HTN Drugs Flashcards
pharmacologic therapy classes for HTN (ABCDs)
*A: angiotensin converting enzyme inhibitors (ACEi) / angiotensin II receptor blockers (ARBs)
*B: beta blockers (BBs)
*C: calcium channel blockers (CCBs)
*D: diuretics
*miscellaneous agents (peripheral alpha-1 receptor blockers, vasodilators, centrally acting agents)
classes of diuretics
*thiazide diuretics
*loop diuretics
*potassium sparing diuretics:
-aldosterone antagonists
-Na+/K+ exchange inhibitors
note: carbonic anhydrase inhibitors and osmotic diuretics are NOT used as anti-hypertensives
what is the first-line choice diuretic for treating HTN in most patients?
*thiazide diuretics
thiazide diuretics - MOA
*inhibits Na+ absorption at DISTAL CONVOLUTED TUBULE (block Na+/Cl- exchange at DCT)
*increased urine output → decreased blood volume → DECREASED BP
note - they also vasodilate to reduce BP
thiazide diuretics - examples
*hydrochlorothiazide (HCTZ)
*chlorthalidone
*metolazone
*chlorothiazide
thiazide diuretics - metabolism
*primarily renal
thiazide diuretics - ADEs
*allergy (rash) [sulfa allergy]
*HYPOKALEMIA
*HYPOMAGNESEMIA
*dehydration
*alkalosis (metabolic)
*nephritis
*gout
thiazide diuretics - uses
*hypertension (first-line medication used in HTN)
*heart failure (volume overload)
hydrochlorothiazide (HCTZ) - drug class, MOA, uses
*thiazide diuretic
*inhibit Na+ absorption at distal convoluted tubule
*used for HTN & heart failure
chlorthalidone - drug class, MOA, uses
*thiazide diuretic
*inhibit Na+ absorption at distal convoluted tubule
*used for HTN & heart failure
metolazone - drug class, MOA, uses
*thiazide diuretic
*inhibit Na+ absorption at distal convoluted tubule
*used for HTN & heart failure
chlorothiazide - drug class, MOA, uses
*thiazide diuretic
*inhibit Na+ absorption at distal convoluted tubule
*used for HTN & heart failure
thiazide diuretics - route & dosing
*PO
*taken once per day
which ions are “wasted” by thiazide diuretics?
*potassium → HYPOKALEMIA
*magnesium → HYPOMAGNESEMIA
loop diuretics - MOA
*inhibit Na+/Cl- absorption at ASCENDING LOOP OF HENLE
loop diuretics - examples
*furosemide (Lasix)
*bumetanide
*torsemide
*ethacrynic acid
loop diuretics - metabolism
*primarily renal
loop diuretics - ADEs
*ototoxicity
*hypokalemia
*hypomagnesemia
*dehydration
*allergy (rash) [sulfa allergy]
*alkalosis (metabolic)
*nephritis
*gout
loop diuretics - route & dosing
*mostly PO or IV
*furosemide - 3x per day (TID)
*bumetanide & torsemide - 2x per day (BID)
which ions are “wasted” by loop diuretics?
*potassium → HYPOKALEMIA
*magnesium → HYPOMAGNESEMIA
furosemide - drug class, MOA, uses
*loop diuretic
*inhibits Na+/Cl- absorption at ascending Loop of Henle
*used for heart failure, HTN, acute/chronic hyperkalemia
note - furosemide is aka Lasix
bumetanide - drug class, MOA, uses
*loop diuretic
*inhibits Na+/Cl- absorption at ascending Loop of Henle
*used for heart failure, HTN, acute/chronic hyperkalemia
torsemide - drug class, MOA, uses
*loop diuretic
*inhibits Na+/Cl- absorption at ascending Loop of Henle
*used for heart failure, HTN, acute/chronic hyperkalemia
loop diuretics - uses
*heart failure (volume overload)
*hypertension
*acute/chronic hyperkalemia
which diuretic causes more urine production compared to the other: loop diuretics or thiazide diuretics?
