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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
endothelial cell function
- decreased permeability - anticoagulant/antithrombotic - vasodilators - growth inhibitors D VAG
26
endothelial cell dysfunction
- increased permeability - procoagulant/prothrombotic - vasoconstrictors - inflammation - growth promoters VIPIG
27
endothelial dysfunction causes increased permeability for
- leukocytes/monocyte adhesion and emigration - platelet adhesion - lipid deposition
28
LDL modifications
- lipid oxidation - ApoB fragmentation - glycation - immune complexes these ENHANCE LDL accumulation in macrophages and peripheral tissues
29
importance of LDL modifications
- increase affinity for scavenger receptors on macrophages | - make LDL stay in periphery instead of go back to the liver
30
effects of LDL modifications
- increased adhesion molecule expression - expression of chemokine, Ck receptors - amplification of platelet activation
31
release of factors from activated platelets, macrophages, or vascular cells leads to
- smooth muscle emigration from media to intima | - macrophage activation
32
intimal/medial thickening: response to vascular injury
- proliferative factors | - neointima formation
33
neointima formation involves in a change in
- smooth muscle cell phenotype | - fibroblast proliferation and collagen production
34
changes in smooth muscle cell phenotype
- lose contractility - gain proliferative and migratory capacity - gain the ability to synthesize extracellular matrix
35
once macrophages have been activated
- macrophages and smooth muscle cells engulf lipid - inflammation HOW TF DO SMOOTH MUSCLE CELLS ENGULF THINGS.
36
cytokine balance in atherogenesis
- tip toward pro inflammatory cytokines
37
after macrophages and smooth muscle cells engulf lipid and inflammation occurs
- smooth muscle proliferation - collagen and other ECM deposition - extracellular lipid - form the fibrofatty atheroma
38
classic atheroma
- raised focal intimal plaque with necrotic lipid core covered by fibrous cap
39
constituents of classic atheroma
- cells - connective tissue extracellular matrix - lipid
40
cells - constituents of classic atheroma
- smooth muscle cells - macrophages - leukocytes
41
connective tissue extracellular matrix - constituents of classic atheroma
- collagen - elastic fibers - proteoglycans
42
lipid - constituents of classic atheroma
- cholesterol and cholesterol esters | - intracellular and extracellular
43
center of larger plaques may contain
- yellow grumous debris | - atheroma
44
fibrous cap composed of
- smooth muscle cells - macrophages - foam cells - lymphocytes - collagen - elastin - proteoglycans - neovascularization
45
necrotic center composed of
- cell debris - cholesterol crystals - foam cells - calcium
46
progression of atherosclerosis
- normal artery - fatty streak - fibrofatty plaque - advanced vulnerable plaque
47
clinical phase progression of atherosclerosis
- aneurysm and rupture - occlusion by thrombus - critical stenosis
48
aneurysm and rupture can happen by
- mural thrombosis - embolization - wall weakening
49
occlusion by thrombus can happen by
- plaque rupture/erosion/hemorrhage - mural thrombosis - embolization
50
critical stenosis can happen by
- progressive plaque growth
51
what kind of lesion is the fatty streak
- early lesion
52
fatty streak possible precursor of
- arthroma
53
is the fatty streak raised?
- not significantly
54
fatty streak disturbance of blood flow
- no disturbance of blood flow
55
fatty streak composed of
- lipid-filled foam cells - with t lymphocytes - and extracellular lipid within intima
56
aortic fatty streaks seen in most western country children by what age?
