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brs (phase 1b) > (cardioresp) vascular endothelium > Flashcards

(cardioresp) vascular endothelium Flashcards

1
Q

where are the majority of endothelial cells found?

A

approx 98% of the endothelial cells reside within the microvasculature

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2
Q

what is the endothelium?

A

thin membrane that lines the inside of the heart and blood vessels

endothelial cells are responsible for releasing substances that control vasoconstriction, vasodilation and enzymes that control blood clotting and platelet adhesion

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3
Q

describe the basic structure of a blood vessel

A

tunica intima = endothelium, subendothelium, internal elastic lamina (smooth muscle + connective tissue)

tunic media = smooth muscle, external elastic membrane

tunica adventitia = vasa vasorum and nerves

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4
Q

what are the three layers of blood vessels?

(except capillaries and venules)

A

tunica adventitia (vasa vasorum, nerves)

tunica media (smooth muscle cells)

tunica intima (endothelium)

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5
Q

what does the tunic adventitia consist of?

A

vasa vasorum and nerves

(connective tissue layer)

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6
Q

what does the tunic media consist of?

A

smooth muscle cells

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7
Q

what does the tunic intima consist of?

A

endothelium

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8
Q

what is the vasa vasorum?

A

small blood vessels that comprise a vascular network supplying the walls of large blood vessels

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9
Q

what is the lamina propia?

A

part of the tunica intima

consists of connective tissue and smooth muscle

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10
Q

what are capillaries?

A

tiny, narrow blood vessels made entirely out of endothelium

where exchange of nutrients and oxygen between the blood and tissues takes place

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11
Q

what are venules?

A

very small branches that collect the blood from the various organs and parts

unite to form veins, which return the blood to the heart

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12
Q

describe the structure of capillaries

A

made up entirely of endothelium, supported by some mural cells (pericytes) and a basement membrane

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13
Q

how do capillaries compare structurally to veins and arteries?

A

capillaries are made up of endothelium and basement membrane with a few, supporting pericytes

whereas larger blood vessels are made up of three different layers: tunica intima, tunica media, and tunica adventitia

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14
Q

what are pericytes and where are they found?

A

contractile cells that wrap around endothelial cells in capillaries and post-capillary venules

control blood flow and homeostasis (i.e. blood-brain barrier)

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15
Q

how small are capillaries?

A

approx 1/10th of the width of a hair (5-10 micrometres)

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16
Q

why is the microvascular endothelium important?

A

promotes tissue homeostasis

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17
Q

what can damage to the endothelium result in?

A

organ dysfunction

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18
Q

how does the microvascular endothelium promote tissue homeostasis?

A

the endothelium is a source of angiocrine factors that are required for the maintenance of tissue homeostasis and organ regeneration

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19
Q

what are angiocrine factors?

A

molecules found in blood vessels’ endothelial cells that can stimulate organ-specific repair activities in damaged or diseased organs + promote tissue homeostasis

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20
Q

which diseases are affected by a dysfunctional endothelium?

A

ischaemia

chronic inflammatory diseases

cancer

diabetes

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21
Q

what is vascular and endothelial heterogeneity?

A

the variety in endothelial cell structure and function depending on time and location and health/disease

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22
Q

what is the significance of tissue-specific microvasculature?

A

the function of the microvasculature is very different in different organs and regions (i.e. is tissue-specific)

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23
Q

how does the microvasculature of the kidney and liver vary compared to that of the brain?

A

liver & kidney = very permeable vasculature for filtration function

(so microvasculature of endothelium looks very different from that in the brain|)

brain = tight vascular endothelium to prevent leakage

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24
Q

define organotypic

A

tissue-specific

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25
Q

what is the significance of endothelial cells and the microvasculature being organotypic?

A

endothelial cells and microvasculature have organotypic (tissue-specific) properties and expression profiles

(depending on time and location)

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26
Q

what are the types of endothelial cell connections?

A

continuous (fenestrated, non-fenestrated)

discontinuous

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27
Q

where are continuous non-fenestrated endothelial cells found?

A

muscle, lung, skin, blood-brain barrier

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28
Q

where are continuous fenestrated endothelial cells found?

A

kidney glomerulus, gastrointestinal tract

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29
Q

where are discontinuous endothelial cells found?

A

liver, marrow sinus

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30
Q

how does the endothelium act as a barrier?

A

vital barrier that separates blood from the tissues

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31
Q

describe the surface area of the endothelium

A

very extensive

= surface area > 1000 m2
= weight > 100 g

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32
Q

describe the size of endothelial cells

A

very flat, about 1-2 µm thick and 10-20 µm in diameter

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33
Q

describe the thickness of the endothelium

A

formed by a monolayer of endothelial cells (one cell thick)

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34
Q

what is the proliferation rate of endothelial cells like?

A

low proliferation rate unless new vessels are required via angiogenesis

+ long life span

(cells undergo contact inhibition and stop proliferating)

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35
Q

when do endothelial cells proliferate?

A

angiogenesis (i.e when new blood vessels are required)

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36
Q

what is the life span of endothelial cells like?

