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Pharm MCQ 2 > Heart Failure Pharmacotherapy > Flashcards

Heart Failure Pharmacotherapy Flashcards

1
Q

What are the 4 medication classes included in GDMT for HFrEF?

A

ARNI/ACE/ARB (aka RAAS inhibitors)
Beta blockers
Aldosterone antagonists (diuretics, usually K+ sparing or thiazide like)
SGLT2 inhibitors

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2
Q

What is the most common cause of HFrEF?

A

Ischemia (CAD, ACS, HTN, etc.)

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3
Q

What are some non-ischemic causes of HFrEF?

A

Idiopathic/congenital
Amyloid, sarcoid, genetic
Drug or toxin induced (chemotherapy)

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4
Q

What are the two classifications of medications in HF?

A

Symptom management medications

Meds that reduce mortality/have a mortality benefit

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5
Q

Does GDMT focus more on symptom management or mortality benefits?

A

Mortality benefits

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6
Q

Which cornerstone medication of GDMT also has evidence to be effective in HFpEF?

A

SGLT2 inhibitors

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7
Q

Examples of HFrEF meds that focus on symptom management

A

Diuretics
Digoxin
Inotropes (in end of life patients)
Vericiguat

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8
Q

Which medications should you use in patients with low renin instead of ACE/ARB/ARNI?

A

Hydralazine + nitrate therapy

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9
Q

Where do ACEs work on the RAAS system?

A

Prevent conversion of angiotensin I to angiotensin II AND prevent conversion of bradykinin into inactive kinins

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10
Q

Where do ARBs work on the RAAS system?

A

Prevent angiotensin II from binding to its receptor

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11
Q

Where do ARNIs work on the RAAS system?

A

Prevent angiotensin II from binding to its receptor (like ARBs)

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12
Q

What is the overall result of ACE and ARB use?

A

Decreased cardiac remodeling and decreased morbidity/mortality

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13
Q

What effect do ACEs and ARBs have on preload and afterload?

A

Decreases both

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14
Q

ADRs of ACEs and ARBs

A

Acute kidney injury (HOWEVER an up to 30% increase in serum creatinine is normal)
Hypotension
Hyperkalemia
Angioedema (much less common with ARBs)

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15
Q

Specific ADRs of ACEs

A

Angioedema and cough (d/t increased bradykinin)

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16
Q

Contraindications of ACEs and ARBs

A

Pregnancy
Bilateral renal artery stenosis
Patients with low renin

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17
Q

What should you do if a patient on an ACE develops a cough?

A

Switch to an ARB

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18
Q

Is there a washout period when switching between ACEs and ARBs?

A

No because they have a similar MOA –> can start next dose of new class when the other one is due

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19
Q

Suffix for ACEs and suffix for ARBs

A

ACEs - pril
ARBs -sartan

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20
Q

Entresto is a combination of…

A

Sacubitril (neprilysin inhibitor) and valsartan (ARB)

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21
Q

What is the overall result of ARNI use?

A

Prevent breakdown of natriuretic peptides (somewhat of a diuretic effect)

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22
Q

ADRS of ARNIs

A

Cough
Angioedema
Hyperkalemia
Hypotension (MC, even more common than in ACEs or ARBS)

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23
Q

ARNI contraindications

A

Pregnancy
Bilateral renal artery stenosis
Potential hx of angioedema with an ACE

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24
Q

ARNI dosing

A

Always BID (can cut tablets in half if unable to tolerate higher doses)

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25
Q

Is there a washout period when switching between ARNIs and ACEs? ARBs?

A

ARNI + ACE = 36 hour washout
ARNI + ARB = no washout (b/c ARNI/Entresto already has an ARB component)

26
Q

T or F: You start patients on the target dose of Entresto when initiating therapy

A

FALSE

27
Q

Beta blockers used for HFrEF

A

Bisoprolol, carvedilol, metoprolol succinate

28
Q

ADRs of BBs

A

Fatigue/exercise intolerance
Bradycardia
Hypotension (minimal)
Sexual dysfunction

29
Q

Contraindications for BBs

A

Sinus bradycardia
2nd or 3rd degree heart block (unless pt has pacemaker)
Active asthma with bronchospasms

30
Q

Which is better for mortality in HFrEF, metoprolol tartrate or succinate?

A

Succinate (50 mg daily) – tartrate has NO MORTALITY BENEFIT

31
Q

What is the overall result of aldosterone antagonist/diuretics/MRA use?

