Teach me everything abouthyoertension, types, treatment of each type with moa of drugs used and in what conditions what antihypertensive drugs is contraindicated and adrs of each drug.

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Here is a comprehensive, textbook-grade guide to hypertension.

HYPERTENSION: A Complete Guide

Sources: Katzung's Basic & Clinical Pharmacology 16e, Lippincott Illustrated Reviews: Pharmacology, Robbins Pathologic Basis of Disease, Harrison's Principles of Internal Medicine 22e

PART 1: DEFINITION AND CLASSIFICATION

Blood pressure (BP) is continuously distributed in populations - there is no sharp normal/abnormal threshold, but clinically accepted definitions are:

Category	Systolic (mmHg)	Diastolic (mmHg)
Normal	< 120	< 80
Elevated	120-129	< 80
Stage 1 Hypertension	130-139	80-89
Stage 2 Hypertension	≥ 140	≥ 90
Hypertensive Crisis	> 180	> 120

Diagnosis requires readings elevated on at least two separate occasions.

PART 2: TYPES OF HYPERTENSION

A. Primary (Essential) Hypertension

Accounts for 90-95% of all cases
No single identifiable cause
Multifactorial: genetic polymorphisms + environmental factors (high salt intake, obesity, sedentary lifestyle, stress, alcohol)
Pathophysiology: baroreceptors and renal BP-control systems appear "set" at a higher level; increased peripheral vascular arteriolar smooth muscle tone
Treatment: lifelong pharmacotherapy + lifestyle modification

B. Secondary Hypertension (5-10% of cases)

Identifiable underlying cause - always investigate in young patients, resistant hypertension, or sudden onset.

Category	Causes
Renal	Acute/chronic glomerulonephritis, polycystic kidney disease, renal artery stenosis, renal vasculitis, renin-secreting tumors
Endocrine	Primary aldosteronism (Conn syndrome), Cushing syndrome, congenital adrenal hyperplasia, pheochromocytoma, thyroid/parathyroid disorders
Drug-induced	Oral contraceptives (estrogens), glucocorticoids, sympathomimetics, NSAIDs, cyclosporine, cocaine, licorice
Cardiovascular	Coarctation of the aorta
Neurogenic	Increased intracranial pressure, sleep apnea
Pregnancy-induced	Preeclampsia/eclampsia

C. Special Subtypes

Subtype	Definition
Isolated Systolic HTN	Systolic ≥ 140, diastolic < 90 - common in elderly due to aortic stiffness
White-coat HTN	Elevated in clinic, normal at home; requires ambulatory BP monitoring
Masked HTN	Normal in clinic, elevated at home
Resistant HTN	BP remains above goal despite optimal 3-drug regimen including a diuretic
Hypertensive Urgency	Severe elevation (>180/>120) WITHOUT target organ damage
Hypertensive Emergency	Severe elevation WITH evidence of acute target organ damage

PART 3: ANTIHYPERTENSIVE DRUG CLASSES - MECHANISMS, USES, CONTRAINDICATIONS, ADRs

CLASS 1: THIAZIDE DIURETICS

Drugs: Hydrochlorothiazide (HCTZ), Chlorthalidone, Indapamide, Metolazone

Mechanism of Action (MOA)

Acutely: Block Na+/Cl- cotransporter in the distal convoluted tubule → increased urinary excretion of Na+ and water → decreased intravascular volume → decreased cardiac output → decreased BP
Chronically (after weeks): Plasma volume normalizes but BP reduction persists because of a direct decrease in peripheral vascular resistance (mechanism not fully understood, possibly via arterial K+ channel opening)

Clinical Uses

First-line for uncomplicated essential hypertension
Elderly patients (especially isolated systolic HTN)
Black patients (respond particularly well)
Combine well with ACE inhibitors, ARBs, beta-blockers, potassium-sparing diuretics
NOT effective when eGFR < 30 mL/min/m² (except metolazone) - use loop diuretics instead

Contraindications

Gout (thiazides raise uric acid - use with caution or avoid)
Hypokalemia (risk of worsening)
Pregnancy (risk to fetus)
Significant renal impairment (eGFR < 30) - ineffective

