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Cardiovascular-First Aid 2017 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Hypertensive drugs that are safe in pregnancy

A

Hydralazine, labetalol, methyldopa, nifedipine

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2
Q

Hypertensive drugs that at protective against diabetic nephropathy

A

ACE inhibitors and ARBs

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3
Q

Hypertensive drugs used with diabetes mellitus

A

ACE inhibitors/ARBs, CCBs, thiazide diuretics, B-blockers

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4
Q

Hypertensive drugs used in HF

A

Diuretics (spironolactone)
ACE inhibitors/ARBs
B-blockers (compensated HF)
Aldosterone antagonist

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5
Q

Hypertensive drug contraindicated in decompensated HF and cardiogenic shock

A

B-blockers

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6
Q

Primary hypertensive drugs

A

Thiazide diuretics
ACE inhibitors/ARBs
Dihydropyridine CCBs

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7
Q

Hypertensive drug that should be avoided in renal artery stenosis

A

Thiazide diuretics

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8
Q

CCBs that act on the heart

A

Non-dihydropyridines: dilitiazem and verapamil

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9
Q

CCBs that act on vascular smooth muscle

A 
CANNN:
Clevidipine
Amlodipine
Nifedipine
Nimodipine
Nicardipine
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10
Q

Dihydropyridine CCB not indicated for HTN

A

Nimodipine

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11
Q

Indicated for HTN, angina, and Raynaud phenomenon

A

Dihydropyridine CCBs (except nimodipine)

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12
Q

CCBs best for vascular smooth muscle

A

Amlodipine = nifedipine > dilitiazem > verapamil

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13
Q

CCBs best for heart

A

Verapamil > dilitiazem > amlodipine = nifedipine

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14
Q

CCBs MOA

A

Block voltage gated L-type Ca channels of cardiac and smooth muscle cells decreasing muscle contractility

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15
Q

CCB indicated for subarachnoid hemorrhage

A

Nimodipine - prevents cerebral vasospasms

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16
Q

CCB indicated for hypertensive urgency or emergency

A

Nicardipine and clevidipine

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17
Q

CCB indicated for HTN, angina, and atrial fibrillation/flutter

A

Non-dihydropyridines verapamil and diltiazem

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18
Q

CCBs that cause cardiac depression, AV block, hyperprolactinemia, constipation

A

Non-dihydropyridines

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19
Q

CCBs that cause peripheral edema, flushing, dizziness, gingival hyperplasia

A

Dihydropyridines

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20
Q

Hypertensive used for severe HTN, HF with organic nitrate and safe to used during pregnancy

A

Hydralazine

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21
Q

Frequently co-administered with hydralazine to prevent reflex tachycardia

A

B-blocker

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22
Q

When is hydralazine contraindicated

A

Angina and CAD

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23
Q

Hypertensive that causes compensatory tachycardia, fluid retention, headache, angina, Lupus-like syndrome

A

Hydralazine

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24
Q

D1 receptor agonist used for hypertensive emergency

A

Fenoldopam

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25
Q

B-blocker used for hypertensive emergency

A

Labetolol

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26
Q

CCB blocker used for hypertensive emergency

A

Clevidipine and Nicardipine

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27
Q

Nitrite used for hypertensive emergency

A

Nitroprusside

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28
Q

D1 receptor agonist used in hypertensive emergency that causes coronary, peripheral, renal, and splanchnic vasodilation

A

Fenoldopam

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29
Q

Antihypertensive used postoperatively that can cause hypotension and tachycardia as side effects

A

Fenoldopam

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30
Q

Short-acting antihypertensive that increases cGMP via direct release of NO

A

Nitroprusside

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31
Q

Can cause cyanide toxicity

A

Nitroprusside

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32
Q

Cause vasodilation by increasing NO in vascular smooth muscle leading to increased cGMP and smooth muscle relaxation

