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shelf pharm > antihypertensive > Flashcards

antihypertensive Flashcards

1
Q

alpha 2 agonists

A

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.

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2
Q

indications for the alpha 2 agonists

A

mild-to-moderate HTN. management in pregnancy

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3
Q

what are the agents for alpha 2 agonists

A

clonidine and methyldopa.

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4
Q

SE of the alpha 2 agonists

A

positive coombs test (methyldopa) CNS depression, edema

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5
Q

what are the interactions with the alpha 2 agonists

A

TCA will decrease the antihypertensive effects of the alpha 2

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6
Q

reserpine mechanism

A

destroys the vesicles that contain NE. thus decrease the outflow. decreases the CO and TPR. decreases the NE, dop, and serotonin in the CNS.

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7
Q

SE of reserpine

A

severe depression. edema. there is increase in GI secretions

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8
Q

contraindications for reserpine

A

peptic ulcer disease, depression.

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9
Q

guanethidine mechanism

A

accumulates in the nerve terminal and inhibits the release of NE.

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10
Q

SE of guanethidine

A

edema, diarrhea,

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11
Q

what class cannot be taken with guanethidine

A

TCA. they will abolish the effects because they block the uptake pump.

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12
Q

alpha 1 blockers agents

A

prazosin, terazosin, doxazosin

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13
Q

alpha 1 blockers effects

A

decrease arteriolar and venous resistance, reflex tachycardia due to the drastic lowering of the BP.

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14
Q

uses of alpha 1 blockers

A

HTN, BPH

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15
Q

SE alpha 1 blockers

A

first dose syncope, orthostatic hypertension, urinary incontinence.

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16
Q

what is the positive about using alpha 1 blockers

A

there is a good effect on lipid profile. decreases LDL and increases HDL.

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17
Q

beta blockers effects

A

they actually work by decreasing the RAAS. although they also cause cardiodepression

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18
Q

beta blockers se

A

fatigue, sexual dysfunction, metabolic perturbations. increase LDL and TG. they can cause DM.

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19
Q

when should beta blocker use be cautioned

A

in asthmatics and vasospastic disorders.

20
Q

hydralazine action

A

decreases the TPR via arteriolar dilation

21
Q

uses of hydralazine

A

moderate to severe HTN. pregnancy management

22
Q

SE of hydralazine

A

SLE-like syndrome. edema. reflex tachycardia.

23
Q

nitroprusside action

A

decreases TPR via arterioles and venules.

24
Q

what are the uses for nitroprusside

A

DOC for hypertensive emergencies.

25
Q

what should be given with nitroprusside

A

nitrites and thiosulfate. this forms met-Hb and protects the electron transport chain from the CN- toxicity of nitroprusside.

26
Q

what are the SE for nitroprusside

A

cyanide toxicity when used for more than 24-48 hrs.

27
Q

minoxidil/diazoxide mechanism

A

opens ATP-dependent potassium channels and causes hyperpolarization of SM resulting in arteriolar vasodilation.

28
Q

uses of minoxidil

A

hypertensive emergencies, severe hypertension, baldness.

29
Q

SE of minoxidil

A

hypertrichosis, hyperglycemia, edema, reflex tachycardia.

30
Q

calcium channel blockers mechanism

A

block L-type channels in the heart and the blood vessels. this decreases CO and TPR.

31
Q

CCB agents

A

verapamil, diltiazem, nifedipine (and the other dipines)

32
Q

which of the CCB acts on the blood vessels

A

the dipine class acts more on the blood vessels than the heart.

33
Q

what is the use of the CCB

A

HTN, angina (esp. vasospastic), antiarrhythmic.

34
Q

SE of the CCB

A

reflex tachycardia, gingival hyperplasia, constipation

35
Q

which of the CCB works on the heart

A

verapamil is more specific for the heart. f

36
Q

ACEi mechanism

A

block the formation of angiotensin II and thus the stimulation of the AT-1 receptor. this decreases aldosterone and vasodilation.

37
Q

what effect does the ACEi have on bradkinin

A

inhibits its degradation.

38
Q

SE of ACEi

A

cough. hyperkalemia. acute renal failure, angioedema.

39
Q

uses of the ACEi

A

mild to moderate HTN. protective of diabetic nephropathy. CHF.

40
Q

ARBs mechanism

A

blocks the angiotensin AT-1 receptor. same result as ACEi but no bradykinin accumulation.

41
Q

what are the contraindications of the ACEi/ARBs

A

pregnancy and renal artery stenosis

42
Q

bosentin uses?

A

pulmonary HTN.

43
Q

mechanism for bosentin

A

ETA receptor antagonist.

44
Q

SE of bosentin

A

HA, flushing, hypotension. -all do to the vasodilatory effects

45
Q

sildenafil mechanism

A

inhibits PDE V. causes pulmonary artery relaxation and decreases pulmonary HTN.

shelf pharm (20 decks)

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