ADRs

ADR	Mechanism
Hypokalemia	Most common - increased Na+ delivery to collecting duct → Na/K exchange
Hyperuricemia / Gout	Compete with uric acid for tubular secretion
Hyperglycemia	Reduce insulin secretion, reduce tissue glucose utilization
Hyperlipidemia	Increase LDL and triglycerides (less with chlorthalidone)
Hyponatremia	Particularly in elderly
Hypomagnesemia	-
Hypercalcemia	Increase calcium reabsorption in distal tubule
Sexual dysfunction	-
Photosensitivity	-

CLASS 2: LOOP DIURETICS

Drugs: Furosemide (Lasix), Bumetanide, Torsemide, Ethacrynic acid

MOA

Block Na+/K+/2Cl- cotransporter (NKCC2) in the thick ascending limb of the loop of Henle → massive natriuresis and diuresis → decreased blood volume → decreased BP. Most powerful diuretics available.

Clinical Uses in Hypertension

Hypertension with chronic kidney disease (eGFR < 30)
Hypertension with heart failure (reduce pulmonary congestion and BP)
Hypertensive emergency (IV furosemide)
Volume overload states

Contraindications

Anuria
Severe hypovolemia/dehydration
Ethacrynic acid: avoid in sulfa allergy patients (only loop diuretic without sulfa group)
Gout (same issue as thiazides but less pronounced)

ADRs

ADR	Note
Hypokalemia	Major risk
Hyponatremia	-
Hypomagnesemia	-
Metabolic alkalosis	H+ loss
Ototoxicity	Especially ethacrynic acid; avoid with aminoglycosides
Hyperuricemia	-
Hyperglycemia	Less than thiazides
Volume depletion / dehydration	-
Azotemia	Pre-renal due to volume depletion

CLASS 3: POTASSIUM-SPARING DIURETICS

Drugs:

Aldosterone antagonists: Spironolactone, Eplerenone
ENaC blockers: Amiloride, Triamterene

MOA

Spironolactone/Eplerenone: Competitively antagonize aldosterone receptors in the collecting tubule → block Na+ reabsorption → natriuresis without K+ wasting. Also block androgens (spironolactone only)
Amiloride/Triamterene: Directly block epithelial sodium channels (ENaC) in the collecting tubule → decreased Na+ reabsorption → reduced K+ secretion

Clinical Uses

Resistant hypertension (spironolactone is highly effective - 4th-line add-on)
Primary aldosteronism (spironolactone is the drug of choice)
Heart failure with reduced EF (spironolactone/eplerenone reduce mortality)
Prevent hypokalemia caused by loop/thiazide diuretics

Contraindications

Hyperkalemia (absolute contraindication)
Severe renal failure (accumulate and cause dangerous hyperkalemia)
Pregnancy (spironolactone: teratogenic due to antiandrogen effects)
Do NOT combine with ACE inhibitors/ARBs without careful K+ monitoring (risk of severe hyperkalemia)

ADRs

Drug	ADR
Spironolactone	Gynecomastia, menstrual irregularities, impotence, decreased libido (antiandrogen effects), hyperkalemia
Eplerenone	Less antiandrogenic (selective), hyperkalemia
Amiloride/Triamterene	Hyperkalemia, nausea, nephrolithiasis (triamterene)

CLASS 4: ACE INHIBITORS (ACEi)

Drugs: Captopril, Enalapril, Lisinopril, Ramipril, Perindopril, Fosinopril, Benazepril, Quinapril, Trandolapril

MOA

Inhibit Angiotensin-Converting Enzyme (ACE) → block conversion of Angiotensin I → Angiotensin II → decreased Ang II → results in:

Vasodilation (less vasoconstriction - arteries and veins)
Decreased aldosterone → less Na+/water retention → decreased blood volume
Decreased sympathetic activity
Accumulation of bradykinin (ACE also normally degrades bradykinin) → additional vasodilation

Clinical Uses (Compelling Indications)

Essential hypertension (first-line, especially in younger/white patients)
Diabetic nephropathy - reduce proteinuria and slow progression (first choice)
Chronic kidney disease - renoprotective
Heart failure with reduced EF - reduce mortality
Post-MI - prevent remodeling
Left ventricular dysfunction
High cardiovascular risk patients

