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PHARM SHELF AND BOARDS > CARDIAC > Flashcards

CARDIAC Flashcards

1
Q

Name 5 drugs commonly used to Tx malignant HTN

A

nitroprusside, nicardipine, clevidipine, labetalol, and fenoldopam

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1
Q

Which aspect of the heart is most sensitive to the effects of Class II antiarrhythmics?

A

AV node

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2
Q

Which lipid-lowering agents act by upregulating LPL?

A

Fibrates

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2
Q

2 clinical indications of cardiac glycosides

A

CHF to increase contractility; Atrial Fibrillation to depress SA node and decrease AV conduction

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3
Q

What are 4 AE of bile acid resins

A

CHOLESTEROL GALLSTONES, decreased fat soluble vitamin absorption (ADEK), GI discomfort, tastes bad

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4
Q

Why does renal failure predispose to digoxin toxicity?

A

decreased clearance

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4
Q

Althought most beta blockers fit into class ____ antiarryhthmics, sotalol is actually a class _________

A

II; III

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5
Q

How does the effect of class IC antiarrhythmics on AP duration differ from Ia and Ib

A

IC does NOT affect AP duration, Ia increases, Ib decreases

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6
Q

What are 5 determinants of myocardial oxygen demand?

A

End Diastolic Volume (preload), Blood Pressure (afterload), heart rate, contractility, and ejection time

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6
Q

What are 2 partial beta agonists that are contraindicated in angina?

A

pindolol and acebutolol

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7
Q

What autoantibodies might you expect in the blood of a patient who is on hydralazine having an AE?

A

anti-histone, these are the autoantibodies present in drug induced lupus, which hydralazine can cause

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8
Q

Which lipid lowering agents do patients not like because they taste bad?

A

bile acid resins

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8
Q

What are 6 EKG findings with digoxin toxicity?

A

increased PR, decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block

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8
Q

What class is quinidine when used to tx the heart? What is its major AE?

A

Class Ia; cinchonism = headache and tinnitus

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9
Q

Name 2 class IC antiarrhythmics

A

propafenone, flecainide

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10
Q

Which class Ia anti-arrhythmic is associated with lupus-like syndrome? What antibodies?

A

procainamide, anti-histone

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12
Q

Which 3 organ systems should you regularly monitor when a person is on amiodarone?

A

LFT’s (hepatoxicity), PFT’s (pulmonary fibrosis), and TFT’s (hypo/hyperthryoidism)

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13
Q

Which CCB’s are most effective on the heart (as opposed to vessels)?

A

Verapamil and diltiazem

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13
Q

What are 4 side effects of hydralazine?

A

Compensatory Tachycardia, Fluid Retention, Nausea, Headache, and LUPUS-LIKE SYNDROME

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13
Q

What are the 3 AE of fibrates?

A

Myositis, hepatoxicity, cholesterol gallstones

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13
Q

What are the 3 AE of Class Ib antiarrhythmics?

A

CNS stimulation or depression and CV depression, also can be a local anesthetic

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14
Q

What are 3 class I anti-arrhythmics

A

quinidine, disopyramide, procainamide

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16
Q

Compare and contrast the effect of BB’s and nitrates on the End Diastolic Volume

A

BB’s increase EDV because they decrease HR and increase filling time; Nitrates decrease EDV by decreasing preload

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16
Q

What is blocked by Class I, II, III, and IV antiarrhythmics?

A

Class I = Na channels, Class II = beta blockers, Class III = K channels, Class IV = Ca channels

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17
Q

What 3 factors predispose to digitalis toxicity?

A

Hypokalemia, renal failure, co-administration of quinidine

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18
Q

What toxicities do ALL class Ia anti-arryhthmics cause?

A

thrombocytopenia and torsades due to QT prolongation

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19
Q

Name 3 bile acid resins

A

Cholestyramine, Colestipol, Colesevelam

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19
Q

What drug is DOC for diagnosing and abolishing SVT?

A

adenosine

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21
Q

Which drugs are first line for increasing HDL?

A

niacin

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21
Q

3 AE of niacin

A

Flushing, Acanthosis nigricans (hyperglycemia), Hyperuricemia (precipitating gout)

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22
Q

Which drug ONLY decreases LDL and does not affect HDL or TG’s?

