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IPC CARDIOLOGY 2 JEN > Heart Failure Medications Pharmacology and PKPD > Flashcards

Heart Failure Medications Pharmacology and PKPD Flashcards

1
Q

What are the Morbidity and Mortality Reducing Drugs?

A

RAAS Inhibition, MRAs, SGLT, BBs, Veno/Vasodilators

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2
Q

What are the RAAS Inhibitors?

A

ACEI/ARB, ARNI

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3
Q

Effects of RAAS Inhibitors on HF?

A

Arteriolar and venous dilation
Decreases aldosterone secretion
Reduces cardiac remodeling

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4
Q

Sacubitril increases…

A

BP and natriuresis

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5
Q

What is the indication for Entresto?

A

HFrEF, HFpEF, HFmrEF

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6
Q

MOA Sacubitril?

A

Neprilysin inhibitor that blocks the breakdown of BNP –> naturesis and vasodilation

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7
Q

MOA Valsartan?

A

Blocks AG II receptor (decreases RAAS cascade)

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8
Q

Most common ADR for Entresto?

A

Hyperkalemia

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9
Q

What happens if the 36 hour wash out period is NOT given with an ACEI?

A

Increase in bradykinin and angioedema

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10
Q

The ARNI has ______ BP lowering effects than an ACEI or ARB alone

A

More

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11
Q

Almost all _____ are renally eliminated?

A

ACEI

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12
Q

ACEI and ARBs are used for which type of HFEF?

A

HFrEF

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13
Q

MRAs Effect on HF?

A

Increases salt and water excretion
Reduces cardiac remodeling

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14
Q

Major Contraindication MRA?

A

Severe kidney impairment
eGFR <30mL/min/1.73m^2 or creatinine >2.5 mg/dL in men or creatinine >2 mg/dL in women
Potassium >5.0 mEq/L

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15
Q

Which MRA is a strong CYP3A4 inhibitor?

A

Eplerenone

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16
Q

ADR Spironolactone?

A

Gynecomastia, breast tenderness, impotence

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17
Q

ADR Eplerenone?

A

Increased TGs

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18
Q

ADRs MRAs

A

Dehydration, hyperkalemia, hyperatremia, dizziness

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19
Q

What are the SGLT inhibitors?

A

Empagliflozin, Dapagliflozin, Sotagliflozin

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20
Q

Which is the SGLT2 inhibitors?

A

Empagliflozin, Dapagliflozin

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21
Q

Which is the SGLT1/2 Inhibitor?

A

Sotagliflozin

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22
Q

SGLT Effects in HF

A

-Increased sodium and water excretion
-Decreased cardiac preload and afterload
-Reduces pulmonary and peripheral edema
-Improves metabolism and efficiency of cardiac muscle

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23
Q

MOA SGLT

A

Increases urine output by osmotic diuresis (glucose excretion)
Increased fibrosis
SGLTI Inhibition: decrease absorption of sodium/glucose

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24
Q

Major Contraindications for Dapagliflozin and Sotagliflozin?

A

eGFR > 25 mL/min/1.73m^2 for initiation
DO NOT need to discontinue if eGFR falls below this while on treatment

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25
Q

Major Contraindication for Empagliflozin?

A

No renal adjustments necessary

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26
Q

ADRs for SGLT?

A

Dehydration, genital mycotic infections/UTI
Hypoglycemia, euglycemic acidosis (stop surrounding surgeries)

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27
Q

How many days prior to surgery should you stop SGLT inhibitors due to euglycemic ketoacidosis?

A

3 days prior to surgery

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28
Q

Which dose may require an adjustment due to SGLT?

A

Loop Diuretic

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29
Q

What are the Beta-Blockers used that have mortality benefit in patients with HF?

A

Carvedilol, Metoprolol Succinate, Bisoprolol

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30
Q

Beta-Blockers effect in HF?

A

Reduces HR
Decreases sympathetic input to cardiac and vascular tissue
Decreases arrhythmias and sudden cardiac death in patients w/ HFrEF mainly due to decrease in sympathetic drive

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31
Q

Major contraindication for Beta-Blocker?

A

Severe bradycardia

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32
Q

DDI of Beta-Blockers?

A

Additive AV nodal blockade with Non-DHP CCB

33
Q

Which are the Vaso/Venodilators associated w HF?

A

Hydralazine and Isosorbide Dinitrate

34
Q

Effects in HF: Hydralazine

A

Reduces afterload –> increased cardiac output

35
Q

Major Contraindication Hydralazine?

A

CAD (causes reflex tachycardia and can cause angina/MI)

36
Q

Effects in HF: Isosorbide Dinitrate

A

Reduces preload –> decreases ventricular stretch

37
Q

ADR Hydralazine?

A

Dizziness, REFLEX TACHYCARDIA, DILE

38
Q

Hydralazine half life?

A

1.5-3 hours

39
Q

Pearls for Hydralazine and combo tablet BiDil?

A

Need to take 3 times daily, not great for adherence!

