Pharmacology Flashcards
(167 cards)
1
Q
Hypertensive drugs that are safe in pregnancy
A
Hydralazine, labetalol, methyldopa, nifedipine
2
Q
Hypertensive drugs that at protective against diabetic nephropathy
A
ACE inhibitors and ARBs
3
Q
Hypertensive drugs used with diabetes mellitus
A
ACE inhibitors/ARBs, CCBs, thiazide diuretics, B-blockers
4
Q
Hypertensive drugs used in HF
A
Diuretics (spironolactone)
ACE inhibitors/ARBs
B-blockers (compensated HF)
Aldosterone antagonist
5
Q
Hypertensive drug contraindicated in decompensated HF and cardiogenic shock
A
B-blockers
6
Q
Primary hypertensive drugs
A
Thiazide diuretics
ACE inhibitors/ARBs
Dihydropyridine CCBs
7
Q
Hypertensive drug that should be avoided in renal artery stenosis
A
Thiazide diuretics
8
Q
CCBs that act on the heart
A
Non-dihydropyridines: dilitiazem and verapamil
9
Q
CCBs that act on vascular smooth muscle
A
CANNN: Clevidipine Amlodipine Nifedipine Nimodipine Nicardipine
10
Q
Dihydropyridine CCB not indicated for HTN
A
Nimodipine
11
Q
Indicated for HTN, angina, and Raynaud phenomenon
A
Dihydropyridine CCBs (except nimodipine)
12
Q
CCBs MOA
A
Block voltage gated L-type Ca channels of cardiac and smooth muscle cells decreasing muscle contractility
13
Q
CCB indicated for subarachnoid hemorrhage
A
Nimodipine - prevents cerebral vasospasms
14
Q
CCB indicated for hypertensive urgency or emergency
A
Nicardipine and clevidipine
15
Q
CCB indicated for HTN, angina, and atrial fibrillation/flutter
A
Non-dihydropyridines verapamil and diltiazem
16
Q
CCBs that cause cardiac depression, AV block, hyperprolactinemia, constipation
A
Non-dihydropyridines
17
Q
Hypertensive used for severe HTN, HF with organic nitrate and safe to used during pregnancy
A
Hydralazine
18
Q
Frequently co-administered with hydralazine to prevent reflex tachycardia
A
B-blocker
19
Q
When is hydralazine contraindicated
A
Angina and CAD
20
Q
Hypertensive that causes compensatory tachycardia, fluid retention, headache, angina, Lupus-like syndrome
A
Hydralazine
21
Q
D1 receptor agonist used for hypertensive emergency
A
Fenoldopam
22
Q
B-blocker used for hypertensive emergency
A
Labetolol
23
Q
Nitrite used for hypertensive emergency
A
Nitroprusside
24
Q
D1 receptor agonist used in hypertensive emergency that causes coronary, peripheral, renal, and splanchnic vasodilation
A
Fenoldopam
25
Antihypertensive used postoperatively that can cause hypotension and tachycardia as side effects
Fenoldopam
26
Short-acting antihypertensive that increases cGMP via direct release of NO
Nitroprusside
27
Can cause cyanide toxicity
Nitroprusside
28
Cause vasodilation by increasing NO in vascular smooth muscle leading to increased cGMP and smooth muscle relaxation
Nitrates
29
Effect of nitrates on vessels at low doses
Veins >> arteries leads to decreased preload
30
Effect of nitrates on vessels at higher doses
Arteries > veins leads to decreased afterload
31
Indications for nitrates
Angina, ACS, pulmonary edema
32
When are nitrates contraindicated
Right ventricular infarction
33
Biochemical precursor of nitric oxide
Arginine
34
Nitrate side effects
Reflex tachycardia, HoTN, flushing, headache and "Monday disease" in industrial exposure
35
Hydralazine MOA
Increase cGMP causing smooth muscle relaxation
36
Effect of hydralazine on vessels
Vasodilates arterioles > veins decreasing afterload
37
Goal of antianginal therapy
Reduce myocardial O2 consumption by decreasing >1 of HR, BP, EDV and contractility
38
Drug given with nitrates to prevent reflex tachycardia
B-blockers
39
B-blockers that should be used with caution in angina
Pinodolol and acebutolol (partial B-agonists)
40
CCB that is similar to B-blockers in effect
Verapamil
41
Partial B-blockers
Pinodolol and acebutolol
42
What are the nitrates
Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
43