A

ezetimibe = decrease in LDL uptake by intestines

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24
Q

What is the treatment for beta blocker OD?

A

glucagon

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25
Q

Why does quinidine predispose to digoxin toxicity?

A

it displaces digoxin from tissue binding sites and decreases its clearance

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26
Q

Why is it that class II antiarrhythmics act so heavily on SA and AV nodes?

A

Because, being beta blockers they decrease Ca currents which are necessary for upstroke in nodal tissue

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28
Q

What is the MOA of hydralazine? What drugs are often co-prescribed and why?

A

It increases cGMP in the ARTERIOLES thereby reducing afterload. It is co-administered with beta-blockers to prevent reflex tachycardia

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29
Q

The effect of adenosine is blocked by what 2 drugs?

A

theophylline and caffeine

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30
Q

What class is procainamide in? Major AE?

A

Class Ia antiarrhythmic; SLE like syndrome with anti-histone abs

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30
Q

Name 4 Class III antiarrhythmics. What is the mnemonic?

A

Amiodarone, Ibutilide, Dofetilide, and Sotalol (AIDS)

31
Q

Why do DM pts get ACE inhibitors?

A

They are protective against diabetic nephropathy

32
Q

Which drug prevents cholesterol reabsorption at the small intestine brush border?

A

Ezetimibe

33
Q

Why would a CCB cause constipation?

A

Because Ca is needed for smooth muscle contraction in the gut

34
Q

In whom (2) is hydralazine contraindicated? Why?

A

Coronary Artery Disease and Angina patients because it causes a reflex tachycardia due to its effect on reducing afterload

35
Q

Which CCB’s are most effective on vascular smooth muscle?

A

Amlodipine and nifedipine

37
Q

How do cardiac glycosides increase contractility AND decrease HR?

A

CONTRACTILITY = inhibition of Na/K pump inhbits the Na/Ca antiport leading to greater Ca in cytoplasm = more contractility? HR is mediated by increasing vagal tone to heart

38
Q

Name 3 class Ib antiarrhythmics

A

Lidocaine, tocainide, mexilitine

39
Q

Which calcium channel is blocked by diltiazem? What about ethosuximide?

A

L type; T type

40
Q

What is the major AE of ibutilide?

A

torsades

41
Q

2 indications for nitrates

A

angina and pulmonary edema

41
Q

What is the MOA of adenosine?

A

it increases K efflux out of the cell and hyperpolarizes it. It is thus the DOC in diagnosing and abolishing supraventricular tachycardia

42
Q

What aspect of cardiac depolarization do ALL class I drugs acts on?

A

all decrease the slope of phase 0 depolarization

43
Q

What cholinergic side effects occur with cardiac glycosides?

A

N/V, diarrhea, BLURRY YELLOW VISION

44
Q

What is “Monday Disease” in industrial exposure?

A

People working with nitrates can develop tolerance to the vasodilating effects and then loss of tolerance during the weekend causes a reflex tach and hypotension with facial flushing on Monday

45
Q

What are the 2 MOA’s of niacin?

A

it inhibits lipolysis in adipose tissue and reduces VLDL secretion from the liver

46
Q

Which drug used in malignant HTN is a D1 agonist?

A

fenoldopam

47
Q

What class is disopyramide in? Major AE?

A

Class Ia antiarrhythmic ; heart failure!

48
Q

What is the antidote to digoxin toxicity?

A

Slowly normalize K, LIDOCAINE, cardiac pacer, anti-digoxin Fab fragments, Mg

49
Q

What is the shortest acting class II antiarrhythmic?

A

ESMOLOL

51
Q

Magnesium is useful for what 2 cardiac conditions?

A

torsades de pointes and digoxin toxicity

53
Q

What is the MOA of nitroprusside?

A

Short acting increase in cGMP to decrease afterload by primarily acting on arterioles

55
Q

Co-administration of what drug predisposes to digoxin toxicity?

A

quinidine

56
Q

Which CCB’s are similar to BB’s in their effect? Which are more similar to nitrates?

A

Similar to BB’s = verapamil and diltiazem; similar to nitrates = nifedipine and amlodipine

57
Q

Which drug are first line for decreasing triglycerides?

A

fibrates

59
Q

How is the effect of nitroglycerin and isosorbide dinitrate different from that of hydralazine?

