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3 Pharma > CAD drugs > Flashcards

CAD drugs Flashcards

1
Q

Oxygen saturation of blood as it returns to the heart

A

MVO2

SVO2

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2
Q

Myocardial O2 supply determined by these factors:

A

1) perfusion pressure

2) intrinsic vascular resistance

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3
Q

Myocardial O2 demand determined by:

A

1) heart rate
2) contractility
3) wall stress
4) MVO2 = HR x SBP

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4
Q

First line drugs in CAD

A

Nitrates

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5
Q

Primary effect of nitroglycerin and related drugs:

A

venous dilation (relaxes all types of smooth muscle)

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6
Q

Secondary effects if nitroglycerin

A

Coronary artery dilation increases supply

Arterial dilation decreases afterload

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7
Q

Disadvantage for chronic use of nitrates?

A

Drug tolerance

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8
Q

Effect of venous dilation on CO?

A

Venodilation increases venous capacitance –> decrease venous return –> decreasing preload and thus decreasing CO

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9
Q

How does the consumption of sulfhydryl groups contribute to nitrate tolerance?

A

Sulfhydryl groups on cell membrane are needed for nitrates to enter cell.

No nitrates will enter the cell if nitrates are constantly given.

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10
Q

How does continuous nitrate use cause receptor down-regulation?

A

vasodilation –> larger blood volume –> sympathetic receptors downregulated

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11
Q

MoA of nitrates:

A

Enter cell membrane –> Nitrification process

NO activates guanylyl cyclase –> increase in cGMP –> Ca release is INHIBITED –> smooth muscle relaxation –> venous dilation

venous dilation –> decreased preload –> decreased CO –> decrease O2 demand

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12
Q

Nitrate drug interactions:

A

Nitrates cannot be taken with other drugs that use cGMP pathway like PDE-5 inhibitors –> severe hypotension

sildenafil, vardenafil, tadalafil

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13
Q

Type of beta blocker for CAD treatment?

A

beta 1 blocker

Decreases oxygen demand by decreasing heart rate.

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14
Q

How do beta blockers enhance coronary blood flow?

A

B1 blockage –> Dereased HR –> Increased diastolic perfusion –> increased filling time

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15
Q

Negative effect of increased filling time?

A

preload inreased –> more force required –> hypertrophy

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16
Q

How do beta blockers reduce MVO2

A

B1 blockage –> Decreased HR and contractility

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17
Q

Why are B blockers without ISA preferred?

A

ISA = partial agonist at receptor

Therefore they will show less decrease in HR.

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18
Q

Why are non-selective 3rd gen BBs unwanted in CAD patients?

A

3rd gen BB (mostly non-selectives) can have alpha antagonistic effect or stimulate NO release –> increase vasodilation –> profound hypotension –> REFLEX TACHYCARDIA –> higher O2 demand for heart

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19
Q

CAD + asthma: what drugs could be used

A

Cardio-selective 3rd gen with partial B2 agonism

Celiprolol

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20
Q

A patient with CAD is on BBs. What drugs should be avoided?

A

CCBs (verapamil, diltiazem)

Anti-arrhythmics (amiodarone)

They have cardiosuppressive effects leading to profound decrease in HR and CO.

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21
Q

BB with highest lipid solubility?

A

propanolol

This is why it can cause lethargy, mental depression, hallucinations

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22
Q

BBs used for early administration after ischemic episodes:

A

IV esmolol

IV metoprolo or atenolol followed by oral metoprolol/atenolol

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23
Q

BBs used for late administration after ischemic episode:

A

BBs without ISA

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24
Q

Two mechanisms of CCBs

A
  1. Block L-type voltage operated channels (VOCs) and receptor operated channels at membrane
  2. Bind to calcium channel protein
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25
Q

CCB group with more vasodilatory effect, less HR effect

A

dihydropyridines

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26
Q

Benzothiazepine

A

Diltiazem

27
Q

Phenylalkylamine

A

Verapamil

28
Q

Second Gen CCB are all this type

A

dihydropyridines

29
Q

Second Gen CCB compared to First Gen?

