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Cardiovascular Flashcards

1
Q

List the 5 CCBs (dihydropyridines).

A 
Amlodipine
Clevidipine
Nicardipine
Nifedipine
Nimodipine
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2
Q

List the 2 CCBs (non-dihydropyridines).

A

Diltiazem

Verapamil

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3
Q

What is the general MOA of CCBs? How do the two classes differ?

A

Block voltage-dependent L-type calcium channels on CARDIAC and SMOOTH MUSCLE to decrease contractility

Dihydropyridines primarily act on vascular smooth muscle (dilate precapillary vessels). Non-dihydropyridines primarily act on cardiac muscle (negative chronotropy)

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4
Q

MOA - hydralazine?

A

Increases cGMP, which causes smooth muscle relaxation -> vasodilates arterioles more than veins, leading to afterload reduction

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5
Q

Why is hydralazine contraindicated in angina/CAD?

A

AE - compensatory tachycardia and angina

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6
Q

Why is hydralazine frequently coadministered with a beta-blocker?

A

Prevent reflex tachycardia

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7
Q

MOA - nitroprusside?

A

Increases cGMP via direct release of NO (short-acting)

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8
Q

Unique AE - nitroprusside?

A

Cyanide toxicity (releases cyanide)

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9
Q

MOA - fenoldopam?

A

D1 receptor agonist, causes coronary, peripheral, renal, and splanchnic vasodilation; decreases BP, increases natriueresis

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10
Q

Indications - fenoldopam?

A

Hypertensive emergency, post-operative hypertension

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11
Q

List the three nitrates.

A

Nitroglycerin
Isosorbide dinitrate
Isosorbide mononitrate

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12
Q

MOA - nitrates.

A

Vasodilate by increasing NO in vascular smooth muscle, leading to increased cGMP and smooth muscle relaxation; dilates veins&raquo_space; arteries to decrease preload

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13
Q

Compare the MOA of hydralazine and nitrates.

A

Both ultimately increase cGMP, which causes smooth muscle relaxation.

Hydralazine - affects arterioles&raquo_space; veins -> afterload reduction

Nitrates - affects veins&raquo_space; arterioles -> preload reduction

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14
Q

What is Monday Disease?

A

Industrial exposure to nitrates leads to a development of tolerance for the vasodilating action during the week and loss of tolerance over the weekend - tachycardia, dizzines, and headache upon re-exposured

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15
Q

When are nitrates specifically contraindicated?

A

Right ventricular infarction

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16
Q

MOA - ranolazine?

A

Inhibits late-phase inward sodium channels in ISCHEMIC MYOCARDIAL CELLS during cardiac repolarization, which ehnahces calcium efflux via the Na/Ca exchanger, reducing oxygen consumption + no effect on HR or contracility

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17
Q

MOA - milrinone

A

Selective PDE-3 inhibitor - increases cAMP accumulation in cardiac myocites, causing increased calcium influx and increased inotrophy/chronotropy; in vascular smooth muscle it does the same, inhibiting MLCK activity -> vasodilation

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18
Q

MOA - statins?

A

Inhibit HMG-CoA reductase to inhibit conversion of HGM-CoA to mevalonate (cholesterol precursor)

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19
Q

Which type of lipid lowering agent decreases mortality in patients with CAD?

A

Statins

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20
Q

List the three bile acid resins.

A
  1. Cholestyramine
  2. Colestipol
  3. Colesevelam
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21
Q

MOA - bile acid resins?

A

Prevents intestinal reabsorption of bile acids, causing the liver to use cholesterol to make more

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22
Q

MOA - ezetimibe?

A

Prevents cholesterol absorption at the Si brush border

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23
Q

List the 3 fibrates.

A

Gemfibrozil
Bezafibrate
Fenofibrate

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24
Q

MOA - fibrates.

A

Upregulates LPL to increase TG clearance, activates PPAR-alpha to induce HDl synthesis

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25
Q

Why do fibrates increase the risk of cholesterol gallstones?