Antianginal that inhibits the late phase of sodium current causing reduction in diastolic wall tension and O2 consumption without affecting contractility
Ranolazine
44
Indications for ranolazine
Refractory angina
45
Antianginal that causes constipation, dizziness, headache, nausea, and QT prolongation
Ranolazine
46
Selective PDE-3 inhibitor indicated for short-term use in acute decompensated HF
Milrinone
47
Milrinone side effects
Arrhythmias and hypotension
48
Milrinone MOA on cardiomyocytes
Increases cAMP causing Ca influx leading to increased inotropy and chronotropy
49
Milrinone MOA on vascular smooth muscle
Increases cAMP inhibiting MLCK and causing general vasodilation
50
Lipid lowering agents that causes myopathy when used with fibrates or niacin
Statins
51
Mechanism of statins
HMG-CoA reductase inhibitors
52
Cholesterol precursor that is inhibited by use of statins
Mevalonate
53
Effect of statins on CAD patients
Decreases mortality
54
Lipid lowering agent that causes hepatotoxicity
Statins
55
Lipid lowering agents that inhibit HMG-CoA reductase
Statins
56
Lipid lowering agent that causes decreased absorption of other drugs and fat soluble vitamins
Bile acid resins
57
Bile acid resin drugs
Cholestyramine
Colestipol
Colesevelam
58
Lipid lowering agent that prevents intestinal reabsorption of bile acids causing liver to use cholesterol to make more
Bile acid resins
59
Lipid lowering agent that slightly increases HDL and triglyceride levels with moderate decrease in LDL levels
Bile acid resins
60
Side effect of Bile acid resins
GI upset
| Decrease absorption of drugs and fat soluble vitamins
61
Lipid lowering agent that causes rare increases in LFTs and diarrhea
Ezetimibe
62
Lipid lowering agent that prevents absorption at intestinal brush border
Ezetimibe
63
Lipid lowering agent with moderate decrease in LDL, minimal to no increase in HDL, and minimal to no decrease in triglyceride levels
Ezetimibe
64
Lipid lowering agent that can cause myopathies and cholesterol gallstones
Fibrates
65
Myopathy risk with fibrates is increased when used in combination with what other lipid lowering agents
HMG CoA reductase inhibitors (statins)
66
Side effect of Ezetimibe
Rare LFTs and diarrhea
67
Fibrate drugs
Gemrfibrozil
Bezafibrate
Fenofibrate
68
Lipid lowering agents with minimal decrease in LDL, minimal increase in HDL and marked decrease in triglyceride levels
Fibrates
69
Lipid lowering agents that activates PPAR-a to induce HDL synthesis
Fibrates
70
Lipid lowering agents upregulate LDL to increase triglyceride clearance
Fibrates
71
Side effect of fibrates
Myopathy (increased with statins) and cholesterol gallstones
72
Side effect of niacin
Flushing
Hyperglycemia
Hyperuricemia
73
Lipid lowering agent that increases risk of gout, diabetes, and can cause acanthosis nigricans
Niacin
74
Lipid lowering agents with moderate decrease in LDL, moderate increase in HDL, and minimal decrease in triglyceride levels
Niacin
75
Lipid lowering agents that inhibit lipolysis in adipose tissue and reduce hepatic VLDL synthesis
Niacin
76
Enzyme that is inhibited by niacin in order to inhibit lipolysis
Hormone-sensitive lipase
77
Drug taken to reduce flushing caused by niacin
NSAIDs
78
Best lipid lowering agent to take to decrease LDL and increase HDL
Niacin
79
Best lipid lowering agent to take to decrease LDL
Statins and PCSK9 inhibitors
80
Best lipid lowering agent to take to decrease triglycerides
Fibrates
81
Lipid lowering agents that cause myalgias, delirium, dementia, and other neurocognitive effects
PCSK9 inhibitors
82
Lipid lowering agents which inactivate LDL receptor degradation increasing removal of LDL from blood
PCSK9 inhibitors
83
Lipid lowering agents with marked decreases in LDL, minimal increases in HDL, minimal decreases in triglycerides
PCKSK9 inhibitors and HMG CoA reductase inhibitors
84
Cardiac glycoside that directly inhibits Na/K/ATPase
Digoxin
85
Digoxin MOA to increase intracellular Ca levels
