Tx of Angina

Question 1

Class of drug that produces potent reduction in preload

Answer 1

Nitrates, reduce venous return by venodilation

Question 2

Names of the non-dihydropyridine CCBs?

Answer 2

Verapamil, Diltiazem

Question 3

Naming system of dihydropyridine CCBs?

Answer 3

all end in “-pine” (Nifedipine, Amlodipine, etc.)

Question 4

Mechanism of action of Non-dihydropyridine CCBs?

Answer 4

Ca2+ channel blockers that predominately reduce heart work by decreasing HR, decreasing contractility, and slowing AV node conduction

Question 5

What medication must you NEVER give with a non-dihydropyridine CCB?

Answer 5

Beta blocker, produces severe bradycardia

Question 6

Mechanism of action of dihydropyridine?

Answer 6

Ca2+ channel blockers that produce potent vasodilation and reduce myocardial O2 demand by reducing afterload

Question 7

What medication must be given with dihydropyridines?

Answer 7

Beta-blockers, they produce a potent reflex tachycardia in response to vasodilation

Question 8

Situations favoring dihydropyridine use?

Answer 8

Sinus Bradycardia, SA/AV block, valvular insufficiency (Aortic or Mitral)

Question 9

Situations favoring non-dihydropyridine use?

Answer 9

Asthma/Bronchospastic COPD, severe peripheral arterial disease (pain at rest), poorly controlled DM (Type I)

Question 10

What significant effect do lipophilic Beta blockers have on hemodynamics?

Answer 10

Reduce afterload (interfere with sympathetic activation in the brain)

Question 11

Which drug class has no effect on Prinzmetal angina?

Answer 11

Beta blockers, can even exacerbate the problem by blockade of B2-mediated coronary vasodilation

Question 12

Main effect of Ranolazine?

Answer 12

reduces the O2 demand of the myocardium

Question 13

Vitally important drug-drug interaction of Ranolazine?

Answer 13

can cause digoxin toxicity by inhibiting P-gp (can increase digoxin effect by 40-60%)

Question 14

Ranolazine is used in which patients?

Answer 14

Those that are refractory and not candidates for revascularization

Question 15

Mechanism of action of Nitrates?

Answer 15

activate guanylate cyclase–> increase intracellular cGMP–>venodilation and coronary artery dilation

Question 16

Biggest problem with Nitrate therapy?

Answer 16

Tolerance

Question 17

Most common ADE of Nitrates?

Answer 17

Headache, causes vasodilation of the meningeal arteries

Question 18

Other ADEs of Nitrates?

Answer 18

Symptoms of hypotension (syncope, orthostatic hypotension, dizziness, reflex tachycardia)

Question 19

What is the most important mechanism of Nitrate tolerance?

Answer 19

Decreased tissue cysteine levels–> they release NO from nitrates

Question 20

Most important drug-drug interaction seen with Nitrates?

Answer 20

Can’t take nitrates with boner pills–> Type V PDE inhibitors cause increased cGMP—> in combo can lead to severe hypotension and even myocardial ischemia

Question 21

What is anginal rebound?

Answer 21

Coronary vasospasm seen with abruptly stopping IV nitroglycerin. Must bridge with transdermal or oral nitro

Question 22

What type Ca2+ channel do CCBs act on?

Answer 22

L-type

Question 23

Why do CCBs not have extensive side effects in other organs?

Answer 23

The L-type Ca2+ channel is primarily only found in the CVS

Question 24

What type of Ca2+ channels mediate neurotransmitter release in neurons?

Answer 24

N-type and P-type

Question 25

Why do dihydropyridines work preferentially on the vasculature?

Answer 25

dihydropyridines (ex. Nifedipine) bind voltage dependently. The voltage in the smooth muscle of the vasculature changes much slower than the heart (so they bind there). This explains reflexive action seen with these drugs

Question 26

Primary ADE seen only with Verapamail?

Answer 26

Constipation

Question 27

ADEs seen with non-dihydropyridines?

Answer 27

Bradycardia, asystole, AV block, CHF (never use in pt with severe CHF)

Question 28

Pregnancy category of all CCBs?

Answer 28

Category C (cross placenta and breast milk)

Question 29

ADEs seen with dihydropyridines?

Answer 29

dizziness, hypotension, HA, peripheral edema (think excessive vasodilation symptoms), Paradoxical exacerbation of angina “coronary steal”

Question 30

Metabolism of CCBs?

Answer 30

CYP3A4

Question 31

Drugs that inhibit CYP3A4?

Answer 31

Cimetidine, Erythromycin, Grapefruit Juice

Question 32

Drugs that induce CYP3A4?

Answer 32

Rifampin, phenobarbital

Question 33

Use of B-blockers with Verapamil/Diltiazem –> good or bad?

Answer 33

risk of SA and AV block. DON’T DO THIS