A

Inhibition of 7-alpha-hydroxylase reduces the conversion of cholesterol to bile acids, increasing the risk of stones

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26
Q

MOA - niacin (B3)?

A

Inhibits lipolysis via hormone-sensitive lipase in adipose tissue; reduces hepatic VLDL synthesis

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27
Q

MOA - alirocumab/evolocumab?

A

Inactivation of LDL-receptor degradation, increasing amount of LDL removed from bloodstream

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28
Q

All lipid-lowering agents decrease LDL. Which categories do so the most?

A

HMG-CoA reductase inhibitors and PCSK9 inhibitors

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29
Q

All lipid-lowering agents increase HDL. Which categories do so the most?

A

Niacin (vitamin B3)

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30
Q

One lipid-lowering agent may slightly increase TG. Which one?

A

Bile acid resins

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31
Q

Which lipid-lowering agent decreases TG the most?

A

Fibrates

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32
Q

What are the general MOA for classes I-IV anti-arrhythmics?

A

I - sodium channel blockers
II - beta blockers
III - potassium channel blockers
IV - calcium channel blockers

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33
Q

List the 3 class IA anti-arrhythmics.

A

Quinidine
Procainamide
Diopyramide

34
Q

MOA - class I?

A

Sodium channel blockade decreases the slope of phase 0, slowing/blocking conduction (especially in depolarized cells - open or inactivated Na+ channels)

35
Q

Class IA anti-arrhythmics are state dependent. What does this mean?

A

They have a greater effect on rapidly depolarizing tissue (more likely to bind).

36
Q

List the 3 class IB anti-arrhythmics.

A
  1. Lidocaine
  2. Mexiletine
  3. Phenytoin
37
Q

List the 2 Class IC anti-arrhythmics.

A
  1. Flecainide

2. Propefanone

38
Q

Compare the class I anti-arrhythmics regarding the following: binding affinity, use dependence, effect on phase 0 upstroke.

A

IA - intermediate binding affinity/use dependence, moderate slowing of phase 0 upstroke

IB - low binding affinity/use dependence, modest slowing of phase 0 upstroke

IC - strong binding affinity/use dependence, drastic slowing of phase 0 upstroke

39
Q

Compare the class I anti-arrhythmics regarding the following: effect on AP duration, ERP, QT interval, conduction velocity

A

IA - increased AP duration, increased ERP, increased QT, decreased conduction velocity

IB - decreased AP duration, decreased ERP

IC - minimal effect on AP duration, significant increase in ERP in AV node/accessory bypass tracts, no effect in Purkinje/ventricular tissue, QRS prolongation, minimal effect on QT interval

40
Q

Which Class I anti-arrhythmic has some potassium channel blocking effects? What effect does this have?

A

IA - prolongs phase 2 and 3, increases ERP

41
Q

Which anti-arrhythmic preferentially affects ischemic tissue?

42
Q

Compare the indications of the Class I anti-arrhythmics.

A

IA - SV (including WPW) and V arrhythmias, especially re-entrant and ectopic SVT and VT; NO action at SA, AV nodes

IB - V arrhythmias, especially in ischemic tissue (post-MI); digitalis-induced arrhythmias

IC - SV (including AFib/Flutter) and V arrythmias

43
Q

Compare the AE of Class I anti-arrhythmics.

A

IA - all cause thrombocytopenia, torsades; quinidine - cinchonism, procainamide - SLE-like syndrome, disopyramide - exacerbates HF

IB - CNS effects

IC - contraindicated in structural and ischemic heart disease

44
Q

Which beta blockers can be used as anti-arrhythmics?

A 
Atenolol
Carvedilol
Esmolol
Metoprolol
Propranolol
Timolol
45
Q

MOA - class II anti-arrhythmics

A

Decrease cAMP -> decrease calcium currents -> decrease slope of phase 4 -> decrease SA/AV node activity, suppress abnormal pacemakers

46
Q

Effect of class II on AV node?

A

AV node is particularly sensitive to class II - they decrease AV conduction velocity, increase PR interval, and prolong conduction time and ERP

47
Q

Indication- class II?