A

Nitrates

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33
Q

Effect of nitrates on vessels at low doses

A

Veins&raquo_space; arteries leads to decreased preload

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34
Q

Effect of nitrates on vessels at higher doses

A

Arteries > veins leads to decreased afterload

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35
Q

Indications for nitrates

A

Angina, ACS, pulmonary edema

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36
Q

When are nitrates contraindicated

A

Right ventricular infarction

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37
Q

Biochemical precursor of nitric oxide

A

Arginine

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38
Q

Nitrate side effects

A

Reflex tachycardia, HoTN, flushing, headache and “Monday disease” in industrial exposure

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39
Q

Hydralazine MOA

A

Increase cGMP causing smooth muscle relaxation

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40
Q

Effect of hydralazine on vessels

A

Vasodilates arterioles > veins decreasing afterload

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41
Q

Exposure to nitrates at work causes tolerance to vasodilatory effects during work week and loss of tolerance over the weekend leading to tachycardia, dizziness, and headache upon re-exposure

A

Monday disease

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42
Q

Goal of antianginal therapy

A

Reduce myocardial O2 consumption by decreasing >1 of HR, BP, EDV and contractility

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43
Q

Drug given with nitrates to prevent reflex tachycardia

A

B-blockers

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44
Q

Effect of nitrates on cardiac function

A 
EDV - decreased
BP - decreased
Contractility - no effect
HR - increased (reflex tachycardia)
Ejection time - decreased
MVO2 - decreased
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45
Q

Effect of B-blockers on cardiac function

A 
EDV - no effect or increased
BP - decreased
Contractility - decreased
HR - decreased
Ejection time - increased
MVO2 - decreased
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46
Q

Effect of nitrates + B-blockers on cardiac function

A 
EDV - no effect or decreased
BP - decreased
Contractility - little to no effect
HR - no effect or decreased
Ejection time - little to no effect
MVO2 - greatly decreased
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47
Q

B-blockers that should be used with caution in angina

A

Pinodolol and acebutolol (partial B-agonists)

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48
Q

CCB that is similar to B-blockers in effect

A

Verapamil

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49
Q

Partial B-blockers

A

Pinodolol and acebutolol

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50
Q

What are the nitrates

A

Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

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51
Q

Antianginal that inhibits the late phase of sodium current causing reduction in diastolic wall tension and O2 consumption without affecting contractility

A

Ranolazine

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52
Q

Indications for ranolazine

A

Refractory angina

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53
Q

Antianginal that causes constipation, dizziness, headache, nausea, and QT prolongation

A

Ranolazine

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54
Q

Selective PDE-3 inhibitor indicated for short-term use in acute decompensated HF

A

Milrinone

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55
Q

Milrinone side effects

A

Arrhythmias and hypotension

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56
Q

Milrinone MOA on cardiomyocytes

A

Increases cAMP causing Ca influx leading to increased inotropy and chronotropy

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57
Q

Milrinone MOA on vascular smooth muscle

A

Increases cAMP inhibiting MLCK and causing general vasodilation

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58
Q

Lipid lowering agents that causes myopathy when used with fibrates or niacin

A

Statins

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59
Q

Mechanism of statins

A

HMG-CoA reductase inhibitors

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60
Q

Cholesterol precursor that is inhibited by use of statins

A

Mevalonate

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61
Q

Effect of statins on CAD patients

A

Decreases mortality

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62
Q

Lipid lowering agent that causes hepatotoxicity

A

Statins

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63
Q

Lipid lowering agents that inhibit HMG-CoA reductase

A

Statins

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64
Q

Lipid lowering agent that causes decreased absorption of other drugs and fat soluble vitamins

A

Bile acid resins

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65
Q

Bile acid resin drugs

A

Cholestyramine
Colestipol
Colesevelam

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66
Q

Lipid lowering agent that prevents intestinal reabsorption of bile acids causing liver to use cholesterol to make more

A

Bile acid resins

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67
Q

Lipid lowering agent that slightly increases HDL and triglyceride levels with moderate decrease in LDL levels

A

Bile acid resins

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68
Q

Side effect of Bile acid resins

A

GI upset

Decrease absorption of drugs and fat soluble vitamins

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69
Q

Lipid lowering agent that causes rare increases in LFTs and diarrhea

A

Ezetimibe

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70
Q

Lipid lowering agent that prevents absorption at intestinal brush border

A

Ezetimibe

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71
Q

Lipid lowering agent with moderate decrease in LDL, minimal to no increase in HDL, and minimal to no decrease in triglyceride levels

