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154 Cards in this Set
- Front
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classification of:
hydrochlorothiazide |
diuretic - thiazide
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classification of:
indapamide |
diuretic - thiazide
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classification of:
chlorthalidone |
diuretic - thiazide
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classification of:
spiranolactone |
diurectic
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classification of:
furosemide |
diuretic - loop diuretics
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classification of:
bumetanide |
diuretic - K+ sparing
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classification of:
triamterene |
diuretic - K+ sparing
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classification of:
amiloride |
diuretic - K+ sparing
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classification of:
methyldopa |
sympatholytics
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classification of:
clonidine |
sympatholytics
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classification of:
guanabenz |
sympatholytic
alpha 2 agonist |
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classification of:
guanadrel |
sympatholytic
adrenergic blocker |
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classification of:
trimethaphan |
sympatholytic
competitive antagonist at ACh receptor |
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classification of:
resperpine |
sympatholytic
irreversible VMAT antagonist |
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classification of:
guanethidine |
sympatholytic
NET uptake 1 blocker |
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classification of:
prazosin |
sympatholytic
a1 antagonist |
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classification of:
phentolamine |
sympatholytic
non-selective alpha antagonist |
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classification of:
propranolol |
sympatholytic
b1 and b2 antagonist |
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classification of:
metoprolol |
sympatholytic
b1 antagonist |
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classification of:
nadolol |
sympatholytic
non-selective beta blocker |
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classification of:
pindolol |
sympatholytic
non-selective Beta blocker B-adrenergic receptor agonist 5HT1A parital agonist/antag |
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classification of:
carvedilol |
sympatholytics
non-selective beta-blocker alpha 1 blocker |
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classification of:
timolol |
non-selective Beta adrenergic receptor antagonist
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classification of:
labetalol |
alpha and beta antagonist
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classification of:
hydralazine |
vasodilator
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classification of:
minoxodil |
vasodilator
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classification of:
diazoxide |
vasodilator
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classification of:
nitroprusside |
vasodilator
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classification of:
nitroglycerin |
vasodilator
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classification of:
nifedipine |
calcium-channel blockers
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classification of:
nicardipine |
calcium-channel blockers
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classification of:
aminodipine |
calcium-channel blockers
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classification of:
felodipine |
calcium-channel blockers
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classification of:
diltiazem |
calcium-channel blockers
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classification of:
verapamil |
calcium-channel blockers
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classification of:
captopril |
ACE inhibitors
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classification of:
enalapril |
ACE inhibitors
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classification of:
lisinopril |
ACE inhibitors
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classification of:
quinapril |
ACE inhibitors
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classification of:
losartan |
angiotensin receptor antagonist
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classification of:
candesartan |
angiotensin receptor antagonist
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classification of:
telmisartan |
angiotensin receptor antagonist
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classification of:
valsartan |
angiotensin receptor antagonist
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general mechanism of diuretics
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lower BP by depleting hte body of sodium and reducing the BV
directly reduce systemic vascular resistance dec BV dec BP |
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thiazides
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hydrochlorothiazide
chlorthalidone |
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loop diuretics
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furosemide
bumetanide torsemide |
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k+ sparing diuretics
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spironolactone
triamterene amiloride |
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general mechanism of sympatholytic
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reducing peripheral vascular resistance
inhibiting CO directly increasing venous pooling in capacitance vessels |
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centrally acting sympatholytic agents
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methyldopa
clonidine guanabenz |
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ganglionic blocking sympatholytic agents
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trimethaphan
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adrenergic neuronal blocking sympatholytic agents
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reserpine
guanadrel guanethidine |
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alpha antagonist sympatholytic agents
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prazosin
phentolamine |
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Beta blocker sympatholytic agents
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propranolol
metoprolol pindolol nadalol betaxolol |
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mixed acting antagonist sympatholytic agents
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labetalol
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arterioal vasodilators
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hydralazine
minoxidil diazoxide |
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arterial and venous vasodilators
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nitroprusside
