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SPR2015_Week3 > Ischemic Heart Disease 1 > Flashcards

Ischemic Heart Disease 1 Flashcards

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1
Q

Progression of atherosclerosis

A

1) Normal
2) Fatty Streak
3) Fibrous plaque
4) Occlusive atherosclerotic plaque
5) Plaque rupture/fissure & thrombosis

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2
Q

what happens in progression from normal to fatty streak

A

1) endothelial injury
2) lipid deposition
3) macrophage + t-cell recruit

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3
Q

what happens in progression from fatty streak to fibrous plaque and becoming occlusive

A

1) activated macrophages (foam cells)
2) smooth muscle prolif –> fibrous cap
3) lipid accumulate in plaque core

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4
Q

what is the effect of occlusive atherosclerotic plauqe

A

effort angina claudication

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5
Q

do you have symptoms with fatty strekas

A

NO, they are SILENT

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6
Q

what happens in progression from occlusive atherosclerotic plaque to plaque rupture/fissure & thrombosis

A

1) plaque disruption
2) thrombus formation
3) vessel occlusion

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7
Q

what are the effects of plaque rupture/fissure + thrombosis

A

1) unstable angina
2) MI
3) stroke
4) critical leg ischemia

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8
Q

Risk factors for CAD

Treatable, with consequent reduced risk

A

1) smoking
2) HTN
3) dyslipidemia

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9
Q

Risk factors for CAD

Treatable but unclear if treatment decr risk

A

1) diabetes/insulin resistance
2) obesity
3) inflammation
4) psych stress
5) sedentary

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10
Q

Risk factors for CAD

Not treatable

A

1) male
2) age
3) genetics

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11
Q

Smoking confers ____ incr in CAD risk

A

50%

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12
Q

Mechanisms of smoking risk

A

– thrombus form, platelet activ, incr fibrinogen

– Aryl hydrocarbon promote atherosclerosis

– endothelial dysfunction and vasospasm

– CO decr myocardial O2 delivery

– Bad effect on lipoproteins (decr HDL)

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13
Q

HTN is a ____ risk

A

graded risk

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14
Q

Mechanism of HTN risk

A

1) incr shear stress on artery wall –> endothelial cell injury
2) incr arterial wall stress –> pathologic cell signaling –> oxidant stress
3) circulating hormones incr (angiotensin/aldosterone/NE) –> effect on artery wall
4) incr in heart work –> LVH

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15
Q

Diabetes and insulin resistance (metabolic syndrome)

Which has greater risk, diabetes or insulin resistance

A

equal but more people with insulin resistance

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16
Q

what are diabetes + insulin resistance assoc with?

A

1) inflammation
2) oxid stress
3) dyslipidemia

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17
Q

Dyslipidemia and risk of CHD

what is dyslipidemic triad?

A

1) high LDL
2) low HDL
3) high triglycerides

each indiv incr risk

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18
Q

Bad effects of LDL cholesterol

A

1) oxidized LDL –> inflamm + athero
2) damage vascular endo
3) deposit in artery wall and taken up in macro > become foam cells
4) activ inflamm cells –> lesions
5) activ platelets –> pro-thrombotic

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19
Q

Beneficial effect of HDL

A

1) inhib LDL oxid
2) inhib tissue factor
3) enhance reverse cholesterol transport
4) stim endo NO prod
5) inhib endo adhesion molec

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20
Q

___ and ___ are independent risk factors for CHD

A

LDL; HDL

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21
Q

Role of inflammation in CHD

A

initaition and progression of atheroslcerosis

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22
Q

what are effects of lipid-laden macrophages

A

pro-inflammatory

found in arterial wall plaque

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23
Q

what are extravascular infalmmation?

A

1) dental
2) respiratory (influenza)
3) immune diseases (RA, lupus)

incr risk of atherosclerosis

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24
Q

what are circulating markers of inflammation?

