HF medication Flashcards

(43 cards)

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
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
c. Metoprolol Succinate
26
What is the mechanism of action of Entresto?
- blocks the peptidase enzyme
27
What is the name of the trial that measured the effects of Entresto vs ACE inhibitor for HF?
-PARADIGM-HF
28
A female begins taking THIS medication for HF and develops acne, hirsutism and gynecomastia. What drug did she take?
- Spironolactone (Aldactone)
29
What were the original vasodilators used for HF?
-Isosorbide dinitrate (Isordil) + Hydralazine (Apresoline) - Isosorbide = venous circulation - Hydralazine = arterial circulation
30
Why does a dose of Digoxin never get fully absorbed?
- gets effluxed by P-gp in the gut
31
Why is Digoxin not commonly used for HF anymore?
- lots of side effects + not disease modifying
32
What is the reason for HR reduction with Digoxin?
- Digoxin mimicks the PNS
33
What is the reason for increased HR contractility with Digoxin?
- Digoxin blocks the Na/K ATPase pump | - will result in Ca++ build up in the cell = increase inotropy
34
What is the correlation between Digoxin effectiveness and potassium?
- hypokalemia will result in increased Digoxin efficacy
35
What are the 3 main adverse effects of Digoxin?
- Nausea, GI upset - Visual disturbances* - Arrhythmias *will be on exam
36
What 2 electrolyte disturbances can worsen Digoxin toxicity?
- Low K+ or/and Mg++
37
What 3 factors may increase Digoxin levels?
- Drug interactions - Impaired kidney function - low lean body mass
38
What is the serum drug level we are aiming for with Digoxin?
< 1 ng/mL *textbook = 0.8 -2 ng/mL
39
This drug inhibits the If (funny channel) of diastolic depolarization in the SA node. a. Ivabradine (Corlanor) b. Digoxin c. Entresto d. Furosemide
a. Ivabradine (Corlanor)
40
When is Ivabradine (Corlanor) indicated? (2)
- add-on therapy in stable symptomatic HF | - those with HF unable to tolerate B-blocker
41
What are the adverse effects of Ivabradine (Corlanor)? (5 listed)
- Bradycardia - A fib - Luminous phenomena - hepatotoxicity - fetal harm
42
What 2 inotropes are used in acutely decompensated disease and how do they work?
- Dobutamine (Dobutrex) = generate cAMP | - Milrinone (Primacor) = block PDE3 to prevent degeneration of cAMP
43
What has been the evolution of HF treatment?
- it has progressed from symptom control to combined symptom control/disease modification