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Cardio Pharm Flashcards

0
Q

What are the l-type channels?

A

On cardiac and smooth muscle

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1
Q

What are the L-type calcium channel blockers?

A

Nifedipine
Verapamil
Diltiazem
Amylodipine

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2
Q

What is the toxicity of calcium channel blockers?

A 
Cardiac depression
AV block
Peripheral edema
Flushing
Dizziness
Constipation
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3
Q

What is the MOA of hydralazine?

A

Increase cGMP causing smooth muscle relaxation –> reduces afterload

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4
Q

What is hydralazine used for?

A

Severe HTN
First line for HTN in pregnancy with methyl dopa (alpha 2 agonist)
Frequently used with beta blockers to prevent reflex tachycardia

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5
Q

What is the toxicity of hydralazine?

A 
Compensatory tachycardia 
Fluid retention
Nausea
Headache
Angina
Lupus-like syndrome
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6
Q

What is the MOA of nitroprusside?

A

Increases cGMP via direct release of NO

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7
Q

What is the draw back to nitroprusside?

A

Releases cyanide!

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8
Q

What is hydralazine contraindicated in?

A

CAD and angina because it causes reflex tachycardia increases the need for oxygen of the heart

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9
Q

What is the MOA of fenoldopam?

A

D1 agonist –> vasodilation of coronary, peripheral, renal, splanchnic arteries
Decreases BP and increases natriuresis

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10
Q

What is the MOA of nitroglycerin?

A

Vaso and venodilator by releasing NO in smooth muscle causing an increase cGMP
Decreases preload and afterload

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11
Q

What is the clinical use of nitroglycerin?

A

Angina

Pulmonary edema

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12
Q

What is the toxicity of nitroglycerin?

A 
Reflex tachycardia 
Hypotension
Flushing 
Headache
Monday disease - due to build up of tolerance during the week, lose it over the weekend (because not using it) and then come Monday causes side effects: tachycardia, dizziness, headache
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13
Q

Which beta blockers are contraindicated in angina?

A

Pindolol and acebutolol - Partial B agonist

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14
Q

Which calcium channel blocker is similar to beta blockers in effect?

A

Verapamil

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15
Q

What is the mech of action of a statin?

A

HMG-CoA reductase inhibitors - inhibit conversion of HMG-CoA to mevalonate

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16
Q

What are the side effects of statins?

A

Hepatotoxicity

Rhabdomyolysis

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17
Q

What is the effect of niacin on lipids?

A

Inhibits lipolysis in adipose tissue
reduces hepatic VLDL secretion into circulation
Effect: decreases circulating lipids

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18
Q

What are the side effects of niacin?

A

Flushing (counteract with aspirin because due to prostaglandins)
Hyperglycemia
Hyperuricemia

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19
Q

What are the bile acid resins?

A

Cholestyramine
Colestipol
Colesevelam

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20
Q

What is the MOA of bile acid resin?

A

Prevents intestinal reabsorption of bile acids

Liver must use cholesterol to make more!

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21
Q

What is the side effect?

A

Bad taste
GI discomfort
Decrease absorption of fat soluble vitamins
Cholesterol gallstones

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22
Q

What is ezetimibe?

A

Cholesterol absorption blocker - prevents absorption at small intestine brush border

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23
Q

What are the side effects of ezetimibe?

A

Increase in LFTs

Diarrhea

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24
Q

What is the MOA of fibrates?

A

Upregulates LPL to increase TG clearance

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25
Q

What are the fibrates?

A

Gemfibrozil
Clofibrate
Bezafibrate
Fenofibrate

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26
Q

What are the side effects of fibrates?

A

Myositis
Hepatotoxicity
Cholesterol gallstones

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27
Q

What lipid med had the best effect on LDL?

A

HMG- CoA reductase

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28
Q

What lipid med has the greatest effect on TGs?

A

Fibrates

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29
Q

Which med has the most effect on HDL?

A

Niacin

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30
Q

What is half life of digoxin?

A

40 hours

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31
Q

What is the bioavailability of digoxin?

A

75%

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32
Q

What percent of digoxin is protein bound?

