antihypertensive Flashcards
alpha 2 agonists
work on the presynaptic receptor that is Gi coupled. this causes a decrease in sympathetic outflow and thus decreased alpha and beta stimulation. this decreases TPR, HR -vasodilates and bradycardia.
indications for the alpha 2 agonists
mild-to-moderate HTN. management in pregnancy
what are the agents for alpha 2 agonists
clonidine and methyldopa.
SE of the alpha 2 agonists
positive coombs test (methyldopa) CNS depression, edema
what are the interactions with the alpha 2 agonists
TCA will decrease the antihypertensive effects of the alpha 2
reserpine mechanism
destroys the vesicles that contain NE. thus decrease the outflow. decreases the CO and TPR. decreases the NE, dop, and serotonin in the CNS.
SE of reserpine
severe depression. edema. there is increase in GI secretions
contraindications for reserpine
peptic ulcer disease, depression.
guanethidine mechanism
accumulates in the nerve terminal and inhibits the release of NE.
SE of guanethidine
edema, diarrhea,
what class cannot be taken with guanethidine
TCA. they will abolish the effects because they block the uptake pump.
alpha 1 blockers agents
prazosin, terazosin, doxazosin
alpha 1 blockers effects
decrease arteriolar and venous resistance, reflex tachycardia due to the drastic lowering of the BP.
uses of alpha 1 blockers
HTN, BPH
SE alpha 1 blockers
first dose syncope, orthostatic hypertension, urinary incontinence.
what is the positive about using alpha 1 blockers
there is a good effect on lipid profile. decreases LDL and increases HDL.
beta blockers effects
they actually work by decreasing the RAAS. although they also cause cardiodepression
beta blockers se
fatigue, sexual dysfunction, metabolic perturbations. increase LDL and TG. they can cause DM.
when should beta blocker use be cautioned
in asthmatics and vasospastic disorders.
hydralazine action
decreases the TPR via arteriolar dilation
uses of hydralazine
moderate to severe HTN. pregnancy management
SE of hydralazine
SLE-like syndrome. edema. reflex tachycardia.
nitroprusside action
decreases TPR via arterioles and venules.
what are the uses for nitroprusside
DOC for hypertensive emergencies.
what should be given with nitroprusside
nitrites and thiosulfate. this forms met-Hb and protects the electron transport chain from the CN- toxicity of nitroprusside.
what are the SE for nitroprusside
cyanide toxicity when used for more than 24-48 hrs.
minoxidil/diazoxide mechanism
opens ATP-dependent potassium channels and causes hyperpolarization of SM resulting in arteriolar vasodilation.
uses of minoxidil
hypertensive emergencies, severe hypertension, baldness.
SE of minoxidil
hypertrichosis, hyperglycemia, edema, reflex tachycardia.
calcium channel blockers mechanism
block L-type channels in the heart and the blood vessels. this decreases CO and TPR.
CCB agents
verapamil, diltiazem, nifedipine (and the other dipines)
which of the CCB acts on the blood vessels
the dipine class acts more on the blood vessels than the heart.
what is the use of the CCB
HTN, angina (esp. vasospastic), antiarrhythmic.
SE of the CCB
reflex tachycardia, gingival hyperplasia, constipation
which of the CCB works on the heart
verapamil is more specific for the heart. f
ACEi mechanism
block the formation of angiotensin II and thus the stimulation of the AT-1 receptor. this decreases aldosterone and vasodilation.
what effect does the ACEi have on bradkinin
inhibits its degradation.
SE of ACEi
cough. hyperkalemia. acute renal failure, angioedema.
uses of the ACEi
mild to moderate HTN. protective of diabetic nephropathy. CHF.
ARBs mechanism
blocks the angiotensin AT-1 receptor. same result as ACEi but no bradykinin accumulation.
what are the contraindications of the ACEi/ARBs
pregnancy and renal artery stenosis
bosentin uses?
pulmonary HTN.
mechanism for bosentin
ETA receptor antagonist.
SE of bosentin
HA, flushing, hypotension. -all do to the vasodilatory effects
sildenafil mechanism
inhibits PDE V. causes pulmonary artery relaxation and decreases pulmonary HTN.
