Brainscape's Knowledge GenomeTM

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


See full index

Renal 2 > PostMT ACE Inhibitors and ARBs > Flashcards

PostMT ACE Inhibitors and ARBs Flashcards

1
Q

ACEIs are approved for tx of what?

A

*HTN in diabetics!

Nephropathy, heart failure, left ventricular dysfunction, acuteMI, prophylaxis of futureCV events.

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

MOA of ACEIs

A

Inhibit ACE (kininase II) and prevent formation of AngII (which then prevents inactivation of bradykinin, a potent vasodilator).

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

How do ACEIs lower BP?

What demographic are they especially good for (v. diuretics)?

A

Decreases peripheral vascular resistance&raquo_space; increased vasodilation
CO and HR not significantly changed, making these agents an excellent choice in Olympic ATHLETES or physically active patients.

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

Which two ACEIs are not prodrugs?

Which has a more frequent dosing? Why?

A

captopril and lisinopril
Captopril = 3-4 times per day with a 1/2life of 2 hours.
Lisinopril = once-daily and has a 1/2life of 12 hours.

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

Adverse effects common to all ACEIs (5).

A

*ARF
*HyperK
*Dry cough
*Angioedema
HypoTension

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

What is a common side effect of ACEIs?

A

ACEI cough

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

When are ACEIs contraindicated? Why?

A

During pregnancy because ACEIs cause:
1st Tri - TERATOGENOUS
2nd Tri - FETAL HYPOTENSION, anuria, renal failure, MALFORMATIONS, DEATH

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

What drug-drug interactions should be avoided with ACEIs (3)?

A

(1) Potassium supplements or (2) potassium sparing diuretics - to avoid hyperkalemia
(3) NSAIDs - which may impair some of the antihypertensive effects of ACEIs by blocking bradykinin-mediated vasodilation, which is partly PG mediate.

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

All ACEIs, except for captopril and lisinopril, are what?

A

Prodrugs with active metabolites.

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

What is special about enalaprilat?

A

Active metabolite of enalapril.

IV administration of this prodrug is approved for hypertensive emergiencies.

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

What is the primary elimination route for ACEIs? What are teh two exceptions and what route are they?

A

Renal is the primary elimination route for most.
Exceptions:
(1) Fosinopril elimination, renal = heaptic
(2) Trandolapril elimination, renal and hepatic

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

What ACEIs (2) have decreased bioavailabilty with food?

A

Captopril and Moexipril

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

What ACEIs have the highest bioavailability? Lowest?

A

Captopril and Perindopril (75%)
Trandolapril (70%)

Moexipril (13%)

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

ARB is what?

A

Angiotensin Receptor Blocker

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

MOA of ARBs

A

ARBs cause selective blockade of AngII receptors (AT1-type).

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

ARBs v. ACEIs - which is a more selective antagonist of angiotensin’s effects and why?

What are the pharmacological differences between ARBs and ACEIs (3)?

A

ARBs have no effect on barkykinin metabolism and therefore are MORE seletive antagonists of angiostensin’s effects than ACE inhibitors.

(1) ARBs reduce activation of AT1 receptors more effectively than ACEIs.
(2) ARBs permit activation of AT2 receptors.
(3) ACEIs increase levels of a number of AC substrates, including bradykinin.

17
Q

What conditions are ARBs used for (5)?

A 
HTN
Diabetic nephropathy
HF
HF or left ventricular dysfunction after acuteMI
Prophylaxis of CV events
18
Q

What How do ARBs inhibit angII?

A 
Blockade of angiotensinII-induced:
Contraction of vascular smooth muscle
Pressor responses
Aldosterone secretion
Changes in renal function
Cellular hypertrophy and hyperplasia
19
Q

Adverse effects of ARBs.

When are they contraindicated (3)?

A

Similar to ACEIs, but cough and angioedema occur at much lower rates.

ARBs are contraindicated during

  • (1) pregnancy
    (2) patients with nondiabetic renal disease
    (3) concomitant use of potassium supplements or potassium sparing diuretics.
20
Q

What ARB is metabolized by CYP450 enzymes into a MORE potent metabolite?

A

Losartan - its peak plasma levels are at 1hr and half life of hours.
Its active metabolite has a peak plasma level of 3 hours and half life of 6-9 hours.

21
Q

Drugs that block renin secretion (2). What do they interfere with?

A

Clonidine and Propranolol.

Several drugs that interfere with SNS inhibit the secretions of renin.

22
Q

MOA of clonidine

A

Agonist of alpha2-receptors in brainstem.

23
Q

What happens when clonidine stimulates alpha2-receptors?

A

Inhibition of sympathetic vasomotor centers, resulting in centrally mediated reduction in renal sympathetic nerve activity.
Ultimately, a reduction of renin secretion.

24
Q

MOA of propranolol.

A

Nonspecific antagonist of adrenergic beta-receptors.

25
Q

What happens when propranolol antagonizes beta-receptors?

A

Propranolol acts on jGm cells by blocking beta1-receptor stimulated release of renin and DECREASES blood pressure. Also does this by decreasing CO and decreasing sympathetic outflow from the CNS.

26
Q

What is an example of a renin inhibitor? Route of administration? Approved treatment of what?

A

Aliskiren. Oral. Treatment of HTN.

27
Q

How is MOA of aliskiren different than ACIs, ARBs, and diuretics?

But what result is similar?

A

Aliskiren produces a decrease in baseline plasma renin activity, in contrast to the rise in plasma renin activity produced by the others.

Aliskiren, ACIs, and ARBs all produce similar decreases in blood pressure.

28
Q

What does aliskiren produce/result in?

A

Dose-dependent REDUCTION in plasma RENIN activity, resulting in decreased angiotensin I and II and aldosterone concentrations.

29
Q

What is the rationale behind polypharmacy?

What is commonly one of the classes of drugs in the combo?

A

Each drug acts on one of a set of interacting, mutually compensatory regulatory mechanisms for maintaining blood pressure. When HTN does not respond adequately to a regimen of one drug, a second drug froma different class with a different MOA is added.

Diuretics!

30
Q

When ARBs are used, which AT-receptor is inhibited, which is stimulated?

A

AT1-receptors are inhibited.

AT2-receptors are stimulated.

31
Q

ACEIs and ARBs inhibit what?

A

RAS

32
Q

MAP=

A

COxTPR

33
Q

Withdrawl HTN from noncompliance iwth what?

A

clonidine

Renal 2 (12 decks)

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