Antihypertensives Flashcards
Hydrochlorothiazide: class
Thiazide diuretic, reduces Na reabsorption in distal tubule
Hydrocholorthiazide: indication
Antihypertensive, diuretic
Lisinopril: class
ACE inhibitor
Lisinopril: indication
Antihypertensive, CHF
Captopril: class
ACE inhibitor
Captopril: indication
Antihypertensive, CHF
Enalapril: class
ACE Inhibitor
Enalapril: indication
Antihypertensive, CHF
Ramipril: class
ACE Inhibitor
Ramipril: indication
Antihypertensive, CHF
Losartan: class
Angiotensin-1 receptor blocker
Losartan: indication
Antihypertensive, diuretic
Nitroprusside: class
Venous and Arterial Vasodilator
Nitroprusside: indication
Antihypertensive, CHF
Hydralazine: class
Arterial vasodilator
Hydralazine: indication
Antihypertensive, CHF
Verapamil: class
Calcium entry blockers
Verapamil: indication
Antihypertensive, antianginal, antiarrhythmic Class IV
Nifedipine: class
Calcium entry blockers
Nifedipine: indication
Antihypertensive, antianginal, antiarrhythmic
Amlodipine: class
Calcium entry blockers
Amlodipine: indication
Antihypertensive, antianginal, antiarrhythmic
Diltiazem: class
Ca entry blocker
Diltiazem: indication
Antihypertensive, antianginal, antiarrhythmic
Nicardipine: class
Ca entry blocker
Nicardipine: indication
Antihypertensive, antianginal, antiarrhythmic
Hydrochlorothiazide: PD
block reuptake of Cl and Na from tubular fluid after glomerular filtration; also appears to cause decrease in SVR via unclear mechanism; will lower BP by up to 10-15 mm in many patients; useful as monotherapy or in combinations; HCTZ most commonly used, but perhaps some slight edge to chlorthalidone (duration, efficacy)
Hydrochlorothiazide: PK
F ~70%, excreted unchanged in urine; short half-life (hours); HCTZ not available in IV formulation; onset 2 h, peak 5 h, duration 10 h
Hydrochlorothiazide: tox
allergy to sulfa antibiotics (?); cause K and Mg depletion; cause Na and Cl depletion, metabolic alkalosis; volume depletion; worsen hyperuricemia
Hydrochlorothiazide: interactions
additive effects with most other antihypertensives
Hydrochlorothiazide: special
more side effects in geriatric patients; Pregnancy Class D; much less effective in patients with reduced GFR
Hydrochlorothiazide: monitor
BP, weight, edema, K, Mg, BUN, creatinine
Lisinopril: PD
inhibits conversion of AT I to AT II by ACE; diminishes both vasocontriction and stimulation of aldosterone secretion by AT II
Lisinopril: PK
well absorbed; onset 1 h, peak 6 h, duration 24 h; once a day is fine; excreted primarily in urine as unchanged drug
Lisinopril: tox
orthostatic hypotension; use with caution in patients with impaired renal function, or renal artery stenosis; be careful in patients on diuretics, or those with aortic stenosis; angioedema, cough; acute renal failure
Lisinopril: interactinos
additive effects with most other antihypertensives; NSAIDs may reduce ability to lower BP; hyperkalemia with KCL, others
Lisinopril: special
often discontinue diuretics prior to beginning use to reduce hypotension; Category C/D in pregnancy, abnormal cartilage development
Lisinopril: monitor
BP, weight, edema, K, BUN, creatinine!!!!!
Why might Lisinopril be best option for preserving renal function?
Inhibits ATII, which causes constriction of efferent arterioles. Can damage glomeruli. But if you dilate the efferent, lowers pressure inside glomerulus, preserves fxn longer. Slows progression of renal failure in diabetics.
Losartan: PD
block stimulation of AT I receptor by angiotensin II, thereby reducing vasoconstriction and production of aldosterone
Losartan: PK
F ~30%; onset 6 h; extensive first pass effect; active metabolite is 40x more potent, much longer half-life
Losartan: tox
dizziness; orthostatic hypotension; worsening of renal failure
Losartan: interactions
additive effects with most other antihypertensives
Losartan: special
Pregnancy class C/D; use care in patients on diuretics, those with renal artery stenosis, those with mitral or aortic stenosis
Losartan: monitor
BP, weight, edema, lytes, BUN, creatinine!!!
