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Cardio Block > Anti-Angina Drugs > Flashcards

Anti-Angina Drugs Flashcards

1
Q

What are 2 examples of nitrate drugs?

A
  1. nitroglycerin

2. isosorbide mononitrate

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2
Q

What are 2 examples of B blockers?

Which is cardioselective?

A
  1. metoprolol- cardioselective

2. propranolol

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3
Q

What are 3 examples of Ca channel blockers?

A
  1. Verapamil
  2. Nifedipine
  3. diltiazem
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4
Q

What are two PDE5 inhibitors?

A
  1. Sildenafil

2. Tadalafil

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5
Q

What is angina pectoris? What are 2 potential causes?

A

It is pain from myocardial ischemia due to:

  1. increased metabolic demands of the heart
  2. Decreased supply of O2 and nutrients
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6
Q

What three factors contribute to the oxygen demand of the heart?

A
  1. Wall tension (preload, afterload)
  2. HR
  3. Contractility
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7
Q

What two factors contribute to the oxygen supply of the heart?

A
  1. A-V O2 difference
  2. myocardial distribution (aortic pressure+ coronary vascular resistance–> coronary blood flow-> Myocardial distribution)
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8
Q

What are the 2 ways to increase O2 supply to the heart?

A
  1. Increase blood flow in coronary circulation

2. redistribute coronary blood flow

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9
Q

Which classes of drugs increase the supply of oxygen to the heart?
Which classes of drugs decrease the demand to the heart?

A
  1. Nitrates and Ca Channel blocker increase supply through vasodilation (reduced coronary vascular resistance)
  2. B-blockers decrease the demand by lowering HR and contractility, Nitrates lower preload, Ca channel blockers decrease afterload (and verapamil and diltiazem decrease HR and contractility)
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10
Q

What are the 2 main hemodynamic effects of B-blockers?

A
  1. reduced myocardial O2 demand by decreasing HR and LV contractility
  2. increased O2 supply by prolonging diastole allowing better perfusion of the subendocardium
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11
Q

What are the 4 major adverse effects/contraindications associated with B-blockers?

A
  1. CNS effects - nightmares, etc
  2. block B2 mediated vasodilation (bad for variant angina like Prinzmetal’s because it cannot counteract the vasospasms)
  3. contraindicated in asthma due to blockage of B2 mediated bronchodilation
  4. CHF or AV block because it will exacerbate hypotension by reducing CO
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12
Q

What drugs are typically combined with B-blockers because they counter each others negative effects?

A

Nitrates.

B-blockers can reduce some of the reflex tachycardia associated with nitrate use

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13
Q

What type of angina might you avoid using a B-blocker with? Why?

A

Variant angina because B2 stimulation would dilate vessels countering the vasospasm(constriction) associated with variant angina. You would not want to block the B2 receptors.

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14
Q

What is the molecular mechanism of calcium antagonists?

What do verapamil and diltiazem do that nifedipine doesn’t?

A

They bind the L-type calcium channel in vascular smooth muscle and decrease calcium entry

Verapamil and diltiazem slow the recovery of Ca channels having direct effects on HR and contractility of the heart.

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15
Q

Where does nifedipine bind on the Ca channel?

A

It sits directly in the channel blocking flow of calcium in.

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16
Q

What are the 3 hemodynamic effects of nifedipine?

A
  1. vasodilation of arterial system to reduce systemic vascular resistance
  2. reduce myocardial O2 demand by decreasing LV afterload (through dilation of peripheral arteries)
  3. increase O2 supply by inhibiting coronary artery constriction and vasospasm, and dilating the coronary arteries to decrease CVR and increase flow
17
Q

Where do verapamil and diltiazem bind on the Ca channel?

A

Near the inactivation gate in the inactive channel which slows reactivation

18
Q

What are the 3 hemodynamic effects of verapamil and diltiazem?

A
  1. Vasodilate and reduce HR/contractility by delaying reactivation of Ca channels
  2. Reduce O2 demand by arterial vasodilation (decreasing afterload)
  3. increase O2 supply by coronary vasodilation and inhibition of coronary constriction which decreases coronary vascular resistance and increases flow
19
Q

What is the molecular mechanism of organic nitrates?

A

Reduce tone of smooth muscle.

  1. Enzymes in vascular smooth muscle metabolize nitroglycerin and isosorbide mononitrate to NO
  2. NO stimulates guanylyl cyclase which increases cGMP
  3. cGMP–> active Protein Kinase
  4. PK-> Sarcoplasmic reticulum to take up Ca
  5. reduced Ca in the cell allows relaxation
20
Q

In addition to the nitrate drugs, what other agents act through NO?

