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
What are the adverse effects of Sildenafil?
- HA, flushing, etc | - Visual impairment with mild blue color tinge, photophobia, and blurred vision
26
What are the contraindications to Sildenafil?
- pregnancy and lactation - patients currently using nitrates/nitrites of any form - Pts taking Alpha blockers
27
What drugs make increase the side effects of Sildenafil?
Inhibitors of CYP3A4, since Sildenafil is metabolized by CYP3A5
28
What is different about Vardenafil and Tadalafil when compared to Sildenafil?
Vardenafil: achieves max plasma concentration sooner (faster onset) Tadalafil: Duration of action is up to 24-36 hrs (allows for spontaneity)