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Pharm 3 test 4 > Heart Failure Drugs > Flashcards

Heart Failure Drugs Flashcards

1
Q

What is the primary treatment goal of heart failure?

A

Alleviation of symptoms, so basic stuff like vasodilators, positive inotropes, etc

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2
Q

What is the secondary treatment goal of heart failure?

A

Prevent progression of cardiac remodeling

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3
Q

Explain what Class I to Class IV of the heart failure classification. Basically, which is worst/best?

A

Class I is the best

Class IV is basically dying in the hospital

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4
Q

What is the most common reason for development of HF?

A

Coronary artherosclerosis and MI’s

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5
Q

Why do diuretics help in HF?

A

Reduction of preload

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6
Q

What’s the only diuretic that’s actually shown to improve morbidity and mortality?

A

Spironolactone

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7
Q

What is the MOA of aldosterone antagonists?

A

Binds to MR receptors, blocking aldosterone from binding there. So reduction in aldosterones functions (Na/K exchange)

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8
Q

What are the two aldosterone antagonists to know?

A

Spironolactone and eplernone

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9
Q

What are the ADEs for aldosterone antagonists?

A

Hyperkalemia (MOST DANGEROUS SIDE EFFECT)
Endocrine Effects-more spironolactone than eplerenone
GI problems
CNS-HA, lethargy

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10
Q

What is the important difference between spironolactone and eplernone?

A

Spironolactone is more likely to act as an androgen receptor antagonist, causing more endocrine issues

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11
Q

Can you use CCB or BBs in HF? why?

A

No nondihydropyradines, cause they reduce contractility

BBs yes cuz they reduce renin secretion

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12
Q

What are the four positive inotropic classes?

A

Cardiac glycosides
Beta adrenergic and dopaminergic agents
Phosphodiasterase inhibitors
Calcium sensitizing agents

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13
Q

What is the cardiac glycoside to know?

A

Digoxin

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14
Q

What is cardiac glycosides MOA?

A

It binds to and inhibits Na/K ATPase, keeping intracellular Na elevated. This activates the Na/Ca pump, pumping Na out in exchange for Ca. More Ca means more contraction
Also, effects baroreceptors responsiveness to change in bp

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15
Q

So to sum it up some, what does cardiac glycosides do

A

Increases contractility, but also increases parasympathetic outflow, decreases sympathetic outflow

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16
Q

Digoxin is a p glycoprotein substrate but not a ____

A

CYP substrate

17
Q

What is digoxins ADEs?

A

Cardiac effects- Arrhythmias

Toxicity- CNS stuff like delerium, also GI and Visual problems

18
Q

What is the treatment for digoxin toxicity?

A

Digibind

19
Q

What is digoxin mainly used for?

A

HF with A fib (see anti arrythmics) IDK

20
Q

What is dobutamines MOA?

A

B1 and B2 agonists

21
Q

What are dobutamines ADEs?

A

Basically stuff you would expect. B1 excess problems like arrhythmias

22
Q

What class is milrinone?

A

Phosphodiasterase 3 inhibitor

23
Q

What is milrinones MOA?

A

Blocks PDE3, leading to increased concentrations of cAMP, leading to increased myocardial contractility and vasodilation in the venous and arterial system

24
Q

What drug class is levosimendan?

A

Calcium sensitizing agent

25
Q

What is levosimendans MOA?

A

Increased interactions between calcium and the contractile proteins, leading to positive inotropic effects

26
Q

Is levosimendan available in the US?

A

NNOOO

27
Q

What can levosimendan cause?

A

Arrhythmias

28
Q

What is the HCN channel blocker?

A

Ivabradine

29
Q

What does HCN channels do?

A

Activated by hyperpolarization and cyclic nucleotides. contributes to diastolic depolarization

30
Q

What is Ivabradines MOA?

A

Blocks HCN channel, reduces pacemaker activity in SA node. So blocking HR is main effect

31
Q

How is ivabradine beneficial in HF?

A

By reducing HR, it creates a more favorable balance between myocardial oxygen demand and it improves diastolic myocardial perfusion

32
Q

How is ivabradine metabolized?

A

CYP3A4

33
Q

What is ivabradines ADEs?

A

Arrhythmias, Phosphenes (floaty sparkles), teratogenix

34
Q

What is the MOA of isosorbide dinitrate\hydralazine?

A

Decreases ventricular filling by increasing venous capacitance

35
Q

What is Nesirtides MOA?

A

Activates BNP receptors which are the guanylyl cyclase type receptors. This leads to increased cGMP, leading to more relaxation. Same concept as sodium nitropresside

36
Q

What does nesirtide do the cardiac system overall?

A

Decreases preload and afterload

37
Q

What is the Neprilysin inhibitor?

A

Sacubitril

38
Q

What is important to understand about sacubitrils delivery considerations?

A

HAS TO BE given with an arb at the minimum. Sacubitril inhibits neprilysin, which is an enzyme that degrades BNP (BNP is a vasodilator and diuretic). But neprilysin also breaks down ANG II. So if you inhibit neprilysin, you have a lot of ANG II floating around

Pharm 3 test 4 (5 decks)

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