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First aid drugs > Step 1 cardiac drugs > Flashcards

Step 1 cardiac drugs Flashcards

1
Q

hydralazine mechanism

A

increases cGMP–smooth muscle relaxation; arterial dilator, reduces afterload

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2
Q

hydralazine use

A

severe hypertension, CHF; first line for HTN in pregnancy with methyldopa

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3
Q

hydralazine coadministered with what? Why?

A

beta blocker; to prevent reflex tachycardia

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4
Q

hydralazine toxicity

A

headaches, nausea, fluid retention, reflex tachycardia, angina, LUPUS LIKE SYNDROME

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5
Q

Ca channel blockers

A

nifedipine, verapamil, diltiazem

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6
Q

Ca channel blocker mechanism

A

block voltage dependent L-type Ca channels of cardiac and smooth muscle–reduce contractility

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7
Q

affinity of Ca channel blockers

A

heart: verapamil > diltiazem > nifedipine

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8
Q

Ca channel blocker use

A

hypertension, angina, arrhythmias, Prinzmetal’s angina, Raynaud’s

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9
Q

Ca channel blocker toxicity

A

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

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10
Q

nitroglycerin, isosorbide dinitrate mechanism

A

release of NO in smooth muscle causes increase in cGMP and smooth muscle relaxation; dilates veins more than arteries; decreases preload

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11
Q

nitroglycerin, isosorbide dinitrate use

A

angina, pulmonary edema; aphrodesiac and erection enhancer

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12
Q

nitroglycerin, isosorbide dinitrate toxicity

A

reflex tachycardia, hypotension, flushing, headache, “Monday disease”

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13
Q

drugs for malignant hypertension

A

nitroprusside, fenaldopam, diazoxide

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14
Q

nitroprusside mechanism

A

increase cGMP via direct release of NO

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15
Q

nitroprusside toxicity

A

releases cyanide (so can cause toxicity)

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16
Q

fenaldopam mechanism

A

dopamine D1 receptor agonist–relaxes renal vascular smooth muscle, splanchnic, peripheral and coronary vessels

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17
Q

diazoxide mechanism

A

opens K channels–hyperpolarizes cell and relax vascular smooth muscle

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18
Q

diazoxide toxicity

A

hyperglycemia (because it reduces insulin release)

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19
Q

class II antiarrhythmic drugs

A

beta blockers–timolol, propanolol, metoprolol, atenolol, esmolol

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20
Q

class II antiarrhythmic mechanism

A

decrease sympathetic tone, slow AV nodal conduction (decreases cAMP and Ca); decrease slope of Phase 4–increase PR interval

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21
Q

class II anti-arrhythmic use

A

V-tach, slowing ventricular rate during atrial fib and flutter (remember they only act on the ventricle!)

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22
Q

class II antiarrhythmic toxicity

A

impotence, exacerbation of asthma, bradycardia, AV block, sedation, sleep disturbances, mask hypoglycemia, metoprolol can cause dylipidemia

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23
Q

class 1a antiarrhythmics

A

procainamide, quinidine, disopyramide

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24
Q

class 1a antiarrhythmic mechanism

A

Na channel blockers, Phase 0 and 3–slow both; intermediate channel blockers; prolong QT and increase refractory period increase AP duration; also have some action at K channels

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25
Q

class 1a antiarrhythmic toxicity

A

arrhythmias (from long QT), procainamide can cause SLE like syndrome, quinidine–cinochism—tinnitus and headache), thrombocytopenia

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26
Q

class 1a antiarrhythmic uses

A

atrial and ventricular arrhythmias (esp reentrant and ectopic and supraventricular tachycardia)

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27
Q

class 1c antiarrhythmics

A

flecainide, encainide, propafenone

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28
Q

class 1c antiarrhythmic mechanism

A

Na channel blockers, slow Phase 0 (no, effect on Phase 3), high Na channel avidity so slow off time, no effect on AP duration

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29
Q

class 1c antiarrhythmic use

A

last resort in refractory arrhythmias; V-tach that progresses to V-fib; intractable SVT

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30
Q

class 1c toxicity

A

contraindicated in MI (proarrhythmic); significantly prolongs refractory period in AV node

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31
Q

class 1b antiarrhythmics

A

lidocaine, mexiletine, tocainide

32
Q

class 1b antiarrhythmic mechanism

A

Na channel blockers; poor avidity–quick on and off; slow Phase 0 but increase Phase 3 slope; decrease AP duration; preferentially rapidly depolarizing or ischemic cells; best for post-MI patients

33
Q

class 1b antiarrhythmic toxicity

A

local anesthetic, CNS stimulation/depression, cardiovascular depression

34
Q

class III antiarrhythmics

A

ibutilide, amiodarone (has I-IV actions), betyrium, sotolol, dofetilide

35
Q

class III antiarrhythmic mechanism

A

block K channels, hyperpolarize to prolong refractory period and AP duration, increase QT interval