A

C-reactive proteins

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25
mechanism of CRP
1) inflamm cells in/out vessel wall (macs/ foams) 2) secrete low level of cytokines (IL-6) 3) taken up in liver 4) liver amplifies low level signal and secrete incr level of CRP
26
What predicts risk of a first CV event in healthy subjects?
1) lipids | 2) inflamm markers
27
what is pathophys of STABLE CAD
1) OBSTRUCTIVE coronary lesion decr flow | 2) cause myocardial ischemia (imbalance btwn coronary O2 delivery + myocardial O2 demand)
28
what is the cardinal symptom of Myocardial ischemia
chest pain = angina pectoris
29
what is unique about coronary circulation?
1) myocardium depends on AEROBIC METAB FOR ENERGY (unlike skeletal) 2) @ rest, near-max amt of O2 extracted from coronary arterial blood 3) LV perfused in DIASTOLE ONLY
30
HOW DO you incr myocardial O2 supply?
incr blood flow rate ONLY
31
what are determinants of myocardial O2 supply?
1) coronary blood flow rate | 2) O2 content in blood
32
what are measures of coronary blood flow rate?
1) Perfusion pressure 2) Perfusion time (1/heart rate) 3) Vascular resistance
33
what is equation for O2 delivery (mmol/min)
Myocardial O2 delivery = coronary blood flow rate x O2 content of arterial blood
34
what is role of perfusion pressure in normal coronary circulation
provides protection from mod change in perfusion pressure
35
where does autoreg occur?
SMALL ARTERIOLES
36
in coronary heart disease, what happens to perfusion pressure?
decr perfusion pressure across EPICARDIAL CORONARY STENOSES
37
dilation of resistance vessels can compensate for ____
pressure drop across stenosis (autoregul) IF pressure gradient too great (due to severe stenosis and/or high flow with exercise ) autoregulation may be exhausted
38
_____ can compensate for pressure drop across stenosis (autoregul)
dilation of resistance vessels
39
what are effects of epicardial coronary stensosi?
decr coronary flow --> myocardial ischemia
40
what is diastolic perfusion time?
LV perfusion MAINLY (b/c compression of intramural coronary vessels during systole)
41
what is effect of tachycardia on diastolic perfusion time
1) incr HR, 2) shorten diastole (fewer # of diastole periods when can perfuse vessels) 3) compromise coronary flow b/c less LV perfusion
42
effect of vasomotor tone
1) vasospasm --> worsen coronary stenosis | 2) vasodilate with Nitro --> treat angina and MI
43
how do you determine oxygen content of arterial blood?
O2 delivery (mol/min) = coronary flow rate x arterial O2 content
44
how can oxygen supply be compromised (2)
1) anemia = less Hb/mL blood | 2) hypoxemia (incomplete saturation of Hb)
45
treatment of chronic stable angina = incr O2 supply perfusion pressure
prevent hypotension
46
treatment of chronic stable angina = incr O2 supply diastolic time
rate-slowing drugs (beta blockers)
47
treatment of chronic stable angina = incr O2 supply coronary resistance
vasodilator (nitrates/Ca2+ blockers) coronary angioplasty + bypass surgery
48
treatment of chronic stable angina = incr O2 supply oxygen content
treat anemia + hypoxemia
49
what are determinants of myocardial O2 demand
1) HR 2) wall tension 3) inotropic state (less energy efficiency)
50
how does wall tension affect myocardial O2 demand
increase with incr wall tension and vessel size determinants = 1) systolic blood pressure 2) cardiac chamber dimesnion
51
Treatment of chronic stable angina: Reducing O2 demand systolic pressure
antihypertensive drugs
52
Treatment of chronic stable angina: Reducing O2 demand HR
rate-slowing drugs (beta blocker, Ca2+ blockers)
53
Treatment of chronic stable angina: Reducing O2 demand wall tension
1) limit XS preload with diuretics + nitrates (decr LV cavity)
54
Treatment of chronic stable angina: Reducing O2 demand inotropic state (contractile stat)
negative inotropes (beta blockers, Ca2+ channel blockers)
55
what is pathophys of unstable coronary syndrome
1) inflamm artery wall 2) weaken fibromuscular cap 3) ABRUPT plaque fissure 4) thrombogenic component (lipid + tissue factor) expose to blood 5) partial/complete thrombosis 6) mycoardial injury + necrosis 7) cardiac dysfunction- death
56
effects of unstable coronary artery disease define unstable angina
near-complete occlusion of vessel with thrombus "threatened heart attack" high risk of recurrence
57
effects of unstable coronary artery disease unstable angina biomarkers
trop negative
58
effects of unstable coronary artery disease unstable angina what happens if you treat successfully
no permanent myocardial damage
59
a
a
60
Unstable coronary disease: Acute Myocardial Infarction define
persistent + severe flow reduction complete vessel occlusion
61
Unstable coronary disease: Acute Myocardial Infarction biomarkers
trop elevated
62
Unstable coronary disease: Acute Myocardial Infarction cardinal symptom
severe + persistent chest pain at rest
63
Unstable coronary disease: Acute Myocardial Infarction what is key to treatment
EARLY REPERFUSION KEY BUT ALSO MAY CAUSE MORE INJURY restore at 30-45 NOT AT 2 hrs
64
Unstable coronary disease: Acute Myocardial Infarction what is late mortality related to?
LV dysfunction
65
consequences of acute coronary obstruction? within minutes
1) diastolic dysfunction (Ca2+ re-uptake impairment) 2) incr LV filling pressure 3) pulm congestion + edema 4) decr ATP, decr pH (systolic dysfunction)
66
consequences of acute coronary obstruction? within minutes do you have ecg signs?
YES
67
consequences of acute coronary obstruction? within minutes SYMPTOMS
1) CHEST PAIN 2) DYSPNEA 3) ARRHYTHMIA
68
consequences of acute coronary obstruction? within hours
1) myocardial necrosis | 2) infarction
69
markers of vascular inflamm + mycoardial injury in unstable CAD?
1) elev CRP | 2) cardiac markers (trop + creatine kinase)
70
Types of CAD damage in smoking
1) more advanced disease at earlier age 2) more predisposed to spontaneous thromboses in coronary vessels
71
reverse cholesterol transport for HDL
HDL remove oxid proinflamm cholest from vessel wall and macrophages to liver for recycling
72
how does inflammation contribute to plaque instability
1) inflamm cells secrete MMPs 2) degrade collagen/elastin in fibro cap 3) plaque instability

SPR2015_Week3 (13 decks)

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