Contraindications

Contraindication	Reason
Pregnancy (all trimesters)	Fetal renal toxicity, oligohydramnios, renal agenesis - absolutely contraindicated
Bilateral renal artery stenosis	Ang II maintains efferent arteriolar tone - blocking it causes acute renal failure
Hyperkalemia	Reduced aldosterone → K+ retention
History of ACEi-induced angioedema	Bradykinin accumulation - switch to ARB
Severe renal impairment	Careful use needed, may worsen function initially
Do NOT combine with ARB or aliskiren	Dual RAAS blockade increases adverse effects without extra benefit

ADRs

ADR	Mechanism
Dry persistent cough (~10-15%)	Bradykinin accumulation in lungs - most common reason for discontinuation
Angioedema (rare but serious)	Bradykinin-mediated; more common in Black patients
Hyperkalemia	Decreased aldosterone
First-dose hypotension	Especially in volume-depleted patients
Acute kidney injury (first weeks)	Reduced GFR - especially in bilateral RAS
Teratogenicity	Fetal renal toxicity
Rash, altered taste	Captopril (sulfhydryl group)
Neutropenia	Rare, more with captopril in renal failure + collagen vascular disease

CLASS 5: ANGIOTENSIN II RECEPTOR BLOCKERS (ARBs)

Drugs: Losartan, Valsartan, Irbesartan, Candesartan, Telmisartan, Olmesartan, Azilsartan

MOA

Selectively block AT1 receptors for Angiotensin II → same end-effects as ACEi (vasodilation, reduced aldosterone, reduced BP) BUT:

Angiotensin II levels actually rise (no negative feedback at AT1) → can act on unblocked AT2 receptors (cardioprotective, antiproliferative)
NO bradykinin accumulation → no cough

Clinical Uses

Same as ACEi: hypertension, diabetic nephropathy, CKD, heart failure, post-MI
Primary indication: ACEi-intolerant patients (especially those with cough or angioedema)
Losartan has uricosuric effect - useful in hypertension + gout

Contraindications

Same as ACEi: Pregnancy (absolutely contraindicated), bilateral renal artery stenosis, hyperkalemia
Do not combine with ACEi (no benefit, increased harm)
History of ACEi-induced angioedema (ARBs can rarely also cause angioedema)

ADRs

Much better tolerated than ACEi
No cough (key advantage over ACEi)
Hyperkalemia, hypotension, renal impairment (same as ACEi but less cough/angioedema)
Rare: angioedema (less than ACEi), dizziness
Teratogenic (same as ACEi)

CLASS 6: DIRECT RENIN INHIBITOR

Drug: Aliskiren (Tekturna)

MOA

Directly inhibits renin (the rate-limiting enzyme of the RAAS) → blocks conversion of angiotensinogen to Angiotensin I → reduces entire downstream RAAS cascade

Clinical Uses

Alternative in hypertension when ACEi/ARBs are not tolerated
Not first-line

Contraindications

Pregnancy (absolutely contraindicated - same mechanism as ACEi/ARB)
Do NOT combine with ACEi or ARB in diabetics or CKD (increased risk of renal failure, hyperkalemia, hypotension)

ADRs

Diarrhea, nausea
Hyperkalemia
Renal impairment
Hypotension

CLASS 7: BETA-BLOCKERS (β-Blockers)

Drugs:

Selective β1 (cardioselective): Atenolol, Metoprolol, Bisoprolol, Betaxolol, Acebutolol
Non-selective (β1+β2): Propranolol, Nadolol, Timolol
α+β blocker: Carvedilol, Labetalol

MOA (Multiple mechanisms)

Decrease cardiac output - block cardiac β1 receptors → reduce heart rate and contractility
Suppress renin release - block β1 receptors in juxtaglomerular cells → less Ang II → less aldosterone
Central sympathetic suppression (especially propranolol) → reduce sympathetic tone
Pre-synaptic β2 blockade → reduce norepinephrine release
Carvedilol/Labetalol add α1 blockade → peripheral vasodilation