A

More vasoselective than 1st

30
Q

Examples of 2nd Gen CCB

A

amlodipine
felodipine

nicardipine
isradipine

31
Q

Examples of 1st Gen CCB

A

nefidipine

32
Q

All CCB are metabolized solely by the liver except?

A

diltiazem

33
Q

Drugs that increase BA of CCB

A

Cimetidine
phenytoin
carbamezapine

34
Q

diltiazem and verapmil increase BA of what drugs?

A

cyclosporine

35
Q

Verapimil effect on digoxin?

A

increased serum levels

36
Q

Lithium levels increase due to which CCB?

A

diltiazem

37
Q

CCB that blocks K channel in smooth muscle inhibiting vasodilation

A

verapamil

38
Q

Effects calcium channel blockers on cardiac muscles

A

Because of the blocked transmembrane calcium current:

1) decreased contractility
2) decrease SA conduction velocity
3) decreased AV conduction velocity

39
Q

Myocardial selectivity of CCB (ranking):

A

verapamil > diltiazem > nifedipine (DHPs)

verapamil has less vasodilation properties

40
Q

CCB that can more likely cause reflex tachycardia

A

DHPs –> nifedipine

41
Q

CCB causing decreased HR

A

verapamil, diltiazem

42
Q

CCB with most sympathetic antagonism

A

diltiazem

less: verapamil, NONE with nifedipine

43
Q

Preferred CCB with AV conduction abnormalities

A

nifedipine

least effect on AV node

44
Q

Preferred CCB with overt heart failure

A

All CCB WORSEN (negative inotropic effects) more commonly with non-DHP

Amlodipine can be used

45
Q

Preferred CCB for hypotension

A

non-DHP

diltiezam, verapamil

46
Q

Preferred CCB with tachycardia, flutter, fibrilliation

A

diltiezam and verapamil

antiarrhythmic effects

47
Q

Preferred CCB with unstable angina

A

NOT nifedipine

in combination with nitrates

48
Q

Preferred CCB with non q-wave myocardial infarction

A

diltiazem can decrease frequency of postinfarction angina

49
Q

Combination of DHP with B-blockers can cause what?

A

AV block

Ventricular depression

50
Q

Action of angiotensin II

A

1) vasoconstriction

2) aldosterone stimulation –> Na and H20 reabsorption

51
Q

How do ACE-I’s decrease remodelling

A

decrease wall stress (load), prevent LV dilatation.

Angiotensin II contributes to remodelling through stimulation of the proto-oncogens c-fos, c-jun, c-myc, transforming growth factor beta (TGF-B), through fibrogenesis and apoptosis

52
Q

Why are ACE-I’s safe to use in patients with ischemic heart disease?

A

they do NOT cause reflex sympathetic activation

53
Q

Adverse effects of ACE-I’s:

A

cough
angioedema

ACE-Inhibitors increase bradykinin which cause cough and angioedema

54
Q

Angiotensin II contributes to remodelling through stimulation of:

A

Pproto-oncogens c-fos, c-jun, c-myc, transforming growth factor beta (TGF-B), through fibrogenesis and apoptosis

55
Q

ACE inhibitors mechanism:

A

Vasodilation
Decrease aldosterone
Increase bradykinin

56
Q

Why do ARBs have more potential for angiotensin block?

A

ARBs block the receptor AT1.

ACE block ACE from forming angiotensin II but other enzymes form angiotensin II.

57
Q

What was the first peptide ARB? Why is it no longer used?

A

Saralasin

Low absorption and short half-life

58
Q

Adverse effects of ARBs

A

cough, hyperkalemia, LBP, dizziness, headache

abnormal taste

59
Q

New drug therapy for myocardial ischemia; rho kinase inhibtor

A

Fasudil

60
Q

New drug therapy for myocardial ischemia; metabolic modulator

A

Trimetazidine

61
Q

New drug therapy for myocardial ischemia; Preconditioning

A

Nicorandil

62
Q

New drug therapy for myocardial ischemia; sinus node inhibition

A

Ivabradine

63
Q

New drug therapy for myocardial ischemia; Late sodium current inhibition

A

Ranolazine

64
Q

New CAD prevent ischemic effects by:

A

targeting metabolic pathways not hemodynamics

3 Pharma (8 decks)

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