*LOOP diuretics produce more urine output compared to thiazide diuretics
potassium sparing diuretics: aldosterone antagonists - examples
*spironolactone
*eplerenone
potassium sparing diuretics: aldosterone antagonists - MOA
*block effects of aldosterone in distal tubules
*competitive aldosterone receptor antagonists in cortical collecting tubule
potassium sparing diuretics: aldosterone antagonists - route & dosing
*PO
*taken once per day
potassium sparing diuretics: aldosterone antagonists - metabolism
*hepatic
potassium sparing diuretics: aldosterone antagonists - ADEs
*HYPERKALEMIA (both spironolactone & eplerenone)
*spironolactone additional ADEs:
-gynecomastia
-breast tenderness
-hirsutism
potassium sparing diuretics: aldosterone antagonists - uses
*heart failure (volume overload; slows progression of HF)
*hypertension
*hyperaldosteronism
*cirrhosis (edema)
spironolactone - drug class, MOA, uses
*aldosterone antagonist, potassium sparing diuretic
*block effects of aldosterone in distal tubules
*used for heart failure, HTN, hyperaldosteronism, and cirrhosis
eplerenone - drug class, MOA, uses
*aldosterone antagonist, potassium sparing diuretic
*block effects of aldosterone in distal tubules
*used for heart failure, HTN, hyperaldosteronism, and cirrhosis
potassium sparing diuretics: Na+/K+ exchange inhibitors - examples
*amiloride
*triamterene
potassium sparing diuretics: Na+/K+ exchange inhibitors - MOA
*inhibit Na+/K+ exchange in collecting duct, distal tubule - secreted into lumen by proximal tubule cells
potassium sparing diuretics: Na+/K+ exchange inhibitors - route & dosing
*PO
*taken once per day
potassium sparing diuretics: Na+/K+ exchange inhibitors - metabolism
*amiloride - renal metabolism
*triamterene - hepatic metabolism
potassium sparing diuretics: Na+/K+ exchange inhibitors - ADEs
*hyperkalemia
*rash
potassium sparing diuretics: Na+/K+ exchange inhibitors - uses
*hypertension (rarely used)
*volume overload
*chronic hypokalemia
calcium channel blockers - MOA in arteries/arterioles (vasculature)
*inhibit Ca2+ transport → VASODILATION → decreased BP
note - dihydropyridine CCBs primarily affect the vasculature
calcium channel blockers - MOA in electrical system of heart
*inhibit Ca2+ transport → decreased HR or decreased contractility
note - non-dihydropyridine CCBs primarily affect the heart tissue (SA/AV node and ventricular myocardium)
calcium channel blockers: 2 subclasses
- non-dihydropyridines (NDHP) → primarily SA & AV node inhibition → decreased HR and ventricular myocardium inhibition → decreased contractility
- dihydropyridines (DHP) → primarily inhibit calcium ions in the vasculature → vasodilation → decreased BP
dihydropyridine CCBs - examples
*nifedipine
*amlodipine (Norvasc)
*R-pine
dihydropyridine CCBs - MOA
*arterial VASODILATORS
*inhibit Ca2+ transport in the vasculature (arteries/arterioles) → VASODILATION → decreased BP
dihydropyridine CCBs - ADEs
*pedal edema
*reflex tachycardia
dihydropyridine CCBs - uses
*hypertension
*stable angina
*vascular vasospasm
dihydropyridine CCBs - metabolism
*hepatic
nifedipine - drug class, MOA, uses
*dihydropyridine calcium channel blocker (DHP CCB)
*inhibits Ca2+ transport in arterial vasculature → arterial VASODILATION → decreased BP
*used for HTN, stable angina, and vascular vasospasm
amlodipine - drug class, MOA, uses
*dihydropyridine calcium channel blocker (DHP CCB)
*inhibits Ca2+ transport in arterial vasculature → arterial VASODILATION → decreased BP
*used for HTN, stable angina, and vascular vasospasm
note - amlodipine is aka Norvasc
non-dihydropyridine CCBs - examples
*verapamil
*diltiazem
non-dihydropyridine CCBs - MOA
*inhibit Ca2+ transport in the heart:
-inhibition in the SA/AV nodes → decreased HR (negative chronotropic effect: verapamil > diltiazem)
-inhibition in the ventricular myocardium → decreased contractility (negative inotropic effect: verapamil > diltiazem)
of the two non-dihydropyridine calcium channel blockers (verapamil & diltiazem), which is more INOTROPIC? which is more CHRONOTROPIC?