Clinical Uses (Compelling Indications)

Hypertension + ischemic heart disease (angina, post-MI) - first choice
Hypertension + heart failure with reduced EF (carvedilol, metoprolol succinate, bisoprolol)
Hypertension + aortic dissection (IV labetalol/esmolol)
Hypertension + hyperthyroidism (propranolol)
Hypertension + migraine prophylaxis (propranolol)
Pheochromocytoma: only AFTER alpha-blockade (to prevent hypertensive crisis)
Hypertensive emergency: IV labetalol, IV esmolol (aortic dissection)

Contraindications

Contraindication	Reason
Asthma / COPD (severe)	β2 blockade → bronchoconstriction (use cardioselective β1 blocker with great caution if needed)
AV block (2nd/3rd degree)	Further suppress AV node conduction
Sinus bradycardia	Worsen bradycardia
Acute decompensated heart failure	Can worsen - only use once stabilized
Peripheral arterial disease (severe)	β2 blockade causes vasoconstriction
Pheochromocytoma without prior alpha-blockade	Unopposed alpha-mediated vasoconstriction → hypertensive crisis
Cocaine-induced HTN	Use of non-selective beta-blocker → unopposed alpha vasoconstriction (use labetalol or benzodiazepines)
Diabetes with hypoglycemia unawareness	Mask tachycardia (warning sign of hypoglycemia); sweating still present

ADRs

ADR	Note
Bradycardia	Most common cardiac effect
Bronchoconstriction	β2 blockade - avoid in asthma
Fatigue, exercise intolerance	Reduced cardiac output
Sexual dysfunction / impotence	-
CNS effects	Depression, vivid dreams, nightmares (especially propranolol - lipophilic, crosses BBB)
Masking hypoglycemia	Especially in type 1 DM
Rebound hypertension	On abrupt withdrawal - taper always
Cold extremities	Peripheral vasoconstriction
Dyslipidemia	Raise triglycerides, lower HDL (except carvedilol)
Weight gain	-

CLASS 8: CALCIUM CHANNEL BLOCKERS (CCBs)

Two Major Subclasses:

A. Dihydropyridines (DHP) - primarily vascular: Nifedipine, Amlodipine, Felodipine, Nicardipine, Clevidipine, Nimodipine, Isradipine

B. Non-Dihydropyridines (non-DHP) - cardiac + vascular:

Phenylalkylamine: Verapamil
Benzothiazepine: Diltiazem

MOA

Block voltage-gated L-type calcium channels in:

Vascular smooth muscle → reduce calcium entry → vasodilation → reduced peripheral resistance → reduced BP
Cardiac muscle (non-DHPs) → reduce contractility and heart rate

DHP CCBs are highly vascular-selective → mainly arterial vasodilation Verapamil and diltiazem reduce cardiac rate and contractility in addition to vasodilation

Clinical Uses

Drug	Best Indications
Amlodipine	First-line HTN; angina; elderly; Black patients; isolated systolic HTN
Verapamil/Diltiazem	HTN + SVT/atrial fibrillation; HTN + angina
Nicardipine IV	Hypertensive emergency
Clevidipine IV	Hypertensive emergency (ultra-short acting)
Nimodipine	Subarachnoid hemorrhage (prevent vasospasm)
All CCBs	Hypertension + Raynaud phenomenon

Contraindications

Contraindication	Drug	Reason
Heart failure with reduced EF	Verapamil, Diltiazem, Nifedipine	Negative inotropes - worsen HFrEF
2nd/3rd degree AV block	Verapamil, Diltiazem	Block AV node conduction
Sick sinus syndrome	Verapamil, Diltiazem	-
Combined with beta-blockers (IV)	Verapamil, Diltiazem	Profound bradycardia/heart block
Pre-excitation syndromes (WPW)	Verapamil	Can accelerate accessory pathway
Hypotension	All CCBs	Worsen vasodilation

ADRs

Drug	ADR
DHP CCBs (amlodipine etc.)	Peripheral edema (ankle), flushing, headache, reflex tachycardia (more with short-acting nifedipine), gingival hyperplasia
Verapamil	Constipation (very common), bradycardia, AV block, negative inotropy, hypotension
Diltiazem	Bradycardia, AV block, edema (less than DHP), constipation (less than verapamil)
Short-acting nifedipine	Avoid in HTN - causes reflex tachycardia and may worsen ischemia

