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Elliot Step 1 > Cardio Drugs > Flashcards

Cardio Drugs Flashcards

1
Q

Regarding CHF, when can beta blockers be used?

A

Only in COMpensated chf

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2
Q

Beta blockers are contraindicated in 2 scenarios (at least 2)

A

Cardiogenic shock and decompensated chf

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3
Q

2 CCBs that act on cardiac muscle primarily

A

Verapail>diltiazem (Verapamil ventricle)

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4
Q

2 CCBs that act on vascular smooth muscle

A

Nifedipine and amlodipine

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5
Q

Medication used in Prinzmetals angina?

A

CCBs

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6
Q

Only CCB not used for arrhythmias?

A

Nifedepine

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7
Q

Toxicity of CCBs?

A

AV block; peripheral edema, flushing, dizziness, constipation

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8
Q

Drug that causes constipation, AV block and peripheral edema?

A

CCB

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9
Q

MOA of hydralazine?

A

Inc cGMP–>smooth muscle relaxation

Vasodilates arterioles> veins (afterload reduction)

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10
Q

Drug that inc cGMP?

A

Hydralazine, nitros, and nitroprusside

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11
Q

Lupus like symptoms with this cardiac drug?

A

Hydralazine and Procainamide

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12
Q

First line therapy for htn in pregnancy?

A

Hydralazine with methyldopa

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13
Q

Hydralazine is coadministered with what drug?

A

Beta blockers– to prevent reflex tachycardia

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14
Q

Drug causes headache, fluid retention, and compensatory tachycardia? When is drug contraindicated?

A

Hydralazine– contraindicated in angina/CAD

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15
Q

Drug contraindicated in angina/CAD?

A

Hydralazine

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16
Q

MOA of nitroprusside? Use?

A

Inc cGMP via direct release of NO– used in malignant hypertension– can cause cyanide poisoning (give nitrite and then thiosulfate)

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17
Q

MOA of Fenoldopam?

A

Dopamine D1 receptor agonist

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18
Q

Isosorbide dinitrate MOA?

A

release NO causing inc in cGMP– dilate veins» ateries–>dec preload

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19
Q

Side effects of Nitro?

A

Flushing; headache– causes monday disease in industrial exposure

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20
Q

Nifedipine is similar to blank; while verapimil is similar to blank?

A

Nifedipine is similar to nitrates

Verapamil is similar to Beta blockers

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21
Q

Partial agonists contraindicated in angina?

A

Pindolol and acebutolol

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22
Q

Causes muscle pain?

A

Statins and fibrates

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23
Q

Increases TG? i.e. not to be given to patient with high TG

A

Bile acid resins (cholestyramine; colestipol, colesevelam)

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24
Q

Prevents intestinal reabsorption of bile acids?

A

Cholestyramine; colestipol; colesevelam

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25
Q

Causes hyperglycemia (lipid med)?

A

Niacin

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26
Q

Lipid med with great effect on HDL?

27
Q

Lipid med causes facial flushing. How is facial flushing treated?

A

Niacin– facial flushing treated with aspirin

28
Q

MOA of niacin (b3)?

A

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

29
Q

Lipid med causes gout?

30
Q

Statin directly blocks production of ?

A

Mevalonate

31
Q

Lipid med that cause cholesterol stones?

A

Bile acid resins (cholestyramine; colestepol; colesevelam); AND Fibrates

32
Q

Most effective in reducing TG? MOA?

A

Fibrates– upregulate LPL–>TG clearance (LPL breaks down TG which are carried via chylomicrons)

33
Q

Ezetimibe MOA? Side effects?

A

Prevents cholesterol uptake from gut. May increase LFTs

34
Q

Lipid drugs that my increaes LFTs?

A

Statins; fibrates; and ezetimibe

35
Q

Cardiac drug with cholinergic side effects including blurry yellow vision?

A

Glycosides

36
Q

How do glycosides decrease heart rate? Use?

A

Via stimulation of vagus nerve– used in Afib and CHF (not used for CHF with normal EF– also Does NOT prolong life in patients with HF– improves quality)

37
Q

Antidotes for glycoside toxicity?

A

Magnesium; lidocain

38
Q

Class 1 antiarrhythmics are state dependent– what does this mean?

A

selectively depress tissue that is frequently depolarized

39
Q

All class 1 block?

A

Na channel blockers

40
Q

Class 1a drugs?

A

Quinidine, procainamide, disopyramide

41
Q

MOA of 1a?

A

Increase AP duration; inc ERP; inc QT interval

42
Q

Causes headache and tinnitus?

43
Q

1a drug toxicities?

A

Thrombocytopenia; torsades

44
Q

1a drug that causes acute heart failure?

A

Disopyramide

45
Q

Class 1B drugs? MOA?

A

Lidocaine, Mexiletine, Tocainide (I’d buy Lidy’s mexican tacos)
Decrease AP duration– preferentially affects ischemic or depolarized tissue

46
Q

Used for post MI arrhythmias?

A

1B– lidocaine, mexiletine, Tocainide

47
Q

Antiarrhythmic with CNS toxicity?

A

1B (lidocaine, mexiletine, tocainide); class II

48
Q

1C drugs? MOA? Use?

A

Flecainide, propafenone– do not increase AP duration

Used for life threatening arrhythmias (significantly prolongs refractory period of AV node)

49
Q

Contraindicated in post MI?

A

1C (flecainide and propafenone)

50
Q

Class II drugs? MOA?

A

Beta blockers
Decreases SA and AV nodal activity by dec cGMP, dec Ca2+ currents.–> suppresses slope of phase 4 (funny channel)– AV node is particularly sensitive

51
Q

Antiarrhythmic that may mask signs of hypoglycemia?

A

Beta blockers

52
Q

Beta blocker that can cause dyslipidemia

A

Metoprolol

53
Q

Class III? MOA?

A

Amiodoraone, Ibutilide, Dofetilide, Sotalol (AIDS) Class III AIDS in heart disease

54
Q

Cardiac drug that causes blue/gray skin deposits resulting in photodermatitis?

A

Class III (Amiodorone, Ibutilide, Dofetilide, Sotalol)

55
Q

Cardiac drug that causes hyperthyroidism?

A

Amiodarone

56
Q

Things to watch out for when giving a patient amiodarone?

A

Liver; thyroid; and pulmonary

57
Q

Cardiac drugs that prolong phase 3?

A

1a and class III

58
Q

Corneal deposits– arrhythmic drug?

A

amiodarone

59
Q

Class IV antiarrhythmics?

A

Verapamil (also used for migraine headaches) and diltiazem

60
Q

Cause constipation flushing and edema?

61
Q

Drugs that cause facial flushing?

A

Niacin, CCBs, Adenosine, and Nitro

62
Q

MOA of adenosine?

A

Increases K+ outside of cells->hyperpolarizing the cells + decrease in incoming calcium. Used to abolish SVT

63
Q

Adenosine effects are blocked by?

A

theophylline and caffeine

64
Q

Drug that hyperpolarizes cell?

Elliot Step 1 (32 decks)

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