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Clinical Exercise Physiology > Vascular Biology of Atherosclerosis > Flashcards

Vascular Biology of Atherosclerosis Flashcards

1
Q

Tunica intima

A

inner layer of vessel wall

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2
Q

The tunica intima is composed of…

A
  1. endothelial layer
  2. internal elastic lamina
  3. subendothelium
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3
Q

endothelial layer

A

monolayer of simple squamous epithelium cells that line the lumen

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4
Q

internal elastic lamina

A

subendothelial basement membrane layer made up of loose connective tissue support endothelium

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5
Q

subendothelium

A

space between endothelium and internal elastic lamina

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6
Q

tunica media

A

middle layer of blood vessel wall

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7
Q

The tunica media is composed of…

A
  1. smooth muscle cell layer
  2. extracellular matrix (ECM)
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8
Q

Smooth muscle cell layer

A

normal smooth muscle cells responsible for smooth muscle vasomotor tone

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9
Q

extracellular matrix (ECM)

A

made up of collagen, elastin, and proteoglycans

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10
Q

collagen

A

load bearing protein

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11
Q

elastin

A

elastic protein functions to cushion vessel during changes in pressure

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12
Q

proteoglycans

A

glycosylated proteins main part of ECM (for structural support)

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13
Q

What are the 2 normal functions of VSMC?

A
  1. contractile function
  2. synthetic function
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14
Q

Contractile functions alter the ?? of the lumen through ?? and ??.

A
  • diameter
  • vasodilation
  • vasoconstriction
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15
Q

Nitric oxide and prostacyclin are examples of?

A

vasodilators

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16
Q

Angiotensin II and endothelin-1 are examples of?

A

vasoconstrictors

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17
Q

Synthetic functions produce ??, ??, and ??; which make up the ?? in the ECM.

A
  • collagen
  • elastin
  • proteoglycans
  • tunica media
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18
Q

Tunica externa

A

outermost layer of blood vessel wall; contains nerve fibers and lymph vessels

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19
Q

The tunica externa is made up of…

A
  1. collagen fiber network
  2. external elastic lamina
  3. vasa vasorum
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19
Q

collagen fiber network

A

reinforces blood vessel and anchors to surrounding tissues

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20
Q

external elastic lamina

A

connective tissue lying immediately outside the smooth muscle of the tunica media

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21
Q

vasa vasorum

A

tiny blood vessels that supply the external layer of blood vessel wall

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22
Q

What are the 5 normal functions of the endothelial layer?

A
  1. barrier function
  2. anti-thrombotic function
  3. vascular tone function
  4. migratory/proliferation of VSMC
  5. anti-inflammatory immune function
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23
Q