A

Ezetimibe

72
Q

Lipid lowering agent that can cause myopathies and cholesterol gallstones

A

Fibrates

73
Q

Myopathy risk with fibrates is increased when used in combination with what other lipid lowering agents

A

HMG CoA reductase inhibitors (statins)

74
Q

Side effect of Ezetimibe

A

Rare LFTs and diarrhea

75
Q

Fibrate drugs

A

Gemrfibrozil
Bezafibrate
Fenofibrate

76
Q

Lipid lowering agents with minimal decrease in LDL, minimal increase in HDL and marked decrease in triglyceride levels

A

Fibrates

77
Q

Lipid lowering agents that activates PPAR-a to induce HDL synthesis

A

Fibrates

78
Q

Lipid lowering agents upregulate LDL to increase triglyceride clearance

A

Fibrates

79
Q

Side effect of fibrates

A

Myopathy (increased with statins) and cholesterol gallstones

80
Q

Side effect of niacin

A

Flushing
Hyperglycemia
Hyperuricemia

81
Q

Lipid lowering agent that increases risk of gout, diabetes, and can cause acanthosis nigricans

A

Niacin

82
Q

Lipid lowering agents with moderate decrease in LDL, moderate increase in HDL, and minimal decrease in triglyceride levels

A

Niacin

83
Q

Lipid lowering agents that inhibit lipolysis in adipose tissue and reduce hepatic VLDL synthesis

A

Niacin

84
Q

Enzyme that is inhibited by niacin in order to inhibit lipolysis

A

Hormone-sensitive lipase

85
Q

Drug taken to reduce flushing caused by niacin

A

NSAIDs

86
Q

Best lipid lowering agent to take to decrease LDL and increase HDL

A

Niacin

87
Q

Best lipid lowering agent to take to decrease LDL

A

Statins and PCSK9 inhibitors

88
Q

Best lipid lowering agent to take to decrease triglycerides

A

Fibrates

89
Q

Lipid lowering agents that cause myalgias, delirium, dementia, and other neurocognitive effects

A

PCSK9 inhibitors

90
Q

Lipid lowering agents which inactivate LDL receptor degradation increasing removal of LDL from blood

A

PCSK9 inhibitors

91
Q

Lipid lowering agents with marked decreases in LDL, minimal increases in HDL, minimal decreases in triglycerides

A

PCKSK9 inhibitors and HMG CoA reductase inhibitors

92
Q

Cardiac glycoside that directly inhibits Na/K/ATPase

A

Digoxin

93
Q

Digoxin MOA to increase intracellular Ca levels

A

Direct inhibition of Na/K/ATPase causing indirect inhibition of Na/Ca exchanger increasing intracellular Ca levels leading to positive inotropy

94
Q

What are the two mechanisms of Digoxin

A

Direct inhibition of Na/K/ATPase leading to positive inotropy
Stimulates vagus causing decreased HR

95
Q

Indications for digoxin

A

HF - increases contractility

A-fib - AV node conduction decreased and SA node depressed

96
Q

Changes seen on ECG with digoxin

A

Increased PR, decreased QT interval and T-wave inversions

97
Q

Digoxin side effects

A

Cholinergic effects, arrhythmias, AV block, hyperkalemia

98
Q

Drugs that displace digoxin from tissue-binding sites and decrease its clearance

A

Verapamil, amiodarone, quinidine

99
Q

Treatment for digoxin toxicity

A
  1. slowly normalize K
  2. cardiac pacemaker
  3. anti-digoxin Fab fragments
  4. give magnesium
100
Q

Side effect of digoxin toxicity that indicates poor prognosis

A

Hyperkalemia

101
Q

Predisposing factor for digoxin toxicity that decreases its clearance

A

renal failure

102
Q

Predisposing factor for digoxin toxicity that is permissive for digoxin binding to K site on Na/K/ATPase

