Anti-anginal drugs Flashcards

1
Q

how long do angina pectoris usually last?

A

15s - 15 mins

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2
Q

what is the immediate cause of angina pectoris?

A

imbalance between myocardial O2 supply and demand

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3
Q

what is the differnce in the vessels in stable angina vs unstable angina

A

both will have narrowed lumen due to a plaque but with unstbale angina the plaque will be ruptured and will have platelet aggregation and thrombus formation

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4
Q

is there plaques or lumen narrowing associated with variant angina?

A

NO, has innappropriate vasopasm

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5
Q

in addition to plaque rupture, what is another cause of unstable angina?

A

if the diseased coronary artery endothelium is unable to produce NO and prostacyclin tha inhibit platelet aggregation and clot formation

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6
Q

variant and unstable angina can result if the endotheiium is unable to make _____ and _____ which inhibit _______ and _______

A

NO and prostacyclin; inhibit platelet aggregation and clot formation

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7
Q

causes of variant/prinzmental angina

A
  • enhanced sympathetics- damaged endothelium cannot make NO
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8
Q

__________ drugs are used to increase oxygen delivery AND decrease oxygen demand

A

vasodilators

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9
Q

what 4 classes of drugs are used to treat angina?

A
  • nitrates: isosorbide dinitrate, nitroglycerin, sodium nitroprusside- beta blockers- calcium channel blockers: amlodipine, nifedipine, diltiazem and verapamil- sodium channel blockers: ranolazine
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10
Q

nitrates cause what to O2

A

decrease in the myocardial oxygen demand via systemic vasodilation
increase oxygen delivery by dilating coronary vessels

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11
Q

what are three functions of NO?

A
  • vasodilation- anti-thrombotic- anti inflammatory(all involve the NO stimulated formation of cGMP)
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12
Q

when is IV nitroglycerin given?

A

unstable angina + acute heart failure

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13
Q

_______ is the first line treatment for acute anginal symptoms

A

sublingual nitroglycerin

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14
Q

what nitrate is given for prophylaxis? and why?

A

isosorbide mononitrate and is given ORALLY

takes longer to see effects (1hr)

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15
Q

how can nitrate tolerance be overcome:

A

daily nitrate free intervals (10-12 hr)

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16
Q

what is the most common AE of nitrates?

A

headache due to cerebral vasodilation

17
Q

high doses of nitrate can cause:

A
  • postural hypotension
  • facial flushing
  • reflex tachycardia
18
Q

_______ is contraindicated with nitrates

A

sildenafil

19
Q

what is the MOA of sildenafil?

A

inhibits the enzymes phosphodiesterase 5 which then will inhibit the breakdown of cGMP leading to an increase in available cGMP causing vasodilation

20
Q

________ is used to treat severe hypertensive emergencies and severe heart failure

A

sodium nitroprusside

21
Q

cyanide intoxication is an AE of ______

A

sodium nitroprusside

22
Q

what patients are recommend to use beta blockers?

A

patients with stable angina and have acute coronary syndrome or those with left ventricular dysfunction

23
Q

beta blockers are contraindicated in the treatment of _______

A

variant angina; don’t want to block the beta2 vasodilatory effect (even when you give a beta 1 selective because selective has some effect on beta2)

24
Q

what drugs are used to treat variant angina?

A

calcium channel blockers or nitrates

NOT BETA BLOCKERS

25
Q

_____ type calcium channels is dominant in cardiac and smooth muscle

A

L type

26
Q

what are the dihydropyradines and what do they act on?

A

nifedipine and amlodipine;

mainly acts on VASCULATURE

27
Q

what should you not give patients who have a preexisting cardiac depression or with an AV conduction abnormalities

A

verapamil (calcium channel blockers that are specific to the heart)

28
Q

digoxin levels can increase when given _____ because it can displace it from its binding sites

A

verapamil (calcium channel blocker)

29
Q

which non dihydropyradine decreases HR more?

A

verapamil

30
Q

MOA of ranolazine?

A

blockade of sodium current that facilitates the calcium entry via Na/Ca exchanger; usually this exchange will bring sodium in and push calcium out but in this when there is angina there is less ATP and so the Na/K ATPase pump doesn’t work so there is more sodium inside the cell thus REVERSING the direction of the Na/Ca exchanger

31
Q

ranolazine lead to _______ intracellular calcium

A

decreased;

32
Q

adverse effects of ranolazine

A

last line treatment; QT interval prolongation

33
Q

treatment regiment for stable angina:

A

nitrates > beta blockers > calcium channel blockers > ranolazine

34
Q

treatment regiment for variant angina?

A

nitroglycerin and calcium channel blockers (NO beta blockers)

35
Q

can you use beta blockers to treat angina in a patient with chronic renal disease?

A

yes, but after giving nitrates, calcium channel blockers have shown to give better outcomes

36
Q

what is the effect on the end diastolic volume when giving beta blockers or calcium channel blockers?

A

EDV will increase (depends on patient)

37
Q

when nitrates + beta blockers or calcium channel blockers are given, what are the effects on:
HR, atrial pressure, EDV, contractility and ejection time?

A
HR: decrease 
atrial pressure: decrease 
EDV: none/decrease 
contractility: none 
ejection time: none