CLASS 9: ALPHA-1 BLOCKERS

Drugs: Prazosin, Doxazosin, Terazosin

MOA

Competitively block α1-adrenergic receptors on vascular smooth muscle → prevent norepinephrine-mediated vasoconstriction → vasodilation of both arterioles and veins → decreased peripheral resistance and venous return → decreased BP

Clinical Uses

Hypertension with benign prostatic hyperplasia (BPH) - ideal combination (relax prostate smooth muscle AND lower BP)
Pheochromocytoma (phenoxybenzamine, phentolamine - irreversible/competitive alpha blockers used pre-op and for crisis)
Resistant hypertension (add-on)
Not first-line for HTN alone (no proven CV outcome benefit)

Contraindications

First-dose orthostatic hypotension (must give first dose at bedtime with caution)
Heart failure (fluid retention with long-term use)
Concurrent use with PDE-5 inhibitors (sildenafil) - severe hypotension

ADRs

ADR	Note
First-dose orthostatic hypotension	Major concern - syncope; give at bedtime initially
Reflex tachycardia	-
Dizziness, lightheadedness	-
Sodium/water retention	Long-term use
Intraoperative floppy iris syndrome	Seen in cataract surgery after doxazosin/tamsulosin use

CLASS 10: CENTRAL SYMPATHOLYTICS (Centrally Acting Agents)

Drugs: Clonidine, Methyldopa, Guanfacine, Moxonidine

MOA

Clonidine: Agonist at α2 receptors (and imidazoline I1 receptors) in the brainstem vasomotor center (nucleus tractus solitarius/rostral ventrolateral medulla) → reduces sympathetic outflow → decreased heart rate, cardiac output, and peripheral resistance → decreased BP
Methyldopa: Prodrug converted to alpha-methylnorepinephrine in the brain → acts as α2 agonist → same mechanism as clonidine. Drug of choice in pregnancy hypertension

Clinical Uses

Methyldopa: Hypertension in pregnancy (safest drug - decades of safety data)
Clonidine: Resistant hypertension (add-on); hypertensive urgency (oral); opioid withdrawal; ADHD
Guanfacine: Hypertension; ADHD
Clonidine patch: When oral compliance is an issue

Contraindications

Clonidine + beta-blocker combination: Risk of severe bradycardia and rebound hypertension on withdrawal
Clonidine: Do NOT stop abruptly (severe rebound hypertension)
Depression (can worsen with methyldopa)
Active hepatic disease (methyldopa can cause hepatotoxicity)

ADRs

Drug	ADR
Clonidine	Dry mouth (very common), sedation, bradycardia, constipation, rebound hypertension on abrupt withdrawal
Methyldopa	Sedation, dry mouth, positive Coombs test (~20%), hemolytic anemia (rare), hepatotoxicity, bradycardia, drug fever, lupus-like syndrome
Both	Sexual dysfunction, orthostatic hypotension

CLASS 11: DIRECT VASODILATORS

Drugs:

Oral: Hydralazine, Minoxidil
Parenteral (emergencies): Nitroprusside, Fenoldopam, Nitroglycerin

MOA

Drug	Mechanism
Hydralazine	Causes vasodilation by releasing nitric oxide (NO) → activates guanylyl cyclase → increased cGMP → smooth muscle relaxation. Dilates arterioles only (not veins)
Minoxidil	Opens ATP-sensitive K+ channels → hyperpolarization of vascular smooth muscle → arteriolar dilation. More potent than hydralazine
Nitroprusside	Releases NO spontaneously → dilates both arterioles and veins → rapidly reduces preload and afterload
Fenoldopam	Selective dopamine D1 receptor agonist → renal and peripheral vasodilation; increases renal blood flow and natriuresis

