIGHER → Stage 1 ✓

Diabetes doesn't change classification — it changes the treatment threshold.

---

📦 SECTION B: SECONDARY HTN

---

• A. Renovascular HTN
• B. Pheochromocytoma
• C. Primary Aldosteronism ✅
• D. Cushing's syndrome

🧠 WHY?

CLUE TRIO:
┌─────────────────────────────────┐
│ Resistant HTN                   │
│ + Hypokalemia                   │
│ + No diuretic use               │
│         ↓                       │
│   Primary Aldosteronism ✓       │
│   (#1 cause of 2° HTN)          │
└─────────────────────────────────┘
Screening test = Aldosterone : Renin Ratio
                 (ARR > 30 = positive)

---

• A. 24-hr urinary cortisol
• B. Aldosterone-renin ratio
• C. 24-hr urinary metanephrines ✅
• D. Renal artery Doppler

🧠 WHY?

5 P's of PHEO:
Pressure ↑ (episodic)
Palpitations
Perspiration
Pain (headache)
Pallor
   ↓
Test = 24-hr urine metanephrines
       (sensitivity ~98%)

---

• A. Renovascular HTN
• B. Coarctation of Aorta ✅
• C. Primary Aldosteronism
• D. Takayasu's arteritis

🧠 WHY?

CLASSIC TRIAD:
①  Radio-femoral pulse delay
②  Upper limb BP > Lower limb BP
③  Rib notching on CXR
          ↓
  Coarctation of Aorta ✓

Confirm → CT Aortogram
Associated → Bicuspid AV, Turner syndrome

---

• A. Diastolic BP
• B. Pulse pressure
• C. Systolic BP ✅
• D. Mean arterial pressure

🧠 WHY?

⚠️ EXAM TRAP — Most think DBP matters more

After 50:  DBP ↓ (vessels get stiff)
           SBP ↑
           Pulse pressure widens

Long-term risk → SBP is the master predictor ✓

---

• A. White coat HTN
• B. Obstructive Sleep Apnea ✅
• C. Primary Aldosteronism
• D. Anxiety

🧠 WHY?

Normal = BP dips ≥10% at night ("dipping")

Non-dipping causes:
┌──────────────────────┐
│ OSA          ← #1   │
│ CKD                 │
│ Diabetes            │
│ Autonomic dysfn     │
└──────────────────────┘
Confirm OSA → Polysomnography

---

📦 SECTION C: TREATMENT

---

• A. Start ACEi immediately
• B. Lifestyle modifications only ✅
• C. Start Thiazide + lifestyle
• D. Refer to cardiologist

🧠 WHY?

Stage 1 HTN drug rule:

10-yr ASCVD < 10%  →  Lifestyle ONLY ✓
10-yr ASCVD ≥ 10%  →  Drug + Lifestyle

His risk = 7%  →  Lifestyle only ✓
Reassess in 3–6 months

---

• A. Na⁺ restriction
• B. DASH diet ✅
• C. Aerobic exercise
• D. Weight loss

🧠 WHY?

BP Reduction Ladder:
┌────────────────────────────────────┐
│ DASH diet         → 8–14 mmHg ✓  │  ← HIGHEST
│ Aerobic exercise  → 4–9 mmHg     │
│ Na⁺ restriction   → 2–8 mmHg     │
│ Weight loss       → ~1 mmHg/kg   │
│ Alcohol reduction → 2–4 mmHg     │
└────────────────────────────────────┘

---

• A. Amlodipine
• B. Chlorthalidone
• C. Lisinopril (ACEi) ✅
• D. HCTZ

🧠 WHY?

Black patients → Low renin state

  ACEi/ARBs work by blocking RAAS
  Less effective when renin is already low
        ↓
  Use CCB or Thiazide as 1st line ✓

(ACEi/ARBs used if DM/CKD/HF = compelling indication)

---

• A. Add cough suppressant, continue lisinopril
• B. Switch to CCB
• C. Switch to Losartan (ARB) ✅
• D. Add thiazide diuretic

🧠 WHY?

ACEi → blocks degradation of BRADYKININ
             ↓
      Bradykinin accumulates
             ↓
        DRY COUGH (10–15% of patients)

Fix: Switch to ARB
ARBs block AT1 receptor directly
→ DO NOT raise bradykinin → NO COUGH ✓

---

• A. HCTZ
• B. Amlodipine
• C. Losartan ✅
• D. Metoprolol

🧠 WHY?

Losartan = only ARB with URICOSURIC effect
  → Inhibits URAT1 transporter
  → ↑ Uric acid excretion

HCTZ → ↑ Uric acid (AVOID in gout!)
Losartan = BP control + gout benefit ✓

---

• A. Beta-blocker
• B. ACEi alone
• C. Long-acting CCB (Amlodipine) ✅
• D. Thiazide diuretic

🧠 WHY?

Asthma + BB = BRONCHOSPASM (contraindicated)

CCB works for BOTH:
✓ HTN → dilates peripheral vessels
✓ Angina → dilates coronary vessels

Amlodipine / Long-acting Nifedipine = ideal ✓

---

• A. ACEi + Thiazide
• B. ACEi + Beta-blocker
• C. ACEi + CCB (Amlodipine) ✅
• D. ARB + CCB

🧠 WHY?

