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Pharmacology > HF medication > Flashcards

HF medication Flashcards

1
Q

What is the NYHA classifications based from?

A
  • based on symptoms
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2
Q

What are the ACC-AHA staging guidelines based from?

A
  • structural disease
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3
Q

Why did they develop a staging system for HF?

A
  • taking into account that the disease is irreversible
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4
Q

Most HF medications have been shown to reduce progression of disease in what type of HF?

A
  • HFrEF
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5
Q

What is the difference between HFrEF and HFpEF? (in terms of LVEDV/EF)

A
  • HFrEF = LVEDV high but EF is low

- HFpEF = LVEDV low but EF is normal

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6
Q

If someone is in acute HF what is the drug to use?

A
  • Loop based diuretics
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7
Q

If a patient is have an acute exacerbation of HF and is not doing well but is already on a loop diuretic what medication can you add for a few days for acute treatment?

a. Amiloride
b. HCTZ
c. Spironolactone
d. Metolazone

A

d. Metolazone

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8
Q

This drug works by inhibiting the NaCl symporter in the thick ascending loop of Henle.

a. Furosemide
b. HCTZ
c. Spironolactone
d. Metolazone

A

a. Furosemide

Loop diuretic

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9
Q

If you are trying to replete someone with low Mg2+ levels what do you need to do?

A
  • replace K+ first
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10
Q

Which loop diuretic can be used for a patient who has a severe sulfa allergy?

a. Furosemide
b. Bumetanide
c. Torsemide
d. Ethacrynic acid

A

d. Ethacrynic acid

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11
Q

T/F: There is NO cross-reactivity between sulfates and sulfonamides.

A

True

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12
Q

T/F: If you have a sulfonamide allergy you can’t use any sulfonamide based drugs.

A

False

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13
Q

How do we usually initiate Furosemide?

A
  • 20 mg by mouth once daily and titrate as needed
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14
Q

Which of the following is NOT an adverse effect of Furosemide?

a. Hyperuricemia
b. Sulfonamide allergy
c. Hyperglycemia
d. Hypercalcemia

A

d. Hypercalcemia

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15
Q

What is an adverse effect that is unique to Loop diuretics and is more common when given in conjunction with aminoglycosides.

A
  • ototoxicity
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16
Q

What role do B-blockers have in patients with HF?

A
  • disease modifying drug for HFrEF
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17
Q

Which B-Blocker has been studied the most for HF?

a. Bisoprolol
b. Carvedilol
c. Metoprolol Succinate
d. Nebivolol

A

c. Metoprolol Succinate

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18
Q

What is the role of RAAS modifiers in patients with HF?

A
  • decrease afterload

* also disease modifying drug

19
Q

Why did Omapatrilat, the first of the vasopeptidase inhibitors, not reach market?

A
  • by blocking the ACE and increasing bradykinin resulted in severe angioedema
20
Q

What is the drug Entresto composed of?

A
  • ARB + neprilysin inhibitor

Sacubitril/Valsartan

21
Q

Why is Entresto used?

A
  • has better results than standard of care for HFrEF
22
Q

What is the most common side effect with Entresto?

A
  • hypotension

* needs to be started on small doses to increase tolerability

23
Q

If a patient is on an ACE inhibitor how long do you have to wait before transitioning to Entresto?

A
  • 36 hrs

* reduce risk of hypotension + angioedema

24
Q

What is the difference between Spironolactone and Eplerenone?

A
  • Eplerenone has fewer off target adverse effects at higher doses
  • usually spironolactone works well in lower doses
25
Q

Which of the following medications is only a B-blocker and not a A + B-blocker?

a. Bisoprolol
b. Carvedilol
c. Metoprolol Succinate
d. Nebivolol
e. Labetalol

A

c. Metoprolol Succinate

26
Q

What is the mechanism of action of Entresto?

A
  • blocks the peptidase enzyme
27
Q

What is the name of the trial that measured the effects of Entresto vs ACE inhibitor for HF?

A

-PARADIGM-HF

28
Q

A female begins taking THIS medication for HF and develops acne, hirsutism and gynecomastia. What drug did she take?

A
  • Spironolactone (Aldactone)
29
Q

What were the original vasodilators used for HF?

A

-Isosorbide dinitrate (Isordil) + Hydralazine (Apresoline)

  • Isosorbide = venous circulation
  • Hydralazine = arterial circulation
30
Q

Why does a dose of Digoxin never get fully absorbed?

A
  • gets effluxed by P-gp in the gut
31
Q

Why is Digoxin not commonly used for HF anymore?

A
  • lots of side effects + not disease modifying
32
Q

What is the reason for HR reduction with Digoxin?

A
  • Digoxin mimicks the PNS
33
Q

What is the reason for increased HR contractility with Digoxin?

A
  • Digoxin blocks the Na/K ATPase pump

- will result in Ca++ build up in the cell = increase inotropy

34
Q

What is the correlation between Digoxin effectiveness and potassium?

A
  • hypokalemia will result in increased Digoxin efficacy
35
Q

What are the 3 main adverse effects of Digoxin?

A
  • Nausea, GI upset
  • Visual disturbances*
  • Arrhythmias

*will be on exam

36
Q

What 2 electrolyte disturbances can worsen Digoxin toxicity?

A
  • Low K+ or/and Mg++
37
Q

What 3 factors may increase Digoxin levels?

A
  • Drug interactions
  • Impaired kidney function
  • low lean body mass
38
Q

What is the serum drug level we are aiming for with Digoxin?

A

< 1 ng/mL

*textbook = 0.8 -2 ng/mL

39
Q

This drug inhibits the If (funny channel) of diastolic depolarization in the SA node.

a. Ivabradine (Corlanor)
b. Digoxin
c. Entresto
d. Furosemide

A

a. Ivabradine (Corlanor)

40
Q

When is Ivabradine (Corlanor) indicated? (2)

A
  • add-on therapy in stable symptomatic HF

- those with HF unable to tolerate B-blocker

41
Q

What are the adverse effects of Ivabradine (Corlanor)? (5 listed)

A
  • Bradycardia
  • A fib
  • Luminous phenomena
  • hepatotoxicity
  • fetal harm
42
Q

What 2 inotropes are used in acutely decompensated disease and how do they work?

A
  • Dobutamine (Dobutrex) = generate cAMP

- Milrinone (Primacor) = block PDE3 to prevent degeneration of cAMP

43
Q

What has been the evolution of HF treatment?

A
  • it has progressed from symptom control to combined symptom control/disease modification

Pharmacology (6 decks)

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