Exam 2: Antianginal Drugs Flashcards

1
Q

How is Prinzmetals angina treated?

A

Nitrates and CCBs

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2
Q

O2 demand depends on cardiac workload, which is determined by what 3 things?

A
  • HR
  • Myocardial contractility
  • Ventricular wall tension
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3
Q

Any increase in HR or contractility increases the need for ***.

A

O2

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4
Q

What 3 things decrease coronary flow?

A

1) shortening diastole when HR increases
2) increased ventricular end-diastolic pressure
3) reduced diastolic arterial pressure

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5
Q

What are the 2 nitrates/nitrites?

A

Nitroglycerin and isosorbide dinitrate

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6
Q

What is the MOA of Nitrates/Nitrites?

A

Uneven vasodilation via NO and cGMP pathway.

Large veins are markedly dilated. Arterioles and precapillry sphincters are less dilated

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7
Q

What is the DOC for any acute angina attack?

A

Nitrates/nitrites

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8
Q

How do nitrates cause anginal relief?

A

Decreases myocardial O2 requirement

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9
Q

Why is the sublingual route for nitrates preferred?

A

It is the fasting acting, and it avoids hepatic destruction

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10
Q

Slow release Nifedipine is indicated only in ** and not in **.

Why?

A

Indicted in HTN, not angina.

It may provoke angina pectoris

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11
Q

What are the beneficial effects of The Dihydropyridines?

A

Vasodilation leading to increased myocardial O2 supply and decreased afterload

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12
Q

What are the harmful effects of Dihydropyridines?

A

Rapid hypotension leading to baroreflex activation causing increased cardiac workload and ischemia

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13
Q

What are the beneficial effects of diltiazem and verapamil?

A

Decreased myocardial contractility.

Bradycardia caused by decreased SA node automaticity and AV node conduction

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14
Q

What are the harmful effects of Verapamil and diltiazem?

A

Potential to cause serious cardiac depression that could end in cardiac arrest, AV block, or HF

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15
Q

How do B-blockers provide anginal relief?

A

Decreased sympathetic activation, leading to decreased cardiac activity and decreased vasoconstriction. Hypotension and bradycardia then cause decreased cardiac workload and decreased Myocardial O2 demand

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16
Q

What kind of angina are b-blockers not useful for?

A

Variant angina, they cant cause coronary vasodilation

17
Q

What are the adverse effects of b-blockers?

A

Bronchocontriction, increased plasma TG, decreased insulin, CNS side effects.

18
Q

What is the MOA of Ranolazine?

A
  • Partial fatty acid oxidation inhibitor (decreased O2 consumption in ischemic tissue)
  • Inhibits late inward sodium current
19
Q

What are the indications for Ranolazine?

A

-Improves coronary circulation by decreasing left ventricular wall stiffness

** Drug of last resort

20
Q

What is the most effect drug combo for angina pectoris?

A

B-blockers and a vasodilator

21
Q

What are the 3 PDE5 inhibitors?

A

Sildenafil, Varenafil, and tadalafil

22
Q

What is the MOA of Sildenafil?

A

Selective inhibitor of cGMP specific phosphodiesterase

23
Q

What are the indications to sildenafil?

A
  • Male ED

- PAH

24
Q

What are the important pharmacokinetics associated with Sildenafil?

A

Max concentration reached within 30-120 minutes

-Metabolized by CYP3A4

25
Q

What are the adverse effects of Sildenafil?

A
  • HA, flushing, etc

- Visual impairment with mild blue color tinge, photophobia, and blurred vision

26
Q

What are the contraindications to Sildenafil?

A
  • pregnancy and lactation
  • patients currently using nitrates/nitrites of any form
  • Pts taking Alpha blockers
27
Q

What drugs make increase the side effects of Sildenafil?

A

Inhibitors of CYP3A4, since Sildenafil is metabolized by CYP3A5

28
Q

What is different about Vardenafil and Tadalafil when compared to Sildenafil?

A

Vardenafil: achieves max plasma concentration sooner (faster onset)

Tadalafil: Duration of action is up to 24-36 hrs (allows for spontaneity)