ACCOMPLISH Trial:

Benazepril + Amlodipine
       vs
Benazepril + HCTZ

→ ACEi + CCB won ✓
  (less CV events despite similar BP control)

∴ Preferred 2-drug combo = ACEi + CCB

---

• A. Reflex tachycardia
• B. Rebound HTN
• C. First-dose orthostatic hypotension ✅
• D. Hyperkalemia

🧠 WHY?

Alpha-1 blockers → block α1 on vessels
                 → sudden vasodilation on standing
                 → BP drops → near-syncope

Called: FIRST-DOSE EFFECT

Prevention:
→ Take first dose at BEDTIME
→ Rise slowly in the morning

That's why alpha-blockers are NOT 1st line for HTN

---

• A. Methyldopa
• B. Nifedipine
• C. Labetalol
• D. Enalapril (ACEi) ✅

🧠 WHY?

ACEi/ARBs in pregnancy =
┌────────────────────────────────────────┐
│  Fetal renal tubular dysplasia         │
│  Oligohydramnios                       │
│  Neonatal renal failure                │
│  Skull hypoplasia                      │
└────────────────────────────────────────┘
        ABSOLUTELY CONTRAINDICATED

SAFE in pregnancy:
Methyldopa ← DOC
Labetalol
Nifedipine (slow release)
Hydralazine (IV for emergencies)

---

📦 SECTION D: COMPELLING INDICATIONS

---

• A. Amlodipine
• B. Chlorthalidone
• C. Lisinopril (ACEi) ✅
• D. Metoprolol

🧠 WHY?

DM + Proteinuria = COMPELLING INDICATION for ACEi/ARB

Why? ACEi →
  ↓ Intraglomerular pressure
  ↓ Proteinuria
  Slows CKD progression
  (Beyond just BP lowering!)

Backed by: RENAAL, IDNT, HOPE trials ✓

---

• A. Amlodipine + Thiazide
• B. ACEi + Beta-blocker + Spironolactone ✅
• C. CCB + ARB
• D. Alpha-blocker + Thiazide

🧠 WHY?

Post-MI + HFrEF (EF <40%) →
┌─────────────────────────────┐
│ ACEi      ← reduces remodel│
│ Beta-blocker ← anti-arrhyth│
│ Spironolactone ← reduces   │
│              mortality      │
└─────────────────────────────┘
RALES + EMPHASIS-HF trials confirm ✓

AVOID: Verapamil/Diltiazem in HFrEF

---

• A. HCTZ
• B. Chlorthalidone
• C. Furosemide (loop diuretic) ✅
• D. Spironolactone

🧠 WHY?

THIAZIDES need to enter tubule lumen to work
  → Secreted by organic acid transporters
  → These fail when eGFR < 30

eGFR < 30 → Thiazides INEFFECTIVE ✓
          → Use LOOP DIURETICS instead
             (Furosemide, Torsemide)

Spironolactone → dangerous hyperkalemia in CKD

---

📦 SECTION E: RESISTANT HTN & EMERGENCIES

---

• A. Add metoprolol
• B. Add Spironolactone 25–50 mg ✅
• C. Add doxazosin
• D. Renal denervation

🧠 WHY?

RESISTANT HTN = ≥ 3 drugs at max dose
                (one MUST be a diuretic)
                + still above target

Best add-on drug = SPIRONOLACTONE ✓
  (PATHWAY-2 trial - beat bisoprolol & doxazosin)

Why it works:
  Most resistant HTN has subclinical aldosterone excess
  Spiro blocks it → dramatic BP drop

Monitor: K⁺ + creatinine

---

• A. Hypertensive urgency
• B. Acute ischemic stroke
• C. Hypertensive Encephalopathy ✅
• D. Subarachnoid hemorrhage

🧠 WHY?

HYPERTENSIVE ENCEPHALOPATHY checklist:
✓ Severe HTN
✓ Confusion/headache/visual disturbance
✓ Papilledema
✓ NO focal neuro signs  ← KEY differentiator
✓ CT normal

MRI → PRES (Posterior Reversible
       Encephalopathy Syndrome)
       Vasogenic edema in occipital regions

Rx: IV Labetalol / Nicardipine
    Reduce MAP by 20–25% in first 1–2 hrs

---

• A. < 160/100 within 6 hours
• B. MAP −25% over 24 hours
• C. SBP < 120 mmHg within MINUTES ✅
• D. SBP < 140 within 1–2 hrs

🧠 WHY?

Diagnosis = AORTIC DISSECTION

Most aggressive BP emergency of all!

Target:  SBP < 120 mmHg
         HR  < 60 bpm
         As FAST as possible

Drug:    IV LABETALOL (1st)  ← α + β blocker
      OR IV Esmolol + Nitroprusside

⚠️ GIVE BB BEFORE Nitroprusside
   (prevents reflex tachycardia from NTP)

---

• A. IV Metoprolol first
• B. IV Phentolamine first, then Propranolol if tachycardia ✅
• C. IV Labetalol only
• D. IV Nitroprusside alone

🧠 WHY?