A

20-40%

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33
Q

What is the MOA of digoxin?

A

Inhibition of the Na/K pump leading to indirect inhibition of Na/Ca exchanger –> increase intracellular calcium (not pumping it out anymore because no more ATP to run antiport)
Positive inotropic
Stimulates vagus –> decrease HR, depresses SA node and decreases conduction at AV node

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34
Q

What is the digoxin used for?

A

A-fib

CHF

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35
Q

What is the toxicity of digoxin?

A

Cholinergic - N/V, diarrhea, blurry yellow vision

ECG - increased PR interval, decreased QT interval, ST scooping, T-wave inversion, arrhythmias, AV block

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36
Q

What conditions predispose to digoxin toxicity?

A

Renal failure (because excreted in urine)
Hypokalemic
Quinidine (displaces digoxin from tissue binding sites, decreases clearance)

37
Q

What is the antidote for digoxin?

A 
Normalize K
Lidocaine
Cardiac pacer
Anti-digoxin Fab fragments
Magnesium
38
Q

What are the class I anti arrhythmics?

A

Quinidine, procainamide, disopyramide

39
Q

What are the effects of the class I anti arrhythmics?

A

Increase action potential duration
Increase effective refractory period
Affect atrial and ventricular arrhythmias especially reentrant and ectopic SVC and VT

40
Q

What is the tox of quinidine?

A

Cinchonism - tinnitus, headache

41
Q

What is the tox of procainamide?

A

Reversible SLE-like syndrome

42
Q

What is the tox of disopyramide?

A

Heart failure

43
Q

What are the toxicities of class I?

A

TCP
Torsades de pointes
Hyperkalemia increases the toxicity of these drugs

44
Q

What are the class b anti-arrythmics?

A

Lidocaine
Mexilitine
Tocainamide

45
Q

What are the effects of class b?

A

Decrease action potential duration

Affect ischemic or de polarized Purkinje and ventricular tissue

46
Q

What are class b used for?

A

Post MI arrhythmias

Digitalis arrhythmias

47
Q

What are the toxicities of class b?

A

Local anesthetic, CNS stimulation/depression, CV depression

48
Q

What are the class c antiarrythmics?

A

Flecainide, propafenone

49
Q

What are class c used for?

A

Intractable SVT
VT that progresses to VF
Last resort - only for patients without structural abnormalities

50
Q

What are the tox of class c?

A

Pro arrhythmic especially post MI

Significantly prolongs refractory period in AV node

51
Q

What are the class II antiarrythmics?

A

Beta blockers

52
Q

What do beta blockers do?

A

Decrease SA and AV nodal activity by decreasing camp and calcium.
Decrease slope of phase 4
Increase PR interval. Esmolol is short acting

53
Q

What are class II used for?

A

VT, SVT

slowing ventricular rate during a-fib, a-flutter

54
Q

What is the tox of class II?

A

Impotence, exacerbation of Asthma, bradycardia , AV nodal block, CHF, sedation, masks hypoglycemia

55
Q

What can metoprolol cause?

A

Dyslipidemia - tx OD with glucagon

56
Q

What can propranolol do?

A

Exacerbate spasm in Prinzmetal’s

57
Q

What are the class III?

A

Amiodarone
Ibutilide
Dofetilide
Sotalol

58
Q

What is the MOA of class III?

A

Increase AP duration
increase ERP
Increase QT interval
Used when other antiarrythmics

59
Q

What is the tox of sotalol?

A

Torsades de pointes

Excessive beta block

60
Q

What is the tox of ibutilide?

A

Torsades

61
Q

What is the tox of amiodarone?

A 
Pulmonary fibrosis
Hepatotoxicity 
Hypothyroidism/hyperthyroid 
Corneal deposits
Blue/gray Skin deposits
Photodermatitis
Constipation
Bradycardia 
AV nodal block
CHF
62
Q

What is unique about amiodarone?

A

Has class I-iV effects because it alters the lipid membrane

63
Q

What are the class IV?

A

Calcium channel blockers: verapamil, diltiazem

64
Q

What is the MOA of class IV?

