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Cardio Exam 2 > Atherosclerosis - Quiz 3 > Flashcards

Atherosclerosis - Quiz 3 Flashcards

1
Q

atherosclerosis accumulation of

within

A
  • progressive accumulation of smooth muscle cells
  • lipids
  • connective tissue
  • within intima
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2
Q

progressive accumulation of smooth muscle cells, lipids, and connective tissue within intima results in

A
  • intimal thickening with atheroma formation
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3
Q

another name for atheroma

A
  • fibrofatty plaque
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4
Q

what can cause ischemia

A
  • narrowing of vessel lumen
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5
Q

atherosclerosis affect on tunica intima

A
  • weakening of tunica intima
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6
Q

what accounts for >50% annual mortality in the US

A
  • major complication of atherosclerosis
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7
Q

what is the leading cause of death in the US

A
  • ischemic heart disease
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8
Q

layers of normal vascular anatomy impacted by atherosclerosis

A
  • intima

- media

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9
Q

constituents of normal vascular anatomy impacted by atherosclerosis

A
  • endothelial cells
  • smooth muscle cells
  • extracellular matrix
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10
Q

extracellular matrix composed of

A
  • elastin
  • collagen
  • glycosoaminoglycans
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11
Q

atherosclerosis affects which artery types

A
  • large (elastic)

- medium (muscular)

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12
Q

examples of large elastic arteries

A
  • aorta

- pulmonary

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13
Q

examples of medium muscular arteries

A
  • coronary

- renal

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14
Q

atherosclerosis is centered in

A
  • vascular wall
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15
Q

atherosclerosis is triggered by

A
  • altered lipid metabolism
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16
Q

atherosclerosis is mediated by

A
  • endothelial dysfunction
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17
Q

contribution factors to the pathogenesis of atherosclerosis

A
  • chronic endothelial injury
  • accumulation of lipoproteins
  • oxidation of accumulated lipoproteins
  • recruitment of inflammatory cells
  • generation and release of growth factors
  • proliferation and migration of cells
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18
Q

chronic endothelial injury due to

A
  • endothelial dysfunction
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19
Q

which lipoproteins are accumulated

A
  • LDL
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20
Q

which inflammatory cells are recruited?

A
  • monocytes/macrophages

- lymphocytes

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21
Q

recruitment of inflammatory cells leads to

A
  • foam cell formation

- fatty streaks

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22
Q

which cells undergo proliferation and migration

A
  • smooth muscle cells

- fibroblasts

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23
Q

result of proliferation and migration of smooth muscle cels and fibroblasts

A
  • fibrous plaque and complex atheroma formation
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24
Q

chronic endothelial injury due to these conditions

A
  • hyperlipidemia
  • hypertension
  • smoking
  • homocysteine
  • hemodynamic factors
  • toxins
  • viruses
  • immune reactions
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25
Q

endothelial cell function

A
  • decreased permeability
  • anticoagulant/antithrombotic
  • vasodilators
  • growth inhibitors

D VAG

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26
Q

endothelial cell dysfunction

A
  • increased permeability
  • procoagulant/prothrombotic
  • vasoconstrictors
  • inflammation
  • growth promoters

VIPIG

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27
Q

endothelial dysfunction causes increased permeability for

A
  • leukocytes/monocyte adhesion and emigration
  • platelet adhesion
  • lipid deposition
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28
Q

LDL modifications

A
  • lipid oxidation
  • ApoB fragmentation
  • glycation
  • immune complexes

these ENHANCE LDL accumulation in macrophages and peripheral tissues

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29
Q

importance of LDL modifications

A
  • increase affinity for scavenger receptors on macrophages

- make LDL stay in periphery instead of go back to the liver

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30
Q

effects of LDL modifications

A
  • increased adhesion molecule expression
  • expression of chemokine, Ck receptors
  • amplification of platelet activation
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31
Q

release of factors from activated platelets, macrophages, or vascular cells leads to

A
  • smooth muscle emigration from media to intima

- macrophage activation

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32
Q

intimal/medial thickening: response to vascular injury

A
  • proliferative factors

- neointima formation

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33
Q

neointima formation involves in a change in

A
  • smooth muscle cell phenotype

- fibroblast proliferation and collagen production

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34
Q

changes in smooth muscle cell phenotype

A
  • lose contractility
  • gain proliferative and migratory capacity
  • gain the ability to synthesize extracellular matrix
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35
Q

once macrophages have been activated

A
  • macrophages and smooth muscle cells engulf lipid
  • inflammation

HOW TF DO SMOOTH MUSCLE CELLS ENGULF THINGS.

