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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
Nitrates effect on MVO2?
Decrease EDV, BP, ejection time and MVO2 Increase contractility and HR as a reflex **Nifedipine is similar
26
Do b-blockers affect preload or afterload?
Afterload
27
B-blockers effect on MVO2?
Decrease BP, HR, contractility, and MVO2 Increase ejection time, and EDV **Verapamil is similar
28
Statins MOA?
Inhibit HMG-CoA reductase
29
Statins effect on lipids?
Major decrease in LDL, minor increase in HDL, minor decrease in triglycerides
30
Statins AE's?
Hepatotoxicity, rhabdomyolysis (especially when used with fibrates and niacin)
31
Niacin MOA?
Inhibits lipolysis in adipose tissue and reduces VLDL synthesis.
32
Niacin effect on lipids?
Moderate decrease in LDL, moderate increase in HDL, minor decrease in triglycerides.
33
Niacin toxicity?
Flushed face (helped by aspirin), hyperglycemia (acanthosis nigricans), and hyperuricemia (exacerbation of gout).
34
What drug class are cholestyramine, colestipol, and colesevelam?
Resins
35
MOA of resins?
Prevent intestinal reabsorption of bile acids, depleting liver stores of cholesterol
36
Resins effect on lipids?
Moderate decrease in LDL, slight increase in HDL, slight increase in triglycerides
37
Resin toxicity?
Patients hate it - tastes bad and causes GI discomfort, decreases absorption of ADEK, cholesterol gallstones
38
MOA of ezetimibe?
Direct prevention of cholesterol absorption at SI brush border
39
Effects of ezetimibe on lipids?
Moderate decrease in LDL; no other effects
40
Ezetimbe toxicity?
Rare elevated LFTs and diarrhea
41
Drug class of gemfibrozil, clofibrate, bezafibrate, and fenofibrates?
Fibrates
42
Fibrate MOA?
Upregulate LPL (lipoprotein lipase), which increases TG clearance; activates PPAR-alpha to induce HDL synthesis
43
Effect of fibrates on lipids?
Minor decrease in LDL, minor increase in HDL, major decrease in triglycerides.
44
Fibrate toxicity?
Myositis (increased risk with statins), hepatotoxicity, cholesterol gallstones (increased risk with resins)
45
MOA of digoxin?
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
Clinical use of digoxin?
CHF, a-fib (decreases conduction at AV node and depression of SA node)
47
Digoxin toxicity?
Cholinergic side effects On ECG - increased PR, decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block Can lead to hyperkalemia
48
What factors predispose a patient to digoxin toxicity?
Renal failure, hypokalemia (digoxin can bind K+ site of Na/K ATPase), verapamil, amiodarone, quinidine
49
Digoxin antidode?
Normalize K+, give anti-digoxin Fab, Mg2+, cardiac pacer for arrhythmias
50
MOA of class I antiarrhythmics?
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
What does it mean to be "state-dependent"?
Drugs work in tissue that is frequently depolarized (tachycardia)
52
Quinidine, procainamide, disopyramide
Class IA antiarrhythmics
53
MOA of class IA antiarrhythmics?
Increase AP duration, increase effective refractory period, increase QT interval
54
Clinical use of IA antiarrhythmics?
Atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.
55
Toxicity of IA antiarrhythmics?
Quinidine - cinchonism (headache, tinnitus) Procainamide - reversible SLE-like syndrome Disopyramide - heart failure All: TdP, thrombocytopenia
56
Lidocaine, mexiletine?
Class IB antiarrhythmics
57
MOA of IB antiarrhythmics
Decrease AP duration. Preferentially work on diseased Purkinje and ventricular tissue
58
Clinical use of IB antiarrhythmics?
Acute ventricular arrhythmias (post-MI); digitalis-induced arrhythmias
59
Toxicity of IB antiarrhythmics?
CNS stimulation/depression, cardiovascular depression
60
Flecainide, propafenone
Class IC antiarrhythmics
61
MOA of IC antiarrhythmics?
Prolongs refractory period in AV node; minimal effect on AP duration
62
Clinical use of IC antiarrhythmics?
SVTs, including a-fib; only a last resort in refractory VT
63
Toxicity of IC antiarrhythmics?
Post-MI, proarrhythmic
64
What are class II antiarrhythmics?
Beta-blockers
65
MOA of beta-blockers?
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
Clinical use of beta-blockers?
SVT, slowing ventricular rate during a-fib and atrial flutter
67
Toxicity of beta blockers?
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
How to treat overdose of beta-blocker?
Glucagon
69
What are class III antiarrhythmics?
K+ channel blockers (amiodarone, ibutilide, dofetilide, sotalol)
70
MOA of class III antiarrhythmics?
Increased AP duration, increased ERP, increased QT interval. Used when other antiarrhythmics fail.
71
Clinical uses of class III antiarrhythmics?
A-fib, atrial flutter, v-tach
72
Toxicity of amiodarone?
Pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, corneal deposits, skin deposits, neurologic effects, constipation, bradycardia, heart block, CHF **Class I-IV effects
73
What to monitor with amiodarone?
PFTs, LFTs, TFTs
74
Toxicity of sotalol?
TdP, excessive beta blockade
75
Toxicity of ibutilide?
TdP
76
What are class IV antiarrhythmics?
Calcium channel blockers (verapamil, diltiazem)
77
MOA of class IV antiarrhythmics?
Decrease conduction velocity, increased ERP, increased PR interval
78
Clinical use of class IV antiarrhythmics?
Prevention of nodal arrhythmias, rate control in a-fib
79
Toxicity of class IV antiarrhythmics?
Constipation, flushing, edema, CHF, AV block, sinus node depression.
80
MOA of adenosine?
Increases K+ out of the cell, inducing hyperpolarization and decreasing calcium current.
81
Use of adenosine?
Abolishing and diagnosing SVT.
82
Adverse effects of adenosine?
Flushing, HTN, chest pain
83
Mg2+ use?
TdP and digoxin toxicity.
84
Class of captopril, enalapril, lisinopril?
ACE inhibitors
85
MOA of ACE inhibitors?
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
MOA of ARBs?
Block angiotensin II receptors, but do not increase bradykinin. No cough or angioedema
87
Clinical uses of ACE inhibitors?
HTN, CHF, proteinuria, diabetic nephrophathy. Prevent unfavorable heart remodeling as a result of chronic HTN.
88
Toxicity of ACE inhibitors?
Cough, angioedema, teratogen, increased creatinine, hyperkalemia, and hypotension.

EOB - Blood Cardio (5 decks)

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