Direct inhibition of Na/K/ATPase causing indirect inhibition of Na/Ca exchanger increasing intracellular Ca levels leading to positive inotropy
86
What are the two mechanisms of Digoxin
Direct inhibition of Na/K/ATPase leading to positive inotropy
Stimulates vagus causing decreased HR
87
Indications for digoxin
HF - increases contractility
| A-fib - AV node conduction decreased and SA node depressed
88
Changes seen on ECG with digoxin
Increased PR, decreased QT interval and T-wave inversions
89
Digoxin side effects
Cholinergic effects, arrhythmias, AV block, hyperkalemia
90
Drugs that displace digoxin from tissue-binding sites and decrease its clearance
Verapamil, amiodarone, quinidine
91
Treatment for digoxin toxicity
1. slowly normalize K
2. cardiac pacemaker
3. anti-digoxin Fab fragments
4. give magnesium
92
Side effect of digoxin toxicity that indicates poor prognosis
Hyperkalemia
93
Predisposing factor for digoxin toxicity that decreases its clearance
renal failure
94
Predisposing factor for digoxin toxicity that is permissive for digoxin binding to K site on Na/K/ATPase
Hypokalemia
95
Class IA antiarrhythmic that causes headache and tinnitus
Quinidine
96
Class IA antiarrhythmic that causes reversible SLE-like syndrome
Procainamide
97
Class IA antiarrhythmic that cause HF
Disopyramide
98
Indicated for atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT
Class IA antiarrhythmics
99
Antiarrhythmic that can cause torsades de pointes
Class IA antiarrhythmics
100
Antiarrhythmics that increase AP, ERP, QT
Class IA antiarrhythmics
101
Antiarrhythmics that decrease AP, ERP, QT
Class IB antiarrhythmics
102
Class I antiarrhythmics with some potassium channel blocking
Class IA antiarrhythmics
103
Class I antiarrhythmic with minimal decrease on slope of phase 0
Class IB antiarrhythmics
104
Class I antiarrhythmic with marked decrease on slope of phase 0
Class IC antiarrhythmics
105
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
Class IC antiarrhythmics
106
Class I antiarrhythmics have the most effect on which phase of action potential
Phase 0
107
Which phase of myocyte action potential is not modulated by any antiarrhythmic
Phase 1 and Phase 4
108
Phase II (plateau phase) of myocyte action potential is blocked by which class of antiarrhythmics
Class IV (CCBs)
109
Antiarrhythmics indicated post-MI for acute ventricular arrhythmias and digitalis-induced arrhythmias
Class IB
110
Sodium channels are blocked by which class of antiarrhythmics
Class I antiarrhythmics
111
Antiarrhythmics that preferentially affect ischemic or depolarized Purkinje and ventricular tissue
Class IB antiarrhythmics
112
Anti-epileptic drug indicated for post-MI acute ventricular arrhythmias or digitalis-induced arrhythmias
Phenytoin
113
Anti-epileptic drug that can fall under Class IB antiarrhythmics
Phenytoin
114
Class I antiarrhythmics that can cause CNS stimulation or depression and cardiovascular depression
Class IB antiarrhythmics
115
Class IB antiarrhythmics
Lidocaine and Mexiletine
116
Class IC antiarrhythmics
Flecainide and Propafenone
117
Class I antiarrhythmic indicated for SVTs, including a-fib
Class IC antiarrhythmics
118
Class I antiarrhythmic used only as a last resort in refractory VT
Class IC antiarrhythmics
119
Antiarrhythmic contraindicated post-MI because of its pro-arrhythmic properties
Class IC antiarrhythmics
120
Mechanism of Class II antiarrhythmics
B-blockers
121
Effect of Class II antiarrhythmics on conductivity of the heart
Decrease SA and AV nodal activity by decreasing cAMP and calcium currents
122
Which phase of the pacemaker action potential is affected by Class II antiarrhythmics
Slope of phase 4 is depressed
123
Very short acting beta blocker
Esmolol
124
Which node is more sensitive to Class II antiarrhythmics
AV node causing increased PR interval
125
Antiarrhytmics indicated for SVT and ventricular control for a-fib and atrial flutter