Clinical Uses

Hydralazine: Third-line oral agent; hypertension with heart failure (combined with nitrates); hypertension in pregnancy (IV form); hypertensive emergency (IV)
Minoxidil (oral): Severe, resistant hypertension - must combine with beta-blocker AND diuretic to prevent reflex tachycardia and fluid retention. Also used topically for alopecia
Nitroprusside IV: Hypertensive emergency (most potent; must monitor cyanide toxicity with prolonged use)
Fenoldopam IV: Hypertensive emergency - particularly beneficial when renal protection is desired

Contraindications

Hydralazine: Coronary artery disease / angina (reflex tachycardia worsens ischemia); dissecting aortic aneurysm; lupus (can trigger drug-induced lupus)
Minoxidil: Pheochromocytoma; pulmonary hypertension
Nitroprusside: Severe hepatic/renal failure (cyanide accumulation); vitamin B12 deficiency; avoid prolonged use (>72h) without monitoring thiocyanate levels

ADRs

Drug	ADR
Hydralazine	Reflex tachycardia, palpitations, headache, nausea, drug-induced lupus (slow acetylators at high doses), sodium/water retention, angina
Minoxidil	Severe reflex tachycardia, hypertrichosis (unwanted facial/body hair - basis of topical use), sodium/water retention, pericardial effusion
Nitroprusside	Cyanide toxicity (prolonged use) → metabolic acidosis, altered mental status; methemoglobinemia; hypotension
Fenoldopam	Hypotension, reflex tachycardia, headache, nausea

PART 4: CONDITIONS AND PREFERRED/CONTRAINDICATED DRUGS

Compelling Indications - Preferred Drugs

Condition	Preferred Drug(s)	Avoid
Diabetes with proteinuria/CKD	ACEi or ARB (first choice)	-
Heart failure with reduced EF (HFrEF)	ACEi/ARB + β-blocker (carvedilol/metoprolol/bisoprolol) + spironolactone + thiazide/loop diuretic	Non-DHP CCBs (verapamil, diltiazem, nifedipine)
Post-MI	ACEi + β-blocker + spironolactone	-
Ischemic heart disease / Angina	β-blocker, long-acting CCB (amlodipine, diltiazem)	Direct vasodilators alone (reflex tachycardia)
Atrial fibrillation / SVT	Verapamil, Diltiazem, β-blockers (rate control)	DHP CCBs (no rate control)
CKD (non-diabetic)	ACEi or ARB	-
Bilateral renal artery stenosis	CCB or alpha-blocker	ACEi, ARB, Aliskiren (reduce GFR)
Hypertension in pregnancy	Methyldopa (first-line), Hydralazine IV, Labetalol IV, Nifedipine	ACEi, ARBs, Aliskiren (all absolutely contraindicated - fetal renal toxicity)
Isolated systolic HTN (elderly)	Thiazide, long-acting DHP-CCB (amlodipine)	Beta-blockers (less effective in elderly)
Pheochromocytoma	Alpha-blocker (phenoxybenzamine) FIRST, then beta-blocker	Beta-blockers alone (hypertensive crisis from unopposed alpha)
Primary aldosteronism	Spironolactone, Eplerenone	-
Hypertension + BPH	Alpha-1 blocker (doxazosin, terazosin)	-
Hypertension + Gout	Losartan (has uricosuric effect) or CCB	Thiazides, Loop diuretics
Hypertension + Migraine	Propranolol, Metoprolol, Verapamil	-
Hypertension + Raynaud	CCB (nifedipine, amlodipine)	Beta-blockers (worsen Raynaud)
Aortic dissection	IV Labetalol, IV Esmolol + nitroprusside	Direct vasodilators alone
Hypertensive emergency	IV Nicardipine, IV Labetalol, IV Nitroprusside (most severe)	Oral nifedipine (unpredictable BP drop)
Cocaine-induced HTN	Benzodiazepines, Phentolamine, Labetalol	Non-selective beta-blockers (propranolol) - unopposed alpha crisis
Resistant HTN	Add spironolactone (4th drug)	-
Hyperthyroidism + HTN	Propranolol	-
Black patients	Thiazide, CCB	ACEi/ARBs (less effective as monotherapy)
COPD/Asthma	CCB, ACEi, ARB, thiazide	Non-selective beta-blockers; even cardioselective with caution

PART 5: HYPERTENSIVE EMERGENCY - TREATMENT OVERVIEW

Definition: BP >180/120 with acute target organ damage (stroke, MI, acute HF, aortic dissection, renal failure, hypertensive encephalopathy, retinal hemorrhage)

Goal: Reduce mean arterial pressure by no more than 25% in the first hour, then to 160/100 over 2-6 hours. Do NOT normalize BP acutely - risk of ischemic stroke, blindness, MI from loss of autoregulation.