Nitroprusside: PD
acts “directly” on vascular smooth muscle to cause dilatation of both veins and arterioles; metabolized to release CN- and NO, which activates guanylate cyclase, leads to production of cGMP from GTP, which then leads to vasodilation; cGMP then hydrolyzed to GMP by PDE
Nitroprusside: PK
only route is iv; rapid onset (minutes) and cessation (minutes), thereby allowing minute-by-minute titration; CN- metabolite is converted to SCN in liver, then excreted in urine; must be given by continuous infusion
Nitroprusside: tox
excessive hypotension; accumulation of CN- and thiocyanate; headache; decreased blood flow to brain
Nitroprusside: interactions
additive effects with most other antihypertensives
Nitroprusside: special
monitor patient VERYclosely—must be in ICU with arterial line; avoid high infusion rates or prolonged infusions, to prevent accumulation of CN-; use with caution in patients with increased intracranial pressure
Nitroprusside: monitor
BP, HR, metabolic acidosis; most often requires arterial line
Hydralazine: PD
“direct” acting vasodilator; seems to act by inducing endothelium to produce NO, which then passes to SM cells and induces production of cGMP, minimal venodilating effect
Hydralazine: PK
given po, im, iv; metabolized extensively in GI mucosa and in liver, eventually excreted as metabolites in urine; F ~40%; onset 30 after po dose, 10 min after iv dose; persist for 2-6 hours
Hydralazine: tox
more dangerous in patients with renal disease, prior stroke, angina; watch for hypotension, edema, occasionally drug-induced lupus
Hydralazine: interactions
additive effects with most other antihypertensives
Hydralazine: special
never use as chronic oral monotherapy for treatment of hypertension, since edema and reflex tachycardia will result; concern giving to patients with CAD
Hydralazine: monitor
BP, weight, edema, BUN, creatinine, symptoms of lupus or angina
Hydralazine: use in pregnancy
Lowers BP in 3rd tri. Used for short period of time, won’t cause lupus.
Verapamil: PD
reduces BP by inhibiting influx of calcium through “slow channels”, thereby dilating peripheral arterioles; produces negative inotropic effect as well; for angina, reduces afterload, thus decreasing oxygen consumption; also, inhibits spasm of coronary arteries in vasospastic angina; blocks reentry paths through AV nodes in paroxysmal SVT
Verapamil: PK
absorbed rapidly, but F ~30%; also available in SR tablets; cleared by kidney and liver (produces active metabolites); onset 2 h po, 1-5 min iv; half-life 6-12 h; may be given po or iv
Verapamil: tox
hypotension, AV block, worsening of CHF, bradycardia
Verapamil: interactions
additive effects with most other antihypertensives; additive toxic effects on heart when given with beta-blockers
Verapamil: special
use reduced doses in patients with both renal and hepatic disease; short-acting nifedipine (and similar CEBs) can increase risk of MI (unclear why); Pregnancy C
Verapamil: monitor
BP, weight, edema
Nifedipine: same class as ?
same as Verapamil
Clonidine: PD
stimulates alpha-2 adrenoceptors in brainstem, thereby leading to down-regulation of sympathetic output
Clonidine: PK
Onset 1 h, duration 8 h, F~85%, also available as cutaneous patch
Clonidine: tox
withdraw gradually because of risk of rebound HTN; risk of bradycardia in sinus node disease; lethargy, fatigue, depression
Clonodine: interaction
additive effects with most other antihypertensives; additive sedation with other CNS drugs
Clonidine: special
Pregnancy class C; avoid in patients with renal insufficiency
Clonidine: monitor
follow BP and HR, fatigue
Methyldopa: class
a2 agonist (central action)
Methyldopa: indication
antihypertensive
Clonidine: class
a2 agonist (central action)
Clonidine: indication
antihypertensive
Trimethaphan: class
NN (ganglionic) blocker
Trimethaphan: indication
Antihypertensive
Reserpine: class
Blocks NE uptake into vesicles
Reserpine: indication
Antihypertensive
Reserpine: PD
binds to vesicles that contain NE or serotonin, preventing their uptake, and ultimately depleting the neuron of NE (or serotonin); this effect takes 2-3 weeks to develop, and including neurons and also the adrenal medulla
Reserpine: PK
good oral bioavailability, but biologic effects take 2-3 weeks to develop (via slow depletion of NE from vesicles)
Reserpine: tox
dizziness; orthostatic hypotension; depression
Reserpine: interaction
additive effects with most other antihypertensives
Reserpine: special
approved by the FDA in 1953!!! First antihypertensive drug approved, and first sympatholytic drug approved by the FDA (remember that in 1960’s, drugs included only reserpine, HCTZ, and hydralazine)
Reserpine: monitor
BP, sympathetic tone, depression!!!!
Reserpine: note
I include this drug to show that this mechanism does work, and for historical interest!! This drug is not used in the long-term management of HTN today in the US, but it is of great historical importance!!
Atenolol: class
B1 blocker
Atenolol: indication
Antihypertensive, antianginal, antiarrhythmic, anti-MI
Prazosin: class
A1 blocker
Prazosin: indication
Antihypertensive, Rx for BHP
Terazosin: class
A1 blocker
Terazosin: indication
Antihypertensive, Rx for BHP
Doxazosin: class
A1 blocker
Doxazosin: indication
Antihypertensive, Rx for BHP
Labetalol: class
A1 and B blocker
Labetalol: indication
Antihypertensive, pheochromocytoma, Hypertensive crisis, pre-eclampsia