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Cardiovascular Medicine-Unit 1 > Drugs Used In Chronic IHD (DSA + Lecture)-Konorev > Flashcards

Drugs Used In Chronic IHD (DSA + Lecture)-Konorev Flashcards

1
Q

Describe 1st pass metabolism of Nitrovasodilators (i.e., nitroglycerin):

A

Significant 1st pass metabolism –> High nitrate reductase activity in the liver (nitrate reducatase activity is saturable)

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2
Q

___ compounds are needed to release NO from nitrates

A

Thiol

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3
Q

Describe the MOA of nitrovasodilators:

A
  • Unknown enzymatic rxn releases NO (role of mt ADH2)
  • Thiol compounds needed to release NO from nitrates
  • Vascular smooth m. relaxation by NO
  • Inhibit platelet aggregation
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4
Q

Describe the sensitivity of vasculature to nitrate-induced vasodilation:

A

Veins > Large arteries > Small arteries and arterioles

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5
Q

What are the effects of nitrates in “Angina of effort”?

A
  • decreased preload

- decreased O2 demand

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6
Q

What are the effects of nitrates in “Vasospastic angina”?

A
  • relaxation of coronary artery vascular smooth muscle

- relieving coronary artery spasm

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7
Q

Describe what happens to the following with development of nitrate tolerance:

  • Thiol compounds?
  • O2 radicals?
  • Autonomics?
  • Salt and water?
A
  • Depletion of thiol compounds
  • Increased generation of O2 radicals
  • Reflex activation of Sympathetic nervous system (Tachycardia, decreased coronary blood supply)
  • Retention of salt and water
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8
Q

What are some adverse effects of nitrates?

A
  • headache (meningeal vasodilation)
  • orthostatic hypotension
  • increased sympathetic discharge –> tachycardia, increased cardiac contractility, increased renal Na and H2O reabsorption
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9
Q

The activation of guanylyl cyclase by nitrates and inhibition of PDE5 by ED drugs concurrently causes prolonged activation of what?

A

cGMP —> Smooth m. relaxation –> erectile tissue and blood vessels

-Combo of nitrates and PDE5 inhibitors causes severe increase in cGMP and a dramatic drop in BP

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10
Q

List the Non-cardioactive (DHP) CCBs:

A

Amlodipine (long-acting)
Nifedipine (short acting)
Nicardipine (short acting)

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11
Q

List the cardioactive (non-DHP) CCBs:

A

Diltiazem

Verapamil

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12
Q

What is the MOA of CCBs?

A
  • Ca mediates smooth m. contraction and enters cells via voltage-dependent Ca channels
  • CCBs block Ca entry to relax vascular smooth m.
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13
Q

What are the anti-angina mechanisms of CCBs?

A
  • Decreased myocardial O2 demand –> dilation of peripheral arterioles (DHP’s more potent vasodilators), and decreased cardiac contractility and heart rate (observed with cardioactive or non-DHP CCB’s)
  • Increased bloody supply
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14
Q

What are the major adverse effects of CCBs?

A
  • Cardiac depression, cardiac arrest and acute heart failure
  • Bradyarrhythmias, AV block
  • Short-acting DHP CCB’s –> vasodilation triggers reflex sympathetic activation
  • Nifedipine (immediate release) increases risk of MI in pts with HTN-slow release and long-acting DHPs are better tolerated
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15
Q

What are some B-blockers indicated in angina?

A

Propanolol
Nadolol
Metoprolol
Atenolol

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16
Q

What is the MOA of B-blockers in angina?

A

Decreased myocardial O2 demand –> decrease in HR leads to improved myocardial perfusion and reduced O2 demand at rest and during exercise, decrease in contractility, decrease in BP leads to reduced afterload

17
Q

What are some adverse effects of B-blockers for angina?

A
  • reduced CO
  • Bronchoconstriction
  • Impaired liver glucose mobilization
  • Produce unfavorable blood lipoprotein profile (increase VLDL and decrease HDL)
  • sedation, depression
  • withdrawal syndrome associated with sympathetic hyperresponsiveness
18
Q

What are some contraindications for using B-blockers for angina?

A
  • Asthma
  • Peripheral vascular disease
  • Raynaud’s syndrome
  • Type 1 diabetic on insulin
  • Bradyarrhythmias and AV conduction abnormalities
  • Severe depression of cardiac function
19
Q

Describe the effect on heart rate with the use of nitrates alone?

A

Reflex increase –> baroreceptor reflex

-undesirable effect

20
Q

Describe the effect on contractility with nitrates alone:

A

Reflex increase –> Baroreceptor reflex

-undesirable effect

21
Q

Describe what happens to end-diastolic volume and ejection time with the use of B-blockers or CCBs:

A

Both increase

-Undesirable effect

22
Q

This drug normalized repolarization of cardiac myocytes and reduces mechanical dysfunction. It does not affect HR, general inotropic state of myocardium, coronary blood flow, or peripheral hemodynamics:

A

Ranolazine

23
Q

The clinical use of this drug is for stable angina which is refractory to standard meds. It decreases angina episodes and improves exercise tolerance in pts taking nitrates, or amlodipine, or atenolol:

A

Ranolazine

24
Q

What are some adverse effects of Ranolazine?

A
  • QT prolongation –> may trigger polymorphic ventricular arrhythmias
  • constipation
  • nausea
  • dizziness
  • headache
25
Q

Ranolazine is metabolized by ___

A

CYP3A4/5 –> DO NOT combine with strong CYP3A inhibitors: antifungal anoles, verapamil

26
Q

Ranolazine inhibits ___

A

CYP2D6 –> increases 1/2 life of Amitriptyline, Fluoxetine, Metoprolol, opiod drugs

27
Q

Increasing coronary blood flow using vasodilators is useful in __ angina which relieves coronary spasm and restores blood flow into the ischemic area

A

Vasospastic (Prinzmetal)

28
Q

The use of vasodilators to increase coronary blood flow is not useful in atherosclerotic (classic) angina and can lead to this phenomenon:

A

Coronary steal phenomenon –> redistribution of blood to non-ischemic areas-associated with the dilation of small arterioles (example-potent arteriolar vasodilators, such as Dipyridamole)

29
Q

Does coronary blood flow occur during systole or diastole?

A

Diastole

30
Q

Nitrate —–> NO Requires metabolic activation by ___

A

ADH2 and Thiols

31
Q

In the development of tolerance to nitrates, increased generation of ___ depletes tissues of NO

A

Superoxide radical

32
Q

Ranolazine inhibits __ current in cardiomyocytes

A

Late Na+

33
Q

What are 4 drug classes used in chronic IHD?

A
  • Nitrates (nitrovasodilators)
  • CCB’s
  • Beta blockers
  • Ranolazine

Cardiovascular Medicine-Unit 1 (6 decks)

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