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Pharmacology > Antianginal / Heart Failure Drugs > Flashcards

Antianginal / Heart Failure Drugs Flashcards

1
Q

Isosorbide Dinitrate

A

Nitrate

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2
Q

Isosorbide Mononitrate

A

Nitrate

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3
Q

Available as oral

A

Isosorbide mononitrate

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4
Q

Available as sublingual (TABLET AND SPRAY), oral, IV, transdermal patch, and topical ointment

A

Nitroglycerine

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5
Q

Nitrate: MOA

A
  • releases nitric oxide (NO) in vascular smooth muscle
  • relaxes venous smooth muscle
  • increases coronary blood flow
  • reduces preload and BP (reflex tachycardia)
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6
Q

Nitrate: indications

A

Angina

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7
Q

Continuous use leads to tolerance

A

Nitrates

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8
Q

Do not use in HF

A
  • Diltiazem
  • Verapamil
    (Nondihydropyridines)
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9
Q

Nitrates: adverse effects

A
  • headache
  • dizziness
  • hypotension
  • reflex tachycardia
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10
Q

Nitrates: interactions

A
  • 5-PDE inhibitors (contraindicated if using nitrates daily)

- do not use within 24 or 72 hours of 5-PDE inhibitors use

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11
Q

Nitroglycerine

A

Nitrate

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12
Q

NifeDIPINE

A

Calcium channel blocker

Dihydropyridine

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13
Q

3A4 inhibitors

A
  • Diltiazem
  • Verapamil
    (Nondihydropyridines)
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14
Q

NicarDIPINE

A

Calcium channel blocker

Dihydropyridine

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15
Q

FeloDIPINE

A

Calcium channel blocker

Dihydropyridine

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16
Q

Diltiazem

A

Calcium channel blocker

Nondihydropyridine

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17
Q

Verapamil

A

Calcium channel blocker

Nondihydropyridine

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18
Q

Calcium channel blockers: MOA

A
  • prevent entry of Ca into cells
  • peripheral vasodilation, decreased afterload
  • coronary vasodilation
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19
Q

Decrease mycocardial contractility, heart rate, and AV node conduction

A

Nondihydropyridine CCBs

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20
Q

Adverse effects of all calcium channel blockers

A

Gingival hyperplasia

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21
Q

Adverse effects of dihydropyridines

A
  • dizziness, headache
  • peripheral edema
  • reflex tachycardia
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22
Q

Adverse effects of nondihydropyridines

A

constipation

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23
Q

Indicated for atrial arrhythmias

A
  • Diltiazem
  • Verapamil
    (Nondihydropyridines)
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24
Q

AmloDIPINE

A

Calcium channel blocker

Dihydropyridine

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25
Q

Increases Digoxin levels

A

Verapamil

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26
Q

B-Blockers

A
  • decreases heart rate and contractility therefore DECREASES OXYGEN DEMAND
  • INCREASES DIASTOLIC FILLING therefore better coronary perfusion increases oxygen supply
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27
Q

Selective B-blockers

A

Atenolol

Metoprolol

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28
Q

Nonselective B-blockers

A

Propranolol

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29
Q

Ranolazine

A

B-blocker

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30
Q

Ranolazine: pharmacokinetics

A

Metabolized by 3A4

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31
Q

Indicated for treatment of CHONIC ANGINA

A

Ranolazine

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32
Q

Should not be used w/ 3A4 inducers or strong 3A4 inhibitors

A

Ranolazine

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33
Q

Warning: QT prolongation (caution w/ other drugs that can cause QT prolongation

A

Ranolazine

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34
Q

Ranolazine: adverse effects

A
  • constipation
  • dizziness
  • headache
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35
Q

How do we treat acute angina?

A
  • sit or lie down
  • NTG under the tongue (do not swallow)
  • wait 5 minutes for pain releif
  • if no pain relief, call 911
  • may repeat 2 more times
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36
Q

Definition of HF

A

Complex CLINICAL SYNDROME that results from any structural or functional impairment of ventricular filling or eject blood

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37
Q

Cardinal manifestations of HF

A
  • dyspnea
  • fatigue
  • may limit exercise tolerance and fluid retention
  • may lead to pulmonary or splanchnic congestion and/or peripheral edema
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38
Q

When is the term “heart failure” preferred over “congestive heart failure?”

A

when patient presents w/o signs/symptoms of volume overload

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39
Q

Pathophysiology of heart failure

A

Reduction in tissue perfusion activates neurohumoral system response

  • Renin-angiotensin-aldosterone system (RAAS)
  • Sympathetic nervous system
40
Q

Pathophysiology of heart failure: RAAS

A
  • vasoconstriction (angiotensin II)
  • Angiotensin II stimulates secretion of aldosterone (causes remodeling and fibrosis) and antidiuretic hormone
  • Angiotensin II causes Na and water retention
  • Angiotensin II leads to cardiac remodeling and fibrosis
41
Q

Pathophysiology of heart failure: SNS

A
  • Vasoconstriction

- cardiac remodeling leading to myocyte death

42
Q

Digoxin

A

Digitalis glycoside

43
Q

Adrenergic agonists

A

Dobutamine

44
Q

Phosphodiesterase inhibitor

A

Milrinone

45
Q

Increase Carbamezapine levels

A
  • Diltiazem
  • Verapamil
    (Nondihydropyridines)
46
Q

What drugs have a positive inotropic effect?

A
  • Digoxin
  • Phosphodiesterase inhibitors (Milrinone)
  • Dobutamine
47
Q

What drugs have a negative inotropic effect?

