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RC Test 3 > B4.050 - Treatment of Angina > Flashcards

B4.050 - Treatment of Angina Flashcards

(89 cards)

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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
what to beta adrenergic antagonists and some Ca entry blockers affect
affect heart rate and contractility
26
what do organic nitrates and calicum entry blockers affect
preload and afterload
27
what do vasodilators, statins, and anti-thrombolytics affect
coronary blood flow, regional myocardial blood flow
28
what are the primary sites of action of pharmacological agenst
reduce O2 demand or enhance O2 supply
29
what do CCBs do
decrease intracellular Ca Blocks calmodulin cascade that leads to contraction of vascular smooth muscle
30
what do beta 2 agonists do
increases cAMP increase cGMP which causes muscle relaxation
31
what does NO do
activator of soluble guanylyl cyclase leading to smooth muscle relaxation
32
what are the 4 drug classes used in angina
1. organic nitrates 2. CCBs 3. beta blockers 4. investigative ones
33
what is ranolazine
reduces intracellular calcium concentration and thus reduces cardiac contractility and work
34
what is allopurinol
inhibits xanthine oxidase which contributes to oxidative stress and endothelial dysfunction
35
which drug prolongs exercise time in patients with angina
allopurinol
36
wht is ivabradine
direct bradycardic agent inhibits hyperpolarization activated sodium channel in sinatrial node
37
what is fasudil
Rho-kinase inhibitor reduces coronary vasospasm in experimental animals
38
where do organin nitrates vasodilate
use enzymes found predominantly on venous side or vasculature, preferentially vasodilates veins
39
what is the one drug that vasodilates both veins and arteries and why
sodium nitroproside does not need enzymes
40
what are the short acting nitrates used for angina
Amyl nitrite - inhalant Nitroglycerin - sublingual Isosorbide dinitrate - sublingual
41
what are long acting nitrates used for angina
Nitroglycerin, oral sustained action Nitroglycerin - 2% ointment Nitroglycerin - slow release, buccal Nitroglycerin - slow release, transderma isosorbide dinitrate - oral isosorbide mononitrate - oral
42
what is sildenafil and why is it important
inhibitor of PDE-5 Can potentiate action of NO in angina --\> sever hypotension, MI
43
Nitrate ion reactis with what and can be used for what type of poisoning
hemoglobin --\> methemoglobin --\> can be used to treat cyanide poisoning because methemoglobin regenerates cytochrome oxidase
44
beneficial effectso of nitrate therapy
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
harmful nitrate effects and their results
reflex increases in HR and contractility - increased myocardial O2 demand Reflex tachycardia - reduced perfusion due to shorter diastole
46
what can you combine NO with to prevent reflex tachycardia
CCB
47
where is NO metabolized
liver
48
why are inhaled or sublingual nitrates quicker
they bypass liver and dissolve right into blood stream
49
routs of administration of NO for acute treatment
inhalation sublingual
50
routes of administratin of NO for chronic treatment
oral transdermal
51
prefered ROA for nitroglycerin and isosorbide dinitrate
sublingual
52
what does sodium notroprusside do
dilates arteries and veins equally
53
can you use sublingual NO for chronic therapy
no
54
how do you minimize tolerance of NO
chronic treatmen use this is common lowest effective dose with nitrate free intervas 10-12 hrs daily
55
acute toxicity of nitrates
strong vasodilation orthostatic hypotension tachycardia throbbing headache
56
what is monday disease
people chronically exposed to nitrates at work would become less tolerant over the weekend and monday would all have headache
57
what type of channel do CCBs block
L type channels in the myocardium and vascular smooth muscles
58
how are calcium channels opened
stimulation of beta receptors
59
what blood vessels are most sensetive to CCBs
arterioles more sensetive than veins
60
what are dihydropyridines
**nifedipine** - binds **1A**, tissue selectivity is **vascular**
61
what does the chemical class benzothiazepine consist of and (CCB)
diltiazem 1B tissue selectivity in between
62
what does the chemical class phenylalkylamine do
**verapamin** - **1C** - **myocardial tissue** selectivity
63
major effects of CCBs
Mainly cardiac effects Decreased contractility, Decreased SA node impulse generation Decreased AV node conduction
64
which CCB has the strongest cardiac effect
Verapamil
65
which CCB is the strongest vasodilator
Nifedipine
66
which CCB has reflex tachycardia
Nifedipine
67
rank order nifedipine, diltiazem and verapamil in their effect on vasodilation (RT) and myocardial depression
68
harmful effects of verapamil and diltiazem
serious cadiac depression could result in cardiac arrest AV block CHF
69
which drug class can affect insulin secretion
CCB
70
what are CCB harmful effects other than mycardial depression and RT
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
what are beta blockers often used for treatment of angina
atenolol metoprolol propranolol nadolol
72
how do beta blockers work
decreasing sympathetic tone to decrease CO
73
what are beta blockers especially useful for
angina associated with effort, reduce myocardial oxygen requirements at rest and during exercise
74
do beta blockers or CCBs produce better outcomes and symptomatic treatment
beta blockers
75
do beta blockers dilate coronary arteries
no
76
what are beta blockers valuble to treat other than exercise induced angina
silent or ambulatory ischemia detected by ECG
77
what drug class reduces amount of ischemic time per day
beta adrenergic blockade
78
harmful effects of beta adrenergic blockade
may induce or worsen CHF whe sympathetic activity is critical to support cardiac performance
79
why are beta blockers potentially harmful in variant angina
slowing HR and prolonging ejection time might increase O2 requirement
80
what drug class may increase plasma TGs and decrease HDL cholesterol
beta blockers
81
which drug class can predispose to diabetes
beta blockers
82
first line therapy for angina pectoris
modify risk factors and add atiplatelet drugs eg. aspirin/clopidogrel plus statins and weight loss
83
effective antianginal therapy will
increase exercise tolerance decrease frequency and duration of myocardial ischemia
84
for variant or angioplastic angina what drugs are most effective
nitrates and CCBs NOT beta blockers
85
drugs for hypertensive pt
CCB or beta blocer
86
normotensive pt drug choice
long actinge nitrate
87
effective drug combos for angina pectoris
beta adrenergic blockers and CCBs 2 CCBs
88
potentially harmful effects of CCBs or beta blockers can be prevented by
combined treatment with nitrates
89
how can reflex tachycardia be minimized
combining nitrates with CCBs or Beta blockers

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