*VERAPAMIL is both more inotropic (decreases contractility more) and more chronotropic (decreases HR more) than diltiazem
non-dihydropyridine CCBs - metabolism
*hepatic (numerous drug-drug interactions)
non-dihydropyridine CCBs - ADEs
*decreased HR
*AV nodal blockade
*hypotension
*constipation
*gingival hyperplasia
*rash
verapamil - drug class, MOA, uses
*non-dihydropyridine calcium channel blocker (NDHP CCB)
*inhibits Ca+ transport in the heart → negative inotropy (decreased contractility) & negative chronotropy (decreased HR)
*used for HTN, stable angina, antiarrhythmic, ventricular rate control, migraine prophylaxis
note - verapamil is more negatively chronotropic & inotropic compared to diltiazem (verapamil decreases HR and contractility more)
diltiazem - drug class, MOA, uses
*non-dihydropyridine calcium channel blocker (NDHP CCB)
*inhibits Ca+ transport in the heart → negative inotropy (decreased contractility) & negative chronotropy (decreased HR)
*used for HTN, stable angina, antiarrhythmic, ventricular rate control, migraine prophylaxis
note - diltiazem is LESS negatively chronotropic & inotropic compared to verapamil (diltiazem decreases HR and contractility LESS)
non-dihydropyridine CCBs - uses
*hypertension
*stable angina
*ventricular rate control
*vascular vasospasm
*migraine prophylaxis
note - NDHP CCBs are class IV antiarrhythmics
how long does amlodipine take to work?
*takes about 3 days to fully kick in
beta blockers - MOA (in HTN)
*block either beta1 receptor (cardioselective) or both beta1 and beta2
*decrease HR/contractility
*decrease BP
cardioselective beta blockers (beta1 blockers) - examples
*metoprolol
*esmolol
*atenolol
*bisoprolol
beta blockers (beta1 & beta2 blockers) - examples
*labetalol (alpha1, beta1, beta2 blockers)
*carvedilol (alpha1, beta1, beta3 blockers)
*propranolol (beta1, beta2 blockers)
beta blockers - ADEs
*drowsiness
*lethargy
*confusion
*broncho-reactive events
*AV nodal blockade
metoprolol - drug class, MOA, uses, metabolism
*beta blocker, specific to beta1 (cardioselective)
*blocking beta1 receptor → decreased HR/contractility, decreased BP
*used in heart failure, HTN (not first line)
*metabolism: cleared by liver with moderate lipophilicity (penetrates blood-brain barrier easily → drowsiness, lethargy, confusion, etc)
labetalol - drug class, receptor activity
*beta blocker
*NON-SPECIFIC: blocks alpha 1, beta 1, and beta 2
carvedilol - drug class, receptor activity
*beta blocker
*NON-SPECIFIC: blocks alpha 1, beta 1, and beta 2
propranolol - drug class, receptor activity, ADEs
*beta blocker
*blocks beta1 AND beta2
*most lipophilic (lipid soluble) beta blocker → high risk of CNS side effects (drowsiness, confusion, lethargy)
angiotensin converting enzyme inhibitors (ACEi) - MOA
*inhibit ACE → decreased AT II → decreased GFR by PREVENTING CONSTRICTION of efferent arterioles
*prevents inactivation of bradykinin (a potent vasodilator) → more bradykinin
note - ACEi are a type of anti-RAS agents
angiotensin converting enzyme inhibitors (ACEi) - examples
*captopril
*enalapril
*lisinopril
*ramipril
note - ACE inhibitors end in -pril
angiotensin converting enzyme inhibitors (ACEi) - ADEs
*HYPERKALEMIA
*ANGIOEDEMA
*acute kidney injury
*COUGH
*hypotension
*avoid use in pregnancy (teratogenic)