A

long life span

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37
Q

what is endothelial cell contact inhibition?

A

abrupt arrest of the cell cycle that occurs between rapidly proliferating cells at the point when a confluent monolayer forms

= control growth and proliferation of endothelium

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38
Q

why is contact inhibition important for the endothelium?

A

to control the growth and proliferation of the endothelium

= preventing uncontrolled growth

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39
Q

what are the key functions of the endothelium?

A

tissue homeostasis and regeneration

permeability

inflammation

vascular tone

angiogenesis

haemostasis & thrombosis

40
Q

which disease is endothelial dysfunction most commonly related to?

A

atherosclerosis

41
Q

why are angiocrine factors essential?

A

for tissue homeostasis

42
Q

endothelial cells are heterogeneous: what does this mean?

A

their function and phenotype depends on their location

43
Q

give examples of substances that are released by endothelial cells to facilitate their function

A
44
Q

what does the resting endothelium stimulate?

A

anti-inflammatory, anti-thrombotic and anti-proliferative pathways

45
Q

what does the activated endothelium stimulate?

A

pro-inflammatory, pro-thrombotic, pro-angiogenic pathways

= triggering coagulation and angiogenesis

46
Q

what can stimulate the activation of the endothelium from its resting state?

A

inflammation, hypertension, hyperglycaemia, viruses, smoking, mechanical stress

47
Q

how do foam cells form as a result of endothelial injury?

A

initial injury

= endothelium activated

= increased endothelial permeability

= increased leukocyte migration and adhesion so leukocytes (and also macrophages) accumulate in the subendothelial space

= subsequent phagocytosis of lipids also in the subendothelial space (by macrophages)

= foam cell formation + plaque growth as the form cell number increases

48
Q

how do foam cells progress to become part of an atherosclerotic plaque? (steps of advanced atherosclerosis)

A

more macrophages accumulate in the subendothelial space

together w the leukocytes, lipids and debris = a necrotic core is formed (i.e. chronic inflammatory lesion)

as part of the response to the initial injury, a fibrous cap forms and walls of the lesion from the lumen

(angiogenesis can also be stimulated as a result from the vasa vasorum in the tunica adventitia)

49
Q

what is the trigger for atherosclerosis?

A

initial injury to the endothelium

(or one of the factors that activate the endothelium = oxidised LDL, hypertension, hyperglycaemia etc)

50
Q

in which area do macrophages accumulate to contribute to an atherosclerotic plaque?

A

subendothelial space

51
Q

how are macrophages converted into foam cells?

A

macrophages in atherosclerotic lesions actively participate in lipoprotein (lipid) ingestion and accumulation giving rise to foam cells filled with lipid droplets

= accumulation of lipid-filled foam cells leads to atherosclerotic plaque growth

52
Q

what is a necrotic core?

A

a core of leukocytes, foam cells, macrophages, debris lipid and dead/dying cells forms due to oxidative stress and depleted ATP levels at the atherosclerotic lesion site

53
Q

explain the significance of the formation of the fibrous cap in atherosclerosis

A

serves as a subendothelial barrier between the vessel lumen and the atherosclerotic necrotic core

54
Q

why is the stimulation of angiogenesis during atherosclerotic plaque formation important?

A

in atherosclerotic plaques, due to the thickening of the arterial wall and inflammation = impaired oxygen delivery

resultant hypoxia causes release of angiogenic factors

angiogenic factors stimulate angiogenesis in the vasa casorum

55
Q

why is angiogenesis of the vasa vasorum specifically, stimulated in atherosclerosis?

A

vasa vasorum supplies the endothelium and muscle of the arteries and veins

so to increase oxygen supply to the atherosclerotic plaque, a lesion of the blood vessel (arterial) wall, the vasa vasorum must be increased via angiogenesis

56
Q

can atherosclerosis happen in veins?

A

it can do rarely = only if they are connected to high-pressure circulatory part of the system

but most often, if not always, happens in arteries as high pressure is though to be a factor required for atherosclerosis

57
Q

define atherogenesis

A

the process of atherosclerotic plaque formation

58
Q

what are the risk factors/stimuli for endothelial cell dysfunction in atherogenesis?

A

hypercholesterolaemia (oxidatively-modified lipoproteins)

hypertension

oxidative stress

proinflammatory cytokines. (IL-1, TNF)

infectious agents

environmental toxins (cigarette smoke, air pollutants)

hameodynamic forces (disturbed blood flow)

diabetes mellitus/sex hormon imbalance/ageing

59
Q

how can hypercholesterolaemia stimulate atherogenesis?

A

increased deposition of oxidatively-modified lipoproteins into the subendothelial space

60
Q

how can sex hormone imbalance stimulate atherogenesis?

A

oestrogen deficiency, menopause

61
Q

which proinflammatory cytokines stimulate atherogenesis?

A

IL-1, TNF

62
Q

which infectious agents stimulate atherogenesis?

A

bacterial endotoxins, viruses

63
Q

which environmental toxins stimulate atherogenesis?

A

cigarette smoke, air pollutants

64
Q

how do haemodynamic forces stimulate atherogenesis?

