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BRS Flashcards (Y2) > Vascular Endothelium > Flashcards

Vascular Endothelium Flashcards

1
Q

Blood vessels are lined by which cells?

A

Endothelial cells

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2
Q

What are the three layers of blood vessels (apart from capillaries and venules)?

A
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3
Q

What percentage of endothelial cells reside within the microvasculature?

A

98%

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4
Q

Describe the structure of capillaries and venules

A

Formed only by endothelium
Supported by some mural cells (pericytes) and a basement membrane

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5
Q

Where does exchange of nutrients and oxygen between blood and tissues occur?

A

Capillaries

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6
Q

What findings suggest that microvascular endothelium promotes tissue homeostasis?

A

Damage to the endothelium can cause organ dysfunction

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7
Q

Are blood vessels just a distribution system?

A

No

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8
Q

Microvascular endothelium are the source of what factors and what are these factors required for?

A

Source of angiocrine factors
Factors are required for maintenance of tissue homeostasis and organ regeneration

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9
Q

Dysfunctional endothelium contributes to which conditions?

A

Contributes to disease more than any other organ:
Ischaemia
Chronic inflammatory diseases
Cancer
Diabetes

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10
Q

Are all blood vessels the same?

A

No, there is vascular and endothelial heterogeneity
Endothelial cells and microvasculature have organotypic (tissue-specific) properties and expression profiles

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11
Q

Describe the structure of endothelial cells

A

Very flat
1-2 micrometers thick and 10-20 micrometers in diameter

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12
Q

How do endothelial cells grow to from the endothelium?

A

Endothelial cells come together to form cell-cell junctions
Establishment of the junction (contains a lot of complex molecular structures) results in growth inhibition - cells stop growing
This is known as contact inhibition

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13
Q

Describe the proliferation rate of endothelial cells

A

Low
Only proliferate during angiogenesis, where new vessels are required

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14
Q

What is the function of endothelial cells?

A

Regulate essential functions of blood vessels:
Vascular tone
Angiogenesis
Permeability
Inflammation
Homeostasis and thrombosis

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15
Q

At rest, what kind of factors are produced by the vascular endothelium?

A

Anti-inflammatory
Anti-thrombotic
Anti-proliferative

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16
Q

When activated, what kind of factors are produced by the vascular endothelium?

A

Pro-inflammatory
Pro-thrombotic
Pro-angiogenic

17
Q

What factors may contribute to chronic activation of the endothelium?

A

Smoking
Viruses
Mechanical stress
Inflammation
High BP
OxLDL
High glucose

18
Q

Over time, what does chronic activation of the endothelium promote and what do these factors lead to?

A

Thrombosis
Leukocyte recruitment
Increased permeability
Ageing of endothelial cells (senescence)
Lead to atherosclerosis

19
Q

What stimuli and risk factors are implicated in endothelial cell dysfunction in atherogenesis?

A
20
Q

What are the four mechanisms of endothelial dysfunction in the pathogenesis of atherosclerosis?

A

Leukocyte recruitment
Permeability
Shear stress
Angiogenesis

21
Q

Describe the leukocyte adhesion cascade

A
22
Q

In physiology, when does leukocyte recruitment occur and where?

A

Takes places during inflammation
Leukocytes adhere to endothelium of post-capillary venules and transmigrate into tissues

23
Q

What is the difference between a capillary and a post-capillary venule?

A

Structure similar but venules have more pericytes

24
Q

How is leukocyte recruitment different in atherosclerosis?

A

Leukocytes adhere to activated endothelium of large arteries and get struck in subendothlial space
Monocytes migrate into subendothelial space -> differentiate into macrophages -> become foam cells (following phagocytosis)

25
Q

How does vascular permeability contribute to atherogenesis?

A

Increased permeability results in leakage of plasma proteins through junctions into the subendothelial space
Lipoprotein trapping (by proteoglycans, ECM) and oxidation
Macrophages phagocytose material -> formation of foam cells

26
Q

Where does atherosclerosis typically occur and why?

A

Branch points - bifurcations and curvatures of the vascular tree
Flow pattern and haemodynamic forces are not uniform in the vascular system - turbulent vs laminar flow

27
Q

Describe blood flow and shear stress in ‘straight’ parts of the arterial tree

A

Laminar blood flow
Wall shear stress is high and directional

28
Q

Describe blood flow and shear stress in the branches and curvatures of the arterial tree. What can this cause?

A

Disturbed/turbulent blood flow
Non-uniform/irregular distribution of low wall shear stress
Can cause chronic endothelial activation

29
Q

Describe the protective effect of laminar blood flow on the vascular endothelium?

A

Promotes
-Antithrombotic and anti-inflammatory factors
-Endothelial survival
-Inhibition of smooth muscle cell proliferation
-Nitric oxide production
Disturbed blood flow promotes the exact opposite

30
Q

Outline the protective effects of NO on the vascular endothelium

A

Essential for health of CVS
- Dilates blood vessels
- Reduces platelet activation
- Inhibits monocyte adhesions
- Reduces proliferation of SMC in vessel wall
- Reduces release of superoxide radicals
- Reduces oxidation of LDL cholesterol (major plaque component)

31
Q

Define angiogenesis

A

Formation of new vessels by sprouting from existing vessels

32
Q

Angiogenesis is essential for what physiological processes?

A

Embryonic development
Menstrual cycle
Wound healing

33
Q

Describe the JANUS paradox of angiogenesis and cardiovascular disease

A

Angiogenesis promotes plaque growth in advanced atherosclerosis
However, therapeutic angiogenesis prevents damage post-ischaemia (e.g. MI)

34
Q

Describe the pathogenesis of atherosclerosis using the response to injury model

A
  1. Endothelial dysfunction
    - Endothlial permeability
    - Leukocyte migration
    - Leukocyte adhesion
  2. Fatty-streak formation
    - Foam-cell formation
  3. Formation of an advanced, complicated lesion
    - Macrophage accumulation
    - Formation of a necrotic core
    - Angiogenesis
35
Q

What processes promote early development of atherosclerotic plaques?

A

Endothelial activation
Leukocyte adhesion
Increased permeability to lipids

36
Q

What is thromboinflammation caused by and which recent disease is it thought to be associated with?

A

Loss of normal antithrombotic and anti-inflammatory functions of endothelial cells - leads to thrombosis and associated inflammation
Occurs in many disorders - thought to occur in COVID 19

37
Q

Describe two possible mechanism of endothelial activation and damage in COVID-19

A
  1. COVID Infection -> cytokine storm -> endothelial activation -> procoagulant switch
  2. Virus enters endothelial cells and causes direct damage (ACE2 expressed in EC?)

BRS Flashcards (Y2) (79 decks)

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