CVS Flashcards

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1
Q

Cholestyramine

  1. mechanism
  2. adverse effects
A

Cholestyramine
1. mechanism: inhibit bile acid cholesterol reabsorption.
(increases TG)
2. adverse effects: GI upset, reduce absorption of fat soluble vitamins

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2
Q

statins

  1. mechanism
  2. adverse effects
A

statins (the only shown to reduce CAD mortality)

  1. mechanism: inhibit HMG-CoA reductase
  2. adverse effects: myopathy, hepatotoxic
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3
Q

Gemfibrozil

  1. mechanism
  2. adverse effects
A

Gemfibrozil (reduce TG alot, reduce VLDL)

  1. mechanism: activates PPAR-a to upregulate LPL to degrade TG , reduce hepatic VLDL synthesis
  2. adverse effects: gallstones (inhibit cholesterol 7a-hydroxylase), myopathy
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4
Q

Niacin

  1. mechanism
  2. adverse effects
A

Niacin (reduce VLDL, increase HDL)

  1. mechanism: inhibits lipolysis in adipose tissue, reduce VLDL synthesis
  2. adverse effects: nice raisin (red , sweet, sour)
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5
Q

Alirocumab

  1. mechanism
  2. adverse effects
A

Alirocumab (reduce LDL alot)

  1. mechanism: PCSK9 inhibitors (deactivate LDL receptor degradation)
  2. adverse effects: myalgia, neurocognitive sx
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6
Q

Ezetimide

  1. mechanism
  2. adverse effects
A

Ezetimide

  1. mechanism: inhibits cholesterol absorption at brush border of small intestines
  2. adverse effects: diarrhea
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7
Q

Which anti-arrhythmics drug is contraindicated in structural/ ischemic heart disease? Which drug should it be replaced with?

A

Class 1C (flecainide, propafenone) replaced with Class 1B (lidocaine, phenytoin, mexiiletine) (with weaker binding strength)

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8
Q

Which anti-arrhythmics drug is contraindicated in pts high risk of torsades de pointes? Why

A

Class 1A (procainamide, quinidine, disopyramide), Class 3 (amiodarone, Ibutilide, dofetilide, Sotalol). Prolong QT

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9
Q

Which part of electrical conduction does each class of anti arrhythmic drug does it effect?

A

1A: sodium (longer AP) less sloppier slope 0
1B: sodium (shorter AP) less sloppier slope 0
1C: sodium (same AP) less sloppier slope 0

2: beta blocker (SA node, AV node activity, longer PR interval) slope 4 of nodal cells
3: potassium (longer QT interval, longer AP) slope 3
4: Calcium (slow down AV node conduction incl depolar & repolar, longer PR interval) prolong slope 1 & 3 of nodal cells

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10
Q

Mechanism of adenosine

A

Increase K+ out of cell (hyperpolarize), blocks calcium channel (slow down AV node conduction)

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11
Q

Mechanism of digoxin

A

block Na/K ATP-ase. Stimulates vagus nerve. Positive inotropy

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12
Q

List 4 changes in aging heart

A
  1. decreased LV chamber apex-to-base dimension
  2. sigmoid shape ventricular septum
  3. myocardial atrophy with collagen deposits
  4. brownish lipofuscin pigment in cardiomyocytes
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