A

SVT (including prevention of rapid ventricular response, aka ventricular rate control, for AFib/Flutter)

48
Q

MOA - class III anti-arrhythmics?

A

Block potassium channels (outward currents during phase 3) -> prolongs repolarization

Increases AP duration, ERP, QT interval

Negative chronotropy

49
Q

List the 4 class III antiarrhythmics.

A

Amiodarone
Dofetilide
Ibutilide
Solatol

50
Q

Which anti-arrhythmic shares properties of all 4 classes?

A

Amiodarone

51
Q

Indication - class III

A

SV and V arrhythmias
(AFib/Flutter - restore and maintain sinus rhythm)

Amiodarone and sotalol for V arrhythmias

52
Q

List the 2 class IV.

A

Verapamil and Diltiazem

53
Q

MOA - class IV

A

Block calcium current in SA/AV nodes -> decreased conduction velocity through AV node, increased ERP and PR interval, prolonged conduction time; no QT prolongation

54
Q

Indication - class IV?

A

SV arrhythmias + rate control (prevent rapid ventricular response) in AFib/Flutter

55
Q

Which anti-arrhythmics affect non-nodal cells? Which affect nodal?

A

Non-nodal - I and III

Nodal - II and IV

56
Q

What phases do each class of anti-arrhythmics affect?

A

I - 0
II - 4
III - 3
IV - 2

57
Q

Effect of classes I and III on AP duration?

A

IA - increase
IB - decrease
IC - no effect
III - increase

58
Q

Which anti-arrhythmic classes don’t increase the ERP?

A

IB (decreases)

IC (no change)

59
Q

Which anti-arrhythmics only affect SV rhythms?

60
Q

Which anti-arrhymics only affect V rhythms?

61
Q

Which anti-arrhythmics affect both SV and V rhythms?

A

IA, IC

III

62
Q

EKG effects of class I?

A

IA - increase QRS and QT
1B - decrease QT
IC - increase QRS

63
Q

EKG effects of class III?

A

Increase QT

64
Q

EKG effects of class II and IV?

A

Increase PR interval

65
Q

Which class IA antiarrhythmic should not be given in heart failure?

A

Diopyramide (will exacerbate heart failure)

66
Q

When is class IC contraindicated?

A

Structural and ischemic heart disease; post MI

67
Q

Which drug class may mask hypoglycemia signs?

A

Beta-blockers

68
Q

Which class III drug does NOT carry a risk of inducing torsades?

A

Amiodarone

69
Q

MOA - digoxin?

A

Inhibits Na/K ATPase, leading to accumulation of Na in the cell and indirect inhibition of the Na/Ca exchanger; this increases intracellular calcium, which leads to positive inotropy; it also stimulates the vagus nerve, decreasing HR

70
Q

Indications - digoxin?

A

Heart failure, AFib

71
Q

AE - digoxin?

A

Cholinergic - N/V, diarrhea, blurry yellow vision, arrhythmias, AV block, hyperkalemia

72
Q

What are 4 miscellaneous anti-arrhythmics?

A

Digoxin
Adenosine
Magnesium
Ivabradine

73
Q

MOA - adenosine?

A

increases potassium efflux from cells, leading to hyperpolarization and decreased calcium current, decreasing AV node conduction

74
Q

Treatment of choice for diagnosing and terminating certain forms of SVT?

75
Q

AE - sense of impending doom

76
Q

Which drugs blunt the effects of adenosine and why?

A

Theophylline and caffeine (both are adenosine receptor antagonists)

77
Q

Indication - magnseium?

A

Torsades and digoxin toxicity

78
Q

MOA - ivabradine?

A

Selective inhibition of funny sodium channels, prolongs phase 4, decreases SA node firing -> negative chronotropy, reduces cardiac O2 requirements

79
Q

Indication - ivabradine?

A

Chronic stable angina who cannot take beta-blockers; chronic HF with reduced EF

80
Q

AE - luminous phenomena/visual brightness?

A

Ivabradine

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