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EOB - Blood Cardio > Cardio Pharm > Flashcards

Cardio Pharm Flashcards

1
Q

First line treatment for primary HTN?

A

Diuretics, ACE inhibitors, ARBs, Ca channel blockers

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2
Q

First line treatment for HTN + CHF?

A

Diuretics, ACE inhibitors, ARBs, B-blockers (compensated ONLY), and aldosterone antagonists

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3
Q

First line treatment for HTN + diabetes?

A

ACE inhibitors (work against diabetic nephropathy), ARBs, Ca channel blockers, diuretics, B-bockers, alpha blockers

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4
Q

Drug class of amlodipine, nimodipine, nifedipine?

A

Dihydropyridines (Ca channel blockers); amlodipine and nifedipine are most active in SM; nimodipine prevents cerebral vasospasm

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5
Q

Drug class of diltalazem?

A

Ca channel blocker (non-dihydropyridine); medium potency in heart and in SM

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6
Q

Drug class of verapamil?

A

Ca channel blocker (non-dihydropyridine); most potent in heart (verapamil = ventricle)

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7
Q

MOA Ca channel blockers?

A

Block voltage dependent L-type calcium channels of both cardiac and smooth muscle, reducing muscle contractility

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8
Q

Use of nifedipine and amlodipine?

A

HTN, angina, Raynaud phenomenon

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9
Q

Only use of nimodipine?

A

SAH

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10
Q

Use of verapamil and diltiazem?

A

HTN, angina, a-fib/flutter

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11
Q

Toxicities of Ca channel blockers?

A

Cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation

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12
Q

Hydralazine MOA?

A

Increases cGMP, causing smooth muscle relaxation

Vasodilates arterioles more than veins, causing afterload reduction

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13
Q

Clinical use of hydralazine?

A

Severe HTN, CHF

First line for pregnancy HTN (with methyldopa, an alpha-2 agonist)

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14
Q

Toxicity of hydralazine?

A

Compensatory tachycardia (give with beta blocker to prevent this), fluid retention, nausea, headache, angina, Lupus-like syndrome.

CI with angina/CAD due to reflex tachycardia

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15
Q

Treatment for HTN crisis?

A

nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam

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16
Q

Nitroprusside MOA?

A

Release of NO to increase cGMP

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17
Q

Toxicity of nitroprusside?

A

Cyanide tox

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18
Q

Fenoldopam MOA?

A

Dopamine D1 receptor agonist causing coronary, peripheral, renal, and splanchnic vasodilation; reduces BP and increases natriuresis.

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19
Q

Nitroglycerin MOA?

A

Increases NO, causing increased cGMP and smooth muscle relaxation; Dilates veins much more than arterioles, reducing preload.

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20
Q

Nitroglycerin Use?

A

Angina, ACS, pulmonary edema

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21
Q

Nitroglycerin Toxicity?

A

Reflex tachycardia (treat with beta blockers), hypotension, flushing, headache, and Monday disease

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22
Q

What is Monday disease?

A

Development of tolerance of nitroglycerin in industrial exposure so that upon re-exposure, experience tachycardia, dizziness, and headache

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23
Q

What are determinants of MVO2 (myocardial oxygen demand)?

A

EDV, BP, HR, contractility

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24
Q

Do nitrates effect preload or afterload?

A

Preload

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25
Q

Nitrates effect on MVO2?

A

Decrease EDV, BP, ejection time and MVO2

Increase contractility and HR as a reflex

**Nifedipine is similar

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26
Q

Do b-blockers affect preload or afterload?

A

Afterload

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27
Q

B-blockers effect on MVO2?

A

Decrease BP, HR, contractility, and MVO2

Increase ejection time, and EDV

**Verapamil is similar

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28
Q

Statins MOA?

A

Inhibit HMG-CoA reductase

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29
Q

Statins effect on lipids?

A

Major decrease in LDL, minor increase in HDL, minor decrease in triglycerides

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30
Q

Statins AE’s?

