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cardio drugs Flashcards

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1
Q

primary essential HTN treatment

A

diuretics, ACE inh, ARBs, Ca2+ channel blockers

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2
Q

HTN with CHF treatment

A

diuretics, ACE inh, ARBs, beta-blockers (compensated CHF, not decompensated or cardiogenic shock), aldosterone antagonists

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3
Q

HTN with DM treatment

A

ACE inhibitors/ARBs, Ca2+ channel blockers, diuretics, beta-blockers, alpha-blockers

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4
Q

MOA of calcium channel blockers

A

block the V-dep L-type Ca++ channels of cardiac and smooth muscle –> reduce muscle contractility

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5
Q

which ca++ channel blockers work on the vascular smooth muscle?

A

amlodipine = nifedipine > diltiazem > verapamil

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6
Q

which ca++ channel blockers work on the heart?

A

verapamil > diltiazem > amlodipine = nifedipine

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7
Q

clinical use of ca++ channel blockers

A

dihydropyridine (except nimodipine): HTN, angina, raynauds
non-dihydropyridine: HTN, angina, atrial fibrillation/flutter
nimodipine: subarachnoid hemorrhage

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8
Q

toxicity of ca++ channel blockers

A

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

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9
Q

amlodipine

A

dihydropine ca++ channel blocker

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10
Q

nimodipine

A

dihydropine ca++ channel blocker

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11
Q

nifedipine

A

dihydropine ca++ channel blocker

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12
Q

diltiazem

A

non-dihydropine ca++ channel blocker

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13
Q

verapamil

A

non-dihydropine ca++ channel blocker

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14
Q

hydralazine MOA

A

inc cGMP –> smooth muscle relaxation, vasodilates arterioles > veins; afterload reductino

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15
Q

clinical use of hydralazine

A

severe HTN, CHF, first line for HTN in pregnancy, methyldopa, with beta blockers to prevent reflex tach

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16
Q

toxicity of hydralazine

A

compensatory tach, fluid retention, nausea, headache, angina, lupus like syndrome

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17
Q

hypertensive emergency drugs

A

nitroprusside, nicardipine, clevidipine, labetalol, fenoldopam

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18
Q

nitroprusside

A

SA
increase cGMP via NO
may cause CN tox beause it releases CN

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19
Q

fenoldopam

A

D1R agaonist - oronary, peripheral, renal and splanchnic vasodilation, decrease BP and natriuresis

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20
Q

MOA of nitroglycerin and isosorbide dinitrate

A

vasodilate via increase NO in vascular smooth muscles –> increased cGMP and smooth muscle relaxation
dilates veins more than arteries
decreased preload

