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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
Why do fibrates increase the risk of cholesterol gallstones?
Inhibition of 7-alpha-hydroxylase reduces the conversion of cholesterol to bile acids, increasing the risk of stones
26
MOA - niacin (B3)?
Inhibits lipolysis via hormone-sensitive lipase in adipose tissue; reduces hepatic VLDL synthesis
27
MOA - alirocumab/evolocumab?
Inactivation of LDL-receptor degradation, increasing amount of LDL removed from bloodstream
28
All lipid-lowering agents decrease LDL. Which categories do so the most?
HMG-CoA reductase inhibitors and PCSK9 inhibitors
29
All lipid-lowering agents increase HDL. Which categories do so the most?
Niacin (vitamin B3)
30
One lipid-lowering agent may slightly increase TG. Which one?
Bile acid resins
31
Which lipid-lowering agent decreases TG the most?
Fibrates
32
What are the general MOA for classes I-IV anti-arrhythmics?
I - sodium channel blockers II - beta blockers III - potassium channel blockers IV - calcium channel blockers
33
List the 3 class IA anti-arrhythmics.
Quinidine Procainamide Diopyramide
34
MOA - class I?
Sodium channel blockade decreases the slope of phase 0, slowing/blocking conduction (especially in depolarized cells - open or inactivated Na+ channels)
35
Class IA anti-arrhythmics are state dependent. What does this mean?
They have a greater effect on rapidly depolarizing tissue (more likely to bind).
36
List the 3 class IB anti-arrhythmics.
1. Lidocaine 2. Mexiletine 3. Phenytoin
37
List the 2 Class IC anti-arrhythmics.
1. Flecainide | 2. Propefanone
38
Compare the class I anti-arrhythmics regarding the following: binding affinity, use dependence, effect on phase 0 upstroke.
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
Compare the class I anti-arrhythmics regarding the following: effect on AP duration, ERP, QT interval, conduction velocity
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
Which Class I anti-arrhythmic has some potassium channel blocking effects? What effect does this have?
IA - prolongs phase 2 and 3, increases ERP
41
Which anti-arrhythmic preferentially affects ischemic tissue?
IB
42
Compare the indications of the Class I anti-arrhythmics.
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
Compare the AE of Class I anti-arrhythmics.
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
Which beta blockers can be used as anti-arrhythmics?
``` Atenolol Carvedilol Esmolol Metoprolol Propranolol Timolol ```
45
MOA - class II anti-arrhythmics
Decrease cAMP -> decrease calcium currents -> decrease slope of phase 4 -> decrease SA/AV node activity, suppress abnormal pacemakers
46
Effect of class II on AV node?
AV node is particularly sensitive to class II - they decrease AV conduction velocity, increase PR interval, and prolong conduction time and ERP
47
Indication- class II?
SVT (including prevention of rapid ventricular response, aka ventricular rate control, for AFib/Flutter)
48
MOA - class III anti-arrhythmics?
Block potassium channels (outward currents during phase 3) -> prolongs repolarization Increases AP duration, ERP, QT interval Negative chronotropy
49
List the 4 class III antiarrhythmics.
Amiodarone Dofetilide Ibutilide Solatol
50
Which anti-arrhythmic shares properties of all 4 classes?
Amiodarone
51
Indication - class III
SV and V arrhythmias (AFib/Flutter - restore and maintain sinus rhythm) Amiodarone and sotalol for V arrhythmias
52
List the 2 class IV.
Verapamil and Diltiazem
53
MOA - class IV
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
Indication - class IV?
SV arrhythmias + rate control (prevent rapid ventricular response) in AFib/Flutter
55
Which anti-arrhythmics affect non-nodal cells? Which affect nodal?
Non-nodal - I and III | Nodal - II and IV
56
What phases do each class of anti-arrhythmics affect?
I - 0 II - 4 III - 3 IV - 2
57
Effect of classes I and III on AP duration?
IA - increase IB - decrease IC - no effect III - increase
58
Which anti-arrhythmic classes don't increase the ERP?
IB (decreases) | IC (no change)
59
Which anti-arrhythmics only affect SV rhythms?
II and IV
60
Which anti-arrhymics only affect V rhythms?
IB
61
Which anti-arrhythmics affect both SV and V rhythms?
IA, IC | III
62
EKG effects of class I?
IA - increase QRS and QT 1B - decrease QT IC - increase QRS
63
EKG effects of class III?
Increase QT
64
EKG effects of class II and IV?
Increase PR interval
65
Which class IA antiarrhythmic should not be given in heart failure?
Diopyramide (will exacerbate heart failure)
66
When is class IC contraindicated?
Structural and ischemic heart disease; post MI
67
Which drug class may mask hypoglycemia signs?
Beta-blockers
68
Which class III drug does NOT carry a risk of inducing torsades?
Amiodarone
69
MOA - digoxin?
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
Indications - digoxin?
Heart failure, AFib
71
AE - digoxin?
Cholinergic - N/V, diarrhea, blurry yellow vision, arrhythmias, AV block, hyperkalemia
72
What are 4 miscellaneous anti-arrhythmics?
Digoxin Adenosine Magnesium Ivabradine
73
MOA - adenosine?
increases potassium efflux from cells, leading to hyperpolarization and decreased calcium current, decreasing AV node conduction
74
Treatment of choice for diagnosing and terminating certain forms of SVT?
Adenosine
75
AE - sense of impending doom
Adenosine
76
Which drugs blunt the effects of adenosine and why?
Theophylline and caffeine (both are adenosine receptor antagonists)
77
Indication - magnseium?
Torsades and digoxin toxicity
78
MOA - ivabradine?
Selective inhibition of funny sodium channels, prolongs phase 4, decreases SA node firing -> negative chronotropy, reduces cardiac O2 requirements
79
Indication - ivabradine?
Chronic stable angina who cannot take beta-blockers; chronic HF with reduced EF
80
AE - luminous phenomena/visual brightness?
Ivabradine

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