Flashcards in pharmacology: antihypertensive drugs Deck (30):
what are the antihypertensive drugs?
drugs altering sympathetic activity:
-alpha 2 agonists (clonidine and mythyldopa)
-drugs interfering with storage vesicles (reserpine and guanethidine)
-alpha 1 blockers (prazosin, doxazosin, terazosin)
direct acting vasodilators:
-NO acting: hydralazine, nitroprusside
-open potassium channels (minoxidil and diazoxide)
ACEIs and ARBs)
what are the alpha 2 agonists? mechanism?
clonidine and methyldopa
mechanism: decrease sympathetic outflow causing decreased TPR and HR
clonidine and methyldopa uses
(alpha 2 agonists)
mild-to-moderate HTN, opiate withdrawal
what is the DOC of hypertensive management in pregnancy?
what are the side effects of clonidine and methyldopa? drug interactions?
SE: positive coomb's (methyldopa), CNS depression, edema
interactions: TCA decrease antihypertensive effects (alpha 2 is trying to lower NE while TCAs are blocking NE reuptake)
what are the drugs that interfere with storage vesicles?
reserpine (destroys vesicles - DEPRESSION) and guanethidine (accumulated into nerve endings by reuptake and inhibit NE release - not clinically relevant)
what are the alpha 1 blockers? mechanism?
-zosin (prazosin, doxazosin, terazosin)
decreased arteriolar and venous resistance
which drugs are used to treat both HTN and BPH? mechanism?
alpha 1 blockers (-ZOSIN) - decreases urinary frequency and nocturia by decreasing the tone of urinary sphincters causing better emptying of the bladder
alpha 1 blocker side effects
first-dose syncope, orthostatic hypotension (decreased preload), urinary incontinence
what are the side effects of beta blockers?
fatigue (CNS depressant)
increased LDLs and TGs (if already high)
*caution with asthma, vasospastic disorders, diabetics)
what are the direct-acting vasodilators?
-drugs acting through NO
hydralazine and nitroprusside
-drugs acting to open potassium channels
minoxidil and diazoxide
hydralazine side effects
SLE like syndrome and slow acetylators
nitroprusside use and side effect
use: hypertensive emergencies (DOC IV)
side effect: cyanide toxicity (co-administered with nitrites and thiosulfate) - can only use for 24-36 hours
drugs altering sympathetic activity vs direct vasodilators?
sympathetic activity: no reflex tachy, risk of orthostatic hypotension, increased PANS activity causing increased secretion which makes it bad for COPD
direct acting vasodilators: reflex tachy, no orthostatic hypotension, no increased PANS (less GI/GU problems), better for COPD
what are the drugs acting to open potassium channels? mechanism?
minoxidil and diazoxide (cause hyperpolarization of smooth muscle which results in arteriolar vasodilation)
minoxidil and diazoxide use and side effects
use: hypertensive emergencies, severe hypertension, baldness (minoxidil is rogaine)
SE: hyertrichosis (too much hair), hyperglycemia (decreased insulin release), edema, reflex tachy
what are the calcium channel blockers? mechanism?
verapamil, diltiazem, dihydropyridiens (-dipines)
block L-trpe Ca channels in heart and blood vessels causing decreased CO and TPR
calcium channel blockers uses and side effects
use: HTN, angina, antiarrhythmics (verapamil and diltizem)
SE: reflex tachy (dipine), gingival hyperplasia (dipines)
what are the ACEIs? mechanism?
block formation of angiotensin II which causes both decreased aldosterone and vasodilation
also prevent bradykinin degradation
what are the ARBs? mechanism?
block AT1 receptors
what is the renin inhibitor?
ACEI and ARB uses
mild-to-moderate HTN, protective of diabetic nephropathy, CHF (prevent remodeling)
ACEI and ARB side effects and contraindication
SE: dry cough (ACEI), hyperkalemia, acute renal failure in renal artery stenosis (no renin to bring more fluid), angioedema
DOC for angina
beta blockers and CCBs
ACEIs and ARBs
DOC heart failure
ACEIs, ARBs, beta blockers
alpha blockers, CCBs, ACEI/ARBs
NO BETA BLOCKERS AND THIAZIDES!!