CHF Pharm Flashcards

(47 cards)

1
Q

Difference between treating HFpEF vs HFrEF

A

Different functional deficiencies of the heart. HFrEF is due to a systolic dysfunction, therefore we can improve the condition by reducing preload and afterload

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2
Q

What is the suffix for ACEi drugs?

A
  • pril

* Captopril, Enalapril, Benzapril, Lisinopril

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3
Q

What is the suffux for ARBs (angiotensin receptor blockers)?

A
  • sartan

* Losartan, Valsartan, Candesartan

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4
Q

Which B-blockers are used to treat heart failure?

A
  • Carvedilol***
  • Metoprolol
  • Bisoprolol
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5
Q

What aspects of HF do ACEi and ARB’s help with?

A

Decreased action of angiotensin II

  • decreased vasoconstriction (decreasing afterload)
  • decreased aldosterone secretion (decreasing preload)
  • decreased cell proliferation and remodeling (vascular stenosis)
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6
Q

Clinical indications for ACEi

*Captopril, Enalapril, Benzapril, Lisinopril

A

HTN, HFrEF, diabetic neuropathy

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7
Q

Classic toxicities associated with ACEi

*Captopril, Enalapril, Benzapril, Lisinopril

A
  • Cough
  • Angioedema
  • Fetal toxicity (teratogenic)
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8
Q

Which ACEi are most commonly prescribed today?

A

Lisinopril, Benazepril

*longer half-life permits 1x/day dosing

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9
Q

ACEi MOA

*Captopril, Enalapril, Benzapril, Lisinopril

A

Competitively binds ACE, preventing the conversion of angiotensin I to angiotensin II

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10
Q

Clinical indications for ARB’s

*Losartan, Valsartan, Candesartan

A

HF if intolerant to ACEi

HTN

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11
Q

Classic toxicities associated with ARB’s

*Losartan, Valsartan, Candesartan

A
  • Cough (not as bad as ACEi)
  • Fetal toxicity (teratogenic)

*angioedema is feared but should not happen

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12
Q

ARB MOA

*Losartan, Valsartan, Candesartan

A

Non-peptide angiotensin II receptor antagonist (AT1)

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13
Q

Which ARB is metabolized to its active form in the liver by CYP enzymes?

*Losartan, Valsartan, Candesartan

A

Losartan

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14
Q

Which ARB is notable for not being a prodrug, therefore it does not need to be metabolized to its active form in the liver?

*Losartan, Valsartan, Candesartan

A

Valsartan

*may be useful in pt intolerant to ACEi who also has liver failure

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15
Q

Which ARB is noteworthy because it is able to irreversibly bind?

*Losartan, Valsartan, Candesartan

A

Candesartan

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16
Q

ACEi and ARB contraindications

A
  • Not tolerated
  • Pregnant (teratogenic)
  • Hypotensive
  • Creatinine .3 mg/dL
  • Hyperkalemia (okay up to 5.5)
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17
Q

Sacubitril MOA

*valsartan/sacubitril

A

Inhibits NEP (enteropeptidase that breaks down BNP and ANP)

  • leads to increased levels of ANP and BNP, which act as a check on RAAS, leading to decreases in all of renin, aldosterone, ADH
  • Considered best initial treatment for HFrEF… but $$$
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18
Q

Which B-blockers can be used in HF?

A

Carvedilol***
Bisoprolol
Metoprolol

*should be given to all HF patients with LVEF <40% unless contraindicated

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19
Q

Clinical indications for Carvedilol

A
  • HFrEF to prevent symptomatic HF
  • rEF after MI or ACS

*Pt must be stable! Don’t want to slow down their heart if they already are not stable. Start with low dose.

20
Q

Carvedilol MOA

A

Non-selective B>a blocker with no sympathomimetic activity

  • Lowers HR
  • keeps heart responsive to sympathetic drive
21
Q

Carvedilol contraindications

A
  • Bronchospastic disease (due to B2 block)
  • Symptomatic bradycardia

WARNING: do not abruptly stop B-blockers, can lead to acute tachycardia, HTN, ischemia

22
Q

Ivabradine MOA

A

Specific inhibition of Funny Na channels in the SA node

  • prolongs diastole and slows HR
  • called hyperpolarization-activated cyclic neucleotide gated (HCN) Funny channels
23
Q

Ivabradine clinical applications

funny channel blocker

A

Treat HR >70 bpm in pt with stable, sinus rhythm, symptomatic HF with LVEF <35% who are on max B-blocker dose or intolerant to B-blockers