A
  • Diltiazem
  • Verapamil
    (Nondihydropyridines)
    DO NOT USE IN HEART FAILURE
48
Q

Positive inotropic definition

A

Increase cardiac CONTRACTILITY

49
Q

Digoxin antidote

A

Digoxin immune Fab

50
Q

Digoxin: pharmacokinetics

A
  • Renally excreted

- Very low therapeutic index (monitor for toxicity)

51
Q

Indicated for HF (reduces morbidity but NOT MORTALITY) and Atrial Fib

A

Digoxin

52
Q

Blurred vision, yellow, green, or blue colors

A

Digoxin

53
Q

Adverse effect includes anorexia, N&V

A

Digoxin

54
Q

Adverse effect includes arrhythmias (most common AV block)

A

Digoxin

55
Q

Digoxin MOA/pharmacologic effect

A

HF: POSITIVE INOTROPIC and NEGATIVE CHRONOTROPIC AND DROMOTROPIC EFFECT
- inhibits Na pump and increases intracellular Na causing more Ca to enter the myocyte, thus INCREASING CONTRACTILITY

Atrial Fib: INCREASES PARASYMPATHETIC TONE and REDUCES SYMPATHETIC TONE

  • slows heart rate
  • slows AV node conduction velocity
56
Q

Can cause seizures

A

Digoxin

57
Q

Amiodarone
Propafenone
Verpamil and diltiazem

A

can increase Digoxin serum levels

58
Q

Used for short term management of acute HF and cardiogenic shock

A

Dobutamine

59
Q

Aluminum and Magnesium containing antacids

Cholestyramine/Colestipol

A

can decrease Digoxin serum levels

60
Q

Precipitate Digoxin toxicity by enhancing pharmacodynamics effects

A

Diuretic induced hypokalemia

61
Q

Can also cause ventricular arrhythmias and hypokalemia can precipitate arrhythmias

A

Digoxin

62
Q

Dobutamine adverse reactions

A
  • tachycardia

- arrhythmias

63
Q

Milrinone indication

A

Short term management of acute HF (usually less than 48 hours)

64
Q

Inhibits type III phosphodiesterase

A

Milrinone

65
Q

Milrinone MOA

A

increases cardiac contractility and relax vascular smooth muscle (vasodilation) by inhibiting type III phospodiesterase

66
Q

Nesiritide adverse effects

A
  • Hypotension

- Renal impairment

67
Q

Nesiritide

A

Vasodilator

68
Q

Form of human b-type natriuretic peptide; causes vasodilation of vascular smooth muscle and vasodilation

A

Nesiritide

69
Q

Indicated for acute DECOMPENSATED HF

A

Nesiritide

70
Q

Dobutamine MOA

A

increases cardiac contractility and hear rate, small effect of preload and decreased afterload

71
Q

Shown to decrease morbidity and mortality in HF patients

A

ACEI

72
Q

Contraindicated in patients w/ a systolic blood pressure of less than 90 mm Hg

A

Nesiritide

73
Q

ACEI w/ NSAIDs

A

Decreases effect of ACEI and may result in decreased renal function, hyperkalemia

74
Q

ACEI w/ Lithium

A

increases lithium levels (leads to toxicity)

75
Q

Thiazolidinediones (Rosiglitazone and Pioglitazone)

A

Should generally be avoided in patients w/ HF

76
Q

Valsartan

A

Angiotensin II Receptor Blocker (ARB)

77
Q

ACEI w/ Spironolactone, Eplerenone, Potassium supplements, ARBs, Trimethoprim

A

Increase potassium levels (hyperkalemia)

78
Q

What should be considered in patients who are intolerant to ACEI such as cough (do not inhibit bradykinin)?

A

ARBs

79
Q

When should you use caution when using ARBs?

A

In people who have developed angioedema while on ACEI.

80
Q

ARB drug interactions

A

same as ACEI drug interactions

81
Q

Hydralazine/Isosorbide Dinitrate

A

Vasodilator

82
Q

What does isosorbide do?

A

relaxes VENOUS smooth muscle

83
Q

When may you use Hydralazine and Isosorbide Dinitrate (Nitrates)?

A

if intolerante to ACEIs or ARBs; can be used as an alternative

84
Q

What does hydralazine do?

A

relaxes ARTERIAL smooth muscle

85
Q

Candesartan

A

Angiotensin II Receptor Blocker (ARB)

86
Q

Indicated in African Americans on optimal therapy w/ ACEIs, B-blockers, and diuretics.

A

Hydralazine and Isosorbide Dinitrate

87
Q

What do B-blockers do?

A

Reduce excessive sympathetic stimulation of the heart
- sympathetic activation also increases activation of RAAS
- chronic stimulation of sympathetic nervous system leads to hypertrophy and apoptosis
- increases cytokines
REDUCES MORTALITY AND MORBIDITY

88
Q

B-blockers and NSAIDs

A

decrease effect of B-blockers

89
Q

Metformin

A

Should generally be avoided in patients w/ HF (in “acute congestive heart failure”)

90
Q

Effects on morbidity and mortality are not known

A

Loop diuretics

91
Q

Antiarrhythmics (except Amiodarone)

A

Should generally be avoided in patients w/ HF

92
Q

Non-DHP CCBs

A

Should generally be avoided in patients w/ HF

93
Q

NSAIDs and COX2 inhibitors

A

Should generally be avoided in patients w/ HF

94
Q

Nondihydropyridines: Indications

A
  • HTN
  • Angina
  • Atrial arrhythmias
95
Q

Strong 3A4 inhibitor/s (e.g. Azole antifungals and clarithromycin) increase levels of…

A

calcium channel blockers (Dihydropyridines and Nondihydropyridines)

Pharmacology (19 decks)

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