A

Hypokalemia

103
Q

Class IA antiarrhythmic that causes headache and tinnitus

A

Quinidine

104
Q

Class IA antiarrhythmic that causes reversible SLE-like syndrome

A

Procainamide

105
Q

Class IA antiarrhythmic that cause HF

A

Disopyramide

106
Q

Indicated for atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT

A

Class IA antiarrhythmics

107
Q

Antiarrhythmic that can cause torsades de pointes

A

Class IA antiarrhythmics

108
Q

Antiarrhythmics that increase AP, ERP, QT

A

Class IA antiarrhythmics

109
Q

Antiarrhythmics that decrease AP, ERP, QT

A

Class IB antiarrhythmics

110
Q

Class I antiarrhythmics with some potassium channel blocking

A

Class IA antiarrhythmics

111
Q

Class I antiarrhythmic with minimal decrease on slope of phase 0

A

Class IB antiarrhythmics

112
Q

Class I antiarrhythmic with marked decrease on slope of phase 0

A

Class IC antiarrhythmics

113
Q

Antiarrhythmics with significant increase in ERP in AV node and accessory bypass tracts, no effect on ERP in Purkinje and ventricular tissue and normal AP duration

A

Class IC antiarrhythmics

114
Q

Class I antiarrhythmics have the most effect on which phase of action potential

A

Phase 0

115
Q

Which phase of myocyte action potential is not modulated by any antiarrhythmic

A

Phase 1 and Phase 4

116
Q

Phase II (plateau phase) of myocyte action potential is blocked by which class of antiarrhythmics

A

Class IV (CCBs)

117
Q

Antiarrhythmics indicated post-MI for acute ventricular arrhythmias and digitalis-induced arrhythmias

A

Class IB

118
Q

Sodium channels are blocked by which class of antiarrhythmics

A

Class I antiarrhythmics

119
Q

Antiarrhythmics that preferentially affect ischemic or depolarized Purkinje and ventricular tissue

A

Class IB antiarrhythmics

120
Q

Anti-epileptic drug indicated for post-MI acute ventricular arrhythmias or digitalis-induced arrhythmias

A

Phenytoin

121
Q

Anti-epileptic drug that can fall under Class IB antiarrhythmics

A

Phenytoin

122
Q

Class I antiarrhythmics that can cause CNS stimulation or depression and cardiovascular depression

A

Class IB antiarrhythmics

123
Q

Class IB antiarrhythmics

A

Lidocaine and Mexiletine

124
Q

Class IC antiarrhythmics

A

Flecainide and Propafenone

125
Q

Class I antiarrhythmic indicated for SVTs, including a-fib

A

Class IC antiarrhythmics

126
Q

Class I antiarrhythmic used only as a last resort in refractory VT

A

Class IC antiarrhythmics

127
Q

Antiarrhythmic contraindicated post-MI because of its pro-arrhythmic properties

A

Class IC antiarrhythmics

128
Q

Mechanism of Class II antiarrhythmics

A

B-blockers

129
Q

Effect of Class II antiarrhythmics on conductivity of the heart

A

Decrease SA and AV nodal activity by decreasing cAMP and calcium currents

130
Q

Which phase of the pacemaker action potential is affected by Class II antiarrhythmics

A

Slope of phase 4 is depressed

131
Q

Very short acting beta blocker

A

Esmolol

132
Q

Which node is more sensitive to Class II antiarrhythmics

A

AV node causing increased PR interval

133
Q

Antiarrhytmics indicated for SVT and ventricular control for a-fib and atrial flutter

A

Class II antiarrhythmics

134
Q

Antiarrhythmics that cause exacerbation of COPD and asthma

A

Class II antiarrhythmics

135
Q

Antiarrhythmics that cause impotence, sedation, and sleep alterations

A

Class II antiarrhythmics

136
Q

Class II antiarrhythmic that can cause dyslipidemia

A

Metoprolol

137
Q

Class II antiarrhythmics that can exacerbate Prinzmetal angina

A

Propranolol

138
Q

Beta blockers that are safe to give alone for cocaine toxicity or pheochromocytoma

A

Carvedilol and Labetalol

139
Q

Antiarrhythmics contraindicated in cocaine toxicity or pheochromocytoma because of unopposed a-agonism