A

All increase cGMP to dilate vessels; however, hydralazine predominately affects arterioles and the nitrates affect veins so they decrease preload

61
Q

Which Class I class is best for MI and which is contraindicated?

A

Class I B = B est; Class I C = C ontraindicated

62
Q

The formation of which molecule is prevented by statins?

A

mevalonate (produced from HMG-CoA reductase)

63
Q

Class IV antiarrhythmics are used to prevent _________ and have this MOA _______

A

nodal arrhythmias (SVT) and they are CCB’s

64
Q

Which subset of class I drugs is particularly useful in treating digitalis toxicity?

A

Class Ib (LIDOCAINE, mexilitine, and tocainide)

65
Q

In which setting of heart failure must you be cautious with the use of beta blockers?

A

Acute decompensated heart failure–they need all the contractility they can get

66
Q

What are the AE of class IC antiarrhythmics?

A

proarrhythmic ESPECIALLY post-MI, and significant prolongation of AV node refractory period

68
Q

Which cardiac drug can cause cyanide toxicity?

A

nitroprusside

68
Q

Which anticonvulsant drug can function as a class Ib antiarrythmic?

A

phenytoin

69
Q

How do class II antiarrhythmics depress abnormal pacemakers?

A

decreasing slope of phase IV depol

70
Q

Which lipid lowering agents can cause cholesterol gallstones and why?

A

Bile acid resins because the liver needs to use cholesterol to create new bile acids; also, fibrates

72
Q

Which drugs are first line for decreasing LDL?

A

statins

74
Q

What effect to BB’s and nitrates have on A) contractility and B) heart rate

A

BB’s decrease contractility and HR but nitrates cause a reflex increase in HR and contractility

75
Q

Name 6 AE of CCB’s

A

Cardiac Depression, AV block, Peripheral edema, flushing (vasodilation), dizziness, and constipation

76
Q

What is first line Tx of HTN in pregnancy?

A

Hydralazine and methyldopa

77
Q

Which drug decreases VLDL secretion from the liver and inhibits lipolysis in fat tissue?

A

Niacin

78
Q

What are 2 AE of ezetimibe?

A

diarrhea (probably osmotic), and rarely, increase in LFTs

79
Q

What is the major AE of sotalol?

A

torsades and excessive beta blockade

80
Q

Compare and contrast the effect of Class Ia antiarrhythmics and Class Ib on the action potential duration

A

Class Ia increases AP duration so is useful for reentrant tachycardias; Class Ib decreases AP duration so is useful for ischemic tissue and POST-MI

81
Q

What electrolyte imbalance may be present with digoxin toxicity?

A

hyperkalemia–a poor prognostic indicator

83
Q

Why does hypokalemia predispose to digoxin toxicity?

A

it is permissive for digoxin to bind to the Na/K pump and have a more potent effect

84
Q

2 AE of statins

A

increased LFT’s (hepatotoxicity) and rhabdomyolysis

85
Q

What is the physiological goal of anti-anginal therapy?

A

Decrease myocardial oxygen demand

86
Q

What is the MOA of fenoldopam?

A

D1 agonist that acts on coronary, peripheral, renal, and splanchnic vessels causing vasodilation to decrease BP and facilitate natriuresis

87
Q

Why does amiodarone have class I, II, III, and IV effects?

A

it alters the lipid membrane, thereby affecting all of the channels

88
Q

Name 2 class IV antiarrhythmics

A

Verapamil and diltiazem

89
Q

What cardiac drug can cause yellow vision?

A

digoxin

90
Q

Why wouldn’t you give propanolol to a person using cocaine?

A

it can exacerbate prinzmetal’s variant angina

91
Q

Why is it that amiodarone can cause hypothyroidism?

A

It is heavily comprised of iodine, this can result in the Wolff-Chaikoff effect in the thyroid whereby there is autoregulation and decreased synthesis of T3/4

92
Q

What does the statement “Class I anti-arryhthmics are state-dependent” mean

A

they selectively act on DEPOLARIZED tissue (i.e. their activity depends on the “state” of the tissue)

93
Q

What is a unique AE of metoprolol? Of propanolol?

A

Metoprolol = dyslipidemia; propanolol = exacerbates prinzmetal angina vasospasm

PHARM SHELF AND BOARDS (13 decks)

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