Anti-anginal drugs Jeff Flashcards

1
Q

What affects supply of coronary blood flow?

A

Aortic diastolic pressure, duration of diastole (time at which ventricles get blood flow through coronary arteries), ejection fraction (if higher, less end-diastolic pressure), O2 delivery (anemia and CAD affecting perfusion)

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2
Q

What affects demand of heart?

A

Heart rate, Intraventricular wall pressure, Pre-load (increase pressure), afterload takes more energy, Contractility, Transluminal wall thickness

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3
Q

What is Prinzmetal’s Angina?

A

It is a variant angina. AKA nocturnal angina b/c recumbent position increases venous return which triggers alpha-adrenergic coronary vasospasm as it activates the stretching pressor response of coronary vaso beds

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4
Q

What is Dipyradamole and what is the mechanism?

A

Fast Acting Vasodilator (Persantine is trade name). It vasodilates to decrease peripheral resistance (more arterial than venodilation)

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5
Q

What are favorable effects of Dipyradamole?

A

Less afterload resulting in higher EF, less end diastolic volume and wall tension, decreased work demand, vasodilation in coronary vasculerature, increased coronary blood flow

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6
Q

Why isn’t dipyradamole used to treat angina?

A

Unfavorable effects occur. Drop in arterial pressure causes baroreceptor stimulation so higher heart rate increasing demand and risk of alpha vasospasm.

ALSO Coronary steal phenomenon (which is when TPR drops and blood goes there b/c little resistance and less flow to coronary arteries. Note: coronary arteries are already dilated after the drug is used, so hypoxic metabolites don’t allow it to reduce pressure enough to cause reperfusion when TPR is so low)

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7
Q

What is Persantine Stress Test?

A

Do it when person can’t do classic stress test. Inject Persantine, dire acting vasodilator, which causes heart to race due to baroreceptor reflex responding to drop in BP to put stress on heart.

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8
Q

How do organic nitrates and nitrites work?

A

Liberate NO to activate guanylate cyclase to make more cGMP to stimulate dephosphorylation dependent inactivation of myosin light chain to vasodilate veins more so than arteries at therapeutic dosage

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9
Q

Advantage of organic nitrates over direct acting vasodilators?

A

Less action on arteries at therapeutic dosage so TPR stays higher to prevent the baroreceptor reflex while still reducing stretching and preload of the heart from decreased venous pressure.

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10
Q

How does decreased preload help with angina?

A

Less stretching puts less pressure on coronary arteries so more blood flow to subendocardium where blood is lacking during angina. Decreases left ventricular pressure and less pulmonary vascular pressure too.

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11
Q

Which drug must you be careful about short shelf life?

A

Nitroglycerine will break down quickly, especially photosensitive so in amber glass bottle. Note: if tongue doesnt burn (from vasodilation), the drug isn’t working

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12
Q

Who gets “Monday Disease,” what are the symptoms, and why does it happen?

A

People who often work with nitroglycerin

Build tolerance during the course of the week and then lose tolerance over the weekend…re-exposure on Monday dilates cranial vessels–> headache

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13
Q

Adverse effects of nitrates?

A

High dose is orthostatic hypotension, meningeal vasodilation. Tolerance, dependence (Monday disease), high dosage can cause methemoglobinemia. IT IS CONTRAINDICATED in phosphodiesterase 5 inhibiters (viagra, cialis, levitra…) b/c that enzyme breaks down cGMP (or NO, which one, Joe?)

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14
Q

Indications of nitrates?

A

Angina, variant angina, CHF

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15
Q

How are nitrates eliminated?

A

Liver for all of them, all protein bound

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16
Q

Which nitrate has a longer half life (5 hours)?

A

Isosorbide-5-mononitrate (notice there is a 5 in the name, like the half life of it)

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17
Q

Which nitrate is fast acting?

A

Amyl Nitrite b/c inhaled and volatile

18
Q

What is isosorbide dinitrate?

A

Works like nitroglycerine but longer acting 40-60 min half life (vs 1-3 mins)

19
Q

What are ways to make nitroglycerin be released slower?

