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SPR2015_Week3 > Ischemic Heart Disease 1 > Flashcards

Ischemic Heart Disease 1 Flashcards

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
Q

mechanism of CRP

A

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

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26
Q

What predicts risk of a first CV event in healthy subjects?

A

1) lipids

2) inflamm markers

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27
Q

what is pathophys of STABLE CAD

A

1) OBSTRUCTIVE coronary lesion decr flow

2) cause myocardial ischemia (imbalance btwn coronary O2 delivery + myocardial O2 demand)

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28
Q

what is the cardinal symptom of Myocardial ischemia

A

chest pain = angina pectoris

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29
Q

what is unique about coronary circulation?

A

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
Q

HOW DO you incr myocardial O2 supply?

A

incr blood flow rate ONLY

31
Q

what are determinants of myocardial O2 supply?

A

1) coronary blood flow rate

2) O2 content in blood

32
Q

what are measures of coronary blood flow rate?

A

1) Perfusion pressure
2) Perfusion time (1/heart rate)
3) Vascular resistance

33
Q

what is equation for O2 delivery (mmol/min)

A

Myocardial O2 delivery = coronary blood flow rate x O2 content of arterial blood

34
Q

what is role of perfusion pressure in normal coronary circulation

A

provides protection from mod change in perfusion pressure

35
Q

where does autoreg occur?

A

SMALL ARTERIOLES

36
Q

in coronary heart disease, what happens to perfusion pressure?

A

decr perfusion pressure across EPICARDIAL CORONARY STENOSES

37
Q

dilation of resistance vessels can compensate for ____

A

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
Q

_____ can compensate for pressure drop across stenosis (autoregul)

A

dilation of resistance vessels

39
Q

what are effects of epicardial coronary stensosi?

A

decr coronary flow –> myocardial ischemia

40
Q

what is diastolic perfusion time?

A

LV perfusion MAINLY (b/c compression of intramural coronary vessels during systole)

41
Q

what is effect of tachycardia on diastolic perfusion time

A

1) incr HR,
2) shorten diastole (fewer # of diastole periods when can perfuse vessels)
3) compromise coronary flow b/c less LV perfusion

42
Q

effect of vasomotor tone

A

1) vasospasm –> worsen coronary stenosis

2) vasodilate with Nitro –> treat angina and MI

43
Q

how do you determine oxygen content of arterial blood?

A

O2 delivery (mol/min) = coronary flow rate x arterial O2 content

44
Q

how can oxygen supply be compromised (2)

A

1) anemia = less Hb/mL blood

2) hypoxemia (incomplete saturation of Hb)

45
Q

treatment of chronic stable angina = incr O2 supply

perfusion pressure

A

prevent hypotension

46
Q

treatment of chronic stable angina = incr O2 supply

diastolic time

A

rate-slowing drugs (beta blockers)

47
Q

treatment of chronic stable angina = incr O2 supply

coronary resistance

A

vasodilator (nitrates/Ca2+ blockers)

coronary angioplasty + bypass surgery

48
Q

treatment of chronic stable angina = incr O2 supply

oxygen content

A

treat anemia + hypoxemia

49
Q

what are determinants of myocardial O2 demand

A

1) HR
2) wall tension
3) inotropic state (less energy efficiency)

50
Q

how does wall tension affect myocardial O2 demand

A

increase with incr wall tension and vessel size

determinants =

1) systolic blood pressure
2) cardiac chamber dimesnion

51
Q

Treatment of chronic stable angina: Reducing O2 demand

systolic pressure

A

antihypertensive drugs

52
Q

Treatment of chronic stable angina: Reducing O2 demand

HR

A

rate-slowing drugs (beta blocker, Ca2+ blockers)

53
Q

Treatment of chronic stable angina: Reducing O2 demand

wall tension

A

1) limit XS preload with diuretics + nitrates (decr LV cavity)

54
Q

Treatment of chronic stable angina: Reducing O2 demand

inotropic state (contractile stat)

A

negative inotropes (beta blockers, Ca2+ channel blockers)

55
Q

what is pathophys of unstable coronary syndrome

A

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
Q

effects of unstable coronary artery disease

define unstable angina

A

near-complete occlusion of vessel with thrombus

“threatened heart attack”

high risk of recurrence

57
Q

effects of unstable coronary artery disease

unstable angina

biomarkers

A

trop negative

58
Q

effects of unstable coronary artery disease

unstable angina

what happens if you treat successfully

A

no permanent myocardial damage

59
Q

a

A

a

60
Q

Unstable coronary disease:

Acute Myocardial Infarction

define

A

persistent + severe flow reduction

complete vessel occlusion

61
Q

Unstable coronary disease:

Acute Myocardial Infarction

biomarkers

A

trop elevated

62
Q

Unstable coronary disease:

Acute Myocardial Infarction

cardinal symptom

A

severe + persistent chest pain at rest

63
Q

Unstable coronary disease:

Acute Myocardial Infarction

what is key to treatment

A

EARLY REPERFUSION KEY BUT ALSO MAY CAUSE MORE INJURY

restore at 30-45 NOT AT 2 hrs

64
Q

Unstable coronary disease: Acute Myocardial Infarction

what is late mortality related to?

A

LV dysfunction

65
Q

consequences of acute coronary obstruction?

within minutes

A

1) diastolic dysfunction (Ca2+ re-uptake impairment)
2) incr LV filling pressure
3) pulm congestion + edema
4) decr ATP, decr pH (systolic dysfunction)

66
Q

consequences of acute coronary obstruction?

within minutes

do you have ecg signs?

A

YES

67
Q

consequences of acute coronary obstruction?

within minutes

SYMPTOMS

A

1) CHEST PAIN
2) DYSPNEA
3) ARRHYTHMIA

68
Q

consequences of acute coronary obstruction?

within hours

A

1) myocardial necrosis

2) infarction

69
Q

markers of vascular inflamm + mycoardial injury in unstable CAD?

A

1) elev CRP

2) cardiac markers (trop + creatine kinase)

70
Q

Types of CAD damage in smoking

A

1) more advanced disease at earlier age

2) more predisposed to spontaneous
thromboses in coronary vessels

71
Q

reverse cholesterol transport for HDL

A

HDL remove oxid proinflamm cholest from vessel wall and macrophages to liver for recycling

72
Q

how does inflammation contribute to plaque instability

A

1) inflamm cells secrete MMPs
2) degrade collagen/elastin in fibro cap
3) plaque instability

SPR2015_Week3 (13 decks)

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