36
Q

class III antiarrhythmic use

A

used when others fail–supraventricular and ventricular tachyarrhythmias

37
Q

class 1b antiarrhythmic use

A

acute ventricular arrhythmias or digitalis-induced arrhythmias

38
Q

class III antiarrhythmic toxicity

A

risk of new arrhythmia (because of long QT)

39
Q

sotolol toxicity

A

torsades de pointes; excessive beta block

40
Q

bretylium toxicity

A

new arrhythmias, hypotension

41
Q

ibulitide toxicity

A

torsades de pointes

42
Q

amiodarone toxicity

A

pulmonary fibrosis, hepatotoxicity, hypo/hyperthyroidism, corneal deposits, blue gray skin deposits and photodermatitis, neurologic effects, constipation, bradycardia, heart block, CHF, P450 inhibitor

43
Q

class IV antiarrhythmics

A

verapamil, diltiazem

44
Q

class IV antiarrhythmic mechanism

A

Ca channel blocker, decreases conduction velocity, increases refractory period and PR interval

45
Q

class IV antiarrhythmic use

A

nodal arrhythmias

46
Q

class IV antiarrhythmic toxicity

A

constipation, flushing, edema, CHF, AV block, sinus node depression; verapamil: gingival hyperplasia

47
Q

adenosine mechanism

A

increases flow of K from AV nodal cells to hyperpolarize the cell and decrease Ca current; very short acting (selective coronary dilator)

48
Q

adenosine use

A

diagnosing and abolishing supraventricular tachycardia

49
Q

adenosine toxicity

A

coronary steal phenomenon, flushing, hypotension, chest pain, effects blocked by theophylline

50
Q

K+ use in arrhythmias

A

depresses ectopic pacemaker cells in hypokalemia (ie digoxin toxicity)

51
Q

Mg 2+ use in arrhythmias

A

tosades de pointes and digoxin toxicity

52
Q

dipyramidole mechanism

A

inhibits breakdown of adenosine (selective coronary vasodilator)

53
Q

dipyramidole toxicity

A

coronary steal phenomenon

54
Q

statin mechanism

A

HMG-CoA reductase inhibitors (inhibit melavonate conversion)

55
Q

effects of statins

A

primarily lower LDL, small decrease in HDL and TG

56
Q

statin toxicity

A

rhabdomyolysis and hepatotoxicity

57
Q

niacin mechanism

A

inhibits lipolysis in adipose tissue; reduces hepatic VLDL secretion into circulation

58
Q

effects of niacin

A

moderate decrease in LDL, increase in HDL, small decrease in TG (acts primarily on HDL)

59
Q

niacin toxicity

A

flushing (take aspirin 30 minutes before), hyperglycemia (acanthosis nigricans), hyperuricemia

60
Q

cholestyramine mechanism

A

prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more (bile acid resin)

61
Q

colestipol mechanism

A

prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more (bile acid resin)

62
Q

colesevelam

A

prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more (bile acid resin)

63
Q

effects of bile acid resins

A

moderate decrease in LDL, slight increase in HDL and triglycerides

64
Q

bile acid resin toxicity

A

patients hate it (GI discomfort and bad taste), decreased absorption of fat soluble vitamins, cholesterol gallstones

65
Q

ezetimibe

A

cholesterol absorption blocker (at small intestine brush border)

66
Q

effects of ezetimibe

A

only effect is lowering LDL (no HDL, TG effects)

67
Q

ezetimibe toxicity

A

rare increase in LFTs

68
Q

gemfibrizol mechanism

A

upregulate lipoprotein lipase (LPL) to increase TG clearance

69
Q

clofibrate mechanism

A

upregulate lipoprotein lipase (LPL) to increase TG clearance

70
Q

bezafibrate mechanism

A

upregulate lipoprotein lipase (LPL) to increase TG clearance

71
Q

fenofibrate mechanism

A

upregulate lipoprotein lipase (LPL) to increase TG clearance

72
Q

effects of fibrates

A

biggest effect is decrease in TG, small decrease in LDL and small increase in HDL

73
Q

fibrate toxicity

A

myositis, hepatotoxicity, cholesterol gallstones

74
Q

digoxin mechanism

A

direct inhibition of Na/K ATPase leads to indirect inhibition of Na/Ca exchanger (increase in intracellular Ca and positive inotropy); stimulates vagus nerve

75
Q

digoxin use

A

CHF, atrial fibrillation

76
Q

digoxin toxicity

A

cholinergic: nausea, vomiting, diarrhea, blurry yellow vision, decreased appetite; increased PR, short QT, scooping, T wave inversion, arrhythmia, hyperkalemia; worse with renal failure, hypokalemia, quinidine

77
Q

digoxin antidote

A

slowly normalize K, lidocaine, Digiband (anti-digoxin fragments), Mg

First aid drugs (10 decks)

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