A

due to disturbed blood flow

65
Q

what are the four mechanisms of atherosclerosis pathogenesis?

A

leukocyte recruitment

vascular permeability

shear stress

angiogenesis

66
Q

explain the leukocyte adhesion cascade

A

inflammatory mediators will activate the endothelium and stimulate them to express surface molecules that facilitate leukocyte adhesion and migration

67
Q

when does leukocyte recruitment into tissues take place?

A

normally, during inflammation

68
Q

how does leukocyte recruitment take place in post-capillary venules?

A

leukocytes adhere to the endothelium of post-capillary venules and transmigrate into tissues

69
Q

compare the structure of a capillary to that of a post-capillary venule

A

capillary = single endothelial cell layer surrounded by basement membrane and pericapillary cells (pericytes)

post-capillary venule = structure similar to capillaries but more pericytes

70
Q

how does leukocyte recruitment differ in atherosclerosis?

A

leukocytes adhere to activated endothelium of large arteries and get stuck in the subendothelial space

71
Q

how do monocytes act in atherosclerosis?

A

migrate into the subendothelial space, differentiate into macrophages and become foam cells that contribute to the atherosclerotic plaque

72
Q

how does vascular permeability vary in atherosclerosis?

A

normally, endothelium regulates the flux of fluids and molecules from the blood to tissues and vice versa

so increased permeability results in leakage of plasma proteins from the blood through the junctions into the subendothelial space (already filled w sticky molecules like proteoglycans and ECM)

= contribute to the atherosclerotic plaque

73
Q

how do plasma proteins contribute to the atherosclerotic plaque?

A

increased vascular permeability results in increased plasma protein leakage into the subendothelial space

74
Q

where does lipoprotein modification take place?

A

subendothelial space

75
Q

explain how increased permeability to lipids increases the risk of atherosclerosis

A

during inflammation, endothelial gaps become wider so = more leaky junctions

lipoproteins that normally would not, are now able to squeeze through the wider junctions and enter the subendothelial space (= increased permeability to lipids)

where they undergo oxidative modification

76
Q

how do foam cells form?

A

the macrophages that migrate to the subendothelial space will combine w the oxidised lipoprotein

= foam cell

77
Q

where do atherosclerotic plaques preferentially occur?

A

at bifurcations and curvatures of the vascular tree

78
Q

why do atherosclerotic plaques preferentially occur where they do?

A

at bifurcations and curvatures of the vascular tree

= flow patterns and hemodynamic forces are not uniform in the vascular system

79
Q

what are the two types of blood flow?

A 
laminar flow (continuous) 
disturbed flow (discontinuous)
80
Q

how is blood flow and wall stress in the straight parts of the arterial tree?

A

blood flow is laminar and wall shear stress is high and directional

81
Q

how is blood flow and wall stress in the branches and curvatures of the arterial tree?

A

blood flow is disturbed with non-uniform and irregular distribution of low wall shear stress

82
Q

what is the protective effect of laminar blood flow on the vascular endothelium?

A

anti-thrombotic, anti-inflammatory factors

endothelial survival

inhibition of SMC proliferation

nitric oxide (NO) proliferation

83
Q

what is the disruptive effect of disturbed blood flow on the vascular endothelium?

A

stimulates thrombosis, inflammation (leukocyte adhesion)

endothelial apoptosis

SMC proliferation

loss of nitric oxide (NO) proliferation

84
Q

what kind of blood flow is associated with high shear stress?

A

laminar blood flow

85
Q

what kind of blood flow is associated with low shear stress?

A

disturbed blood flow

86
Q

why is nitric oxide important for the endothelium?

A

has protective effects on the vascular endothelium

87
Q

why is smooth muscle cell proliferation harmful?

A

contributes to vascular lesion formation

88
Q

list the functions of nitric oxide in the endothelium

A

dilates blood vessels

reduces platelet activation

inhibits monocyte adhesion

reduces proliferation of SMC in the vessel wall

reduces release of superoxide radicals

reduces oxidation of LDL cholesterol (major component of plaques)

89
Q

define angiogenesis

A

the formation of new vessels from existing vessels

(via endothelial cell activation and proliferation)

90
Q

what triggers angiogenesis?

A

hypoxia

91
Q

foe which processes is angiogenesis essential?

A

embryonic development

menstrual cycle

wound healing

92
Q

in which scenario can angiogenesis be particularly harmful?

A

when an atherosclerotic plaque becomes a chronic inflammatory condition

= stimulates angiogenesis to contribute to plaque growth (i.e. advanced atherosclerotic plaques)

93
Q

in which scenario can angiogenesis be particularly useful?

A

when angiogenesis can be induced to revascularise and prevent the loss of ischaemic tissue

94
Q

where does leukocyte trasnmigration occur?

A

post-capillary venules

95
Q

what is thromboinflammation and why does it occur?

A

loss of the normal anti-thrombotic and anti-inflammatory functions of endothelial cells causes thrombosis with associated inflammation

= thromboinflammation

(occurs in sepsis, ischaemia etc)

brs (phase 1b) (71 decks)

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