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BRS YR2 > Vascular Endothelium > Flashcards

Vascular Endothelium Flashcards

1
Q

What are the 3 layers of blood vessels (from outermost to innermost)?

A
  • tunica adventitia
  • tunica media
  • tunica intima
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2
Q

What makes up the tunica adventitia?

A
  • vasa vasorum
  • nerves
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3
Q

What makes up the tunica media?

A
  • external elastic membrane
  • smooth muscle
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4
Q

What makes up the tunica intima?

A
  • internal elastic membrane
  • lamina propria
  • endothelium
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5
Q

What is the lamina propria?

A
  • smooth muscle
  • connective tissue
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6
Q

What are capillaries and venules comprised of?

A
  • endothelium
  • pericytes (mural cells)
  • basement membrane
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7
Q

What happens at capillaries?

A

exchange of nutrients and oxygen between blood and tissues

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8
Q

What does the microvascular endothelium do?

A
  • source of angiocrine factors
  • promote tissue homeostasis and organ regeneration
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9
Q

What is the impact of a dysfunctional endothelium?

A
  • contributes to disease
  • ischemia
  • chronic inflammatory diseases
  • cancer
  • diabetes
  • atherosclerosis
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10
Q

Do endothelium cells vary?

A
  • yes, they have organotypic properties and expression profiles
  • have structural, functional and molecular differences
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11
Q

What are the properties of endothelial cells in the muscle, lung, skin and blood brain barrier?

A

continuous non-fenestrated

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12
Q

What are the properties of endothelial cells in the kidney glomerulus, GI tract?

A

continuous fenestrated

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13
Q

What are the properties of endothelial cells in the liver and marrow?

A

discontinuous

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14
Q

What are the properties of endothelial cells?

A
  • very flat
  • about 1-2 micrometers thick
  • about 10-20 micrometers in diameter
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15
Q

What is contact inhibition?

A

when the junctions of 2 cells join and establishes a junction causing the cells to stop growing

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16
Q

What is the lifespan of endothelial cells?

A
  • long
  • low proliferation rate
    (unless angiogenesis is necessary)
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17
Q

What are the functions of endotheliun?

A
  • vascular tone
  • permeability
  • angiogenesis
  • haemostasis and thrombosis
  • inflammation
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18
Q

What happens when the endothelium is at rest?

A

promotion of:

  • anti-inflammatory
  • anti-thrombotic
  • anti-proliferative
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19
Q

What happens when the endothelium is activated?

A

promotion of:

  • pro-inflammatory
  • pro-thrombotic
  • pro-angiogenic
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20
Q

What activates the endothelium?

A
  • smoking
  • viruses
  • mechanical stress
  • inflammation
  • high BP
  • OxLDL
  • high glucose
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21
Q

What happens when there is long term/chronic activation of the endothelium?

A
  • thrombosis
  • senescence
  • permeability
  • leukocyte recruitment
    all cause: atherosclerosis
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22
Q

What are the characteristics of endothelial dysfunction in atherosclerosis?

A
  • endothelial permeability
  • leukocyte migration
  • endothelial adhesion
  • leukocyte adhesion
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23
Q

What happens in the fatty-streak formation in atherosclerosis?

A
  • smooth muscle migration
  • foam cell formation
  • t cell activation
  • adherence and aggregation of platelets
  • adherence and entry of leukocytes
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24
Q

What happens in the formation of an advanced, complicated lesion of atherosclerosis?

A
  • macrophage accumulation
  • formation of a necrotic core
  • angiogenesis
  • fibrous cap formation
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25
Q

What are the triggers of endothelial dysfunction in atherogenesis?

A
  • oxidative stress
  • pro-inflammatory cytokines
  • infectious agents
  • environmental toxins
  • haemodynamic forces
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26
Q

What are the risk factors of endothelial dysfunction causing atherogenesis?

A
  • hypercholesterolaemia
  • DM/metabolic syndrome
  • hypertension
  • sex hormonal imbalance
  • ageing
27
Q

What are the mechanisms that contribute to the development of atherosclerosis?

A
  • leukocyte recruitment
  • permeability
  • shear stress
  • angiogenesis
28
Q

What happens in the leukocyte adhesion cascade?

A
  • capture
  • rolling and arrest (activation)
  • adhesion
  • spreading
  • paracellular and transcellular transmigration
29
Q

When and where does leukocyte recruitment normally occur?

A

during inflammation, leukocytes adhere to the post-capillary venules before entering the tissues

30
Q

What is the structure of a capillary?

A
  • endothelial cells
  • basement membrane
  • pericapillary cells (pericytes)
31
Q

What is the difference in the structure of a capillary and a post-capillary venule?

A

venules have more pericytes (pericapillary cells)

32
Q

Where does leukocyte recruitment occur in atherosclerosis?

