Coronary Artery Disease Flashcards

1
Q

What is the most important contributor to ECG/electrophysical changes of ischemia?

A

increased K+ leakage

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2
Q

Why is aspirin given to patients with CAD?

A

Proven to reduce adverse events (MI, CVA, death); for those w/stable angina, unstable angina, acute MI, prophylaxis

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3
Q

What is a drug that may be given for CAD if allergic to aspirin? Why is it not really used?

A

Ticlopidine

Causes Neutropenia and, rarely, TTP and has not shown a decrease in adverse events in pts w/ stable angina

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4
Q

What are 2 thienopyridine antiplatelet agents that are more potent alternatives to aspirin? How do they work?

A

Clopidogrel (plavix)
Prasugrel
inhibits ADP binding to P2Y12 (inhibits platelet aggregation)

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5
Q

In what patients are Clopidogrel and Prasugrel used? Which one has serious toxicity effects and is limited to use in healthy patients under 75?

A

Used in patients with stent placement as an antithrombotic

Prasugrel is very potent and assoc. with increased bleeding events

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6
Q

Which drug is a ADP receptor blocker that inhibits platelet aggregation but has a black box warning against use with aspirin doses above 100mg?

A

Ticagrelor

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7
Q

What is the mechanism of action and therapeutic use of Dipyridamole?

A

Mech: Dipyridamole inhibits the phosphodiesterase enzymes that normally break down cAMP (increasing cellular cAMP levels and blocking the platelet response to ADP); inhibits the cellular reuptake of adenosine into platelets, red blood cells and endothelial cells leading to increased extracellular concentrations of adenosine.
Use: patients with peripheral vascular disease if NO CAD present

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8
Q

What are 4 effects of Angiotensin II?

A
  1. vasoconstriction of arterioloes
  2. increased GFR since caused more constriction in efferent arterioles of glomerulus
  3. stimulates aldosterone release
  4. stimulates ADH release
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9
Q

What are the therapeutic uses of ACEI?

A

Often used as an add-on antihypertensive for anyone with chronic kidney disease/proteinuria, CHF, left ventricular hypertrophy, or post-MI (prevents left ventricular remodeling); reduces incidence of future CAD events, may reduce risk of diabetes

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10
Q

What are 4 side effects and 4 contraindications of ACEIs?

A

SE: Dry cough (10-30%), angioedema, hyperkalemia (decreased aldosterone), hypotension
Contraindicated in: pregnancy, renal artery stenosis, hyperkalemia, and prior angioedema (no ARB allowed, either); caution in renal failure

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11
Q

What are 3 therapeutic effects of Beta-blockers?

A
  1. decrease O2 demand of heart (decrease contractility, HR)
  2. Class II antiarrhythmics
  3. increase AP duration / refractory period
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12
Q

What are 4 contraindications to Beta-blocker use?

A
  1. severe bradycardia
  2. high degree AV block
  3. sick sinus syndrome
  4. unstable LV failure / acute HF
    (also relative contraindication is asthma, severe depression, peripheral vascular disease)
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13
Q

What part of the vascular system predominates in Nitrates effects? What are the effects?

A

Venous dilation –> reduces ventricular preload –> reduces ventricular wall stress –> reduced O2 demand

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14
Q

Which drugs can be used to treat Prinzmetal’s angina?

A
  • Nitrates (causes dilation of coronary arteries and collateral vessels which increases O2 delivery and relieves coronary vasospasm)
  • Ca+ channel blockers (dihydropyridines)
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15
Q

What are 4 contraindications for use of Nitrates?

A
  1. Hypertrophic cardiomyopathy
  2. Severe aortic stenosis
    (since in both, need adequate preload to generate contraction force)
  3. Significant hypotension
  4. Use of phosphodiesterase inhibitors [viagra]
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16
Q

Besides vasodilatory effects, what are 2 other actions of endothelial-derived NO?

A
  1. inhibits platelet aggregation

2. inhibits leukocyte-endothelial interactions (anti-inflammatory)

17
Q

What are 4 side effects of Nitrates?

A
  1. tolerance- need infrequent dosing or “nitrate free” periods to counteract
  2. headaches (may diminish with long-term use)
  3. hypotension
  4. Bezold-Jarisch reflex (cardiac receptors sense decreased preload which causes increase in vagal input and sinus bradycardia)
18
Q

What is the mechanism of action of felodipine and others in its class?

A

(Ca+ channel blockers)
Interact with L-type voltage gated plasma membrane Ca channel –> decreased calcium entry into vascular smooth muscle cell, preventing contraction

19
Q

Which subclass of Ca+ channel blockers are vasoselective and which are more heart-specific? What are the consequences?

A

Dihydropyridines are vasoselective
–> dilate coronary arteries and arteriolar resistance vessels which may relieve coronary vasospasm and decrease arterial pressure
Non-dihydropyridines are heart-specific
–> true negative ionotropes, decrease firing of aberrant pacemaker sites, decrease HR

20
Q

Name a 1st generation dihydropyridine. Name 3 2nd generation. What is the difference?

A

1st generation: Nifedipine
2nd generation: Amlodipine, Felodipine, Isradipine
*1st generation not as selective and has some negative ionotropic effects

21
Q

What are 2 Non-dihydropyridines?

A

Verapamil

Diltiazem

22
Q

In what patients are Ca+ channel blockers contraindicated?

A

Contraindicated in overt decompensated heart failure, bradycardia, sinus node dysfunction, high-degree AV block

23
Q

What is the most common side effect of Ca+ channel blockers? What are 6 others?

A
  • Most common- constipation
  • hypotension
  • worsening HF
  • peripheral edema
  • headache
  • flushing
  • bradycardia / AV block (non-dihydro’s)