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BRS YEAR 2 > Cardio - Vascular Endothelium > Flashcards

Cardio - Vascular Endothelium Flashcards

1
Q

Where do the majority of endothelial cells reside

A

98% are found in the microvasculature

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2
Q

What is the basic structure of the blood vessels

A

Tunica adventitia
Tunica media
Tunica Intima

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3
Q

What is in the tunica adventitia

A

Vasa Vasorum

Nerves

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4
Q

What is in the tunica media

A

External elastic membrane

Smooth muscle

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5
Q

What is in the tunica intima

A

Internal elastic membrane
Lamina propria
Basement membrane
Endothelium

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6
Q

Where does the typical blood vessel structure not apply in the vasculature

A

Venules and capillaries

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7
Q

What’s in the lamina propria

A

Smooth muscle and connective tissue

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8
Q

What are vasa vasorum

A

Blood vessels that supply to larger vessels

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9
Q

What do capillaries and venules consist of

A

Endothelial monolayer with supporting mural cells called pericytes and a surrounding basement membrane

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10
Q

How do we know that endothelial cells contribute to tissue homeostasis

A

We have seen that endothelial cell damage can lead to dysfunction of the respective organ - therefore it is a source of angiocrine factors that promote tissue homeostasis and organ regeneration

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11
Q

What diseases can a dysfunctional endothelium contribute to

A

Cancer
Diabetes
Chronic Inflammatory disease
Ischaemia

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12
Q

What is meant by heterogenous endothelial cells

A

Endothelial cells and microvasculature have organotypic properties and expression profiles relevant to their specific tissue

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13
Q

What are the capillaries of the kidney and liver like

A

Very permeable to allow for constant transport

(Kidney = fenestrated continuous, 
Liver = discontinuous)
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14
Q

What are the capillaries of the brain like

A

Tight blood brain barrier to restrict entry and access to brain

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15
Q

Describe the morphology of endothelial cells

A

Flat
Large surface area
Form a monolayer

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16
Q

How do endothelial cells form a monolayer

A

Contact inhibition - junctions form between 2 endothelial cells and this triggers them to stop growing

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17
Q

What cells typically form monolayers

A

Only endothelial and epithelial cells

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18
Q

Describe the life span or proliferation rate of endothelial cells

A

Very long lifespan and low proliferation rate unless new blood vessels are needed for angiogenesis

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19
Q

What essential functions of blood vessels are controlled by endothelial cells

A 
Vascular tone
Inflammation
Permeability 
Haemostasis and thrombosis 
Angiogenesis
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20
Q

How do endothelial cells control angiogenesis

A

Matrix products e.g. proteoglycans

Growth factors e.g. IGF-1

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21
Q

How do endothelial cells control vascular tone and permeability

A

Vasoconstrictors e.g. ACE

Vasodilators e.g. NO

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22
Q

How do endothelial cells control inflammation

A

Adhesion molecules e.g. ICAMs

Inflammatory mediators e.g. IL-1

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23
Q

How do endothelial cells control thrombosis and haemostasis

A

Procoagulants e.g. VWF

Anticoagulants e.g. heparin

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24
Q

What are the properties of resting endothelium

A

Anti-inflammatory
Anti-thrombotic
Anti-proliferative

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25
Q

What are the properties of active endothelium

A

Pro-inflammatory
Pro-thrombotic
Pro-proliferative

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26
Q

What is a physiological switch from resting to active endothelium

A

Occurs in a controlled time and space in order to respond to an event - occurs as part of haemostasis

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27
Q

What causes chronic endothelial activation and what are the effects of this?

(hint - LIST)

A

When we have chronic activation for example from the triggers for atherosclerosis, we get chronic activation. Over time, this causes thrombosis, senescence, leukocyte recruitment, and increased permeability.

28
Q

List examples of things that can cause activation of endothelium (SHIVHOM)

A 
Smoking
Hypertension
Inflammation
Viruses
High glucose
OxLDL
Mechanical stress
29
Q

What is the accepted model form the pathogenesis of atherosclerosis

A

Response to Injury model

30
Q

What is the model for atherosclerosis

A

We get initial injury, this causes endothelial activation and as a result there’s increased permeability, increased leukocyte recruitment and adhesion leading to subsequent transmigration. Transmigration of leukocytes leads to their accumulation in the sub endothelial space - their phagocytosis causes foam cell formation.
As we get more and more advanced, we get more and more macrophage accumulation. They then die and form a necrotic core which forms an inflammatory lesion, and then stimulated angiogenesis from the vasa vasorum in the adventitia

31
Q

What are the stimuli and risk factors for atherosclerosis

A 
Hypercholesterolaemia 
Diabetes mellitus/ metabolic syndrome
Hypertension 
Sex hormonal balance
Ageing 
Oxidative stress
Proinflammatory cytokines
Infectious agents
Environmental toxins 
Haemodynamic forces

O PHISH HEAD

32
Q

What are the 4 mechanisms contributing to the formation of atherosclerotic plaques

A

Leukocyte recruitment
Permeability
Shear stress
Angiogenesis

33
Q

Describe the adhesion cascade

A

Classical cascade for leukocyte recruitment - endothelium expresses various molecules to prompt response e.g. ICAM.
Cells roll and then find a junction through which they can migrate to work within the tissue during an inflammatory response