A

Hepatotoxicity, rhabdomyolysis (especially when used with fibrates and niacin)

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31
Q

Niacin MOA?

A

Inhibits lipolysis in adipose tissue and reduces VLDL synthesis.

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32
Q

Niacin effect on lipids?

A

Moderate decrease in LDL, moderate increase in HDL, minor decrease in triglycerides.

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33
Q

Niacin toxicity?

A

Flushed face (helped by aspirin), hyperglycemia (acanthosis nigricans), and hyperuricemia (exacerbation of gout).

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34
Q

What drug class are cholestyramine, colestipol, and colesevelam?

A

Resins

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35
Q

MOA of resins?

A

Prevent intestinal reabsorption of bile acids, depleting liver stores of cholesterol

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36
Q

Resins effect on lipids?

A

Moderate decrease in LDL, slight increase in HDL, slight increase in triglycerides

37
Q

Resin toxicity?

A

Patients hate it - tastes bad and causes GI discomfort, decreases absorption of ADEK, cholesterol gallstones

38
Q

MOA of ezetimibe?

A

Direct prevention of cholesterol absorption at SI brush border

39
Q

Effects of ezetimibe on lipids?

A

Moderate decrease in LDL; no other effects

40
Q

Ezetimbe toxicity?

A

Rare elevated LFTs and diarrhea

41
Q

Drug class of gemfibrozil, clofibrate, bezafibrate, and fenofibrates?

A

Fibrates

42
Q

Fibrate MOA?

A

Upregulate LPL (lipoprotein lipase), which increases TG clearance; activates PPAR-alpha to induce HDL synthesis

43
Q

Effect of fibrates on lipids?

A

Minor decrease in LDL, minor increase in HDL, major decrease in triglycerides.

44
Q

Fibrate toxicity?

A

Myositis (increased risk with statins), hepatotoxicity, cholesterol gallstones (increased risk with resins)

45
Q

MOA of digoxin?

A

Direct inhibition of Na+/K+/ATPase leads to indirect inhibition of Na+/Ca+ exchanger/antiport, increasing Ca2+ and causing positive inotropy. Also stimulates vagus nerve, decreasing HR.

46
Q

Clinical use of digoxin?

A

CHF, a-fib (decreases conduction at AV node and depression of SA node)

47
Q

Digoxin toxicity?

A

Cholinergic side effects
On ECG - increased PR, decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block
Can lead to hyperkalemia

48
Q

What factors predispose a patient to digoxin toxicity?

A

Renal failure, hypokalemia (digoxin can bind K+ site of Na/K ATPase), verapamil, amiodarone, quinidine

49
Q

Digoxin antidode?

A

Normalize K+, give anti-digoxin Fab, Mg2+, cardiac pacer for arrhythmias

50
Q

MOA of class I antiarrhythmics?

A

Na channel blockers

Slow or block conduction (especially in depolarized cells), decrease slope of phase 0 depolarization, and increase threshold for firing in abnormal pacemaker cells.

51
Q

What does it mean to be “state-dependent”?

A

Drugs work in tissue that is frequently depolarized (tachycardia)

52
Q

Quinidine, procainamide, disopyramide

A

Class IA antiarrhythmics

53
Q

MOA of class IA antiarrhythmics?

A

Increase AP duration, increase effective refractory period, increase QT interval

54
Q

Clinical use of IA antiarrhythmics?

A

Atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.

55
Q

Toxicity of IA antiarrhythmics?

A

Quinidine - cinchonism (headache, tinnitus)
Procainamide - reversible SLE-like syndrome
Disopyramide - heart failure

All: TdP, thrombocytopenia

56
Q

Lidocaine, mexiletine?

A

Class IB antiarrhythmics

57
Q

MOA of IB antiarrhythmics

A

Decrease AP duration. Preferentially work on diseased Purkinje and ventricular tissue

58
Q

Clinical use of IB antiarrhythmics?

A

Acute ventricular arrhythmias (post-MI); digitalis-induced arrhythmias

59
Q

Toxicity of IB antiarrhythmics?