A

Ointment lasts 4-8 hours, nitroglycerin impregnated transdermal discs (fancy word for patch) are absorbed over 24 hours

20
Q

What are phenylalkylamines? (and specific drug)

A

Ca2+ channel blocker (and it is Verapamil).

21
Q

What are dihydropyridines?

A

Calcium channel blocker acting especially in (peripheral?) vasculature and not as much heart. END IN PINE. Nifedipine, nicardipine, amlodipine

22
Q

What are benezothiazepines? (specific drug)

A

Ca2+ channel blocker (and it is diltiazem).

23
Q

What are diarylaminoprpylamines? (specific drug)

A

Ca2+ channel blocker (and it is bepridil).

24
Q

What is vasodilating, negative inotropic, suppression of SA automaticity and depression of AV conduction effects of phenylalylamines?

What effects do phenylalylamines have on vasodilation? Inotropicity? SA automaticity? and AV conduction depression?

(Jeff, I got a little confused in reading this…but after writing an example myself I realize how tough it is to write a flashcard for this)

A

Verapamil is strong vasodilation and negative inotropic. Very strong depression of SA and AV node

Verapamil:

Strong vasodilator

Strongly negative inotropic

Very strongly depresses SA automaticy

Very strongly depresses AV conduction

(If you like yours better, keep it that way)

25
Q

What is vasodilating, negative inotropic, suppression of SA automaticity and depression of AV conduction effects of dihydropyridines?

A

If it ends in pine, it has high vasodilating properties and little to no effect on heart inotropics, SA or AV nodes

26
Q

What is vasodilating, negative inotropic, suppression of SA automaticity and depression of AV conduction effects of benzothiazepines?

A

Diltiazem has moderate effect on vasodilation and a 2 of 5 for negative inotropic effect but strongly suppresses SA and AV node (though not quite as well as verapamil [5 and 4 for SA and AV respectively)

27
Q

What is vasodilating, negative inotropic, suppression of SA automaticity and depression of AV conduction effects of diarylaminoprpylamines?

A

Beripidil is weak vasodilator with 4 of 5 for negative inotropic and great SA and AV nodal slowing

28
Q

Ca2+ channel for vasodilation?

A

Go with pines. Sums up the section well.

29
Q

What calcium channel blockers can be used for pectoris angina?

A

Any will work

30
Q

What Ca2+ blockers can be used for Prinzmetals angina?

A

Anything not ending in pine.

Dihydropyridines–having a stronger peripheral vasodilation effect–cause hypotension–>tachycardia via baroreceptor reflex

31
Q

What are the selective Beta-1 Beta blockers?

A

Metoprolol, Atenolol, Acebutulol. (MAA)

32
Q

Nonselecive Beta Blockers

A

Propranolol, timolol, nadolol, pindolol. (if it ends in lol and does not start with M or A, because they are not MAA, the beta1 cardio selective)

33
Q

Benefit of beta blockers for treating angina?

A

Less rate so less demand.

34
Q

Unfavorable effects of beta blockers?

A

Incfreased filling time, so more end-diastolic tension, Negative inotropics, increased risk of ALPHA VASOSPASM

35
Q

Adverse effect of Beta blockers?

A

Bradycardia (duh), depression of contractility (duh), Impedence of AV conduction (just menitoned bradycardia, so duh), May aggravate variant angina (alpha vasospasm) WHICH DECREASES coronary blood flow and worsens transluminal distribution of coronary blood flow.

36
Q

3 uses of beta blockers?

A

Suraventricular arrhythmias, typical anginas with organic nigtrats, antihypertensives. (also cheating golfers to relax while putting and stuff)

37
Q

What two conditions can be made worse by calcium channel blockers?

A

sick sinus syndrome and CHF

38
Q

What calcium channel blockers can cause reflexive tachycardia?

A

Ending in pine can cause it because it canc ause hypotension.

39
Q

If you are about to lower blood pressure, what can you do to stop the baroreceptor reflex to prevent tachycardia?

A

Beta blockers are great here, will stop the stimulation for faster heart rate.

40
Q

What is a slow acting and long acting “pine”?

A

Amlodipine? More like amSLOWdipine. LOL THANKS JOE.