B4.050 - Treatment of Angina Flashcards

1
Q

what are the 3 risk factors for CAD

A

High BP High LDL Smoking

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2
Q

how many americans have one of the 3 risk factors for CAD

A

50%

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3
Q

what medical conditions increase risk of heart disease

A

DM Obesity Poor diet Physical inactivity Excessive alcohol

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4
Q

what is angina pectoris

A

chest pain when amount of blood delivered to heart cannot supply enough oxygen to satisfy myocardial requirement

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5
Q

what is the primary symptom of heart disease

A

angina pectoris

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6
Q

what is used for immediate relief of angina pectoris

A

organic nitrates (Nitroglycerin)

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7
Q

what is used as prophylaxis for angina pectoris

A

CCB and Beta blockers

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8
Q

how is angina pectoris pain described

A

strangling, vise like, constricting, suffocating. crushing, heavy, sqeezing

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9
Q

how is angina pectoris described in vague situations

A

only mild pressure, numbing, nausea, sweating, SOB

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10
Q

what is the site of chest pain in angina pectoris

A

usually retrosternal often radiating down the left arm or may also involve the right or both arms

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11
Q

etiology of classic atherosclerotic angina of effort

A

atheromatous obstruction of large coronaries especially with exercise

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12
Q

what is the treatment for angina of effort

A

if uncontrolled by drugs may require coronary bypass or angioplasty

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13
Q

what is variant or angioplastic prinzmetals angina

A

spasms or constriction in atherosclerotic coronary vessels

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14
Q

what is the treatment for prinzmetals angina

A

relieved by nitrates or CCBs

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15
Q

what does oxygen demand depend on

A

cardiac workload which is determined by

1. contractility (major det of O2 consumption)

  1. heart rate
  2. wall stress
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16
Q

cornerstone drugs for angina

A

CCBs and beta blockers

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17
Q

what is the main source of energy in the heart

A

fatty acid oxidation

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18
Q

what does trimetazidine do

A

shifts myocardial metabolism towards greater use of glucose to potentially reduce oxygen demand without affecting hemodynamics

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19
Q

what is a pFOX inhibitor

A

inhibits fatty acid oxidation to try and shift energy use from fatty acid oxidation to glycolysis

Trimetazidine

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20
Q

what is O2 delivery directly related to

A

perfusion pressure and duration of diastole

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21
Q

what happens with increased diastole time

A

increased O2 delivery

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22
Q

what is vascular bed resistance determined by

A

metabolic products

autonomic activity

various drugs

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23
Q

damage to endothelium of coronary vessels causes what

A

increase in vascular resistance

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24
Q

what can increase O2 supply

A

mechanical intervention

Stents

Angioplasty

Coronary bypass surgery

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25
Q

what to beta adrenergic antagonists and some Ca entry blockers affect

A

affect heart rate and contractility

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26
Q

what do organic nitrates and calicum entry blockers affect

A

preload and afterload

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27
Q

what do vasodilators, statins, and anti-thrombolytics affect

A

coronary blood flow, regional myocardial blood flow

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28
Q

what are the primary sites of action of pharmacological agenst

A

reduce O2 demand or enhance O2 supply

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29
Q

what do CCBs do

A

decrease intracellular Ca

Blocks calmodulin cascade that leads to contraction of vascular smooth muscle

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30
Q

what do beta 2 agonists do

A

increases cAMP

increase cGMP which causes muscle relaxation

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31
Q

what does NO do

A

activator of soluble guanylyl cyclase leading to smooth muscle relaxation

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32
Q

what are the 4 drug classes used in angina

A
  1. organic nitrates
  2. CCBs
  3. beta blockers
  4. investigative ones
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33
Q

what is ranolazine

A

reduces intracellular calcium concentration and thus reduces cardiac contractility and work

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34
Q

what is allopurinol

A

inhibits xanthine oxidase which contributes to oxidative stress and endothelial dysfunction

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35
Q

which drug prolongs exercise time in patients with angina

A

allopurinol

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36
Q

wht is ivabradine

A

direct bradycardic agent

inhibits hyperpolarization activated sodium channel in sinatrial node

37
Q

what is fasudil

A

Rho-kinase inhibitor reduces coronary vasospasm in experimental animals

38
Q

where do organin nitrates vasodilate

A

use enzymes found predominantly on venous side or vasculature, preferentially vasodilates veins

39
Q

what is the one drug that vasodilates both veins and arteries and why

A

sodium nitroproside

does not need enzymes

40
Q

what are the short acting nitrates used for angina

A

Amyl nitrite - inhalant

Nitroglycerin - sublingual

Isosorbide dinitrate - sublingual

41
Q

what are long acting nitrates used for angina

A

Nitroglycerin, oral sustained action

Nitroglycerin - 2% ointment

Nitroglycerin - slow release, buccal

Nitroglycerin - slow release, transderma

isosorbide dinitrate - oral

isosorbide mononitrate - oral

42
Q

what is sildenafil and why is it important

A

inhibitor of PDE-5

Can potentiate action of NO in angina –> sever hypotension, MI

43
Q

Nitrate ion reactis with what and can be used for what type of poisoning

A

hemoglobin –> methemoglobin –> can be used to treat cyanide poisoning because methemoglobin regenerates cytochrome oxidase

