antihypertensive Flashcards

(45 cards)

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

indications for the alpha 2 agonists

A

mild-to-moderate HTN. management in pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the agents for alpha 2 agonists

A

clonidine and methyldopa.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

SE of the alpha 2 agonists

A

positive coombs test (methyldopa) CNS depression, edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the interactions with the alpha 2 agonists

A

TCA will decrease the antihypertensive effects of the alpha 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

SE of reserpine

A

severe depression. edema. there is increase in GI secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

contraindications for reserpine

A

peptic ulcer disease, depression.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

guanethidine mechanism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

SE of guanethidine

A

edema, diarrhea,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what class cannot be taken with guanethidine

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

alpha 1 blockers agents

A

prazosin, terazosin, doxazosin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

alpha 1 blockers effects

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

uses of alpha 1 blockers

A

HTN, BPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

SE alpha 1 blockers

A

first dose syncope, orthostatic hypertension, urinary incontinence.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

beta blockers effects

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

beta blockers se

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
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.
26
what are the SE for nitroprusside
cyanide toxicity when used for more than 24-48 hrs.
27
minoxidil/diazoxide mechanism
opens ATP-dependent potassium channels and causes hyperpolarization of SM resulting in arteriolar vasodilation.
28
uses of minoxidil
hypertensive emergencies, severe hypertension, baldness.
29
SE of minoxidil
hypertrichosis, hyperglycemia, edema, reflex tachycardia.
30
calcium channel blockers mechanism
block L-type channels in the heart and the blood vessels. this decreases CO and TPR.
31
CCB agents
verapamil, diltiazem, nifedipine (and the other dipines)
32
which of the CCB acts on the blood vessels
the dipine class acts more on the blood vessels than the heart.
33
what is the use of the CCB
HTN, angina (esp. vasospastic), antiarrhythmic.
34
SE of the CCB
reflex tachycardia, gingival hyperplasia, constipation
35
which of the CCB works on the heart
verapamil is more specific for the heart. f
36
ACEi mechanism
block the formation of angiotensin II and thus the stimulation of the AT-1 receptor. this decreases aldosterone and vasodilation.
37
what effect does the ACEi have on bradkinin
inhibits its degradation.
38
SE of ACEi
cough. hyperkalemia. acute renal failure, angioedema.
39
uses of the ACEi
mild to moderate HTN. protective of diabetic nephropathy. CHF.
40
ARBs mechanism
blocks the angiotensin AT-1 receptor. same result as ACEi but no bradykinin accumulation.
41
what are the contraindications of the ACEi/ARBs
pregnancy and renal artery stenosis
42
bosentin uses?
pulmonary HTN.
43
mechanism for bosentin
ETA receptor antagonist.
44
SE of bosentin
HA, flushing, hypotension. -all do to the vasodilatory effects
45
sildenafil mechanism
inhibits PDE V. causes pulmonary artery relaxation and decreases pulmonary HTN.