A

Decreases conduction velocity, increases ERP, increase PR,

65
Q

What are class IV used for?

A

In prevention of nodal arrythmias

66
Q

What is the MOA of adenosine as an antiarrythmic?

A 
Increase K efflux hyper polarizing the cell and decreases spontaneous calcium channels
Short acting (15 seconds)
67
Q

What is the DOC for diagnosing/taxing SVT?

A

Adenosine

68
Q

What is the tox of adenosine?

A

Flushing
Hypotension
Chest pain

69
Q

What blocks adenosine?

A

Caffeine

Theophylline

70
Q

What is magnesium used for?

A

Effective in torsades and digoxin tox

71
Q

Which antiarrythmic causes bradycardia and QT prolongation?

A

Sotalol - class 3 K-blocking and beta blocker

72
Q

How do beta blockers work as antiarrythmics?

A

Slow AV nodal conduction and phase 4 depolarization of cardiac pacemaker cells
Phase 4 is mediated by sodium channels that depolarize spontaneously

73
Q

What phase do calcium channel blockers slow?

A

Phase 0 of pacemaker cells - the opening of voltage gated calcium channels
Phase 2 of myocyte action potential - calcium influx through calcium channels that balances K efflux

74
Q

What side effects is verapamil associated with?

A

Gingival hyperplasia
Constipation
AV nodal block

75
Q

What is ergonovine?

A

An ergot alkaloid that stimulates serotonin and alpha adrenergic receptors

76
Q

What is ergonovine used for?

A

Testing for Prinzmetal’s angina by provoking an attack

77
Q

How is procainamide metabolized?

A

By acetylation

78
Q

What is the MOA of an ARB?

A

Blocks Ang I receptors thereby blocking the effects of angiotensin II
Will have increased renin and Ang I and Ang II but decreased aldosterone and vasodilation. No change in bradykinin

79
Q

How does metoprolol work in lowering bp?

A

Blocks B1 in heart and in Jg apparatus thereby decreasing the level of circulating renin.

80
Q

What is the MOA of nesirtide?

A

Recombinant form of BNP - dilates arterioles and venules by activating guanylate cycle and increasing cGMP. Also causes diuresis/natriuresis and decreases bp

81
Q

What can nesirtide be used for?

A

Decompensated left ventricular dysfunction leading to CHF

82
Q

On which part of the EKG do beta blockers act?

A

Increase the PR interval

83
Q

Which phase of the ventricular depolarization graph do class IA agents act on?

A

Prolong phase 0 - decrease sodium influx so that the upstroke isn’t as rapid
Prolong phase 3 - slow K efflux for slow repolarization
Increase AP duration, ERP, and QT interval

84
Q

What effects do class IB agents have on the ventricular action potential graph?

A

Shorten phase 3 - so increase efflux of K and repolarization, also decreases ERP
Decreases duration of the action potential
Have affinity for rapidly de polarizing cells (best for ischemic cells)

85
Q

What effect do class IC agents have on the ventricular action potential curve?

A

Slows phase 0 - slow the opening of sodium channels so the upstroke isn’t as rapid.
Has no effect on action potential duration
Works within the QRS interval
May significantly prolong the refractory period in the AV node (PR interval)
Have highest affinity for non-resting sodium channel - have more effect on normal myocardium

86
Q

What phase do beta blockers act in?

A

Prolong phase 4 - decreases current through funny sodium channels so decreases rate of depolarization
Also decreases calcium influx thru channels that usually augment phase 4 by decreasing camp
Slows conduction through the SA and AV node (increases PR interval)

87
Q

What effects do class 3 agents have on the ventricular action potential curve?

A

Increase phase 3 - decrease potassium efflux

Increases AP duration, QT interval and ERP

88
Q

What is the toxicity of sotalol?

A

Torsades and excessive beta block

89
Q

What is the toxicity of ibutilide?

A

Torsades

90
Q

What phases do calcium channel blockers act on?

A

Slow phase 0 - calcium influx causing the upstroke in the SA node
Slow phase 4 - decreasing calcium flow that normally augments this period - slows diastolic depolarization
Decreases conduction velocity, increases ERP, increases PR interval

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