Endothelial layer: barrier function

A

restrict passage of large molecules into subendothelial space

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24
Endothelial layer: anti-thrombotic function
- secretes anti-clotting factors - secretes platelet inhibitors/anti-aggregation factors
25
example of anti clotting factors
heparin sulfate
26
example of platelet inhibitors/anti-aggregation factors
nitric oxide
27
Endothelial layer: vascular tone function
- increased secretion of vasodilators - decreased secretion of vasoconstrictors
28
example of vasodilator
nitric oxide
29
examples of vasoconstrictor
endothelin-1
30
Endothelial layer: migratory/proliferation of VSMC function
inhibits migration of VSMCs from media to intima
31
Endothelial layer: anti-inflammatory immune function
- suppress leukocyte (WBC) adhesion to endothelial wall - suppress expression of chemokines (attract WBCs) on endothelial wall - suppress expression of adhesion molecules (adhere WBCs)) on endothelial wall
32
arteriosclerosis
generic term for thickening of the blood vessel (arterial) wall
33
"athero"
gruel or wax; corresponds to the lipid/necrotic core area at the base of the athersclerotic plaque
34
concentric lesion
thickening of tunica media of artery
34
"sclerosis"
hardening; referring to the fibrous cap of the plaque's luminal edge
34
atherosclerosis
eccentric arteriosclerosis
35
What causes concentric lesions?
proliferation of VSMCs
36
Concentric lesion can be described visually as...
symmetric narrowing of the vessel (arterial) lumen
37
Disease of Aging
concentric lesion
38
Concentric lesions typically referred to as...
arteriosclerosis
39
eccentric lesion
tunica intima thinkening (subendothelial) of artery
40
Eccentric lesion can be visually described as...
asymmetric narrowing of vessel wall
41
What causes eccentric lesions?
accumulation of oxidized lipids, macrophages, VSMCs, platelets, tissue factor
42
Eccentric lesion develop from - immature "??" into "??" - ?? that protudes into lumen of artery
- fatty streak - mature plaque - lesion
43
Eccentric lesions are typically called...
atherosclerosis
44
# Development of Eccentric lesions fatty streaks
earliest form of eccentric lesion
45
# Development of Eccentric lesions Fatty streak are made up of subendothelial accumulation of ??.
foam cells
46
# Development of Eccentric lesions ?? are macrophages that take up oxidized and modified lipids.
Foam cells
47
# Development of Eccentric lesions appearance of fatty streaks
yellow, minimally raised lesions
48
# Development of Eccentric lesions When do fatty streaks appear?
very young age; teens - vets
49
# Development of Eccentric lesions Fibrous plaques
advanced eccentric lesion
50
# Development of Eccentric lesions Fibrous plaques protude into lumen and ?? blood flow.
inhibit (% stenosis)
51
Fibrous plaques have an outer ?? of ?? and ?? that separates lipid core from blood.
- fibrous cap - collagen - SMCs
52
# Development of Eccentric lesions 5 Common sites of arterial atherosclerosis
1. abdominal aorta and iliac arteries (bifurcation) 2. proximal coronary arteries 3. thoracic aorta, femoral and popliteal arteries 4. internal carotid arteries 5. cerebral arteries
53
Manifestations of atherosclerotic disease
1. Coronary artery disease (CAD) 2. Cerebrovascular disease (CVA) 3. Peripheral vascular disease (PVD)
54
Examples of coronary artery disease (CAD)
- myocardial ischemia - myocardial infarction
55
myocardial ischemia
angina pectoris
56
myocardial infarction (MI)
heart attack
57
Examples of Cerebrovascular disease (CVA)
- ischemic stroke - hemorrhagic stroke
58
ischemic stroke
embolism or thrombus occludes artery and brain region becomes ischemic
59
hemorrhagic stroke
weakened blood vessel ruptures and bleeds, eg. ruptured aneurysm
60
Example of peripheral vascular disease
leg "claudication"
61
leg "claudication"
pain due to plaques in lower extremity arteries (iliac, femoral, popliteal)
62
What are the 3 hypothesis of athersclerosis plaque development?
1. aging hypothesis 2. lipid hypothesis 3. endothelial dysfunction / injury hypothesis
63
Aging hypothesis
progressive thickening of medial layer of arterial wall (arteriosclerosis) until lumen is blocked
64
lipid hypothesis
cholesterol builds up on arterial walls and eventually blocks lumen
65
endothelial dysfunction / injury hypothesis
- toxic substances and/or physical injury to endothelial wall is the primary event in atherogenesis - followed by prolonged inflammatory repsonse and fatty streak formation leading to athersclerotic mature plaque
66
# Normal vs Activated Endothelial Cells normal nitric oxide
normal
67
# Normal vs Activated Endothelial Cells promotion of vasodilation
normal
68
# Normal vs Activated Endothelial Cells inhibits platelet aggregation
normal
69
# Normal vs Activated Endothelial Cells inhibition of VSMC migration
normal
70
# Normal vs Activated Endothelial Cells inhibition of VSMC proliferation
normal
71
# Normal vs Activated Endothelial Cells inhibition of leukocyte (WBC) adhesion to endothelium
normal
72
# Normal vs Activated Endothelial Cells reduced NO bioavailability
activated
73
# Normal vs Activated Endothelial Cells increased vasocontriction
activated
74
# Normal vs Activated Endothelial Cells increased permability to molecules/cells
activated
75
# Normal vs Activated Endothelial Cells decreased anti-thrombotic properties
activated