angiotensin II receptor blockers (ARBs) - MOA
*selectively block binding of angiotensin II to AT1 receptor
*prevents vasoconstriction of arterioles
angiotensin II receptor blockers (ARBs) - examples
*losartan
*candesartan
*valsartan
note - ARBs end in -sartan
angiotensin II receptor blockers (ARBs) - ADEs
*hyperkalemia
*angioedema
*acute kidney injury
*hypotension
*avoid use in pregnancy (teratogenic)
aliskiren - drug class, MOA, ADEs
*renin inhibitor
*MOA: direct renin inhibitor → blocks conversion of angiotensinogen to angiotensin I → ultimately prevents vasoconstriction
*ADEs: hyperkalemia, angioedema, acute kidney injury, hypotension, avoid use in pregnancy (teratogenic)
doxazosin - drug class, MOA, ADEs, uses
*peripheral alpha-1 receptor blocker
*MOA: blocks alpha-1 receptors in peripheral vasculature → vasodilation
*ADEs: first dose syncope, dizziness, lethargy
*use: 4th or 5th line drug for HTN
hydralazine - drug class, MOA, ADEs, uses
*vasodilator
*MOA: increases cGMP → smooth muscle relaxation (VASODILATION)
*ADEs: reflex tachycardia, drug induced lupus
*use: 4th or 5th line drug for HTN
minoxidil - drug class, MOA, ADEs, uses
*vasodilator
*MOA: increases cGMP → smooth muscle relaxation (VASODILATION)
*ADEs: hair growth, sodium/water retention
*use: 4th or 5th line drug for HTN
clonidine - drug class, MOA, ADEs, uses
*alpha-2 receptor agonist
*MOA: stimulate alpha-2, blunting sympathetic nervous system
*ADEs: DRY MOUTH, SEDATION, mental status changes, confusion, REBOUND HYPERTENSION if abruptly stopped
*use: 4th or 5th line drug for HTN
methyldopa - drug class, MOA, ADEs, uses
*alpha-2 receptor agonist
*MOA: stimulate alpha-2, blunting sympathetic nervous system
*ADEs: dry mouth, sedation, mental status changes, confusion
*use: 4th or 5th line drug for HTN
“compelling indications” in HTN treatment - defined
*clinical scenario where HTN & another existing comorbidity can be treated with a single drug
compelling indication tx: HTN + HFrEF
*thiazides
*loops
*ACEi
*ARBs
*BBs
*aldosterone blockers
compelling indication tx: HTN + HFpEF
*thiazide
*loops
*ACEi
*ARBs
*BBs
*aldosterone blockers
compelling indication tx: HTN + post-MI
*BB
*ACEi
*ARBs
*aldosterone blockers
compelling indication tx: HTN + coronary artery disease
*BB
*ACEi
*CCBs
*thiazides
compelling indication tx: HTN + diabetes
*thiazides
*ACEi
*ARBs
*CCBs
compelling indication tx: HTN + chronic kidney disease
*ACEi
*ARBs
compelling indication tx: HTN + recurrent stroke prevention
*thiazides
*ACEi
compelling indication tx: HTN + atrial fibrillation/flutter
*BBs
*NDHP CCBs (for ventricular rate control)
compelling indication tx: HTN + PREGNANCY
*nifedipine
*methyldopa
*labetalol
*hydralazine
drug-related HTN
*corticosteroids → fluid retention
*cocaine, amphetamines → vasoconstrictors
*cyclosporine/tacrolimus
*caffeine/nicotine → vasoconstrictors
*NSAIDs → fluid retention
*oral contraceptives → fluid retention
*decongestants → vasoconstrictors
*herbal products
antihypertensive medications for hypertensive emergency/urgency
*nitroglycerin (venodilator)
*nitroprusside (arterial/venodilator)
*nicardipine (CCB)
*clevidipine (CCB)
*esmolol (beta1 selective BB)
*labetalol (nonselective BB)
*enalaprilat (ACEi)
*hydralazine (arterial vasodilator)