44
Q

beneficial effectso of nitrate therapy

A
  1. pronouced dilation of large veins - reduced preload, O2 demand, cardiac work
  2. redistribution of regional coronary artery blood flow - from normal to ischemic areas due to perferential dilation of large epicardial arteries
  3. mild arteriolar dilation to reduce afterload and O2 demand in heart
45
Q

harmful nitrate effects and their results

A

reflex increases in HR and contractility - increased myocardial O2 demand

Reflex tachycardia - reduced perfusion due to shorter diastole

46
Q

what can you combine NO with to prevent reflex tachycardia

A

CCB

47
Q

where is NO metabolized

A

liver

48
Q

why are inhaled or sublingual nitrates quicker

A

they bypass liver and dissolve right into blood stream

49
Q

routs of administration of NO for acute treatment

A

inhalation

sublingual

50
Q

routes of administratin of NO for chronic treatment

A

oral

transdermal

51
Q

prefered ROA for nitroglycerin and isosorbide dinitrate

A

sublingual

52
Q

what does sodium notroprusside do

A

dilates arteries and veins equally

53
Q

can you use sublingual NO for chronic therapy

A

no

54
Q

how do you minimize tolerance of NO

A

chronic treatmen use this is common

lowest effective dose with nitrate free intervas 10-12 hrs daily

55
Q

acute toxicity of nitrates

A

strong vasodilation

orthostatic hypotension

tachycardia

throbbing headache

56
Q

what is monday disease

A

people chronically exposed to nitrates at work would become less tolerant over the weekend and monday would all have headache

57
Q

what type of channel do CCBs block

A

L type channels in the myocardium and vascular smooth muscles

58
Q

how are calcium channels opened

A

stimulation of beta receptors

59
Q

what blood vessels are most sensetive to CCBs

A

arterioles more sensetive than veins

60
Q

what are dihydropyridines

A

nifedipine - binds 1A, tissue selectivity is vascular

61
Q

what does the chemical class benzothiazepine consist of and (CCB)

A

diltiazem 1B tissue selectivity in between

62
Q

what does the chemical class phenylalkylamine do

A

verapamin - 1C - myocardial tissue selectivity

63
Q

major effects of CCBs

A

Mainly cardiac effects

Decreased contractility,

Decreased SA node impulse generation

Decreased AV node conduction

64
Q

which CCB has the strongest cardiac effect

A

Verapamil

65
Q

which CCB is the strongest vasodilator

A

Nifedipine

66
Q

which CCB has reflex tachycardia

A

Nifedipine

67
Q

rank order nifedipine, diltiazem and verapamil in their effect on vasodilation (RT) and myocardial depression

A
68
Q

harmful effects of verapamil and diltiazem

A

serious cadiac depression could result in

cardiac arrest

AV block

CHF

69
Q

which drug class can affect insulin secretion

A

CCB

70
Q

what are CCB harmful effects other than mycardial depression and RT

A

inhibition of insulin secretion

interference with platelet aggregation

verapamil and diltiazem may reduce digoxin renal clearance

they should not be used in patients with ventricular dysfunction or SA/AV node disturbances

71
Q

what are beta blockers often used for treatment of angina

A

atenolol

metoprolol

propranolol

nadolol

72
Q

how do beta blockers work

A

decreasing sympathetic tone to decrease CO

73
Q

what are beta blockers especially useful for

A

angina associated with effort, reduce myocardial oxygen requirements at rest and during exercise

74
Q

do beta blockers or CCBs produce better outcomes and symptomatic treatment

A

beta blockers

75
Q

do beta blockers dilate coronary arteries

A

no

76
Q

what are beta blockers valuble to treat other than exercise induced angina

A

silent or ambulatory ischemia detected by ECG

77
Q

what drug class reduces amount of ischemic time per day

A

beta adrenergic blockade

78
Q

harmful effects of beta adrenergic blockade

A

may induce or worsen CHF whe sympathetic activity is critical to support cardiac performance

79
Q

why are beta blockers potentially harmful in variant angina

A

slowing HR and prolonging ejection time might increase O2 requirement

80
Q

what drug class may increase plasma TGs and decrease HDL cholesterol

A

beta blockers

81
Q

which drug class can predispose to diabetes

A

beta blockers

82
Q

first line therapy for angina pectoris

A

modify risk factors and add atiplatelet drugs

eg. aspirin/clopidogrel plus statins and weight loss

83
Q

effective antianginal therapy will

A

increase exercise tolerance

decrease frequency and duration of myocardial ischemia

84
Q

for variant or angioplastic angina what drugs are most effective

A

nitrates and CCBs

NOT beta blockers

85
Q

drugs for hypertensive pt

A

CCB or beta blocer

86
Q

normotensive pt drug choice

A

long actinge nitrate

87
Q

effective drug combos for angina pectoris

A

beta adrenergic blockers and CCBs

2 CCBs

88
Q

potentially harmful effects of CCBs or beta blockers can be prevented by

A

combined treatment with nitrates

89
Q

how can reflex tachycardia be minimized

A

combining nitrates with CCBs or Beta blockers