76
# Normal vs Activated Endothelial Cells increased VSMC migration into intimal space
activated
77
# Normal vs Activated Endothelial Cells increased VSMC proliferation
activated
78
# Normal vs Activated Endothelial Cells increased leukocyte attraction and adhesionto endothelial wall
activated
79
# Normal vs Activated Endothelial Cells increased production of reactive oxygen species (ROS)
activated
80
Factors that contribute to endothelial dysfunction or injury
- genetic predisposition - hypertension - diabetes - smoking - aging - inactivity - obesity - inflammation - infection
81
what is the central feature of endothelial dysfunction?
reduced NO
82
Reactive oxygen species (ROS)
normal by-product of aerobic metabolism
83
Free radicals
- unpaired electron in outer orbit - very reactvie molecules - oxidize lipids, proteins, and DNA - cell damage
84
examples of ROS
- superoxide anion radical (O2-) - peroxynitrite (ONOO-)
85
antioxidant enzymes provide an ?? to ROS.
electron
86
Antioxidant enzymes prevent ?? and ??.
- oxidative damage - NO degradation
87
The most common antioxidant enzyme is ...
superoxide dismutase (SOD)
88
SOD function
reduces O2- to hydrogen peroxide (H2O2)
89
3 types of SOD
1. Copper Zinc SOD (CuZnSOD) 2. Manganese SOD (MnSOD) 3. Extracellular SOD (ecSOD)
90
Location of copper zinc SOD
cytoplasm
91
location of manganese SOD
mitochondria
92
location of extracellular SOD
extracellular bound to endothelial cell
93
Endothelial injury occurs at branch points called..
bifurcations
94
Regions of laminar flow and shear stress: - eNOS? - NO? - SOD?
- increased expression - increased production - increased expression
95
Regions of turbulent or oscillatory flow: - eNOS? - SOD? - NO? - ROS?
- decreased values - decreased values - decreased availability - increased production
96
# LDL entry and modification LDL cholesterol enters ??.
subendothelial space
97
# LDL entry and modification LDL is "??" increasing residence time in subendo space.
"trapped"
98
# LDL entry and modification LDL can accumulate in part due to ?? LDL and ??.
- elevated circulating - hypertension
99
# LDL entry and modification LDL is ??
modified
100
# LDL entry and modification LDL becomes ?? by ROS or ?? by hyperglycemia in diabetes. | key step in atherogenesis
- oxidized - glycated
101
# LDL entry and modification Modified LDL (mLDL) increases endothelial cell expression of...
1. adhesion molecules 2. chemokines
102
# LDL entry and modification adhesion molecules function
attract and adhere monocytes to endothelial layer
103
# LDL entry and modification adhesion molecules examples
- VCAM-1 - ICAM-1 - P-selectin - E-selectin
104
# LDL entry and modification chemokine function
direct migration of monocytes to subendothelial space (diapedesis)
105
# Recruitment and migration of leukocytes Monocyte migration is initiated by...
MCP-1
106
# Recruitment and migration of leukocytes MCP-1
signal to attract monocytes into the subendothelial space
107
# Recruitment and migration of leukocytes Once in the ??, monocytes are stimulated by ??.
monocyte colony stim factor (M-CSF)
108
# Recruitment and migration of leukocytes M-CSF
increases expression of scavenger receptors on monocytes
109
# Recruitment and migration of leukocytes With increased scavenger receptors, monocytes differentiate into...
macrophages
110
# Recruitment and migration of leukocytes Macrophages ingest ?? via scavenger receptors and then become ??.
- mLDL - foam cells
111
# Recruitment and migration of leukocytes 4 secretion of foam cells
1. inflammatory cytokines 2. superoxide 3. matrix metalloproteinases (MMP's) 4. tissue factor
112
# Recruitment and migration of leukocytes examples of inflammatory cytokines
IL-1 and TNF-alpha
113
# Recruitment and migration of leukocytes superoxide function
propagates further expression of adhesion and MCP-1 = positive feedback loop
114
# Recruitment and migration of leukocytes Matrix metalloproteinases function
degrades fibrous cap of developing plaque
115
# Recruitment and migration of leukocytes tissue factor function
stimulates coagulation cascade when exposed to blood
116
# Recruitment and proliferation of VSMCs 4 steps: Transition "fatty streak" to "mature plaque"
1. migration of VSMCs to subendothelial space 2. proliferation of VSMCs into intima from media 3. VSMC secretion of connective tissue 4. foam cell secretions
117
# Recruitment and proliferation of VSMCs foam cells secrete:
1. platelet derived growth factor (PDGF) 2. inflammatory cytokines (IL-1 and TNF-alpha)
118
# Recruitment and proliferation of VSMCs foam cell secretions functions (3)
1. promote VSMC migration into subendothelial spsace 2. proliferation of VSMCs 3. synthesis of collagen matrix
119
# Stable vs Vulnerable plaque thick fibrous cap
stable
120
# Stable vs Vulnerable plaque small lipid pool
stable
121
# Stable vs Vulnerable plaque few inflammatory cells
stable
122
# Stable vs Vulnerable plaque dense extracellular matrix (collagen)
stable
123
# Stable vs Vulnerable plaque many VSMCs secreting EC matrix
stable
124
# Stable vs Vulnerable plaque thin fibrous cap
vulnerable
125
# Stable vs Vulnerable plaque large lipid pool
vulnerable
126
# Stable vs Vulnerable plaque many inflammatory macrophage cells with tissue factor
vulnerable
127

Clinical Exercise Physiology (9 decks)

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