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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
Q

Endothelial layer: anti-thrombotic function

A
  • secretes anti-clotting factors
  • secretes platelet inhibitors/anti-aggregation factors
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25
Q

example of anti clotting factors

A

heparin sulfate

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26
Q

example of platelet inhibitors/anti-aggregation factors

A

nitric oxide

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27
Q

Endothelial layer: vascular tone function

A
  • increased secretion of vasodilators
  • decreased secretion of vasoconstrictors
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28
Q

example of vasodilator

A

nitric oxide

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29
Q

examples of vasoconstrictor

A

endothelin-1

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30
Q

Endothelial layer: migratory/proliferation of VSMC function

A

inhibits migration of VSMCs from media to intima

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31
Q

Endothelial layer: anti-inflammatory immune function

A
  • 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
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32
Q

arteriosclerosis

A

generic term for thickening of the blood vessel (arterial) wall

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33
Q

“athero”

A

gruel or wax; corresponds to the lipid/necrotic core area at the base of the athersclerotic plaque

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34
Q

concentric lesion

A

thickening of tunica media of artery

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34
Q

“sclerosis”

A

hardening; referring to the fibrous cap of the plaque’s luminal edge

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34
Q

atherosclerosis

A

eccentric arteriosclerosis

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35
Q

What causes concentric lesions?

A

proliferation of VSMCs

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36
Q

Concentric lesion can be described visually as…

A

symmetric narrowing of the vessel (arterial) lumen

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37
Q

Disease of Aging

A

concentric lesion

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38
Q

Concentric lesions typically referred to as…

A

arteriosclerosis

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39
Q

eccentric lesion

A

tunica intima thinkening (subendothelial) of artery

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40
Q

Eccentric lesion can be visually described as…

A

asymmetric narrowing of vessel wall

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41
Q

What causes eccentric lesions?

A

accumulation of oxidized lipids, macrophages, VSMCs, platelets, tissue factor

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42
Q

Eccentric lesion develop from
- immature “??” into “??”
- ?? that protudes into lumen of artery

A
  • fatty streak
  • mature plaque
  • lesion
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43
Q

Eccentric lesions are typically called…

A

atherosclerosis

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44
Q

Development of Eccentric lesions

fatty streaks

A

earliest form of eccentric lesion

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45
Q

Development of Eccentric lesions

Fatty streak are made up of subendothelial accumulation of ??.

A

foam cells

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46
Q

Development of Eccentric lesions

?? are macrophages that take up oxidized and modified lipids.

A

Foam cells

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47
Q

Development of Eccentric lesions

appearance of fatty streaks

A

yellow, minimally raised lesions

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48
Q

Development of Eccentric lesions

When do fatty streaks appear?

A

very young age; teens - vets

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49
Q

Development of Eccentric lesions

Fibrous plaques

A

advanced eccentric lesion

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50
Q

Development of Eccentric lesions

Fibrous plaques protude into lumen and ?? blood flow.

A

inhibit (% stenosis)

51
Q

Fibrous plaques have an outer ?? of ?? and ?? that separates lipid core from blood.

A
  • fibrous cap
  • collagen
  • SMCs
52
Q

Development of Eccentric lesions

5 Common sites of arterial atherosclerosis

A
  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
Q

Manifestations of atherosclerotic disease

A
  1. Coronary artery disease (CAD)
  2. Cerebrovascular disease (CVA)
  3. Peripheral vascular disease (PVD)
54
Q

Examples of coronary artery disease (CAD)

A
  • myocardial ischemia
  • myocardial infarction
55
Q

myocardial ischemia

A

angina pectoris

56
Q

myocardial infarction (MI)

A

heart attack

57
Q

Examples of Cerebrovascular disease (CVA)

A
  • ischemic stroke
  • hemorrhagic stroke
58
Q

ischemic stroke

A

embolism or thrombus occludes artery and brain region becomes ischemic

59
Q

hemorrhagic stroke

A

weakened blood vessel ruptures and bleeds, eg. ruptured aneurysm

60
Q

Example of peripheral vascular disease

A

leg “claudication”

61
Q

leg “claudication”

A

pain due to plaques in lower extremity arteries (iliac, femoral, popliteal)

62
Q

What are the 3 hypothesis of athersclerosis plaque development?

A
  1. aging hypothesis
  2. lipid hypothesis
  3. endothelial dysfunction / injury hypothesis
63
Q

Aging hypothesis

A

progressive thickening of medial layer of arterial wall (arteriosclerosis) until lumen is blocked

64
Q

lipid hypothesis

A

cholesterol builds up on arterial walls and eventually blocks lumen

65
Q

endothelial dysfunction / injury hypothesis

A
  • 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
Q

Normal vs Activated Endothelial Cells

normal nitric oxide

67
Q

Normal vs Activated Endothelial Cells

promotion of vasodilation

68
Q

Normal vs Activated Endothelial Cells

inhibits platelet aggregation

69
Q

Normal vs Activated Endothelial Cells

inhibition of VSMC migration

70
Q

Normal vs Activated Endothelial Cells

inhibition of VSMC proliferation

71
Q

Normal vs Activated Endothelial Cells

inhibition of leukocyte (WBC) adhesion to endothelium

72
Q

Normal vs Activated Endothelial Cells

reduced NO bioavailability

73
Q

Normal vs Activated Endothelial Cells

increased vasocontriction

74
Q

Normal vs Activated Endothelial Cells

increased permability to molecules/cells

75
Q

Normal vs Activated Endothelial Cells

decreased anti-thrombotic properties

76
Q

Normal vs Activated Endothelial Cells

increased VSMC migration into intimal space

77
Q

Normal vs Activated Endothelial Cells

increased VSMC proliferation

78
Q

Normal vs Activated Endothelial Cells

increased leukocyte attraction and adhesionto endothelial wall

79
Q

Normal vs Activated Endothelial Cells

increased production of reactive oxygen species (ROS)

80
Q

Factors that contribute to endothelial dysfunction or injury

A
  • genetic predisposition
  • hypertension
  • diabetes
  • smoking
  • aging
  • inactivity
  • obesity
  • inflammation
  • infection
81
Q

what is the central feature of endothelial dysfunction?