A

Decreased sodium/water retention
Fibrosis (cardiac remodeling)
Decreased morbidity/mortality

32
Q

Examples of MRAs

A

Spironolactone (non-selective antagonist)
Eplerenone (selective antagonist)

33
Q

ADRs of spironolactone

A

Gynecomastia (b/c it is non selective, it also binds androgen pathways)
Hyperkalemia
Hypotension

34
Q

ADRs of eplerenone

A

Hyperkalemia
Hypotension
NO GYNECOMASTIA (b/c this is selective)

35
Q

MRA contraindications

A

Hyperkalemia
Poor kidney function (SCr > 2 in females, SCr > 2.5 in males)

36
Q

Where do SGLT2 inhibitors work in the nephron?

A

Proximal tubule

37
Q

Examples of SGLT2 inhibitors

A

Dapagliflozin (Farxiga)
Empagliflozin (Jardiance)

38
Q

ADRS of SGLT2 inhibitors

A

Euglycemic DKA (blood sugar not high)
Dyslipidemia
Increased urination
UTIs

39
Q

SGLT2 inhibitor contraindications

A

Pregnancy (2nd and 3rd trimesters)
eGFR < 20 for Jadiance
eGFR < 25 for Farxiga

40
Q

True or false: SGLT2i dosing for HF is fixed

A

TRUE – changes when dosing for diabetes

41
Q

What is the result of using hydralazine?

A

Direct ARTERIAL vasodilator –> decreases afterload

42
Q

What is the result of using nitrate therapy (isosorbide dinitrate)?

A

Direct VENOUS vasodilator –> decreases preload

43
Q

When should you use hydralazine/nitrate therapy?

A

Patients who cannot tolerate ACE/ARB/ARNI (d/t renal function, hyperkalemia, or presence of ADRs)
Patients with low renin (AA)
Pregnancy

44
Q

ADRs of hydralazine/nitrate therapy

A

Headache, dizziness
Hypotension with reflex tachycardia
Lupus like syndrome @ high doses

45
Q

Hydralazine/nitrate contraindications

A

PDE-5 inhibitors (sildenafil, tadalafil) –> decreases BP TOO much

46
Q

Do loop diuretics reduce mortality or manage symptoms?

A

Manage symptoms

47
Q

Where do loop diuretics work?

A

Loop of Henle of the nephron

48
Q

What symptoms do loop diuretics address?

A

Relieve pulmonary congestion (“wet” patients) and peripheral edema

49
Q

Examples of loop diuretics

A

Furosemide (lasix)
Torsemide (Demadex)
Bumetanide (Bumex)

50
Q

Loop diuretics ADRs

A

Electrolyte disturbances:
- Hypokalemia
- Hypomagnesemia
- Hyperuricemia
Ototoxicity @ high doses

51
Q

Should you take loop diuretics in the morning or at night?

A

In the morning to avoid peeing during the middle of the night

52
Q

Which is more potent, furosemide or bumetanide?

A

Furosemide (IV, more potent than oral)

53
Q

Digoxin MOA?

A

Inhibits Na/K/ATPase pump –> increase calcium concentration intracellularly –> positive inotropic effect –> increased contractility and CO

54
Q

Does digoxin have a mortality benefit?

A

NO - strictly sx management

55
Q

Digoxin has a narrow therapeutic index. What are some signs of digoxin toxicity?

A

N/V
Anorexia
Bradycardia
Visual disturbances

56
Q

At what dose do you common see digoxin toxicity?

A

> 2 ng/mL

57
Q

How is digoxin eliminated?

A

Renally, so consider kidney function when dosing and dose based on ideal body weight

58
Q

When do SGLT2 inhibitors have the most benefit in HFpEF?

A

When the EF is closer to 50% (b/c it’s more like HFrEF at that point)

59
Q

Mainstay of HFpEF treatment?

A

Symptom management and lowering of BP

60
Q

BP goal for managing HFpEF?

A

<130/80 mmHg

61
Q

When can ARNI be useful in HFpEF?

A

If BP is very uncontrolled

62
Q

What are some medications to avoid in HF?

A

Non DHP CCBs
NSAIDs (increase fluid retention and therefore increase risk of AKI)
Arrhythmia meds
COX 2 inhibitors
Estrogens and androgens
Cardiotoxic agents

Pharm MCQ 2 (24 decks)

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