Heart Drugs Flashcards

1
Q

Calcium Channel blockers tissue selectivity vascular smooth muscle

A

Vascular smooth muscle: alodipine= nifedipine > diltiazem > verapamil

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2
Q

Ca channel blocker tissues selectivity for heart

A

Verapamil> diltiazem > amlodipine = nifedipine

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3
Q

Ca channel blocker toxicity

A

Av block, peripheral edema, dizziness, constipation, cardiac depression

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4
Q

Hydralazine mechanism

A

Increase cGMP to relax smooth muscle which vasodilation of arteries more than veins so after load is lower

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5
Q

Co administered with hydralazine and why

A

Beta blocker for reflex tachycardia

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6
Q

Treatment for pregnancy hypertension

A

Hydralazine plus methyldopa

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7
Q

Hydralazine sides

A

Compensatory tachycardia (so no in angina or cad) , fluid retention, nausea, lupus like, angina

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8
Q

Nitroprusside mechanism

A

Short acting increase cGMP via NO release

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9
Q

Nitroprusside tox

A

Has cyanide so cyanide toxicity

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10
Q

Fenoldopam

A

Dopamine d1 receptor agonist, vasodilation including coronary renal and splanchnic, decrease bp and increase naturesis

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11
Q

Calcium Channel blockers drugs

A

Nifedipine, verapamil , diltiazem, amlodipine

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12
Q

Nitroglycerin/ isosorbide dinitrate: mechanism and clincial use

A

vasodialation (veins) by NO release -> cGMP increase

used for angina and pulmonary edema

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13
Q

nitroglyerin/ isosorbide dinitrate toxicity

A

reflex tachycardia, hyoptension, flushing, headache, monday’s disease in industry exposure

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14
Q

what do statins stop HMG-CoA from becoming?

A

mevalonate

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15
Q

side effects of statins

A

hepatotoxicity, rhabdomyolysis

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16
Q

statins effect on : LDL, HDL, Triglycerides

A

way down, up, down

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17
Q

niacin effect on LDL HDL Triglycerides

A

down, up, down

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18
Q

bile acid resin effect on LDL HDL Triglyceries

A

down, slightly up, slightly up

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19
Q

niacin: other name and mech

A

vitamin b3, inhibits lipolysis in adipose, reduces hepatic VLDL secretion

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20
Q

niacin sides

A

red flushed face (fix with aspirin), hyperglycemia (causing acanthosis nigricans), hyperuricemia (exacerbates gout)

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21
Q

bile acid resins and effects

A

cholestyramine, colestipol, colesevelam. prevents reabsorption of bile so liver must use cholesterol to make more

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22
Q

bile acid resins sides

A

tastes bad, gi discomfort, cholesterol gallstones, cant absorb fat soluble vitamins

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23
Q

ezetimibe

A

Cholestrol absorption blockers. rarely causes high LFTs and diarrhea

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24
Q

Fibrates

A

drives down triglycerides a lot, activates lipoprotein lipase. tox: myositis, hepatotox, cholestrol gallstones

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25
Q

Class I Antiarrhythmics are what?

A

Na channel blockers

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26
Q

Class IA drugs

A

Quinidine, Procainamide, Disopyramide

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27
Q

Class IA actions

A

increase AP duration, increase effective refractory period, increase QT interval.

28
Q

Class IA uses

A

atrial and ventricular arrythmias. especially reentrant currents and ectopic supraventricular or ventricular tachycardia

29
Q

Quinidine tox and class

A

Class IA. cinchonism = headache and tinnitus

30
Q

Procainamide tox and class

A

Class IA. reversible SLE-like syndrome

31
Q

disopyramide tox and class

A

heart failure

32
Q

Class IA shared toxicities

A

thrombocytopenia, torsades de pointes due to high QT interval

33
Q

Class IB drugs

A

Lidocaine, Mexilentine, Tocainide

34
Q

Class IB actions

A

decrease AP duration. preferentially targets ischemic or depolarized purkinje and ventricular tissue

35
Q

Class IB uses

A

acute ventricular arrhythmias especially post MI and digitalis arrhythmias

36
Q

Digoxin availability and action

A

75% available, 1/2 life is 40 hrs. directly inhibits Na/K ATPase, thus indirectly inhibits Na/Ca

37
Q

Digoxin effects

A

increases intracellular Ca -> positive inotropy. stimulates vagus nerve -> lower heart rate. improves contractility. slows down the AV node and depresses SA node

38
Q

Digoxin use

A

CHF (contractility), atrial fib (slowed AV node conduction and SA depression)

39
Q

Digoxin tox

A

Cholinergic effects: nausea, comiting, diarrhea, blurry yellow vision (van Gogh)
ECG: increase PR, down QT, ST scooping, T-wave inversion, arrhythmia, av block
hyperkalemia - bad sign

40
Q

Digoxin tox predisposing factors

A

renal failure, hypokalemia, quinidine

41
Q

Antidote to digoxin poisoning

A

slowly normalize K, lidocain, cardiac pacer, anti-digoxin Fab fragments, Mg.

42
Q

Class IC drugs

A

Flecainide, propafenone

43
Q

Class IC uses

A

last resort for refractory tachyarrhythmias without structural anomaly

44
Q

Class IC effects

A

no effect on AP duration

45
Q

Class IC tox

A

proarrhythmic (post MI, so contraindicated). prolongs refractory period of AV node a lot

46
Q

class two anti arrythmics: drugs and type of drug

A

beta blockers: metoprolol, propranolol, esmolol, atenolol, timolol

47
Q

shortest acting betablocker?

A

esmolol

48
Q

beta blocker actions on the heart

A

Decreases SA and AV node actiity by decrease cAMP and Ca currents. Makes phase 4 have a shallower long slope.

AV node hit more

49
Q

class II uses

A

v tach, svt, slowing ventricle during a fib/flutter

50
Q

beta blocker toxicity

A

impotence, asthma attack, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations), mask signs of hyperglycemia

51
Q

special sides of metoprolol

A

dyslipidemia. treat with high dose glucagon

52
Q

special sides of propranolol

A

can exacerbate vasospasm of Prinzmetals (cyclical) angina

53
Q

Class III drugs and type

A

Potassium Channel Blocker. Amiodarone, Ibutilide, Dofetilide, Sotalol

54
Q

Class III effects and use

A

increase AP duration, increase ERP, used when other antiarrythmics fail (like IC), increase QT

55
Q

Sotalol tox

A

torsades de pointes, excessive beta block

56
Q

ibutilide tox

A

torsades

57
Q

amiodarone tox

A

pulmanary fibrosis, hepatotox, hypo/hyperthyroid (amiodorone is 40% iodine), corneal deposits, blue/grey skin deposits, neurological effects, constipation, CV (bradycardia, heart block, CHF)

58
Q

Amiodarone special precautions

A

check PFTs, LFT, and TFTs

59
Q

what makes amiodarone unique

A

has class I, II, III, and IV effects (plus iodine effects) cause it disrupts membrane

60
Q

Class IV drugs and type

A

Ca channel blockers, Verapmil and diltiazen

61
Q

Class IV effects

A

decrease conduction velocity, increase: ERP, PR

62
Q

Class IV use

A

prevent nodal arrhytmias

63
Q

Adenosine mech

A

increase K out of cells -> hyperpolarize

64
Q

Adenosine use

A

best drug for diagnose and treat supraventricular tachy. very short acting (15 secs)

65
Q

Adenosine tox

A

flushing, hypotension, chest pain. Fix with: theophyllin or caffeine

66
Q

Mg use

A

torsades de pointes and digoxin toxicty