Agent	Route	Best For
Nicardipine	IV infusion	Most hypertensive emergencies
Labetalol	IV bolus/infusion	Aortic dissection, pregnancy (eclampsia), stroke
Esmolol	IV infusion	Aortic dissection, perioperative
Nitroprusside	IV infusion	Most severe emergency (titratable) - watch cyanide
Fenoldopam	IV infusion	Emergency + renal protection needed
Hydralazine	IV	Eclampsia, pregnancy
Phentolamine	IV	Pheochromocytoma crisis, cocaine
Nitroglycerin	IV	Emergency + ACS or flash pulmonary edema
Clevidipine	IV	Perioperative / ICU

PART 6: SUMMARY TABLE - DRUG CLASS QUICK REFERENCE

Drug Class	MOA Summary	Key Indication	Key Contraindication	Key ADR
Thiazide diuretics	Block DCT Na+/Cl- transporter	First-line HTN; elderly; Black patients	Gout; severe renal failure	Hypokalemia, hyperuricemia, hyperglycemia
Loop diuretics	Block TAL NKCC2	HTN + CKD/HF	Anuria; dehydration	Hypokalemia, ototoxicity
K-sparing diuretics	Block aldosterone/ENaC	Resistant HTN; primary aldosteronism	Hyperkalemia; renal failure	Hyperkalemia; gynecomastia (spironolactone)
ACE inhibitors	Block ACE → no Ang II	Diabetic nephropathy; HFrEF; post-MI	Pregnancy; bilateral RAS; angioedema history	Dry cough; angioedema; hyperkalemia
ARBs	Block AT1 receptor	ACEi-intolerant; diabetic nephropathy	Pregnancy; bilateral RAS	No cough; hyperkalemia; rare angioedema
Beta-blockers	Block β-adrenoceptors	HTN + angina; HTN + HFrEF; post-MI	Asthma; AV block; pheochromocytoma (alone)	Bradycardia; bronchospasm; fatigue; mask hypoglycemia
DHP CCBs (amlodipine)	Block L-type Ca channels (vascular)	Elderly; isolated systolic HTN; angina	HFrEF (caution with nifedipine)	Ankle edema; flushing; reflex tachycardia (nifedipine)
Non-DHP CCBs	Block L-type Ca channels (heart+vessels)	HTN + AF; HTN + angina	HFrEF; AV block; WPW	Bradycardia; constipation (verapamil)
Alpha-1 blockers	Block α1 receptors → vasodilation	HTN + BPH; pheochromocytoma	Heart failure (fluid retention)	First-dose orthostatic hypotension
Central sympatholytics	α2 agonist → reduce sympathetic outflow	Pregnancy (methyldopa); resistant HTN (clonidine)	Abrupt withdrawal (clonidine); active liver disease (methyldopa)	Dry mouth; sedation; rebound HTN (clonidine withdrawal); Coombs+ (methyldopa)
Hydralazine	Release NO → arteriolar vasodilation	Pregnancy (IV); HF (+ nitrate)	CAD alone; aortic dissection; lupus	Reflex tachycardia; drug-induced lupus
Minoxidil	Open K+ channels → hyperpolarization	Severe/resistant HTN	-	Hypertrichosis; tachycardia; fluid retention
Nitroprusside	NO donor → arterial + venous dilation	Most severe hypertensive emergency	Prolonged use → cyanide toxicity	Cyanide/thiocyanate toxicity

Sources: Katzung's Basic & Clinical Pharmacology 16e (pp. 270-290), Lippincott Illustrated Reviews: Pharmacology (pp. 286-317), Robbins Pathologic Basis of Disease (pp. 2599-2610), Harrison's Principles of Internal Medicine 22e

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