24
Q

Ivabradine contraindicatoins

funny channel blocker

A

-ADHF, hypotension, bradycardia, heart block, arrhythmia

25
Spironolactone, Eplerenone MOA
Competitive antagonist of aldosterone receptors *Eplerenone is more selective to aldosterone receptor * K sparing diuretic (aldosterone inhibition) * Antagonizes pro-fibrotic effects of aldosterone on local vasculature
26
Spironolactone clinical applications
- Reduce fibrosis HFrEF and post-MI HF | - Counteracts K loss induced by other diuretics in treatment of HTN, HF
27
How do diuretics help with HF?
Decrease edema (congestion)
28
Loop diuretic MOA Furosemide, Toresemide, Bumetanide Ethactynic acid
Block Na K 2Cl cotransporter in the TAL * Prevents reabsorption of Na, K, Cl * Prevents paracellular reabsorption of Ca and Mg
29
Clinical applications of loop diuretics Furosemide, Toresemide, Bumetanide Ethactynic acid
- Edema - HF (decreases preload) - HTN *also works in pt with low GFR (unlike thiazides)
30
What toxicities are associated with loop diuretics (furosemide)?
Hypokalemia, Hyponatremia, Hypochloremia (inhibition of NKCC cotransporter) * also hypomagnesemia and hypocalcemia * hyperglycemia and hyperuricemia * **Ototoxicity * **Sulfonamide! allergy risk
31
Which loop diuretic is not a sulfonamide, and can therefore be used in patients with sulfa allergies?
Ethacrynic acid
32
Diuretic use in HF (1st line, 2nd line, 3rd line)
1. Loop diuretic 2. add K sparing diuretic if needed (hypokalemia) 3. add thiazide if more diuresis needed
33
Thiazide diuretic MOA *Hydrochlorothiazide, Chlorothiazide, Chlorthlidone, Metolazone
Inhibits Na reabsorption via blocking Na/Cl cotransporter in the DCT *K-losing diuretic
34
Clinical applications of thiazide diuretics *Hydrochlorothiazide, Chlorothiazide, Chlorthlidone, Metolazone
- HTN - Ca nephrolithiasis - Adjunct tx in HF *not effective in pt with low GFR
35
What toxicities are associated with thiazide diuretics? *Hydrochlorothiazide, Chlorothiazide, Chlorthlidone, Metolazone
- Hypokalemia, Hyponatremia, Hypomagnesemia, Hypocholoremia | * Sulfonamide!!!
36
What thiazide diuretic is *long acting*, and commonly used as an adjunct diuretic in heart failure?
Metolazone
37
Nitrate drug MOA *Nitroglycerin, Isosorbide dinitrate
MOA: forms NO, more prominently causes venodilation
38
Clinical application for nitrate drugs
- Angina pectoris | - Acute decompensated HF (ADHF)
39
Which nitrate drug is administered orally and has a slower onset of action, and may specifically be used for HFrEF
Isosorbide dinitrate
40
What drug causes direct vasodilation of arterioles and is specifically indicated for African Americans with HFrEF?
Hydralazine * hydralazine/isosorbide nitrate combo drug * can also treat HTN *may cause drug induced lupus-like synd
41
How do vasodilators help in the treatment of HFrEF?
Reduced afterload (decreased work needed to be done by heart)
42
Digoxin MOA
inhibition of Na/K ATPase in myocardial cells, indirectly stimulating Na/Ca exchanger, leading to increased Ca within the myocardial cell * increased Ca = increased contractility * suppresses AV conduction via increased vagal tone, slowing HR
43
Clinical application of Digoxin
Not commonly used any longer * Controls Afib * HF * can only be administered if HR is normal
44
What happens in digoxin toxicity?
Ca overload can cause arrhythmias
45
Major Digoxin drug interaction
Diuretics * digoxin competes with K at the Na/K ATPase * diuretics cause hypokalemia * hypokalemia increases digoxin binding, increasing likelihood of toxicity
46
Sympathomimetics used to treat acute decompensated HF in the ER (rescue therapy) *indicated if symptomatic hypotension with end-organ dysfunction despite adequate filling pressures
Dobutamine, Dopamine
47
Milrinone MOA
PDE3 inhibitor, increases cAMP and therefore contractility *used as inotropic therapy in pt unresponsive to dobutamine or dopamine