A
  1. Ach
  2. Bradykinin
  3. atrial natriuretic factor
  4. nitroprusside
21
Q

What are the hemodynamic effects of nitrates on myocardium?

A
  1. dilate peripheral veins decreasing LV preload
  2. dilate peripheral arterioles to decrease LV afterload

They have a larger effect on veins

22
Q

How do nitrates reduce myocardial oxygen demand?

A
  1. dilate peripheral venules reducing venous pressure and decreasing LV preload. Decreased preload decreases end-diastolic volume which decreases wall tension
  2. dilating peripheral arterioles reducing LV afterload
23
Q

What reflex can the body have to nitrates?

A

Dilates veins-> reduced preload-> reduced end-diastolic volume-> reduced wall tension BUT

The dilated veins can causes a mild reflex sympathetic stimulation which increases HR and contractility to minimize the fall in CO

24
Q

What are the two major side effects to using nitrates?

A
  1. Flushing because of dilated veins in head and neck

2. Headaches due to meningeal vein dilation

25
Q

What are the 5 ways nitrates increase myocardial oxygen supply?

A
  1. inhibiting coronary vasoconstriction
  2. dilate epicardial vessels (selective for larger vessels)
  3. reduce severity of stenosis in diseased coronary vessels by increasing epicardial contribution
  4. collateral coronary flow to areas of myocardium supplied by occluded or diseased coronary arteries
  5. redistribution of blood flow to ischemic regions
26
Q

What is the absorption of nitroglycerin? (what is the preparation, time for effect to begin, duration of action)

A

Sublingual (more rapid absorption) or oral
1-5 minutes to begin effect
Duration of action: 20-30 minutes

27
Q

How must nitroglycerin tablets be stored?

A

They are very unstable so they need to be protected from moisture, sunlight and temperature

28
Q

`What is the bioavailability of nitroglycerin?

A

10-20% due to hepatic first pass (another reason why sublingual is the preferred route of administration)

29
Q

For topical preparations of nitroglycerin, what is the absorption rate? How long do the effects of the drug last?
What are the 2 preparations for topical delivery?

A

absorbed in an hour and last 4-8.

  1. in a lanolin-petrolatum base applied to skin
  2. adhesive patch where nitro is delivered at a constant rate dependent of the surface area of the patch
30
Q

What is the half life of nitroglycerin? How is it excreted?

A

1-3 minutes and it is excreted renally

31
Q

What is the absorption of isosorbide dinitrate? (preparation, time for affect, duration of action)

A

It is sublingual or oral. Max effect in 6 minutes and lasts an hour (longer acting than nitroglycerin)

At high oral doses, it can produce sustained hemodynamic/antianginal effects because the parent compound persists and the metabolites it degrades to are also active

32
Q

What is the bioavailability of isosorbide dinitrate?

A

10-20% due to a substantial hepatic first pass

33
Q

What is the fate of isosorbide dinitrate in the body? What is the half life?

A

It is metabolized in the liver to an active metabolite isosorbide-5-mononitrate.
Half life of dinitrate is 45 minutes
Half life of mononitrate is 2-5 hours

34
Q

What is the downfall of frequent use of nitrates?

How can this be avoided?

A

Frequent, continuous or repeated exposure to high doses of nitrates can lead to a decrease in their effects (“nitrate tolerance”)
Isosorbide dinitrate overuse can cause decreased hemodynamic effect AND cross-tolerance to nitroglycerin

This can be avoided with 8-12hour nitrate free intervals a day to allow recovery of response

35
Q

What are the 2 major adverse effects of nitrate drugs?

A
  1. headache due to dilation of meningeal vessels with vertigo, dizziness, flushing and postural hypotension
  2. GI intolerance with high doses of nitrates
36
Q

What drug is absolutely contraindicated with nitroglycerin?

A

PDE5 inhibitors like sildenafil and tadalafil (Viagra and Cialis) which treat ED and idiopathic pulmonary atrial hypertension

37
Q

What is the mechanism of action of sildenafil and tadalafil?

A

They are PDE5 inhibitors so they block the breakdown of cGMP, enhancing NO effects.
If they are used with nitrates, they cause a dangerous drop in BP due to excessive dilation

38
Q

What is PDE6 inhibitor?

A

It blocks degradation of cGMP in the retina and can cause visual disturbances

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