40
Q

Major Contraindication for Isosorbide Dinitrate

A

PDE5

41
Q

ADR Isosorbide Dinitrate

A

Headaches, dizziness, syncope

42
Q

MOA Isosorbide Dinitrate

A

Forms the free radical nitric oxide which in smooth muscle activates guanylate cyclase which
increases guanosine 3’5’ monophosphate (cGMP) leading to smooth muscle relaxation.
Produces a vasodilator effect on the peripheral veins and arteries with more prominent
effects on the veins.

43
Q

Key PKPD Isosorbide Dinitrate

A

Dependent in formulation, oral bioavailability is low bc of first pass hepatic metabolism (10-20%)

44
Q

Loop Diuretics Effect in HF

A

Increased excretion of salt and water
Reduces cardiac preload and afterload
Reduces pulmonary and peripheral edema

45
Q

Loop Diuretics key note**

A

Improves symptoms of HF, fluid overload, SOB, that is when loop diuretics are use completely for symptom control, they do not reduce mortality in patients with HF

46
Q

Major Contraindications Loop Diuretics

A

Anuria (no urine)

47
Q

DDI Loop Diuretics

A

Increased risk of ototoxicity if used with aminoglycosides

48
Q

BBW Loop Diuretics (Furosemide)

A

Potent diuretic at high doses can lead to profound fluid and electrolyte loss

49
Q

Bioavailability of Loop Diuretics

A

Furosemide is 40-70%
The rest are 90 and above

50
Q

Diuretic Resistance: What do you do if there is increased distal sodium reabsorption (chronic loop diuretic use)?

A

ADD Thiazide to the loop

51
Q

Diuretic Resistance: Poor delivery to site of effect: reduced GFR, HF, gut enema

A

INCREASED dose of loop diuretic

52
Q

When do you increase the threshold of diuretics?

A

Chronic use, AKI/CKD, HF (gut edema)

53
Q

What is the ceiling dose for a loop diuretic?

A

Once you hit a good dose, an increase in dose 80 vs 120 won’t do anything different to the patient, so no need to go up.

54
Q

Which two medications require food to ensure adequate absorption?

A

Ivabradine (Corlanor)
Vericiguat (Verquvo)
These drugs are also BOTH indicated for HFrEF only

55
Q

MOA of Ivabradine?

A

Impacts the ‘funny’ channel in the SA node

56
Q

DDI Ivabradine

A

Major substrate of CYP3A4

57
Q

Major Contraindications Ivabradine

A

Severe hepatic impairment, acute decompensated HF, clinically significant hypotension, sick sinus syndrome, sinoatrial block, third degree AV block

58
Q

ADR Ivabradine

A

Bradycardia, afib

59
Q

MOA Vericiguat

A

Enhances production of cGMP by directly stimulating sGC independent of NO and enhances sGC sensitivity to endogenous NO, thereby increasing cGMP production. Increased levels of cGMP lead to smooth muscle relaxation and vasodilation

60
Q

Major Contraindication Vericiguat?

A

Pregnancy

61
Q

ADR Vericiguat?

A

Hypotension, anemia

62
Q

DDI Vericiguat?

A

Category X: use in combination with PDE5 inhibitors

63
Q

Pearls Vericiguat?

A

Formulation may include lactose
Must have a negative pregnancy test prior to initiation

64
Q

Which drug is the Cardiac Glycoside?

A

Digoxin

65
Q

Digoxin effects in HF?

A

Increases cardiac contractility
Increases parasympathetic tone of heart (decreases sinus rate, AV conduction)

66
Q

Digoxin indication?

A

HFrEF, rate control for afib

67
Q

MOA Digoxin

A

Inhibition of the sodium/potassium ATPase pump in myocardial cells results in a transient
increase of intracellular sodium, which in turn promotes calcium influx via the sodium-
calcium exchange pump leading to increased contractility.
May improve baroreflex sensitivity.

68
Q

ADR Digoxin?

A

Arrhythmia, heart block, GI and neurological side effects

69
Q

DDI Digoxin

A

Major substrate of PgP, minor substrate of CYP3A4

70
Q

Monitoring for Digoxin?

A

Heart rate and rhythm

71
Q

Monitoring for Digoxin…what is the serum concentration trough goal?

A

Ideally 0.5-0.9 ng/mL

72
Q

ADR Digoxin?

A

Tachycardia, bradycardia, anorexia, nausea, vomiting

73
Q

Distribution of Digoxin?

A

HIGH volume of distribution: once absorbed, it is widely distributed into the tissues, takes 6-8 hours for that

73
Q

Pearls Digoxin?

A

Almost exclusively used for patients with HFrEF and afib
BEERS criteria (not ideal for older patients)

74
Q

Heart:Serum Concentration Digoxin?

A

70:1

75
Q

Excretion of Digoxin?

A

2/3 excreted unchanged by the kidneys , renal clearance is proportional to creatinine clearance, half life is 36-40 hours in normal renal function (worse in patients w bad renal function)

76
Q

Digoxin Levels

A

Toxic effects may occur BEFORE therapeutic effects are detected
Levels must be drawn after distribution period, ideally at least 10-12 hours, levels should be drawn at steady state: 5-7 days after initiation

77
Q

What are the morbidity drugs?

A

Diuretics, If Channel Inhibitor, Soluble Cyclase Stimulator, Cardiac Glycoside

IPC CARDIOLOGY 2 JEN (6 decks)

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