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

B4.050 Treatment of Angina Flashcards

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1
Q

etiology of CAD

A

mainly due to obstruction of coronaries by atheromatous plaques

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2
Q

leading cause of death in US

A

heart disease
both women and men
CAD is principle type of heart disease

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3
Q

three major risk factors of CAD

A

high BP
high LDL cholesterol
smoking
49% of americans have one of the three at least

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4
Q

other risk factors of CAD

A 
diabetes
overweight/ obesity
poor diet
physical inactivity
excessive alcohol use
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5
Q

what is angina pectoris

A

primary symptom of heart disease, refers to chest pain resulting from myocardial ischemia

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6
Q

characterize angina pectoris

A

chest pain when amount of blood delivered to heart by coronary arteries cannot supply enough O2 to satisfy myocardial requirement
oxygen need exceeds oxygen supply

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7
Q

for immediate relief of angina

A

organic nitrates (nitroglycerin)

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8
Q

for prophylaxis for angina

A

CCBs and B blockers

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9
Q

describe pain associated with angina

A

severe chest pain described as: strangling, constricting, suffocating, crushing, heavy, or squeezing
chest discomfort may be vague (esp in women) and accompanied by numbing, nausea, sweating, SOB
usually retrosternal; often radiating down left arm though may involve both arms
typically relieved within minutes by rest or w nitro

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10
Q

2 types of angina

A

classic/ atherosclerotic

variant/ angiospastic / prinzmetals

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11
Q

etiology of classic angina

A

atheromatous obstruction of large coronaries

especially present w exercise

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12
Q

treatment of classic angina

A

if uncontrolled by drugs, may require coronary bypass or angioplasty

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13
Q

etiology of variant angina

A

spasm or constriction of in atherosclerotic coronary vessels

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14
Q

treatment of variant angina

A

relieved by nitrates or CCBs

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15
Q

what determines oxygen demand of myocardium

A

cardiac workload:

  1. contractility (major determinant)
  2. HR
  3. wall stress (IV pressure, ventricular volume, wall thickness)
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16
Q

what drugs help with myocardial ischemia?

A

drugs that reduce cardiac size, rate, or force and therefore reduce cardiac oxygen demand
CCBs, B-blockers

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17
Q

what is the main energy source in the heart and why is it significant

A

fatty acid oxidation

required more oxygen than glycolysis

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18
Q

mechanism of trimetazidine

A

shift myocardial metabolism towards greater use of glucose
has potential to reduce O2 demand without affecting hemodynamics
called pFOX inhibitors: partially inhibit fatty acid oxidation

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19
Q

what determines O2 supply

A

O2 delivery

extraction (better when blood speed is slower moving through vessels)

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20
Q

how might additional O2 be supplied to the myocardium

A

ONLY by increasing O2 delivery through coronary blood flow

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21
Q

what are the determinants of O2 delivery through coronary blood flow

A

directly related to perfusion pressure and duration of diastole
inversely proportional to coronary vascular resistance, determined by: metabolic products, autonomic activity, various drugs
damage to endothelium of coronary vessels increases vascular resistance

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22
Q

what are some mechanical interventions that can increase O2 supply

A

stent
angioplasty
coronary bypass surgery

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23
Q

how do CCBs impact vascular tone

A

decrease intracellular Ca2+

Ca2+ needed in pathway to myosin/actin contraction

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24
Q

why does increasing cAMP relax vascular smooth muscle

A

cAMP phosphorylates MLCK which prevents it from phosphorylating myosin light chains allowing them to contract

