Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

what are the ACE (angiotensin converting enzyme) inhibitors

A

captopril, enalapril, lisinopril

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

clinical uses of ACE inhibitors

A

hypertension (first line for primary)
heart failure
myocardial infarction
albuminuria in non pregnant patients

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

why aren’t ACE inhibitors first line agents for blacks and elderly

A

because the RAAS system is less active in them

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

how does ACE inhibitors work?

A
  • it blocks conversion of angiotensin I to angiotensin II hence reducing its vasoconstrictive activity and release of aldosterone
  • blocks degradation of bradykinin and stimulates release of vasodilators such as prostacyclin and prostaglandin E2
  • increase in renin since no neg feedback from angiotensin II
  • slight increase in serum creatinine
  • rise in K+ levels in blood if renal insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how do you dose the ACE inhibitors

A

enalapril and lisinopril given once a day while captopril given two to three times daily

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

adverse effects of ACE inhibitors

A

CATCHH
Cough (due to bradykinin)
Angioedema
Teratogen (fetal renal malformation; renal failure in those with bilateral renal artery stenosis)
Creatinine (increased due to decreased GFR)
Hypotension
Hyperkalemia (due to reduction in aldosterone)

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

ACE inhibitors are contraindicated in who

A

bilateral renal artery stenosis (no vasoconstriction by angiotensin II on the efferent arteriole to help maintain glomerular capillary pressure and filtration)
hyperkalemia (due to reduction in aldosterone release hence less sodium absorption so less K excretion)
pregnancy (teratogen – fetal renal malformation)

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

what are the angiotensin II receptor blockers (ARBs)

A

Losartan

Valsartan

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

clinical use of ARBs (angiotensin II receptor blockers)

A

hypertension and heart failure

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

when do you switch from an ACE inhibitor to an ARB if they both work almost the same way

A

when the patient is experiencing the bradykinin mediated dry ass cough

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

when do ARBs work equally effective in black/oldies as it does in whites/youngings

A

when combined with calcium channel blockers

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

mechanism of ARBs

A
  • they block the receptor that mediates the effects of angiotensin II hence no vasoconstriction or release of aldosterone
  • don’t block the breakdown of bradykinin so no dry ass cough or angioedema (as seen in ACE Inhibitors)
  • since angiotensin II not activating its receptor, no negative feedback on renin release so renin still high
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what are the adverse effects of ARBs?

A

hypotension
hyperkalemia (due to less aldosterone secretion hence less Na absorption so less K excretion)
angioedema
diarrhea
acute renal failure (no vasoconstriction on efferent arterioles from angiotensin II if bilateral renal artery stenosis so reduced glomerular capillary pressure and filtration)

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

contraindication of ARBs

A

pregnancy (fetal renal malformation)
bilateral renal artery stenosis
hyperkalemia

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

what are the calcium channel blockers (CCB)

A 
VAND
Verapamil (diphenalkylamine)
Amlodipine (dihydropyridine)
Nifedipine (dihydropyridine)
Diltiazem (benzothiazepine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

clinical use of CCBs

A

hypertension, angina, arrhythmias

17
Q

why would you combine CCBs with ARBs or ACE Inhibitors

A

because it is considered the first line drug treatment for hypertension for blacks/elderly

18
Q

which one of the CCBs can you safely combine with beta blockers and why?

A

the dihydropyridines (amlodipine and nifedipine) because of their cardio depressant effects

19
Q

mechanism of CCBs

A
  • block voltage gated L type calcium channels on vascular smooth muscle, cardiac myocytes, and cardiac nodal tissue thereby stopping calcium from entering these cells
  • this leads to smooth muscle relaxation, decreased myocardial force, decreased HR
  • the dihydropyridines (in comparison to the non-dihydropyridines) only act on vascular smooth muscle hence evoke a reflex tachycardia
20
Q

knowing that dihydropyridines only act on vascular smooth muscle while the other work on both vascular SM and cardiac tissue, what do you use each type to treat

A

dihydropyridines - hypertension
verapamil - angina and cardiac arrhythmias (could be used for hypertension)
diltiazem - hypertension, angina, arrhythmias

21
Q

adverse effects of CCBs

A

dihydropyridines - reflex tachycardia, peripheral edema, dizziness, flushing, headache, gingival hyperplasia

non-hydropyridines (verapamil and diltiazem) - cardiac conduction abnormalities, constipation (v), anorexia, nausea, peripheral edema, hypotension

22
Q

contraindications for CCBs

A

bradycardia, conduction defects, heart failure

esp don’t give verapamil and diltiazem

23
Q

alpha 1 antagonists increase the risk for CHF, so what conditions would you save alpha 1 antagonist as the treatment for hypertension

A

in men with BPH because drugs like tamsulosin are used to treat both BPH and hypertension

24
Q

why should you give a small first dose to those on alpha 1 antagonist for tx for hypertension

A

some patients have precipitous (dangerously high) drop in BP after first dose

25
Q

adverse effects of alpha 1 antagonist

A

sodium and water retention hence why a diuretic should be given in combination

26
Q

what are the direct vasodilators

A

hydralazine

minoxidil

27
Q

clinical uses of direct vasodilators

A

hydralazine - moderate to severe hypertension, heart failure, pregnant women with preeclampsia

minoxidil - severe hypertension and alopecia androgenetica

28
Q

adverse effects of direct vasodilators

A

hydralazine - hypotension, reflex tachycardia and sodium and H2O retention, reversible lupus like syndrome,

minoxidil - hypotension, reflex tachycardia and sodium and H20 retention

29
Q

when are beta blocker considered first line as an anti hypertensive

A

in patients with coronary heart disease, heart failure, or post MI

30
Q

adverse effects of beta blockers

A
  • drug withdrawal (abrupt cessation of beta blocker causes unstable angina, MI, tachycardia and etc because of upregulation of beta receptors)
  • CV effects (bradycardia etc)
  • disturbed lipid metabolism
  • hypoglycemia
  • bronchoconstriction
  • CNS effect (reduced sexual function and fatigue)
31
Q

contraindications for beta blockers

A

reactive airway disease (asthma and COPD)

pts with sinus bradycardia and partial AV block

Pharmacology (79 decks)

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