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21
Q

clinical use of nitroglycerin and isosorbide dinitrate

A

angina, ACS, PE

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22
Q

nitroglycerine and isosorbide dinitrate toxicity

A

reflex tach, hypoTN, flushing, headache

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23
Q

MOA of HMG - CoA reductase inhibitors

A

inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor

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24
Q

Side effects of statins

A

hepatotoxicity

rhabdomyolysis

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25
MOA of niacin
inhibits lipolysis in adipose tissue, reduces hepatic VLDL synthesis
26
Side effects of niacin
red flushed face which is decreased with aspirin or long term use hyperglycemia (acanthosis nigricans) hyperuricemia (exacerbates gout)
27
what are the bile acid resins?
cholestyramine, colestipol, colesevelam
28
MOA of bile acid resins
prevent intestinal reabsorption of bile acids, liver must use cholesterol to make more
29
side effects of bile acid resins
tastes bad, GI discomfort, decreased absorption of fat soluble vitamins, cholesterol gallstones
30
MOA of fibrates
upregulates LPL leading to TG clearance | activates PPAR-a to induce HDL synthesis
31
side effects of fibrates
myositis (increased risk of concurrent statins) hepatotoxicity cholesterol gallstones
32
cardiac glycoside drug
digoxin
33
moa of cardiac glycoside
direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca++ exchanger/antiport --> increased intracellular calcium --> positive inotropy --> vagus nerve stimulation --> decreased HR
34
clinical use of cardiac glycosides
CHF, atrial fib
35
toxicity of cardiac glycosides
cholinergic: nausea, vomiting, diarrhea, blurry yellow vision, hyperkalemia
36
what does ECG show with cardiac glycoside use?
``` increased PR decreased QT ST scooping T wave inversion arrhythmia AV block ```
37
what factors predispose to toxicity
renal failure, hypokalemia, verapamil, amiodarone, quinidine
38
antidote to cardiac glycoside use
slowly normalize k+, cardiac pacer, anti-digoxin Fab fragments, Mg2+
39
quinidine
class 1a
40
procainamide
class 1a
41
disopyramide
class 1a
42
lidocaine
class 1b
43
mexiletine
class 1b
44
flecainide
class 1c
45
propafenone
class 1c
46
metoprolol
class 2
47
propranolol
class 2
48
esmolol
class 2
49
atenolol
class 2
50
timolol
class 2
51
carvedilol
class 2
52
amiodarone
class 3
53
ibutilide
class 3
54
dofetilide
class 3
55
sotalol
class 3
56
verapamil
class 4
57
diltiazem
class 4
58
class 1 antiarrhythmics moa
Na+ channel blockers, slow or block conduction decrease slope of phase 0 depolarization and increased threshold for firing in abnormal pacemaker cells state dependent hyperkalemia causes increased toxicity
59
moa of class 1a
increased AP duration, increased effective refractory period, increased QT
60
clinical use of class 1a
both atrial and ventricular arrhythmias, especially reentrant and ectopic SVT and VT
61
toxicity of class 1a
cinchonism, reversible SLE like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades de points due to increased QT
62
MOA of class 1b
Myositis (increased risk of concurrent statins) hepatotoxicity cholesterol gallstones
63
clinical use of class 1b
acute ventricular arrhythmias, digitalis induced arrhythmias. Best post-MI
64
toxicity
CNS stimulation/depression, cardiovascular depression
65
MOA of class 1c
prolongs refractory period in AV node | minimal effect on AP duration
66
clinical use of class 1c
SVTs, including atrial fib last resort in refractory VT
67
toxicity of class 1c
proarrhythmic, especially post-MI contraindicated in structural and ischemic heart disease
68
MOA of class 2
decrease SA and AV nodal activity by decreasing cAMP and ca++ currents suppresses abnormal pacemaker by decreasing slope of phase 4
69
clinical use of class 2
SVT, slowing ventricular rate during atrial fibrillation and atrial flutter
70
toxicity of class 2
``` impotence COPD, asthma exacerbation cardiovascular effects, CNS effects metoprolol: dyslipidemia propanolol: exacerbates vasospasm in Prinzmetal angina contraindiated in cocaine users ```
71
how do you treat class 2 overdose?
glucagon
72
class 3 moa
K+ channel blocker AP duration increase with increased ERP increase QT
73
clinical use of class 3
atrial fibrillation, atrial flutter, ventricular tach (amiodarone, sotalol)
74
toxicity of sotalol
torsades de points, excessive beta blockade
75
toxicity of ibutilide
torsades de points
76
toxicity of amiodarone
pulmonary fibrosis, hepatotoxicity, hypothyroidism, hyperthyroidism, corneal deposits, skin deposits, photodermatitis, neurological effects, constipation, cardiovascular effects
77
moa of class 4
ca++ channel blocker, decreased conduction velocity, increased ERP, PR interval increase
78
clinical use of class 4
prevention of nodal arrhythmias, rate control in atrial fibrillation
79
toxicity of class 4
constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
80
what are the other antiarrhythmics
adenosine, Mg++
81
adenosine
increased K+ out of cells --> hyperpolarizing the cell and decreasing calcium current used for diagnosing and abolishing supraventricular tachycardia very short acting (15 seconds) adverse effects: flushing, hypotension, chest pain effects blocked by theophylline and caffeine
82
mg2+
effective in torsades de points and digoxin

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