34
Q

What happens to children without a functioning cascade

A

Die after a few months as they can’t protect themselves from inflammation

35
Q

Where does physiological leukocyte migration most typically happen

A

Post-capillary venules - they enter into tissues by squeezing through the cell and chewing up the BM before entering

36
Q

What is the difference between venule and capillary structure

A

Venules have more pericytes than capillaries

37
Q

Where does pathological leukocyte migration happen

A

Large arteries

38
Q

What is the problem with leukocyte migration in large arteries

A

They can’t chew past the various layers of the larger arteries so they get stuck in the sub endothelial space

39
Q

What is the vascular endothelium

A

Layer of cells controlling the flux of fluids and molecules in there blood to and from tissues

40
Q

What is the significance of increased permeability

A

Increase in plasma proteins leaking through to the sub endothelial space which as sticky ECM and proteoglycans

41
Q

What is lipoprotein trapping

A

When the endothelium is activated with increased permeability, we get lipoproteins travelling into the sub endothelial space.
They bind to proteoglycans causing their oxidation.
Macrophages which have also inappropriately migrated into the sub endothelial space will phagocytose the oxidated LDL to form foam cells

42
Q

Where does atherosclerosis preferentially occur

A

Bifurcations and curvatures of the vascular tree

43
Q

Why does atherosclerosis target bifurcations and curvatures

A

Varying flow pattern and balance of haemodynamic forces along the vasculature

44
Q

What’s the difference between straight arteries and branches/curvatures

A

Straight arteries = laminar flow that has a high directional shear stress

Branches/curvatures = disturbed turbulent flow that’s irregularly distributed to give a low wall shear stress

45
Q

What does laminar flow promote

A
  • Anti-thrombotic factors such as thrombomodulin
  • Anti-inflammatory factors
  • Endothelial survival
  • Inhibition of SMC proliferation
  • NO production
46
Q

What does disturbed or turbulent flow promote

A 
Thrombosis 
Inflammation
Endothelial apoptosis 
SMC proliferation
Loss of NO production
47
Q

What the role of nitric oxide (6)

A 
Dilates blood vessels 
Reduces LDL oxidation
Reduces superoxide radical release
Reduces SMC proliferation 
Inhibits monocyte adhesion 
Reduces platelet activation
48
Q

What is angiogenesis

A

Formation of new blood vessels sprouting from existing blood vessels

49
Q

What triggers angiogenesis

A

Generally hypoxia causes downstream signalling to endothelial cells, this up-regulating factors to initiate angiogenesis through the release of angiogenic factor production

50
Q

What is angiogenesis involved with

A

Embryonic development
Menstrual cycle
Wound healing
Also seen in some diseases

51
Q

What is the janus paradox of angiogenesis in CVD

A

It has both a beneficial and harmful role in cardiovascular disease

52
Q

How is angiogenesis good in CVD

A

We can induce angiogenesis downstream of blocked arteries to prevent damage from ischaemia

53
Q

How is angiogenesis bad in CVD

A

lesions become chronic inflammatory diseases of blood vessels to stimulate angiongenesis in the vasa vasorum of the adventitia which contributes to plaque growth

54
Q

What is the significance of COVID-19 with endothelial activation - how does this present clinically?

A

There may be a systemic endothelial activation therefore loss of haemostasis due to the presence of local in situ thrombosis in COVID, and how many COVID patients experience both venous and arterial thrombi

55
Q

What does coagulopathy mean for prognosis

A

Increase in D-dimer and fibrinogen, and correlates with a poor prognosis

56
Q

What is recommended for COVID patients at risk from coagulopathy

A

Anti-thrombotic therapy - under review

57
Q

What are CEC - how do they relate to anti-thrombotic therapy

A

Circulating endothelial cells (marker for injury -shed form damage) - found in severe COVID - however anti-coagulation in COVID patients showed a reduction in CEC

58
Q

What is thrombo-inflammation

A

Loss of resting endothelium anti-thrombotic/inflammatory properties therefore we get thrombosis associated with inflammation in COVID

59
Q

When does thromboinflammation occur

A

COVID and other systemic inflammatory disorders

60
Q

How does COVID disrupt endothelial function

A 
Bleeding/thrombosis
Inflammation
Change to permeability
Change in vascular tone
Change in redox balance

Causes endothelial activation

61
Q

What are the mechanisms for activation and damage of endothelium with COVID

A

SARS-CoV2 Infection leads to cytokine storm therefore massive inflammatory reaction. This causes endothelial activation and a consequent procoagulant switch

62
Q

How does COVID cause direct damage to endothelial cells

A

2 possible mechanisms:

  1. Cytokine storm
  2. SARS-CoV2 enters endothelial cells and causes direct damage
63
Q

Where is ACE2 expressed

A

Epithelial cells, not in endothelial cells

64
Q

Does COVID replicate in endothelial cells?

A

No

65
Q

What is the clinical significance of looking at COVID’s role with reference to the endothelium

A

drugs that reduce endothelial activation may be beneficial in COVID-19 patients however the drug screen is still ongoing

BRS YEAR 2 (37 decks)

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