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Pharm Test 4 > Antianginals and Agents for Erectile Dysfunction > Flashcards

Antianginals and Agents for Erectile Dysfunction Flashcards

1
Q

MOA of Nitroglycerin:

A

Prodrug metabolized to NO in VSM by mitochondrial aldehyde dehydrogenase-2 causing venous and arterial dilation. Venous dilation predominates- reduces preload

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2
Q

At high doses of nitroglycerin what cardiovascular effect takes place?

A

Reflex tachycardia if dilation if systemic arteries reduces MAP.

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3
Q

True/ False: Nitroglycerin has a direct vasodilating effect on spastic coronary arteries?

A

True

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4
Q

Continued use of nitroglycerin causes tolerance. What is the mechanism?

A

current theory is nitrate-mediated inactivation of ALDH2 that reduces production of NO.

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5
Q

Adverse Effects of Nitroglycerin

A

Headache, Orthostatic Hypotension, Reflex tachycardia

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6
Q

Drug Interactions of Nitroglycerin

A
  • Vasodilator drugs for ED (sildenafil)- NTG can precipitate severe refractory hypotension and possible MI if taken within 24 hours of PDE-5 inhibitors.
  • Alcohol-inhibits ALDH2 and accentuates orthostatic hypotension
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7
Q

Name the 2 subclasses of calcium channel blockers and list the drugs in those subclasses.

A

1) Dihydropyrimidines: Nifedipine (only effects on vasculature)
2) Heart rate-lowering: Verapamil and diltiazem (direct effects on the heart and vasculature)

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8
Q

Cardiovascular effects of nitroglycerin at usual doses?

A

no direct inotropic or chronotropic effects; no changes in BP.

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9
Q

If the patient takes their first dose of nitroglycerin and it does not terminate angina symptoms within 5 minutes, what should that patient do?

A

Contact EMS

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10
Q

MOA for calcium channel blockers

A

1) Block inward flow of Ca2+ through voltage gated L-type calcium channels by binding to the channel alpha1 subunit.
2) Produce marked decrease in transmembrane calcium current (intracellular Ca2+ decreases) in vascular smooth muscle, cardiac myocytes, and nodal tissue.

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11
Q

Effect of Calcium Channel blockers?

A

All are effective vasodilators of both peripheral and coronary arteries; the predominant effect is to decrease afterload and thus reduce oxygen demand.
-Especially useful in relaxing coronary artery vasospasms to increase O2 supply in variant angina.

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12
Q

True or false: CCBs are effective prophylaxis against angina attacks?

A

True

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13
Q

True or false: Immediate release nifedipine should be used for angina attacks?

A

False- nifedipine should not be used due to reflex tachycardia. Long-acting preparations or 2nd gen agents are preferred.

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14
Q

True/false? CCBs are equally efficacious as beta blockers with regard to controlling angina and there is evidence for survival benefit.

A

False: There is not evidence for a survival benefit for CCBs.

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15
Q

Does Nifedipine have greater inhibitory action on VSM or the myocardium?

A

VSM- Much less depression of myocardial contractility and minimal effects on SA nodal automaticity and AV conduction velocity compared to non-DHPs

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16
Q

You should avoid grapefruit juice while taking Nifedipine because it is metabolized by:

A

CYP3A4

17
Q

Verapamil and diltiazem differ from DHPs how?

A

Act on SA and AV nodal tissue and thus can decrease heart rate and contractility; less potent vasodilators than DHPs.

18
Q

Diltiazem vs. Verapemil: Which drug produces less cardiac depression and it better tolerated by most patients?

A

Diltiazem

19
Q

Verapemil and Diltiazem are contraindicated in what syndrome?

A

Sick sinus syndrome.

20
Q

Adverse effects of CCBs: Be specific

A

1) Bradyarrythmias (Ver, dil)
2) Reflex tachycardia (nifed)
3) Cardiac depression (ver,dil)
4) Flushing, peripheral edema (nifed)
5) Constipation (ver)

21
Q

Beta Adrenergic Receptor antagonist prototype

A

Propranolol

22
Q

MOA of Propranolol:

A

1) Decreases HR, contractile force, systemic BP (afterload) which decreases myocardial oxygen demand.
2) Negative chronotropism increases perfusion of myocardium during diastole
3) Decrease resting HR to some extent, but the effect on exercise-induced tachycardia is much more pronounced.

23
Q

The goal in administering propranolol is a dose titrated to maintain resting HR at ___ BPM and limit peak HR during exertion to ____ BPM

A

55 BPM, 110 BPM

24
Q

True/False: Propranolol is effective in reducing the severity and frequency of stable anginal attacks

A

True

25
Q

True/false: Propranolol reduces mortality by decreasing the incidence of sudden cardiac death?

A

True

26
Q

True/False: Propranolol is useful for vasospastic angina.

A

False: Propranolol is not useful for vasospastic angina and may worsen the condition (due to unopposed alpha-adrenergic receptor activity).

27
Q

Adverse effects of propranolol:

A

1) Potential for acute adverse effects on ventricular function (Beta 1).
2) Increase airway resistance.
3) Can precipitate acute MI on sudden withdrawal.
4) Agents with intrinsic beta1 receptor agonist activity (pinodol) are contraindicated.
5) Fatigue, depression and sexual dysfunction.

28
Q

What is the preferred initial agent in patients with CAD who present with stable angina (post-MI and CHF) because of proven survival benefit; especially effective in patients with silent ischemia?

A

A beta blocker.

29
Q

Asthma/COPD, coronary vasospasm are indications for which anginal therapy?

A

CCBs

30
Q

Beta blocker combined with HRL-CCB can cause what symptoms?

A

Severe bradycardia, heart block, and heart failure.

31
Q

Prototype PDE5 inhibitor for erectile dysfunction

A

Sildenafil (Viagra)

32
Q

MOA of sildenafil

A

Selective competitive inhibition of PDE-5 (in VSM of corpora cavernosum).

1) Prolongs activity of NO/cGMP
2) Preferentially relaxes smooth muscle or corpora cavernosa= more blood flow
3) No effect in absence of sexual stimulation- Parasympathetics must be intact

33
Q

Side effects of Sildenafil

A

1) Headache and flushing (PDE1), nasal congestion, dyspepsia.
2) Abnormal vision-blue color tinge, blurring, light sensitivity
3) Risk of sudden hearing loss
4) Priapism- treat with vasoconstrictors

34
Q

Drug interaction of sildenafil

A

Can potentiate the effects of organic nitrates and alpha blockers.

35
Q

Sildenafil is metabolized by what enzyme?

A

CYP3A4

Pharm Test 4 (8 decks)

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