Drugs for Hypertension Flashcards
Captopril Lisinopril Enalaprilat Benazepril Enalapril Fasinopril Moexipril Perindopril Quinapril Ramipril Trandolapril
ACEI
Mechanism:
decrease angiotensin II–>decreased vasoconstriction–>decreased aldosterone–> decrease Na+ and H2O
Decreased bradykinin breakdown–>vasodilation
1st line therapy: diabetes, chronic kidney disease, coronary artery disease, LVD, previous ischemic stroke
Pharmacokinetics: cleared by kidney, reduce dose in pts with high renin
Avoid use: pregnancy, bilateral renal artery stenosis, angioedema, high-normal K+, hyperkalemia, volume depletion
Favorable: low-normal K+, prediabetic, albuminuria
Adverse effects: hypotension, coughing (bradykinin), angioedema, increased K+, acute renal failure, fetopathic potential, skin rash
Elderly African Americans respond poorly
Losartan Candesartan Irbesartan Valsartan Telmisartan Olmesartan Eprosartan
ARBs
Mechanism:
binds angiotensin II type 1 receptor–>decrease effects of Ang-II
1st line therapy: diabetes, chronic kidney disease, coronary artery disease, LVD, used when intolerance to ACEI
Avoid use: pregnancy, bilateral renal artery stenosis, high-normal K_, hyperkalemia, volume depletion
Favorable: low-normal K+, prediabetes
Nifedipine
Amlodipine
Felodipine
Dihydropyridine Calcium Channel Blocker
Mechanism: vasodilator (10:1 vascular: cardiac)
1st line therapy: diabetes, coronary artery disease
Avoid use: LVD, peripheral edema, high-normal HR or tachycardia
Favorable: Reynaud syndrome, elderly w/ isolated systolic hypertension
Verapamil
Diltiazem
Non-dihydropyridine calcium channel blocker
Mechanism: vasodilator (1:1 vascular: cardiac)
1st line therapy: diabetes, alternative to beta blockers in coronary artery disease
Avoid use: 2nd or 3rd heart block, LVD, peripheral edema, low-normal heart rate
Favorable: Reynaud syndrome, migraine headache, high-normal HR or tachycardia
Chlorthiazide
Hydrochlorothiazide
Thiazide diuretics
Mechanism: inhibit NaCl reabsorption in DCT, vasodilation
1st line therapy: LVD, previous ischemic stroke, add on for diabetes and coronary artery disease
Avoid: prior allergic reaction to sulfa-type drugs, gout, hyponatremia, hypokalemia, prediabetes, elevated fasting glucose (causes hyperglycemia)
Favorable: osteoporosis, high-normal K+
Propranolol
Metoprolol
Pindolol
Labetolol
Beta blockers
Mechanism: block beta receptors (some block alpha as well–>labetalol)
1st line therapy: coronary artery disease, LVD, add on therapy for diabetes
Favorable: migraine headache, tachyarrhythmia, high-normal HR or tachycardia, hyperthyroidism, essential tremor, preoperative hypertension
Spironolactone
Eplerenone
Aldosterone antagonist
Mechanism: bind aldosterone receptor–>decrease Na+ and H2O retention
Add on therapy: resistant HTN, coronary artery disease, LVD
Favorable: low-normal K+, chronic kidney disease
Unfavorable: high-normal K_
Prazosin
Doxazosin
Terazosin
Alpha 1-andrenergic receptor blockers
Mechanism: selective at vascular smooth muscle alpha 1 receptors (a1»>a2)
Used with diuretics; lowers LDL, TG, and total cholesterol
Adverse effects: tolerance to antihypertensive effect, reflex tachycardia, sexual dysfunction
Clonidine
Alpha-2 agonist
Mechanism: stimulate alpha-2–>decrease NE release
Therapy: pts who can’t take meds by mouth (patch form), pts prone to early morning surge in BP
Adverse effect: rebound hypertension if stopped abruptly
Optimally used with diuretic to diminish fluid retention
alpha-methyldopa
Alpha-2 agonist
Mechanism: stimulate alpha-2–>decrease release of NE
Therapy: gestational HTN, and chronic HTN in pregnancy (safe use)
Adverse effects: anticholinergic side effects, hepatotoxicity, Direct Coomb’s test
Hydralazine
Arterial vasodilator
Mechanism:
decrease IP3-induced Ca2_ release from smooth muscle SR–>decreas contraction
Open Ca2+ activated K+ channels in smooth muscle–>relaxation
Relaxes arterioles
Therapy: add-on to manage resistant HTN (severe chronic kidney disease), gestational HTN
Adverse effect: lupus, compensatory tachycardia and Na+ retention–>use in combo with diauretic and Beta blocker or NDHP CCB
Minoxidil
Arterial Vasodilator
Mechanism:
activate ATP-dependent K+ channels–>relax arteriolar VSMCs
Cardiac effect: decrease BP, increase blood flow to heart, increase cardiac output, increased renal blood flow
Therapy: severe refractory hypertension, in combo with beta blockers and diuretics
Adverse effects: fluid and salt retention, reflex increase in myocardial contractility, hypertrichosis
Sodium nitroprusside
Arterial Vasodilator
Mechanism:
donates NO–>cGMP-mediated Ca2+ sequestration–>VENOdilation–>decrease afterload and preload
Use: intravenous agent for HTN emergencies and rapid management of CHF
Adverse effect: methemoglobinemia, cyanide poisoning, cell death due to inhibition of cellular respiration
Aliskiren
Direct renin inhibitor
Mechanism:
bind catalytic site of renin–>prevent cleaving angiotensinogen–>no Ang-I
Therapy: newer drug, monotherapy or in combo
Lowers BP when used in comb with thiazide, ACEI, ARB, or CCB
Adverse: hyperkalemia, kidney failure in pts with bilateral renal artery stenosis, NEVER use in pregnancy, orthostatic hypotension
Reserpine
Rauwolfia alkaloid
Mechanism:
block transport of NE into storage granules–>depletes NE from nerve endings
Therapy: rarely used due to side effects; combo with thiazide diuretics
Adverse effects: sedation, depression, decreased CO, orthostatic hypotension, increased parasympathetic activity