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general mechanism for vasodilators
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relaxing vascular smooth muscle therby dilating resistance vessels
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general mechanism for ACE inhibitors
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block the synthesis of the potent vasoconstrictor, AT II, and salt retaining hormone, aldosterone
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ACE inhibitors
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captopril
enalapril lisinopril quinapril |
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general mechanism for ARBs
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directly antagonize the effects of AT II on the angiotensis receptor (type 1 AT-R)
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ARBs
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losartan
candesartan valsartan telmisartan irbesartan |
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drugs acting at vasomotor center
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methyldopa
clonidine guanabenz guanfacine |
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drugs acting at sympathetic nerve terminals
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guanethidine
guanadrel reserpine |
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drugs acting at B-receptors of heart
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propranolol
other B-blockers |
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drugs acting at sympathetic ganglia
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trimethaphan
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drugs acting at angiotensin receptors of vessels
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losartan
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drugs acting at alpha receptors of vessels
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prazosin
other alpha blockers |
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drugs acting at vascular smooth muscles
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hydralazine
verapamil minoxidil nitroprusside diazoxide other CCBs |
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drugs acting at kidney tubules
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thiazides
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drugs acting at B-receptors of juxtaglomerular cells that release renin
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propranolol
other Beta-blockers |
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CO or TPR:
B blockers |
CO
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CO or TPR:
peripherally acting sympathomimetics |
CO
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CO or TPR:
diuretics |
CO
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CO or TPR:
ACE inhibitors |
CO
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CO or TPR:
Beta blockers |
CO
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CO or TPR:
peripherally acting sympatholytics |
TPR
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CO or TPR:
CCBs |
TPR
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CO or TPR:
oral vasodilators |
TPR
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CO or TPR:
ACE inhibitors |
TPR
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CO or TPR:
centrally acting sympatholytics |
CO
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CO or TPR:
B blockers (on dec symp flow) |
TPR
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proposed mechanism of thiazide diurestics
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dec sodium, water retention
dec blood volume dec cardiac output dec peripheral resistance dec in BP |
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adverse effects of thiazide diuretics
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potassium depletion
hyponatremia metabolic alkalosis hypomagnesemia hyperuricermia and gout hypercalcemia hyperglycemia hyperlipidemia insulin resistance hypersensitivity resistance (fever, rash, purpura, anaphylaxis) contras: chronic arrhytmias and ischemic heart disease |
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adverse effects of loop diuretics
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hearing loss
watery diarrhea |
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adverse effects of K+ sparing diuretics
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hyperkalemia
megaloblastic anemia |
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therapeutic uses of thiazides
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manage HTN
more effective in african americans (susceptible to effects of volume expansion) |
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therapeutic uses of loop diuretics
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HTN in pts with advanced renal disease b/c of potent natriuretic properties and intrinsic ability to augment renal blood flow
multiple times a day |
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therapeutic uses of K+ sparing diuretics
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less potent
minimize K= depeletion used in combo with other drugs |
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frequent HTN Tx combos
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ACE Is and Ca+ channel blockers
ACE I and diuretics ARBs and diuretics B-blockers and diuretics |
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mechanism of centrally acting sympatholytics
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lower BP by dec symp flow originiating in vasomotor centers
don't interfere with sensitivity of these centers to baroreceptor control |
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methyldopa metabolism
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to alpha-methyl dopamine and then to alpha methylnorepi. it can be stored in noradrengergic receptors and replace NE as NT
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methyldopa action
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after release from NE receptors, it acts on alpha 2 receptors which decrease symp outflow
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clonidine action
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alpha 2 agonist
dec BP by directly stimulating central a2 receptors |
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methyldopa in older pts
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CO might be dec as a result of dec HR and SV (secondary to relaxation of veins and a reduction in preload)
renal blood flow is maintained and renal fxn unchanged |
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clonidine effects
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lowers BP by an effect on both CO and peripheral resistance
supine: reduce HR and SV upright: symp to vasculature is increased, clonidine reduces vascular resistance |
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adverse effects of methyldopa and clonidine
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sedation
