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Flashcards in CHF therapy Deck (39)
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1
Q

What is the most important therapy to start at risk CHF patients on?

A

ACE inhibitors/ARBs–> prevents cardiac remodeling associated with AngII/Aldosterone

2
Q

What is the indication for Beta-blocker therapy in CHF patients?

A

The second the Ejection Fraction drops

3
Q

What therapy is changed around in late, severe CHF?

A

Remove any beta-blockers, put the pt on beta-agonist (must preserve any remaining cardiac function)

4
Q

Angiotensin II/Aldosterone mitogenic effects?

A

Hypertrophy of cardiac myocytes, hypertrophy of vascular smooth muscle, cardiac/vascular fibrosis and remodeling, and atherosclerosis

5
Q

Detrimental effect of ventricular fibrosis?

A

Decreased compliance, less function

6
Q

Pregnancy class of ACE inhibitors/ARBs?

A

Severely teratogenic, NEVER GIVE TO PREGNANT WOMEN

7
Q

ADEs of ACE inhibitors not present in ARBs?

A

ARBs do not increase bradykinin levels or produce dry, irritating cough

8
Q

Once a CHF patient begins having edema, what therapy needs to be started?

A

Diuretics (normally HCTZ first, then furosemide)

9
Q

Main reason why beta-blockers are efficacious in heart failure?

A

reduce the deleterious effects of chronically elevated Norepi and Epi –> overactivity of SNS causes down regulation of B receptors –> B blocker therapy allows for a regeneration of the beta receptors, improving Cardiac function

10
Q

Nebivolol special effect?

A

potentiates NO in the vasculature (only approved for HTN in the United States, not CHF)

11
Q

Carvedilol special effect?

A

functions as an alpha1-antagonist, reduces reflex vasoconstriction

12
Q

Best beta blocker for CHF?

A

Carvedilol

13
Q

Aldosterone antagonists?

A

Spironolactone, eplerenone

14
Q

What medication can you not take with diuretics?

A

NSAIDs

15
Q

Hemodynamic effect of diuretics that is beneficial to CHF patients?

A

reduced preload

16
Q

What is a high ceiling diuretic?

A

A diuretic that can cause a very high amount of diuresis (Furosemide)

17
Q

Do ACE inhibitors/ARBs have diuretic effects?

A

Yes, they reduce Na+ retention by preventing aldosterone release

18
Q

Spironolactone, Eplerenone beneficial effects besides diuresis?

A

prevent the mitogenic effects of aldosterone (combines with AngII–> fibrosis)

19
Q

Mechanism of action of Hydralazine?

A

Vasodilator that acts directly on arterial smooth muscle (effective for CHF, reduced afterload)

20
Q

What causes release of the natriuretic peptides (ANP/BNP)

A

volume and pressure expansion

21
Q

What causes release of the natriuretic peptides (ANP/BNP)

A

volume and pressure expansion (elevated in CHF)

22
Q

Effects of ANP/BNP?

A

Promote vasodilation, venodilation, natriuresis. Reduce preload, inhibit renin/aldosterone release, inhibit Na+ reabsorption, promote afferent arteriole dilation

23
Q

What is Neseritide?

A

Recombinant human BNP

24
Q

MOA of Neseritide?

A

binds to BNP receptor in vascular smooth muscle–> veno-and vasodilation via cGMP (reduce preload/afterload)

25
Q

Naming system for ACE inhibitors?

A

End in “-pril” (Lisonopril)

26
Q

Naming system for ARBs?

A

End in “-tan” (Losartan)

27
Q

Where do ACE inhibitors work?

A

Block AngI–>AngII conversion in lung endothelium

28
Q

Life threatining ADE seen in ACE inhibitors?

A

Severe angioedema due to inhibition of Bradykinin metabolism (more prevalent in African Americans)

29
Q

Who respond less favorably to ACE inhibitors?

A

African Americans and low-renin hypertensives

30
Q

Advantageous effect of ACE inhibitors for diabetics?

A

Preserves their renal function

31
Q

Most common ADEs with ACE inhibitors?

A

1st dose hypotension, a dry, irritating cough

32
Q

Direct Renin Inhibitor?

A

Aliskiren

33
Q

Drug drug interactions seen with Aliskerin?

A

Inhibits p-glycoprotein pumps (don’t prescribe with erythromycin/amiodarone

34
Q

What does Digoxin inhibit?

A

Na+/K+ ATPase

35
Q

How does Digoxin cause its intended effect

A

Na+/K+ ATPase inhibition–> increase in intracellular Na+–>reversal of Na:Ca pump–> increase intracellular Ca2+ and therefore contractility

36
Q

Ionotropes only increase what?

A

Stroke Volume

37
Q

Unusual ADE seen in early Digoxin toxicity

A

Blurry blue-green halos in the eyes

38
Q

What is Digibind?

A

anti-Digoxin antibody used in digoxin toxicity rescue

39
Q

Digoxin’s therapeutic window?

A

Extremely narrow, toxicity is very easy to cause