A

CNS stimulation/depression, cardiovascular depression

60
Q

Flecainide, propafenone

A

Class IC antiarrhythmics

61
Q

MOA of IC antiarrhythmics?

A

Prolongs refractory period in AV node; minimal effect on AP duration

62
Q

Clinical use of IC antiarrhythmics?

A

SVTs, including a-fib; only a last resort in refractory VT

63
Q

Toxicity of IC antiarrhythmics?

A

Post-MI, proarrhythmic

64
Q

What are class II antiarrhythmics?

A

Beta-blockers

65
Q

MOA of beta-blockers?

A

Decrease SA and AV node activity via decreasing cAMP, which decreases calcium currents. Decreases slope of phase 4 (funny channel depolarization), which slows it!

AV node is particularly sensitive, raises PR interval

66
Q

Clinical use of beta-blockers?

A

SVT, slowing ventricular rate during a-fib and atrial flutter

67
Q

Toxicity of beta blockers?

A

Impotence, exacerbation of COPD and asthma, bradycardia, AV block , CHF, sedation, sleep alterations. MAY MASK SIGNS OF HYPOGLYCEMIA. Metoprolol can cause dyslipidemia, propranolol can exacerbate vasospasm in Prinzmetal angina. Contraindicated in cocaine users (risk of unopposed alpha-adrenergic receptor agonist activity).

68
Q

How to treat overdose of beta-blocker?

A

Glucagon

69
Q

What are class III antiarrhythmics?

A

K+ channel blockers (amiodarone, ibutilide, dofetilide, sotalol)

70
Q

MOA of class III antiarrhythmics?

A

Increased AP duration, increased ERP, increased QT interval. Used when other antiarrhythmics fail.

71
Q

Clinical uses of class III antiarrhythmics?

A

A-fib, atrial flutter, v-tach

72
Q

Toxicity of amiodarone?

A

Pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, corneal deposits, skin deposits, neurologic effects, constipation, bradycardia, heart block, CHF

**Class I-IV effects

73
Q

What to monitor with amiodarone?

A

PFTs, LFTs, TFTs

74
Q

Toxicity of sotalol?

A

TdP, excessive beta blockade

75
Q

Toxicity of ibutilide?

A

TdP

76
Q

What are class IV antiarrhythmics?

A

Calcium channel blockers (verapamil, diltiazem)

77
Q

MOA of class IV antiarrhythmics?

A

Decrease conduction velocity, increased ERP, increased PR interval

78
Q

Clinical use of class IV antiarrhythmics?

A

Prevention of nodal arrhythmias, rate control in a-fib

79
Q

Toxicity of class IV antiarrhythmics?

A

Constipation, flushing, edema, CHF, AV block, sinus node depression.

80
Q

MOA of adenosine?

A

Increases K+ out of the cell, inducing hyperpolarization and decreasing calcium current.

81
Q

Use of adenosine?

A

Abolishing and diagnosing SVT.

82
Q

Adverse effects of adenosine?

A

Flushing, HTN, chest pain

83
Q

Mg2+ use?

A

TdP and digoxin toxicity.

84
Q

Class of captopril, enalapril, lisinopril?

A

ACE inhibitors

85
Q

MOA of ACE inhibitors?

A

Block angiotensin converting enzyme, so ATII cannot be produced, which prevents constriction of efferent arterioles in kidney. Also decreases production of aldosterone, which reduces blood volume.

Block inactivation of bradykinin, a vasodilator.

86
Q

MOA of ARBs?

A

Block angiotensin II receptors, but do not increase bradykinin. No cough or angioedema

87
Q

Clinical uses of ACE inhibitors?

A

HTN, CHF, proteinuria, diabetic nephrophathy. Prevent unfavorable heart remodeling as a result of chronic HTN.

88
Q

Toxicity of ACE inhibitors?

A

Cough, angioedema, teratogen, increased creatinine, hyperkalemia, and hypotension.

EOB - Blood Cardio (5 decks)

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