mental lassitude impaired concentration depression (clonidine) dry mouth (clonidine) increase in prolactin secretion (methyldopa) positive coombs test (methyldopa) acute withdrawal can lead to life-threatening HTN crisis (clonidine) |
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clonidine works well with
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vasodilator because reflex inc in HR and CO that results from the vasodilator will be reduced or prevented with clonidine
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mechanism of action of ganglionic blocking agents
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competitive antagonists at all autonomic ganglia with ACh for nicotinic receptors
-results in pooling of blood in venous capacitance vessels; -hypotensive effect -direct vasodilation via release of histamine |
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use of trimethaphan
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HTN
HTN crises acute aortic dissection control BP during neurosurgery |
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adverse effects of ganglionic blocking agents
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due to blockade of both para and symp ganglia
tachycardia mydriasis cycloplegia tone/motility of GI dry mouth dec urination vasodilation pooling/ dec venous return heart contractions neuromuscular blockade |
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reserpine mechanism of action
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blocks uptake of biogenic amines into storage vesicles (VAT) in symp neurons and central CA neurons
depletion of these NTs (amines, NE, DA, serotonin) |
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adverse effects of resperpine
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drowsiness
lethargy parasymp (bradycardia, salivation, miosis, diarrhea, nausea, nasal congestion) severe depression with suicidal ideations |
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therapeutic uses of reserpine
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readily penetrates the brain
BP reduced in supine and erect position symp intact in low doses: dec CO and peripheral resistance |
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mechanism of action of guanethidine
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taken into symp nerve terminals to prevent release of symp transmitters and may also deplete NT stores
low bioavailbility |
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effect of guanethidine
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dec in BP due to venous pooling and reduced venous return
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adverse effects of guanethidine
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orthostatic hypoTN
lower incidence of diarhea |
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guanthedine is often used in combo with what drug
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diuretics to manage salt retention
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alpha-adrenergic antagonists mechanism of action
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prazosin: blocking postjunctional a1 recetpors without affecting a2
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effect of alpha-adrenergic antagonists
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reduces peripheral vascular resistance
dilates both arterioles and viens and reduces BP in both the supine and standing position tachycardia only with first dose high protein binding and 3 hour elimination halflife |
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beta-adrenergic antagonists mechanism of action
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competitive antagonists to B-receptors
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effects of beta-adrenergic antagonists
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negative inotropic and chronotropic effects in heart
slow atrioventricular conduction and increase PR interval |
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suggested mechanisms of antiHTN effect of beta-adrenergic antagonists
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dec CO
block B receptors in CNS inhibit renin release block prejunctional b receptors reduce venous return and BV reduce periph vascular resistance reduce vascular compliance reset baros attenuation of pressure reponse to CAs with exercise and stress |
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beta-adrenergic antagonists with LAA
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propranolol
pindolol metoprolol carvedilol labetalol (little) |
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beta-adrenergic antagonists with ISA
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pindolol
labetalol (little) |
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beta-adrenergic antagonists with selectivity
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metoprolol (b1)
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adverse effects of beta-adrenergic antagonists
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bradycardia, hypoTN, dec CO, cold extremities, precipitate or aggravate periph vascular dz
provoke asthmatic attacks in susceptible pts impair symp mediated rebound to hypoglycemia fatigue lethargy vivid dreams nightmares depression memory loss |
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therpeutic uses of beta-adrenergic antagonists
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essential HTN
ischemic heart dz management supraventricular arrhythmias idiopathis hypertrophic subaortic stenosis, pheochromocytoma, glaucoma, hyperthyroidism, anxiety, non-parkinsonian tremor, migraine, portal HTN, urinary incontinence, useful in alcohol withdrawal |
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mixed acting adrenergic antagonists : labetaolol and carvedilol
mechanism of action |
block B1, B2, and a
L - weak intrinsic sympathomimetic activity and LAA C - no intrin sympathomim and LAA |
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uses of labetalol and carvedilol
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L: dec vascular resistance therefore dec BP
L:IV for HTN crisis C: anti-oxidant |
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three broad categories of vasodilators
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oral
parenteral calcium channel blockers (Oral and parenteral) |
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oral vasodilators
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hydralazine
minoxidil |
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parenteral vasodilators
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sodium nitroprusside
diazoxide |
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CCB vasodilators
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fenoldopam
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hydrazaline mechanism of action
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dilation of arteries and arterioles but not veins
releases NO and activates K channels produces widespread vasodilation |
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hydrazaline effects and used in combo with what?
