Tx of Angina Flashcards
Class of drug that produces potent reduction in preload
Nitrates, reduce venous return by venodilation
Names of the non-dihydropyridine CCBs?
Verapamil, Diltiazem
Naming system of dihydropyridine CCBs?
all end in “-pine” (Nifedipine, Amlodipine, etc.)
Mechanism of action of Non-dihydropyridine CCBs?
Ca2+ channel blockers that predominately reduce heart work by decreasing HR, decreasing contractility, and slowing AV node conduction
What medication must you NEVER give with a non-dihydropyridine CCB?
Beta blocker, produces severe bradycardia
Mechanism of action of dihydropyridine?
Ca2+ channel blockers that produce potent vasodilation and reduce myocardial O2 demand by reducing afterload
What medication must be given with dihydropyridines?
Beta-blockers, they produce a potent reflex tachycardia in response to vasodilation
Situations favoring dihydropyridine use?
Sinus Bradycardia, SA/AV block, valvular insufficiency (Aortic or Mitral)
Situations favoring non-dihydropyridine use?
Asthma/Bronchospastic COPD, severe peripheral arterial disease (pain at rest), poorly controlled DM (Type I)
What significant effect do lipophilic Beta blockers have on hemodynamics?
Reduce afterload (interfere with sympathetic activation in the brain)
Which drug class has no effect on Prinzmetal angina?
Beta blockers, can even exacerbate the problem by blockade of B2-mediated coronary vasodilation
Main effect of Ranolazine?
reduces the O2 demand of the myocardium
Vitally important drug-drug interaction of Ranolazine?
can cause digoxin toxicity by inhibiting P-gp (can increase digoxin effect by 40-60%)
Ranolazine is used in which patients?
Those that are refractory and not candidates for revascularization
Mechanism of action of Nitrates?
activate guanylate cyclase–> increase intracellular cGMP–>venodilation and coronary artery dilation
Biggest problem with Nitrate therapy?
Tolerance
Most common ADE of Nitrates?
Headache, causes vasodilation of the meningeal arteries
Other ADEs of Nitrates?
Symptoms of hypotension (syncope, orthostatic hypotension, dizziness, reflex tachycardia)
What is the most important mechanism of Nitrate tolerance?
Decreased tissue cysteine levels–> they release NO from nitrates
Most important drug-drug interaction seen with Nitrates?
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
What is anginal rebound?
Coronary vasospasm seen with abruptly stopping IV nitroglycerin. Must bridge with transdermal or oral nitro
What type Ca2+ channel do CCBs act on?
L-type
Why do CCBs not have extensive side effects in other organs?
The L-type Ca2+ channel is primarily only found in the CVS
What type of Ca2+ channels mediate neurotransmitter release in neurons?
N-type and P-type
Why do dihydropyridines work preferentially on the vasculature?
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
Primary ADE seen only with Verapamail?
Constipation
ADEs seen with non-dihydropyridines?
Bradycardia, asystole, AV block, CHF (never use in pt with severe CHF)
Pregnancy category of all CCBs?
Category C (cross placenta and breast milk)
ADEs seen with dihydropyridines?
dizziness, hypotension, HA, peripheral edema (think excessive vasodilation symptoms), Paradoxical exacerbation of angina “coronary steal”
Metabolism of CCBs?
CYP3A4
Drugs that inhibit CYP3A4?
Cimetidine, Erythromycin, Grapefruit Juice
Drugs that induce CYP3A4?
Rifampin, phenobarbital
Use of B-blockers with Verapamil/Diltiazem –> good or bad?
risk of SA and AV block. DON’T DO THIS