A

Beta blockers (except carvedilol and labetalol)

140
Q

Beta blockers that are non-selective alpha and beta antagonists

A

Carvedilol and Labetalol

141
Q

Treatment for beta blocker toxicity

A

Glucagon, Atropine, Saline (GAS)

142
Q

Drugs contraindicated with beta blockers due to worsening of HoTN and conduction abnormalities

A

TCAs

143
Q

Class III antiarrhythmics

A

Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)

144
Q

Class III antiarrhythmics mechanism of action

A

Increase AP, ERP, an QT

145
Q

Antiarrhythmics which increase AP, ERP, an QT by affecting phase 3

A

Class III antiarrhythmics

146
Q

Antiarrhythmics with markedly prolonged repolarization

A

Class III antiarrhythmics

147
Q

Class III antiarrhythmic indicated for ventricular tachycardia

A

Amiodarone and Sotalol

148
Q

Indication for Class III antiarrhythmics

A 
Atrial flutter and a-fib
Ventricular tachycardia (Amiodarone and Sotalol only)
149
Q

Class III antiarrhythmics that causes torsades de pointes and excessive beta blockade

A

Sotalol

150
Q

Antiarrhytmics that can cause torsades de pointes

A

Sotalol, Ibutilide and Class IA antiarrhythmics

151
Q

Antiarrhythmic with Class I, II, III, and IV effects

A

Amiodarone

152
Q

What labs need to be drawn when using Amiodarone

A

PFTs, LFTs, and TFTs

153
Q

Pulmonary side effect of Amiodarone

A

Pulmonary fibrosis

154
Q

Endocrine side effect of Amiodarone

A

Hypo or hyperthyroidism

155
Q

GI effect of Amiodarone

A

Hepatotoxicity

156
Q

Skin effects of Amiodarone

A

Blue/gray skin deposits resulting in photodermatitis

157
Q

Eye effects of Amiodarone

A

Corneal deposits

158
Q

Cardiovascular effects of Amiodarone

A

Bradycardia, heart block, HF

159
Q

Channels blocked by Class III antiarrhythmics

A

Potassium channels

160
Q

Class IV antiarrhythmics

A

Diltiazem and Verapamil

161
Q

Effect of Class IV antiarrhythmics on pacemaker action potential

A

Decrease conduction velocity, increased ERP, and PR interval

162
Q

Antiarrhythmics that decrease conduction velocity, increased ERP, and PR interval of pacemaker action potential

A

Class IV antiarrhythmics

163
Q

Antiarrhythmics indicated for prevention of nodal arrhythmias and rate control in a-fib

A

Class IV antiarrhythmics

164
Q

Antiarrhythmics that cause constipation, flushing, edema, HF, AV block, and sinus node depression

A

Class IV antiarrhythmics

165
Q

Class IV antiarrhythmics block which channels

A

Calcium channels

166
Q

Drug of choice in diagnosing and terminating certain forms of SVT

A

Adenosine

167
Q

Antiarrhythmic that decreases AV node conduction by increasing K out of cell causing hyperpolarization and decreased intracellular calcium

A

Adenosine

168
Q

Duration of action of Adenosine

A

About 15 seconds

169
Q

Adenosine receptor antagonist that blunt the affects of adenosine

A

Caffeine and theophylline

170
Q

Antiarrhythmic that causes flushing, HoTN, CP, sense of impending doom and bronchospasms

A

Adenosine

171
Q

Given for treatment of torsades de pointes and digoxin toxicity

A

Magnesium

172
Q

Antiarrhythmic indicated for chronic stable angina in patients who cannot take B-blockers

A

Ivabradine

173
Q

Antiarrhythmic indicated for reduced ejection fraction and chronic HF

A

Ivabradine

174
Q

Antiarrhythmic that selectively inhibits I-funny channels, prolonging slow depolarization phase (phase 4)

A

Ivabradine

175
Q

Antiarrhythmic that causes luminous phenomena or visual brightness, HTN and bradycardia

A

Ivabradine

Cardiovascular-First Aid 2017 (5 decks)

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