GOLDEN RULE in Pheo Crisis:

ALPHA-BLOCK FIRST ← ALWAYS
THEN beta-block

Why?
If BB given first:
  β2 vasodilators blocked
  α1 vasoconstriction UNOPPOSED
          ↓
  PARADOXICAL HTN worsening ← dangerous!

Sequence:
Phentolamine (IV α-blocker)
      ↓
Propranolol (if tachycardia persists)

---

• A. IV Labetalol + oral nifedipine
• B. IV MgSO₄ + IV Hydralazine or Labetalol ✅
• C. Emergency C-section immediately
• D. IV Furosemide + oral methyldopa

🧠 WHY?

ECLAMPSIA = Pre-eclampsia + SEIZURES

Two simultaneous priorities:

① MgSO₄ IV ← stops/prevents seizures
             (NOT a normal anticonvulsant!)
             Works by ↓ NMDA excitability
             + vasodilation

② Hydralazine or Labetalol IV ← control BP

③ Definitive = DELIVERY

MgSO₄ Toxicity ladder:
Loss of DTRs → Resp depression → Cardiac arrest
Antidote = IV Calcium Gluconate

---

• A. Lower to < 130/80 immediately
• B. Only treat if BP > 220/120; reduce MAP 15% over 24 hrs ✅
• C. IV Labetalol to reach < 140/90 now
• D. No treatment needed

🧠 WHY?

Ischemic penumbra = LOST autoregulation
  Depends entirely on systemic BP for perfusion

Aggressively lower BP = EXTEND the infarct ← dangerous!

RULES:
No thrombolytics → treat only if BP > 220/120
                   → reduce by 15% over 24 hrs

With thrombolytics → treat if BP > 185/110
                     (before and during infusion)

---

📦 SECTION F: SIDE EFFECTS

---

• A. Add antihistamine, continue lisinopril
• B. IV steroids + switch to ARB
• C. Stop lisinopril; epinephrine if severe; switch to ARB ✅
• D. Stop lisinopril; ARBs also cause this — use CCB only

🧠 WHY?

ACEi ANGIOEDEMA:
  Bradykinin-mediated (NOT IgE)
  Can occur months to YEARS after starting!

Antihistamines/Steroids = NOT very effective
  (it's bradykinin, not histamine)

Severe → IV Epinephrine + Airway management

Future drug:
→ ARB safe (no bradykinin effect)
→ ~ 5-10% cross-reactivity (use with caution)

NEVER rechallenge with any ACEi ✓

---

• A. Amlodipine + HCTZ
• B. Lisinopril + Spironolactone ✅
• C. Metoprolol + amlodipine
• D. Furosemide + nifedipine

🧠 WHY?

ACEi (Lisinopril):
  ↓ Ang II → ↓ Aldosterone → ↓ K⁺ excretion

Spironolactone: Blocks aldosterone receptor → ↓ K⁺ excretion

TOGETHER = additive hyperkalemia ← dangerous!

This is why ACEi + MRA combo requires close K⁺ + renal monitoring

---

• A. Start amlodipine
• B. Restart Clonidine; taper slowly ✅
• C. Start phentolamine (suspected pheo)
• D. IV Nitroprusside

🧠 WHY?

CLONIDINE REBOUND:
  Central α2 agonist suddenly removed
            ↓
  Sympathetic SURGE
            ↓
  Severe rebound HTN + tachycardia + tremors

Fix = Restart clonidine → taper gradually

Same logic → Never stop BB abruptly in IHD (can precipitate MI from sympathetic rebound)

---

📦 BONUS RAPID-FIRE VIVA

---

---

Grade IV = Hypertensive Emergency → treat with IV drugs immediately.

---

✅ CORRECT ANSWER = NO

Hypertensive URGENCY = no target organ damage

Rapid BP lowering →
  Ischemia of pressure-dependent organs
  (brain, heart, kidney)

Correct approach:
① Restart stopped medications
② Start/adjust oral antihypertensives
③ Outpatient follow-up in 24–72 hours
④ NO ER admission required in most cases

"Treat the patient, not the number" ✓

---

🎯 QUICK DRUG CHEAT SHEET

CONDITION            BEST DRUG
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
DM + proteinuria  → ACEi or ARB
Pregnancy         → Methyldopa (DOC)
HTN + Gout        → Losartan
HTN + BPH         → Alpha-blocker (Doxazosin)
HTN + Asthma      → CCB (avoid BB)
HTN + Angina      → CCB or BB (if no asthma)
HTN + Post-MI     → ACEi + BB + Spiro
HTN + HFrEF       → ACEi + BB + Spiro
HTN + Black pt    → CCB or Thiazide (1st line)
HTN + Raynaud's   → CCB (Nifedipine)
HTN + OSA         → Treat OSA first!
Resistant HTN     → Add Spironolactone
Pheo crisis       → Phentolamine FIRST, then BB
Aortic dissection → Labetalol IV (fastest target!)
Eclampsia         → MgSO₄ + Hydralazine/Labetalol
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

---