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36
Q

cytokine balance in atherogenesis

A
  • tip toward pro inflammatory cytokines
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37
Q

after macrophages and smooth muscle cells engulf lipid and inflammation occurs

A
  • smooth muscle proliferation
  • collagen and other ECM deposition
  • extracellular lipid
  • form the fibrofatty atheroma
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38
Q

classic atheroma

A
  • raised focal intimal plaque with necrotic lipid core covered by fibrous cap
39
Q

constituents of classic atheroma

A
  • cells
  • connective tissue extracellular matrix
  • lipid
40
Q

cells - constituents of classic atheroma

A
  • smooth muscle cells
  • macrophages
  • leukocytes
41
Q

connective tissue extracellular matrix - constituents of classic atheroma

A
  • collagen
  • elastic fibers
  • proteoglycans
42
Q

lipid - constituents of classic atheroma

A
  • cholesterol and cholesterol esters

- intracellular and extracellular

43
Q

center of larger plaques may contain

A
  • yellow grumous debris

- atheroma

44
Q

fibrous cap composed of

A
  • smooth muscle cells
  • macrophages
  • foam cells
  • lymphocytes
  • collagen
  • elastin
  • proteoglycans
  • neovascularization
45
Q

necrotic center composed of

A
  • cell debris
  • cholesterol crystals
  • foam cells
  • calcium
46
Q

progression of atherosclerosis

A
  • normal artery
  • fatty streak
  • fibrofatty plaque
  • advanced vulnerable plaque
47
Q

clinical phase progression of atherosclerosis

A
  • aneurysm and rupture
  • occlusion by thrombus
  • critical stenosis
48
Q

aneurysm and rupture can happen by

A
  • mural thrombosis
  • embolization
  • wall weakening
49
Q

occlusion by thrombus can happen by

A
  • plaque rupture/erosion/hemorrhage
  • mural thrombosis
  • embolization
50
Q

critical stenosis can happen by

A
  • progressive plaque growth
51
Q

what kind of lesion is the fatty streak

A
  • early lesion
52
Q

fatty streak possible precursor of

A
  • arthroma
53
Q

is the fatty streak raised?

A
  • not significantly
54
Q

fatty streak disturbance of blood flow

A
  • no disturbance of blood flow
55
Q

fatty streak composed of

A
  • lipid-filled foam cells
  • with t lymphocytes
  • and extracellular lipid within intima
56
Q

aortic fatty streaks seen in most western country children by what age?

A
  • 10
57
Q

what stage lesion is the fibrofatty plaque

A
  • intermediate
58
Q

fibrofatty plaque raised

A
  • focal raised lesions causing disturbance of blood flow
59
Q

fibrofatty plaque composed of

A
  • fibrous cap

- lipid core

60
Q

what stage of lesion is the complicated lesion

A
  • advanced
61
Q

calcification of complicated lesions

A
  • patchy or massive calcification
62
Q

results of complicated lesion

A
  • focal rupture or ulceration of luminal surface
  • intra-plaque hemorrhage
  • superimposed thrombosis
  • weakening of tunica intima
63
Q

focal rupture or ulceration of luminal surface can cause

A
  • exposure of thrombogenic constituents

- atheroembolization

64
Q

intra-plaque hemorrhage may induce

A
  • plaque rupture
65
Q

what may cause weakening of tunica media

A
  • thinning of tunica media

- loss of elastic tissue with aneurysmal dilation

66
Q

process of fatty streak development

A
  • endothelial dysfunction
  • lipoprotein entry and modification
  • leukocyte recruitment
  • foam cell formation
67
Q

endothelial dysfunction

A
  • secondary to shear stress

- increased LDL concentration

68
Q

lipoprotein entry and modification

A
  • intimal accumulation of LDL proteins

- oxidation and glycation of lipoproteins

69
Q

leukocyte recruitment

A
  • endothelial cells and smooth muscle cells induce expression of adhesion molecules and release chemoattractants
  • increase monocytes
  • increase T cell recruitment
70
Q