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25
what drugs increase cAMP
B2 agonists | not used in angina
26
what is the mechanism of action of nicorandil
K+ channel opener | prevents depolarization
27
how does increasing cGMP relax vascular smooth muscle?
cGMP dephosphorylates myosin light chains preventing them from relaxing
28
how does NO work to relax muscle?
activator of soluble guanylyl cyclase | guanylyl cyclase is involved in converting GTP to cGMP
29
how does sildenafil work
inhibits PDE5, which normally breaks down cGMP | if you inhibit the breakdown, you have more free cGMP, thus more relaxation
30
how do organic nitrates, CCBs, and B blockers decrease myocardial O2 demand?
decrease - HR - ventricular volume - BP - contractility
31
what is 4th drug group used in angina?
recently approved | ranolazine
32
mechanism of action of ranolazine
reduces intracellular calcium concentration and thus reduces contractility and work
33
mechanism of action of allopurinol
inhibits xanthine oxidase (which contributes to oxidative stress and endothelial dysfunction) high doses prolong exercise time in patients w angina
34
direct bradycardic agent
ivabradine
35
mechanism of action of ivabradine
inhibit hyperpolarization activated sodium channel in the SA node
36
rho-kinase inhibitor
fasudil
37
mechanism of action of fasudil
reduce coronary vasospasm in experimental animals
38
where do nitrates primarily work and why
venous side | this is where enzymes are primarily found
39
why does sodium nitroprusside act on both veins and arteries
doesn't require enzymes to work
40
what can endogenously release NO
endothelial cells
41
what is the mechanism of action of NO
activate guanylyl cyclase GC can then convert GTP to cGMP CGMP dephosphorylates myosin light chains relaxation
42
2 types of nitrates
short acting 3-60 min | long acting 2-10 hours
43
routes of administration of short acting nitrates
inhalant | sublingual
44
routes of administration of long acting nitrates
``` oral ointment buccal transdermal chewable ```
45
4 primary nitrates
``` amyl nitrite (short only) nitroglycerin (short or long) isosorbide dinitrate (short or long) isosobide mononitrate (long only) ```
46
other effects of NO
erection via relaxation of corpora cavernosa increased cGMP in platelets decreases aggregation nitrite ion reaction with hemoglobin can cause methemoglobinemia
47
3 primary mechanisms by which nitrate therapy is beneficial
1. pronounced dilation of large veins to reduce preload, myocardial O2 demand, and cardiac work 2. redistribution of regional coronary blood flow from normal to ischemic areas due to preferential dilation of large epicardial arteries 3. mild arteriolar dilation to reduce afterload and myocardial O2 demand
48
harmful effects of nitrates
reflex tachycardia and contractility - increased myocardial O2 demand - reduced perfusion due to shortened diastole
49
how to prevent harmful effects of nitrates
add B-blocker of CCB to nitrate administration
50
issue with oral nitrates
rapidly metabolized by hepatic reductase | fast acting drugs bypass the liver
51
fastest acting nitrate preparations
inhaled amyl nitrite | IV sodium nitroprusside
52
sublingual nitroglycerin pharmacokinetics
``` used for immediate angina relief rapid action (onset 1-3 min), short (duration 10-30 min), but not suitable for maintenance or chronic therapy ```
53
how do you minimize tolerance from nitrates?
during chronic treatment use lowest effective dose with nitrate free intervals of 10-12 hrs daily
54
acute nitrate toxicity
strong vasodilation resulting in orthostatic hypotension, tachycardia, and throbbing headaches
55
"Monday disease"
manufacturers that are chronically exposed to high nitrate levels become tolerant after a weekend away from nitrates, get headache and dizziness on Mondays bc tolerance diminishes
56
2 important cardio actions of intracellular calcium
triggers contraction in myocardium and vascular smooth muscle required for pacemaker activity of SA node and for conduction through AV node
57
how are Ca2+ channels regulated in heart and vascular smooth muscle
opened by stimulation of B receptors to enhance calcium entry closed by CCBs to inhibit calcium entry
58
which muscles are most sensitive to CCBs
vascular smooth muscles, bronchiolar, GI, and uterine | arterioles more sensitive than veins
59
how is CCB tissue selectivity established
L-type Ca channel has 3 different binding sites (1A, 1B, 1C) 1A = vascular 1B = combo 1C = myocardial
60
what happens on the molecular level with a CCB binds to a calcium channel?
pores close on calcium channel | decrease of transmembrane Ca currents
61
major cardiac effects of CCBs
decreased contractility decreased SA node impulse generation decreased AV node conduction
62
discuss differences in tissue selectivity and how they impact HR
nifedipine (dihydropyridines) strongest vasodilator, verapamil strongest cardiac effects, diltiazem in between HR increased by nifedipine bc of reflex tachy after vasodilation, HR decreased by verapamil due to SA and AV depression
63
beneficial effects of dihydropyridines
coronary vasodilation > increased myocardial O2 supply | vasodilation of systemic arteries > decreased afterload
64
harmful effect of dihydropyridines
increased risk of MI pronounced hypotension > reflex tachy > increased cardiac workload short acting CCB should be avoided in patients with HTN
65
beneficial effects of verapamil/diltiazem
reduced SA automaticity and AV conduction | decreased myocardial contractility and bradycardia > reduced cardiac workload
66
harmful effect of verapamil and diltiazem
the potential for serious cardiac depression that could result in -cardiac arrest -AV block -CHF don't use in pts with ventricular dysfunction of SA-AV node disturbances
67
other CCB effects
inhibition of insulin secretion interference with platelet aggregation flushing, edema, dizziness, nausea, constipation
68
how do verapamil and diltiazem enhance digoxin toxicity
reduce digoxin renal clearance to increase plasma digoxin
69
B blockers used in angina
atenolol metoprolol sometimes propranolol, nadolol
70
when are B blockers especially useful
management of angina associated with effort | reduce myocardial O2 requirements at rest and during exercise
71
which is better for angina, B blockers or CCBs?
B blockers produce better outcomes and symptomatic treatment
72
what have B blockers been shown to do in patents with heart disease
reduce mortality in patients with MI | improve survival and prevent stroke in hypertensive pts
73
beneficial effects of B blockers in angina
decreased sympathetic activity > decreased contractility, HR, and vasoconstriction > decreased cardiac workload > decreased O2 demand direct vasodilation by some B blockers bradycardia prolongs diastole and increases perfusion time
74
harmful effect of B blockers
may induce or worsen CHF whenever sympathetic activity is critical to support cardiac performance
75
goals of effective antianginal therapy
increase exercise tolerance | decrease frequency and duration or myocardial ischemia
76
which drugs are more effective for variant angina
nitrates and CCBs | B-blockers do not dilate spastic coronary blood vessels
77
angina therapy for hypertensive patient
monotherapy w slow release CCB or B blocker
78
angina therapy for normotensive patient
long acting nitrates
79
most effective drug combos
``` B blocker + CCB 2 CCBs (vera and nife) ```
80
how can harmful effects of CCBs or B blockers be avoided?
combined treatment w nitrates

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