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Cardiology Exam > HTN Drugs > Flashcards

HTN Drugs Flashcards

1
Q

pharmacologic therapy classes for HTN (ABCDs)

A

*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)

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2
Q

classes of diuretics

A

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

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3
Q

what is the first-line choice diuretic for treating HTN in most patients?

A

*thiazide diuretics

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4
Q

thiazide diuretics - MOA

A

*inhibits Na+ absorption at DISTAL CONVOLUTED TUBULE (block Na+/Cl- exchange at DCT)

note - they also vasodilate to reduce BP

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5
Q

thiazide diuretics - examples

A

*hydrochlorothiazide (HCTZ)
*chlorthalidone
*metolazone
*chlorothiazide

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6
Q

thiazide diuretics - metabolism

A

*primarily renal

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7
Q

thiazide diuretics - ADEs

A

*allergy (rash) [sulfa allergy]
*HYPOKALEMIA
*HYPOMAGNESEMIA
*dehydration
*alkalosis (metabolic)
*nephritis
*gout

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8
Q

thiazide diuretics - uses

A

*hypertension (first-line medication used in HTN)
*heart failure (volume overload)

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9
Q

hydrochlorothiazide (HCTZ) - drug class, MOA, uses

A

*thiazide diuretic
*inhibit Na+ absorption at distal convoluted tubule
*used for HTN & heart failure

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10
Q

chlorthalidone - drug class, MOA, uses

A

*thiazide diuretic
*inhibit Na+ absorption at distal convoluted tubule
*used for HTN & heart failure

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11
Q

metolazone - drug class, MOA, uses

A

*thiazide diuretic
*inhibit Na+ absorption at distal convoluted tubule
*used for HTN & heart failure

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12
Q

chlorothiazide - drug class, MOA, uses

A

*thiazide diuretic
*inhibit Na+ absorption at distal convoluted tubule
*used for HTN & heart failure

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13
Q

thiazide diuretics - route & dosing

A

*PO
*taken once per day

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14
Q

which ions are “wasted” by thiazide diuretics?

A

*potassium → HYPOKALEMIA
*magnesium → HYPOMAGNESEMIA

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15
Q

loop diuretics - MOA

A

*inhibit Na+/Cl- absorption at ASCENDING LOOP OF HENLE

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16
Q

loop diuretics - examples

A

*furosemide (Lasix)
*bumetanide
*torsemide
*ethacrynic acid

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17
Q

loop diuretics - metabolism

A

*primarily renal

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18
Q

loop diuretics - ADEs

A

*ototoxicity
*hypokalemia
*hypomagnesemia
*dehydration
*allergy (rash) [sulfa allergy]
*alkalosis (metabolic)
*nephritis
*gout

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19
Q

loop diuretics - route & dosing

A

*mostly PO or IV
*furosemide - 3x per day (TID)
*bumetanide & torsemide - 2x per day (BID)

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20
Q

which ions are “wasted” by loop diuretics?

A

*potassium → HYPOKALEMIA
*magnesium → HYPOMAGNESEMIA

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21
Q

furosemide - drug class, MOA, uses

A

*loop diuretic
*inhibits Na+/Cl- absorption at ascending Loop of Henle
*used for heart failure, HTN, acute/chronic hyperkalemia

note - furosemide is aka Lasix

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22
Q

bumetanide - drug class, MOA, uses

A

*loop diuretic
*inhibits Na+/Cl- absorption at ascending Loop of Henle
*used for heart failure, HTN, acute/chronic hyperkalemia

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23
Q

torsemide - drug class, MOA, uses

A

*loop diuretic
*inhibits Na+/Cl- absorption at ascending Loop of Henle
*used for heart failure, HTN, acute/chronic hyperkalemia

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24
Q

loop diuretics - uses

A

*heart failure (volume overload)
*hypertension
*acute/chronic hyperkalemia

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25
Q

which diuretic causes more urine production compared to the other: loop diuretics or thiazide diuretics?

A

*LOOP diuretics produce more urine output compared to thiazide diuretics

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26
Q

potassium sparing diuretics: aldosterone antagonists - examples

A

*spironolactone
*eplerenone

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27
Q

potassium sparing diuretics: aldosterone antagonists - MOA

A

*block effects of aldosterone in distal tubules
*competitive aldosterone receptor antagonists in cortical collecting tubule

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28
Q

potassium sparing diuretics: aldosterone antagonists - route & dosing

A

*PO
*taken once per day

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29
Q

potassium sparing diuretics: aldosterone antagonists - metabolism

A

*hepatic

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30
Q

potassium sparing diuretics: aldosterone antagonists - ADEs

A

*HYPERKALEMIA (both spironolactone & eplerenone)
*spironolactone additional ADEs:
-gynecomastia
-breast tenderness
-hirsutism