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vascular resistance is dec more prominently in cerebral, coronary, renal, and splanchnic than in skeletal, muscle, or skin; little effect in non-vascular smooth m
diuretics and B-blockers |
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adverse effects of hydrazaline
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headahce, nausea, anorexia, palpitations, sweating, and flushin
ischemic HD pts: reflex tachycardia and symp stim resulting in angina and cardiac arrythmias arthralgia and skin rashes |
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therapeutic uses of hydrazaline
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always with diuretic and B-blocker
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minoxidil mechanism of action
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opening K channels in vascular smooth muscle cells; results in stabilization of cell membrane, thus, inhibiting cell contraction; relaxes arterioles but not veins; longer acting; produces profound reflex activation of symp nervous system
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adverse effects of mioxidil
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tachycardia
palpitations angina edema (if not combined with B-blocker, diuretic) headache sweating hypertrichosis |
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mioxidil therapeutic uses
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HTN
rogaine |
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mechanism of action of sodium nitroprusside
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dilates arteries and veins which results in reduced arteriolar resistance and venous return
release of NO which activates GC resulting in inc of cGMP |
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adverse effects of sodium nitroprusside
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accumulation of cyanide
(cyanide intox tx: sodium thiosulfate) |
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therpeutic use of sodium nitroprusside
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HTN emergencies and cardiac failure
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diazoxide mechanism of action
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opening K channels resulting in stabilization of RMP
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effect of diazoxide
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IV: rapid fall in vascular resistance and mean arterial pressure
tachycardia 4-12 hours |
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adverse effects of diazoxide
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hyperuricemia
severe hyperglycemia excessive falls in BP angina ischemia cardiac failure |
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mechanism of action of CCBs
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inhibit calcium influx into arterial smooth m cells by blocking L-type Ca+ channels
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nifedipine action
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selective effects on arterial resistance vessels, which reduces BP (afterload)
results in reflex increase in HR and contractility |
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side effects of nifedipine
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hypotension
headache peripheral edema |
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diltiazem effects
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decrease BP and inc coronary blood flow
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diltiazem side effects
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only seen in 2-5%
peripheral edema AV conduction delays fall in CO |
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verapamil effects
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coronary and peripheral vasodilating effects
negative inotropic agent |
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verapamil side effects
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8-10%
cardiodepression cardiac conduction delays peripheral edema headache constipation |
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ACE inhibitors mechanism of action
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blocks conversion of angiotensin I to angiotensin II
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ACE inhibitors effect
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lower BP by decreasing periph resistance
less effective in pts with low renin essential HTN |
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captopril effect
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increases level of bradykinin by preventing its inactivation
fall in aldosterone synthesis and reflex increase in plasma renin activity reduction in ventricular afterload, it augments CO in CHF pts |
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captopril side effects
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hyperkalemia b/c of effect on aldosterone synthesis
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use of captopril
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HTN
CHF left ventricular dysfunction after MI diabetic nephropahty |
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capto can be used iwth
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thiazide diuretics
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enalapril metabolism
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pro-drug converted by deesterification to a converting enzyme inhibitor
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enalapril adverse effects
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hypotension
acute renal failure (in renal dz pts) decrease in renal function is attributed to a dec in AT II dry cough accomp by wheezing and angioedema due to inc in bradykinin |
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angiotensin receptor antagonists mechanism
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blocking AT II receptor and have no effect on bradykinin metabolism
more complete blockade of effects of AT II by directly antagonizing the interaction of AT II with its receptor |
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ARB prototype
selectivity |
losartan
AT1 selective |
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ARB effects
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decrease peripheral arterial pressure (afterload) and cardiac venous return (preload)
lower BP indep of RAAS |