- 10
57
what stage lesion is the fibrofatty plaque
- intermediate
58
fibrofatty plaque raised
- focal raised lesions causing disturbance of blood flow
59
fibrofatty plaque composed of
- fibrous cap | - lipid core
60
what stage of lesion is the complicated lesion
- advanced
61
calcification of complicated lesions
- patchy or massive calcification
62
results of complicated lesion
- focal rupture or ulceration of luminal surface - intra-plaque hemorrhage - superimposed thrombosis - weakening of tunica intima
63
focal rupture or ulceration of luminal surface can cause
- exposure of thrombogenic constituents | - atheroembolization
64
intra-plaque hemorrhage may induce
- plaque rupture
65
what may cause weakening of tunica media
- thinning of tunica media | - loss of elastic tissue with aneurysmal dilation
66
process of fatty streak development
- endothelial dysfunction - lipoprotein entry and modification - leukocyte recruitment - foam cell formation
67
endothelial dysfunction
- secondary to shear stress | - increased LDL concentration
68
lipoprotein entry and modification
- intimal accumulation of LDL proteins | - oxidation and glycation of lipoproteins
69
leukocyte recruitment
- endothelial cells and smooth muscle cells induce expression of adhesion molecules and release chemoattractants - increase monocytes - increase T cell recruitment
70
foam cell formation
- monocytes engulf oxidized LDL and become foam cells
71
plaque progression process
- intima continues to thicken - evolution of the fatty streak and calcification - fibrous capsule - luminal narrowing
72
intima continues to thicken due to
- smooth muscle cell proliferation | - increased leukocyte recruitment
73
fibrous capsule due to
- smooth muscle cell apoptosis | - lipid rich core surrounded by fibrous capsule
74
luminal narrowing
- plaque growth into lumen causes flow limitation
75
result of luminal narrowing
- claudication | - angina
76
claudication will occur if flow limitation is in
- peripheral vessels
77
angina will occur if flow limitation is in
- coronary circulation
78
which fibrous capsules are more stable
- thicker | - cause more narrowing through
79
which types of lesions are reversible
- those leading to fatty streak development
80
complications of atherosclerosis
- ischemia (due to luminal stenosis) - acute infarcts (due to acute thombosis, atheroembolization or thromboembolism) - artery remodeling (leads to aneurysm formation and/or rupture)
81
complications of atherosclerosis - ischemia due to
- luminal stenosis
82
complications of atherosclerosis - acute infarcts due to
- acute thrombosis secondary to plaque rupture or intra-plaque hemorrhage - embolization of plaque fragments or thrombus
83
major complications of atherosclerosis
- MI - sudden cardiac death - chronic ischemic heart disease - aortic aneurysms - cerebral infarction - ischemic encephalopathy - PVD - mesenteric occlusion
84
arterial distribution of atherosclerosis from highest to lowest incidence
- abdominal aorta - coronary arteries - popliteal arteries - descending thoracic aorta - internal carotids - circle of willis
85
modifiable risk factors for atherosclerosis
- smoking - hypertension - dyslipidemia - diabetes - sedendary lifestyle
86
non-modifiable risk factors for atherosclerosis
- age - sex - family history/genetics
87
what hormone is protective against atherosclerosis
- estrogen
88
Characteristics of Unstable Plaque/Plaque Rupture
- Thin fibrous cap - Intense Inflammation - High Oxidative Burden - Abundant Macrophages - Large Lipid Core - Increased MMPs/TF
89
Characteristics of a Stable Plaque (not likely to rupture)
- Thick Fibrous Cap - Mild Inflammation - Mild Oxidative Burden - Low Macrophage Content - Small Lipid core
90
Progression of (Coronary) Atherosclerosis From Pre-Clinical Phase to Clinical Phase
Pre-Clinical Phase: -Normal artery > Fatty Streak > Fibrofatty Plaque > Advanced Plaque Clinical Phase: - Aneurysm and Rupture - Occlusion by Thrombus - Critical Stenosis
91
Vulnerable plaques are prone to
erosion or rupture, and therefore thrombus formation
92
The presence of a Fibrous Cap and Lipid Core occurs in
Fibrofatty Plaque (after fatty streak)
93
What do you see in a Fatty Streak
Lipid-filled foam cells with T lymphocytes and extracellular lipid within intima
94
Endothelial Cell Properties/Functions (7)
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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