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31
Q

potassium sparing diuretics: aldosterone antagonists - uses

A

*heart failure (volume overload; slows progression of HF)
*hypertension
*hyperaldosteronism
*cirrhosis (edema)

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32
Q

spironolactone - drug class, MOA, uses

A

*aldosterone antagonist, potassium sparing diuretic
*block effects of aldosterone in distal tubules
*used for heart failure, HTN, hyperaldosteronism, and cirrhosis

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33
Q

eplerenone - drug class, MOA, uses

A

*aldosterone antagonist, potassium sparing diuretic
*block effects of aldosterone in distal tubules
*used for heart failure, HTN, hyperaldosteronism, and cirrhosis

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34
Q

potassium sparing diuretics: Na+/K+ exchange inhibitors - examples

A

*amiloride
*triamterene

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35
Q

potassium sparing diuretics: Na+/K+ exchange inhibitors - MOA

A

*inhibit Na+/K+ exchange in collecting duct, distal tubule - secreted into lumen by proximal tubule cells

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36
Q

potassium sparing diuretics: Na+/K+ exchange inhibitors - route & dosing

A

*PO
*taken once per day

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37
Q

potassium sparing diuretics: Na+/K+ exchange inhibitors - metabolism

A

*amiloride - renal metabolism
*triamterene - hepatic metabolism

38
Q

potassium sparing diuretics: Na+/K+ exchange inhibitors - ADEs

A

*hyperkalemia
*rash

39
Q

potassium sparing diuretics: Na+/K+ exchange inhibitors - uses

A

*hypertension (rarely used)
*volume overload
*chronic hypokalemia

40
Q

calcium channel blockers - MOA in arteries/arterioles (vasculature)

A

*inhibit Ca2+ transport → VASODILATION → decreased BP

note - dihydropyridine CCBs primarily affect the vasculature

41
Q

calcium channel blockers - MOA in electrical system of heart

A

*inhibit Ca2+ transport → decreased HR or decreased contractility

note - non-dihydropyridine CCBs primarily affect the heart tissue (SA/AV node and ventricular myocardium)

42
Q

calcium channel blockers: 2 subclasses

A
  1. non-dihydropyridines (NDHP) → primarily SA & AV node inhibition → decreased HR and ventricular myocardium inhibition → decreased contractility
  2. dihydropyridines (DHP) → primarily inhibit calcium ions in the vasculature → vasodilation → decreased BP
43
Q

dihydropyridine CCBs - examples

A

*nifedipine
*amlodipine (Norvasc)
*R-pine

44
Q

dihydropyridine CCBs - MOA

A

*arterial VASODILATORS
*inhibit Ca2+ transport in the vasculature (arteries/arterioles) → VASODILATION → decreased BP

45
Q

dihydropyridine CCBs - ADEs

A

*pedal edema
*reflex tachycardia

46
Q

dihydropyridine CCBs - uses

A

*hypertension
*stable angina
*vascular vasospasm

47
Q

dihydropyridine CCBs - metabolism

A

*hepatic

48
Q

nifedipine - drug class, MOA, uses

A

*dihydropyridine calcium channel blocker (DHP CCB)
*inhibits Ca2+ transport in arterial vasculature → arterial VASODILATION → decreased BP
*used for HTN, stable angina, and vascular vasospasm

49
Q

amlodipine - drug class, MOA, uses

A

*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

50
Q

non-dihydropyridine CCBs - examples

A

*verapamil
*diltiazem

51
Q

non-dihydropyridine CCBs - MOA

A

*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)

52
Q

of the two non-dihydropyridine calcium channel blockers (verapamil & diltiazem), which is more INOTROPIC? which is more CHRONOTROPIC?

A

*VERAPAMIL is both more inotropic (decreases contractility more) and more chronotropic (decreases HR more) than diltiazem

53
Q

non-dihydropyridine CCBs - metabolism

A

*hepatic (numerous drug-drug interactions)

54
Q

non-dihydropyridine CCBs - ADEs

A

*decreased HR
*AV nodal blockade
*hypotension
*constipation
*gingival hyperplasia
*rash

55
Q

verapamil - drug class, MOA, uses

A

*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)

56
Q

diltiazem - drug class, MOA, uses

A

*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)

57
Q

non-dihydropyridine CCBs - uses

A

*hypertension
*stable angina
*ventricular rate control
*vascular vasospasm
*migraine prophylaxis

note - NDHP CCBs are class IV antiarrhythmics

58
Q

how long does amlodipine take to work?

