Angina II Flashcards

1
Q

Does angiotensin II cause more vasoconstriction in the efferent or afferent arterioles of the glomerulus.

A

Efferent. This results in blood building up in the glomerulus, which increases glomerular pressure.

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2
Q

What are angiotensin II’s 3 functions?

A
  1. Vasoconstriction
  2. Aldosterone release
  3. ADH release
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3
Q

ACEIs increase levels of what?

A

Bradykinin, since ACE is responsible for degrading bradykinin. Bradykinin is a vasodilator and may cause cough and angioedema.

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4
Q

What are the side effects of ACEIs?

A
  • Dry cough
  • Hyperkalemia (from decreased aldosterone release)
  • Hypotension
  • Angioedema (rare, but serious)
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5
Q

What did a few trials prove about the nature of ACEI’s impact on reduction of MI and mortality?

A

That it could not be attributed to blood pressure decrease alone. In fact, one study showed that ACEIs don’t have any significant effect on BP (recall from an earlier lecture that ACEIs and ARBs have no effect on plasma volume).

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6
Q

What two effects do beta blockers have?

A
  • Anti-ischemic: decreases contractility and heart rate, thus decreasing myocardial oxygen demand.
  • Anti arrhythmic: inhibits sympathetic influences on cardiac electrical activity.
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7
Q

What are the contraindications for beta-blocker use?

A
  • Severe bradycardia
  • High degree AV block
  • Sick Sinus Syndrome
  • Unstable LV failure

Also: asthma depression and peripheral vascular disease.

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8
Q

What group of people will beta-blockers NOT benefit?

A

People with previous long-term cardiac disease (i.e. an MI more than 1 yr old or CAD without MI).

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9
Q

How do nitrates work?

A

They get reduced to NO, which eventually forms cGMP, which inhibits calcium entry into the cell. This results in smooth muscle relaxation and thus, vasodilation.

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10
Q

What do nitrates do to help CAD?

A

They cause dilation of large coronary arteries, which increases myocardial oxygen delivery, as well as relieves coronary vasospasm.

Venous dilation usually predominates, reducing venous pressure and resulting in less preload. The decreased preload results in less wall stress, reducing myocardial oxygen demand and improving subendocardial blood flow.

It also inhibits platelet aggregation and inhibits leukocyte-endothelial interactions (anti-inflammatory).

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11
Q

What are the contraindications for nitrates?

A
  • Hypertrophic cardiomyopathy (patients need a larger preload to generate a contractile force)
  • Severe aortic stenosis (probably the same reason)
  • Significant hypotension
  • Use of phosphodiesterase inhibitors used to treat erectile dysfunction (PDE inhibitors inhibit cGMP degradation).
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12
Q

What is the only first generation dihydropyridine?

A

Nifedipine. First generations have some negative ionotropic effect. (Second gens are more vasoselective).

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13
Q

What are the effects of non-dihydropyridines.

A
  • Vasodilation
  • True negative ionotropes (decrease myocardial activity)
  • Decrease firing rate of aberrant pacemaker sites
  • Decrease conduction velocity and prolong repolarization, thus decreasing heart rate.
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14
Q

What are the two non-dihydropyrimidines?

A

Verapamil (relatively selective for myocardium; less effective as a systemic vasodilator) and Diltiazem

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