A
  • adhere to the activated endothelium of of large arteries and are stuck in the sub-endothelial space
  • monocytes differentiate into macrophages and then foam cells in the subendothelial space
33
Q

What happens when there is increased permeability of the endothelium?

A
  • leakage of plasma proteins through the junctions into the subendothelial space
  • LDL enters the subendotheial space and becomes OxLDL which further activates endothelial cells
  • macrophages take up OxLDL and become foam cells
34
Q

What happens to blood flow in the straight parts of the arterial tree?

A
  • laminar blood flow
  • high and directional wall shear stress
35
Q

What happens to blood flow in the branches and curvatures of the arterial tree?

A
  • disturbed blood flow
  • non-uniform and irregular distribution of low wall shear stress
36
Q

What does laminar blood flow promote?

A
  • anti-thrombotic, anti-inflammatory factors
  • endothelial survival
  • inhibitions of SMC proliferation
  • NO production
37
Q

What does disturbed blood flow promote?

A
  • thrombosis, inflammation (leukocyte adhesion)
  • endothelial apoptosis
  • SMC proliferation
  • loss of NO production
38
Q

What is the role of NO?

A

key regulator of vascular function

  • reduces OxLDL
  • vasodilation
  • reduces platelet activation
  • inhibits monocyte adhesion
  • reduces release of superoxide radicals
  • reduces SMC proliferation
39
Q

What is angiogenesis?

A

formation of new blood vessels by sprouting from existing ones

40
Q

What is angiogenesis triggered by?

A

hypoxia

41
Q

What is angiogenesis essential for?

A
  • embryonic development
  • wound healing
  • menstrual cycle
42
Q

What is the double role of angiogenesis?

A
  • promotes plaque growth
  • theraputic angiogenesis prevents damage post-ischemia
43
Q

What is pathological angiogenesis associated with?

A

advanced atherosclerotic plaques

44
Q

What is associated with a poor prognosis with a COVID infection?

A
  • increased D-Dimers
  • increased fibrinogen
45
Q

Where are the majority of endothelial cells?

A

capillaries

46
Q

What is thromboinflammation?

A

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

47
Q

How does covid cause endothelial dysfunction?

A
  • cytokine storm
  • endothelial activation
  • procoagulant switch
48
Q

What are the 2 possible ways that SARS-CoV2 causes endothelial damage?

A
  • cytokine storm secondary to the infection causes the endothelial damage
  • SARS-CoV2 enters the cells and causes direct damage (no evidence)
49
Q

What functions of blood vessels and tissues does the endothelium control?

A
  • vascular tone
  • angiogenesis
  • haemostasis and thrombosis
  • inflammation
  • permeability
50
Q

How do endothelial cells regulate thrombosis and haemostasis?

A

Antithrombotic and procoagulant factors

51
Q

How do endothelial cells regulate angiogenesis?

A

Growth factors (e.g IGF) and matrix products

52
Q

How do endothelial cells regulate vascular tone and permeability?

A

Vasconstricting and vasodilating factors

53
Q

How do endothelial cells regulate inflammation?

A

Inflammatory modulators and adhesion molecules

54
Q

How are the transcriptional signatures of individual cells examined?

A
  • single cell RNAseq
  • shown on a seurat cluster graph, each dot is a cell and each cell is grouped according to the similarities in their gene expression
55
Q

What influences the phenotype of endothelial cells?

A

Tissue-specific microenvironment

56
Q

How are new blood vessels formed?

A

Sprouting angiogenesis

57
Q

Which pathologies does angiogenesis play a role in?

A

Cancer
Retinopathies
Atherosclerosis
Chronic inflammatory diseases
Ischemic diseases
Vascular malformations

58
Q

What is an angiogenic switch?

A
  • tumour cells in large tumours secrete angiogenic factors that stimulate new vessel formation by endothelial cells in adjacent vessels
  • this facilitates tumour growth and metastasis
59
Q

What is Von Willebrand disease?

A
  • most common hereditary bleeding disorder (1/100)
  • caused by dysfunction of Von Willebrand factor
60
Q

How is VWD treated?

A

VWF or DDAVP

61
Q

What causes severe, intractable bleeding in the GIT in patients eith VWD?

A
  • Vascular malformations in the gut blood vessels
  • cannot be treated with VWF replacement
62
Q

What is the role of VWF in haemostasis?

A
  • mediates platelet adhesion to the subendothelium and platelet aggregation
  • stabilises circulating coagulation Factor VIII
63
Q

What is the role of VWF in angiogenesis?

A
  • regulates growth factor signalling (VEGFR2:Ang-2)
64
Q

Where do atheroscleoritc plaques usually occur and why?

A
  • at bifurcations and curvaturesof the vascular tree
  • flow patterns and haemodynamic forces are not uniform in the vascular system

BRS YR2 (67 decks)

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