A

*takes about 3 days to fully kick in

59
Q

beta blockers - MOA (in HTN)

A

*block either beta1 receptor (cardioselective) or both beta1 and beta2
*decrease HR/contractility
*decrease BP

60
Q

cardioselective beta blockers (beta1 blockers) - examples

A

*metoprolol
*esmolol
*atenolol
*bisoprolol

61
Q

beta blockers (beta1 & beta2 blockers) - examples

A

*labetalol (alpha1, beta1, beta2 blockers)
*carvedilol (alpha1, beta1, beta3 blockers)
*propranolol (beta1, beta2 blockers)

62
Q

beta blockers - ADEs

A

*drowsiness
*lethargy
*confusion
*broncho-reactive events
*AV nodal blockade

63
Q

metoprolol - drug class, MOA, uses, metabolism

A

*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)

64
Q

labetalol - drug class, receptor activity

A

*beta blocker
*NON-SPECIFIC: blocks alpha 1, beta 1, and beta 2

65
Q

carvedilol - drug class, receptor activity

A

*beta blocker
*NON-SPECIFIC: blocks alpha 1, beta 1, and beta 2

66
Q

propranolol - drug class, receptor activity, ADEs

A

*beta blocker
*blocks beta1 AND beta2
*most lipophilic (lipid soluble) beta blocker → high risk of CNS side effects (drowsiness, confusion, lethargy)

67
Q

angiotensin converting enzyme inhibitors (ACEi) - MOA

A

*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

68
Q

angiotensin converting enzyme inhibitors (ACEi) - examples

A

*captopril
*enalapril
*lisinopril
*ramipril

note - ACE inhibitors end in -pril

69
Q

angiotensin converting enzyme inhibitors (ACEi) - ADEs

A

*HYPERKALEMIA
*ANGIOEDEMA
*acute kidney injury
*COUGH
*hypotension
*avoid use in pregnancy (teratogenic)

70
Q

angiotensin II receptor blockers (ARBs) - MOA

A

*selectively block binding of angiotensin II to AT1 receptor
*prevents vasoconstriction of arterioles

71
Q

angiotensin II receptor blockers (ARBs) - examples

A

*losartan
*candesartan
*valsartan

note - ARBs end in -sartan

72
Q

angiotensin II receptor blockers (ARBs) - ADEs

A

*hyperkalemia
*angioedema
*acute kidney injury
*hypotension
*avoid use in pregnancy (teratogenic)

73
Q

aliskiren - drug class, MOA, ADEs

A

*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)

74
Q

doxazosin - drug class, MOA, ADEs, uses

A

*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

75
Q

hydralazine - drug class, MOA, ADEs, uses

A

*vasodilator
*MOA: increases cGMP → smooth muscle relaxation (VASODILATION)
*ADEs: reflex tachycardia, drug induced lupus
*use: 4th or 5th line drug for HTN

76
Q

minoxidil - drug class, MOA, ADEs, uses

A

*vasodilator
*MOA: increases cGMP → smooth muscle relaxation (VASODILATION)
*ADEs: hair growth, sodium/water retention
*use: 4th or 5th line drug for HTN

77
Q

clonidine - drug class, MOA, ADEs, uses

A

*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

78
Q

methyldopa - drug class, MOA, ADEs, uses

A

*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

79
Q

“compelling indications” in HTN treatment - defined

A

*clinical scenario where HTN & another existing comorbidity can be treated with a single drug

80
Q

compelling indication tx: HTN + HFrEF

A

*thiazides
*loops
*ACEi
*ARBs
*BBs
*aldosterone blockers

81
Q

compelling indication tx: HTN + HFpEF

A

*thiazide
*loops
*ACEi
*ARBs
*BBs
*aldosterone blockers

82
Q

compelling indication tx: HTN + post-MI

A

*BB
*ACEi
*ARBs
*aldosterone blockers

83
Q

compelling indication tx: HTN + coronary artery disease

A

*BB
*ACEi
*CCBs
*thiazides

84
Q

compelling indication tx: HTN + diabetes

A

*thiazides
*ACEi
*ARBs
*CCBs

85
Q

compelling indication tx: HTN + chronic kidney disease

A

*ACEi
*ARBs

86
Q

compelling indication tx: HTN + recurrent stroke prevention

A

*thiazides
*ACEi

87
Q

compelling indication tx: HTN + atrial fibrillation/flutter

A

*BBs
*NDHP CCBs (for ventricular rate control)

88
Q

compelling indication tx: HTN + PREGNANCY

A

*nifedipine
*methyldopa
*labetalol
*hydralazine

89
Q

drug-related HTN

A

*corticosteroids → fluid retention
*cocaine, amphetamines → vasoconstrictors
*cyclosporine/tacrolimus
*caffeine/nicotine → vasoconstrictors
*NSAIDs → fluid retention
*oral contraceptives → fluid retention
*decongestants → vasoconstrictors
*herbal products

90
Q

antihypertensive medications for hypertensive emergency/urgency

A

*nitroglycerin (venodilator)
*nitroprusside (arterial/venodilator)
*nicardipine (CCB)
*clevidipine (CCB)
*esmolol (beta1 selective BB)
*labetalol (nonselective BB)
*enalaprilat (ACEi)
*hydralazine (arterial vasodilator)

Cardiology Exam (47 decks)

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