Class II antiarrhythmics
126
Antiarrhythmics that cause exacerbation of COPD and asthma
Class II antiarrhythmics
127
Antiarrhythmics that cause impotence, sedation, and sleep alterations
Class II antiarrhythmics
128
Class II antiarrhythmic that can cause dyslipidemia
Metoprolol
129
Class II antiarrhythmics that can exacerbate Prinzmetal angina
Propranolol
130
Beta blockers that are safe to give alone for cocaine toxicity or pheochromocytoma
Carvedilol and Labetalol
131
Antiarrhythmics contraindicated in cocaine toxicity or pheochromocytoma because of unopposed a-agonism
Beta blockers (except carvedilol and labetalol)
132
Beta blockers that are non-selective alpha and beta antagonists
Carvedilol and Labetalol
133
Treatment for beta blocker toxicity
Glucagon, Atropine, Saline (GAS)
134
Drugs contraindicated with beta blockers due to worsening of HoTN and conduction abnormalities
TCAs
135
Class III antiarrhythmics
Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)
136
Class III antiarrhythmics mechanism of action
Increase AP, ERP, an QT
137
Antiarrhythmics which increase AP, ERP, an QT by affecting phase 3
Class III antiarrhythmics
138
Antiarrhythmics with markedly prolonged repolarization
Class III antiarrhythmics
139
Class III antiarrhythmic indicated for ventricular tachycardia
Amiodarone and Sotalol
140
Indication for Class III antiarrhythmics
```
Atrial flutter and a-fib
Ventricular tachycardia (Amiodarone and Sotalol only)
```
141
Class III antiarrhythmics that causes torsades de pointes and excessive beta blockade
Sotalol
142
Antiarrhytmics that can cause torsades de pointes
Sotalol, Ibutilide and Class IA antiarrhythmics
143
Antiarrhythmic with Class I, II, III, and IV effects
Amiodarone
144
What labs need to be drawn when using Amiodarone
PFTs, LFTs, and TFTs
145
Pulmonary side effect of Amiodarone
Pulmonary fibrosis
146
Endocrine side effect of Amiodarone
Hypo or hyperthyroidism
147
GI effect of Amiodarone
Hepatotoxicity
148
Skin effects of Amiodarone
Blue/gray skin deposits resulting in photodermatitis
149
Eye effects of Amiodarone
Corneal deposits
150
Cardiovascular effects of Amiodarone
Bradycardia, heart block, HF
151
Channels blocked by Class III antiarrhythmics
Potassium channels
152
Class IV antiarrhythmics
Diltiazem and Verapamil
153
Effect of Class IV antiarrhythmics on pacemaker action potential
Decrease conduction velocity, increased ERP, and PR interval
154
Antiarrhythmics that decrease conduction velocity, increased ERP, and PR interval of pacemaker action potential
Class IV antiarrhythmics
155
Antiarrhythmics indicated for prevention of nodal arrhythmias and rate control in a-fib
Class IV antiarrhythmics
156
Antiarrhythmics that cause constipation, flushing, edema, HF, AV block, and sinus node depression
Class IV antiarrhythmics
157
Class IV antiarrhythmics block which channels
Calcium channels
158
Drug of choice in diagnosing and terminating certain forms of SVT
Adenosine
159
Antiarrhythmic that decreases AV node conduction by increasing K out of cell causing hyperpolarization and decreased intracellular calcium
Adenosine
160
Duration of action of Adenosine
About 15 seconds
161
Adenosine receptor antagonist that blunt the affects of adenosine
Caffeine and theophylline
162
Antiarrhythmic that causes flushing, HoTN, CP, sense of impending doom and bronchospasms
Adenosine
163
Given for treatment of torsades de pointes and digoxin toxicity
Magnesium
164
Antiarrhythmic indicated for chronic stable angina in patients who cannot take B-blockers
Ivabradine
165
Antiarrhythmic indicated for reduced ejection fraction and chronic HF
Ivabradine
166
Antiarrhythmic that selectively inhibits I-funny channels, prolonging slow depolarization phase (phase 4)
Ivabradine
167
Antiarrhythmic that causes luminous phenomena or visual brightness, HTN and bradycardia
Ivabradine
