Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Abbey pharm shelf/step > pharmacology: antihypertensive drugs > Flashcards

pharmacology: antihypertensive drugs Flashcards

1
Q

what are the antihypertensive drugs?

A

drugs altering sympathetic activity:

  • alpha 2 agonists (clonidine and mythyldopa)
  • drugs interfering with storage vesicles (reserpine and guanethidine)
  • alpha 1 blockers (prazosin, doxazosin, terazosin)
  • beta blockers

direct acting vasodilators:

  • NO acting: hydralazine, nitroprusside
  • open potassium channels (minoxidil and diazoxide)

calcium-channel blockers

  • verapamil, diltiazem
  • dihydropyridines (-dipines)

diuretics

ACEIs and ARBs)
ACEIs: prils
ARBs: sartan

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

what are the alpha 2 agonists? mechanism?

A

clonidine and methyldopa

mechanism: decrease sympathetic outflow causing decreased TPR and HR

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

clonidine and methyldopa uses

A

(alpha 2 agonists)

mild-to-moderate HTN, opiate withdrawal

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

what is the DOC of hypertensive management in pregnancy?

A

methyldopa

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

what are the side effects of clonidine and methyldopa? drug interactions?

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the drugs that interfere with storage vesicles?

A

reserpine (destroys vesicles - DEPRESSION) and guanethidine (accumulated into nerve endings by reuptake and inhibit NE release - not clinically relevant)

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

what are the alpha 1 blockers? mechanism?

A

-zosin (prazosin, doxazosin, terazosin)

decreased arteriolar and venous resistance

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

which drugs are used to treat both HTN and BPH? mechanism?

A

alpha 1 blockers (-ZOSIN) - decreases urinary frequency and nocturia by decreasing the tone of urinary sphincters causing better emptying of the bladder

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

alpha 1 blocker side effects

A

first-dose syncope, orthostatic hypotension (decreased preload), urinary incontinence

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

what are the side effects of beta blockers?

A

cardiovascular depression
fatigue (CNS depressant)
sexual dysfunction
increased LDLs and TGs (if already high)

*caution with asthma, vasospastic disorders, diabetics)

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

what are the direct-acting vasodilators?

A

-drugs acting through NO
hydralazine and nitroprusside

-drugs acting to open potassium channels
minoxidil and diazoxide

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

hydralazine side effects

A

SLE like syndrome and slow acetylators
edema
reflex tachycardia

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

nitroprusside use and side effect

A

use: hypertensive emergencies (DOC IV)

side effect: cyanide toxicity (co-administered with nitrites and thiosulfate) - can only use for 24-36 hours

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

drugs altering sympathetic activity vs direct vasodilators?

A

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

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

what are the drugs acting to open potassium channels? mechanism?

A

minoxidil and diazoxide (cause hyperpolarization of smooth muscle which results in arteriolar vasodilation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

minoxidil and diazoxide use and side effects

A

use: hypertensive emergencies, severe hypertension, baldness (minoxidil is rogaine)
SE: hyertrichosis (too much hair), hyperglycemia (decreased insulin release), edema, reflex tachy

17
Q

what are the calcium channel blockers? mechanism?

A

verapamil, diltiazem, dihydropyridiens (-dipines)

block L-trpe Ca channels in heart and blood vessels causing decreased CO and TPR

18
Q

calcium channel blockers uses and side effects

A

use: HTN, angina, antiarrhythmics (verapamil and diltizem)
SE: reflex tachy (dipine), gingival hyperplasia (dipines)
constipation (verpamil)

19
Q

what are the ACEIs? mechanism?

A

-prils
block formation of angiotensin II which causes both decreased aldosterone and vasodilation
also prevent bradykinin degradation

20
Q

what are the ARBs? mechanism?

A

-sartans

block AT1 receptors

21
Q

what is the renin inhibitor?

A

aliskiren

22
Q

ACEI and ARB uses

A

mild-to-moderate HTN, protective of diabetic nephropathy, CHF (prevent remodeling)

23
Q

ACEI and ARB side effects and contraindication

A

SE: dry cough (ACEI), hyperkalemia, acute renal failure in renal artery stenosis (no renin to bring more fluid), angioedema
contraindication: pregnancy

24
Q

DOC for angina

A

beta blockers and CCBs

25
Q

DOC diabetes

A

ACEIs and ARBs

26
Q

DOC heart failure

A

ACEIs, ARBs, beta blockers

27
Q

DOC post-MI

A

beta blockers

28
Q

DOC BPH

A

alpha blockers

29
Q

DOC dyslipidemias

A

alpha blockers, CCBs, ACEI/ARBs

NO BETA BLOCKERS AND THIAZIDES!!

30
Q

what is used for treatment of pulmonary HTN?

A

bosentan, sildenafil (inhibits PDE, increasing cGMP, pulmonary artery relaxation)

Abbey pharm shelf/step (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions