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BRS YR2 > Vascular Endothelium > Flashcards

Vascular Endothelium Flashcards

1
Q

What are the 3 layers of blood vessels?

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

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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

a source of angiocrine factors required to 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

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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
21
Q

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

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

What are the characteristics of endothelial dysfunction in atherosclerosis?

A
  • endothelial permeability
  • leukocyte migration
  • endothelial adhesion
  • leukocyte adhesion
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
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
25
Q

What are the triggers of endothelial dysfunction in atherogenesis?

A
  • oxidative stress
  • pro-inflammatory cytokines
  • infectious agents
  • environmental toxins
  • haemodynamic forces
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
  • spreading
  • between the junctions
29
Q

When and where does leukocyte recruitment normally occur?

A

during inflammation, adherence to the post-capillary venules before entering the tissures

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

to the activated endothelium of of large arteries and are stuck in the sub-endothelial space
- monocytes differentiate into macrophages and then foam cells

33
Q

What happens when there is increased permeability of the endothelium?

A

leakage of plasma proteins through the junctions into the subendothelial space

34
Q

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

A
  • laminar blood flow

- high an 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
    if therapeutic:
  • 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
  • SARS-CoV2 infection
  • 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)

BRS YR2 (70 decks)

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