A

reduced NO

82
Q

Reactive oxygen species (ROS)

A

normal by-product of aerobic metabolism

83
Q

Free radicals

A
  • unpaired electron in outer orbit
  • very reactvie molecules
  • oxidize lipids, proteins, and DNA - cell damage
84
Q

examples of ROS

A
  • superoxide anion radical (O2-)
  • peroxynitrite (ONOO-)
85
Q

antioxidant enzymes provide an ?? to ROS.

86
Q

Antioxidant enzymes prevent ?? and ??.

A
  • oxidative damage
  • NO degradation
87
Q

The most common antioxidant enzyme is …

A

superoxide dismutase (SOD)

88
Q

SOD function

A

reduces O2- to hydrogen peroxide (H2O2)

89
Q

3 types of SOD

A
  1. Copper Zinc SOD (CuZnSOD)
  2. Manganese SOD (MnSOD)
  3. Extracellular SOD (ecSOD)
90
Q

Location of copper zinc SOD

91
Q

location of manganese SOD

A

mitochondria

92
Q

location of extracellular SOD

A

extracellular bound to endothelial cell

93
Q

Endothelial injury occurs at branch points called..

A

bifurcations

94
Q

Regions of laminar flow and shear stress:
- eNOS?
- NO?
- SOD?

A
  • increased expression
  • increased production
  • increased expression
95
Q

Regions of turbulent or oscillatory flow:
- eNOS?
- SOD?
- NO?
- ROS?

A
  • decreased values
  • decreased values
  • decreased availability
  • increased production
96
Q

LDL entry and modification

LDL cholesterol enters ??.

A

subendothelial space

97
Q

LDL entry and modification

LDL is “??” increasing residence time in subendo space.

A

“trapped”

98
Q

LDL entry and modification

LDL can accumulate in part due to ?? LDL and ??.

A
  • elevated circulating
  • hypertension
99
Q

LDL entry and modification

LDL is ??

100
Q

LDL entry and modification

LDL becomes ?? by ROS or ?? by hyperglycemia in diabetes.

key step in atherogenesis

A
  • oxidized
  • glycated
101
Q

LDL entry and modification

Modified LDL (mLDL) increases endothelial cell expression of…

A
  1. adhesion molecules
  2. chemokines
102
Q

LDL entry and modification

adhesion molecules function

A

attract and adhere monocytes to endothelial layer

103
Q

LDL entry and modification

adhesion molecules examples

A
  • VCAM-1
  • ICAM-1
  • P-selectin
  • E-selectin
104
Q

LDL entry and modification

chemokine function

A

direct migration of monocytes to subendothelial space (diapedesis)

105
Q

Recruitment and migration of leukocytes

Monocyte migration is initiated by…

106
Q

Recruitment and migration of leukocytes

MCP-1

A

signal to attract monocytes into the subendothelial space

107
Q

Recruitment and migration of leukocytes

Once in the ??, monocytes are stimulated by ??.

A

monocyte colony stim factor (M-CSF)

108
Q

Recruitment and migration of leukocytes

M-CSF

A

increases expression of scavenger receptors on monocytes

109
Q

Recruitment and migration of leukocytes

With increased scavenger receptors, monocytes differentiate into…

A

macrophages

110
Q

Recruitment and migration of leukocytes

Macrophages ingest ?? via scavenger receptors and then become ??.

A
  • mLDL
  • foam cells
111
Q

Recruitment and migration of leukocytes

4 secretion of foam cells

A
  1. inflammatory cytokines
  2. superoxide
  3. matrix metalloproteinases (MMP’s)
  4. tissue factor
112
Q

Recruitment and migration of leukocytes

examples of inflammatory cytokines

A

IL-1 and TNF-alpha

113
Q

Recruitment and migration of leukocytes

superoxide function

A

propagates further expression of adhesion and MCP-1 = positive feedback loop

114
Q

Recruitment and migration of leukocytes

Matrix metalloproteinases function

A

degrades fibrous cap of developing plaque

115
Q

Recruitment and migration of leukocytes

tissue factor function

A

stimulates coagulation cascade when exposed to blood

116
Q

Recruitment and proliferation of VSMCs

4 steps: Transition “fatty streak” to “mature plaque”

A
  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
Q

Recruitment and proliferation of VSMCs

foam cells secrete:

A
  1. platelet derived growth factor (PDGF)
  2. inflammatory cytokines (IL-1 and TNF-alpha)
118
Q

Recruitment and proliferation of VSMCs

foam cell secretions functions (3)

A
  1. promote VSMC migration into subendothelial spsace
  2. proliferation of VSMCs
  3. synthesis of collagen matrix
119
Q

Stable vs Vulnerable plaque

thick fibrous cap

120
Q

Stable vs Vulnerable plaque

small lipid pool

121
Q

Stable vs Vulnerable plaque

few inflammatory cells

122
Q

Stable vs Vulnerable plaque

dense extracellular matrix (collagen)

123
Q

Stable vs Vulnerable plaque

many VSMCs secreting EC matrix

124
Q

Stable vs Vulnerable plaque

thin fibrous cap

A

vulnerable

125
Q

Stable vs Vulnerable plaque

large lipid pool

A

vulnerable

126
Q

Stable vs Vulnerable plaque

many inflammatory macrophage cells with tissue factor

A

vulnerable

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