foam cell formation

A
  • monocytes engulf oxidized LDL and become foam cells
71
Q

plaque progression process

A
  • intima continues to thicken
  • evolution of the fatty streak and calcification
  • fibrous capsule
  • luminal narrowing
72
Q

intima continues to thicken due to

A
  • smooth muscle cell proliferation

- increased leukocyte recruitment

73
Q

fibrous capsule due to

A
  • smooth muscle cell apoptosis

- lipid rich core surrounded by fibrous capsule

74
Q

luminal narrowing

A
  • plaque growth into lumen causes flow limitation
75
Q

result of luminal narrowing

A
  • claudication

- angina

76
Q

claudication will occur if flow limitation is in

A
  • peripheral vessels
77
Q

angina will occur if flow limitation is in

A
  • coronary circulation
78
Q

which fibrous capsules are more stable

A
  • thicker

- cause more narrowing through

79
Q

which types of lesions are reversible

A
  • those leading to fatty streak development
80
Q

complications of atherosclerosis

A
  • ischemia (due to luminal stenosis)
  • acute infarcts (due to acute thombosis, atheroembolization or thromboembolism)
  • artery remodeling (leads to aneurysm formation and/or rupture)
81
Q

complications of atherosclerosis - ischemia due to

A
  • luminal stenosis
82
Q

complications of atherosclerosis - acute infarcts due to

A
  • acute thrombosis secondary to plaque rupture or intra-plaque hemorrhage
  • embolization of plaque fragments or thrombus
83
Q

major complications of atherosclerosis

A
  • MI
  • sudden cardiac death
  • chronic ischemic heart disease
  • aortic aneurysms
  • cerebral infarction
  • ischemic encephalopathy
  • PVD
  • mesenteric occlusion
84
Q

arterial distribution of atherosclerosis from highest to lowest incidence

A
  • abdominal aorta
  • coronary arteries
  • popliteal arteries
  • descending thoracic aorta
  • internal carotids
  • circle of willis
85
Q

modifiable risk factors for atherosclerosis

A
  • smoking
  • hypertension
  • dyslipidemia
  • diabetes
  • sedendary lifestyle
86
Q

non-modifiable risk factors for atherosclerosis

A
  • age
  • sex
  • family history/genetics
87
Q

what hormone is protective against atherosclerosis

A
  • estrogen
88
Q

Characteristics of Unstable Plaque/Plaque Rupture

A
  • Thin fibrous cap
  • Intense Inflammation
  • High Oxidative Burden
  • Abundant Macrophages
  • Large Lipid Core
  • Increased MMPs/TF
89
Q

Characteristics of a Stable Plaque (not likely to rupture)

A
  • Thick Fibrous Cap
  • Mild Inflammation
  • Mild Oxidative Burden
  • Low Macrophage Content
  • Small Lipid core
90
Q

Progression of (Coronary) Atherosclerosis

From Pre-Clinical Phase to Clinical Phase

A

Pre-Clinical Phase:
-Normal artery > Fatty Streak > Fibrofatty Plaque > Advanced Plaque

Clinical Phase:

  • Aneurysm and Rupture
  • Occlusion by Thrombus
  • Critical Stenosis
91
Q

Vulnerable plaques are prone to

A

erosion or rupture, and therefore thrombus formation

92
Q

The presence of a Fibrous Cap and Lipid Core occurs in

A

Fibrofatty Plaque (after fatty streak)

93
Q

What do you see in a Fatty Streak

A

Lipid-filled foam cells with T lymphocytes and extracellular lipid within intima

94
Q

Endothelial Cell Properties/Functions (7)

A
  1. Maintenance of Permeability Barrier
  2. Modulate Coagulation (Anticoag/Antithrombotic/Fibrinolytic v. Prothrombotic)
  3. ECM Production (collagen, proteoglycans)
  4. Modulate Blood Flow and Vascular Reactivity
  5. Regulate Inflammation/Immunity
  6. Regulate Cell Growth
  7. Oxidation of LDL

Cardio Exam 2 (29 decks)

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