Angina Pectoris Flashcards

1
Q

Classic Angina vs Variant Angina

A

CA: occlusion of the coronary arteries resulting from the formation of atherosclerotic plques
VA: spontaneous vasoconstriction of coronary arteries

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2
Q

When do symptoms occur for CA?

A

Exertion/stress

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3
Q

Risk Factor for CA?

A

High Cholesterol

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4
Q

Origin of VA?

A

Genetic

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5
Q

When do symptoms occur for VA?

A

At Rest

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6
Q

General Drug mechanisms used to treat stable angina pectoris (2)

A
  1. Drugs that reduce o2 demand

2. Drugs that increase o2 supply

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7
Q

How can drugs reduce o2 demand?

A

Decrease cardiac work by:

  1. Decrease HR
  2. Decrease force of contraction
  3. Decrease Preload
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8
Q

What is used to treat stable angina pectoris (5)

A
  1. Organic Nitrates
  2. Beta Blockers
  3. CCBs
  4. Combo therapy
  5. Surgery
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9
Q

Beneficial effects of vasodilators in the treatment of angina (2)

A
  1. Dilation of veins
  2. Dilation of the coronary arteries
    * dilating arterioles is NOT beneficial for tx of angina
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10
Q

What are CCBs particularily useful for? What are they not effective against?

A
  1. Variant Angina

2. Classic Angina

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11
Q

How do organic nitrates effect o2 supply and demand?

A
  1. Dilate veins = Decrease preload and o2 demand

2. Dilate large arteries = increase o2 supply

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12
Q

What type of angina are organic nitrates used for?

A

Both Classic and Variant

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13
Q

Most important nitrate drugs are (3)?

A
  1. Nitroglycerine
  2. Isosorbide Di-nitrate
  3. Isosorbide Mono-Nitrate
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14
Q

How is nitroglycerine administered and why?

A

Sublingually or transdermally because it is inactivate by 1st pass metabolism

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15
Q

What limits the utility of nitrate drugs for tx?

A

Tolerance

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16
Q

What are the compensatory responses to nitrate drugs?

A

Reflex tachycarida

*May require co-therapy w/ Beta blocker

17
Q

Toxic effects of Nitrate Drugs?

A

Headache: 30%
Flushing/sweating
Hypotension

18
Q

Mechanism of action of nitrate drugs

A
  1. Denitration
  2. Cross membrane to vascular smooth muscle cell
  3. Combines w/ guanylyl cyclase to convert GTP to cGMP
  4. cGMP opens K channel causing hyperpolarization and smooth muscle relaxation
19
Q

How do beta blockers help treat angina?

A

Block Beta-Adrenergic receptors causing:

  1. Decreased HR
  2. Decreased contractile Force
    - -> Decrease O2 Demand
20
Q

what type of angina are Beta blockers used for?

A

Classic Only

-may precipitate vasospasms in people w/ variant angina

21
Q

What should beta blockers be given with? why?

A

Organic nitrates

Blocks increases in o2 demand resulting from reflex tachycardia

22
Q

What should you avoid doing w/ beta block therapy that could precipitate a heart attack?

A

Avoid rapid termination

23
Q

How do CCBs work in general?

A

Block L-Type Voltage Dependent Calcium channels on cardiac and/or Vascular smooth muscle

24
Q

What are the non-cardioactive CCBs

A
  • Amlodipine

- Nifedipine

25
Q

Cardioactive CCBs?

A

Verapmil

26
Q

Beneficial CCB effects?

A
  1. Arterial Dilation: increased O2 supply

2. Cardiac Suppression: Decreased o2 demand

27
Q

Which CCBs can decrease the rate and force of contraction of the heart?

A

Cardioactive CCBs = verapmil

28
Q

What angina are CCBs used for?

A

BOTH
1st choice for VA - cardioactive CCB
Effect w/ Stable, but used when nitro and Beta blocks are ineffective of problematic

29
Q

What type of CCB do you use for monotherapy of angina?

A

Cardioactive CCB

30
Q

What type of CCB do you use in combination w/ a beta blocker?

A

always a non-cardioactive CCB (amildopine, nifedipine)

31
Q

What do anti-platelet drugs do for preventing acute MI?

A

They prevent clotting

use Aspirin and ADP blockers

32
Q

When to use ADP blockers over aspirin?

A

For higher risk individuals
Post MI
Post PCI surgery

33
Q

Fibrinolytic Drugs vs Angioplasty effectivness?

A
tPA = 50%
Angioplasty = 90%
34
Q

What fibrinolytic drug is most effective and how is it taken

A

Urokinase - taken IV w/ heparin

-best if given w/in 5-6 hours, in ambulance