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CardioRespiratory 2 > Vascular Endothelium > Flashcards

Vascular Endothelium Flashcards

1
Q

x % of all endothelial cells reside within the (micro)vasculature?

A

98%

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2
Q

WHat is the basic structure of blood vessels?

A

Three layers:

TUnica Adventitia
Tunica Media
Tunica Intima

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3
Q

What is the tunica adventita made of?

A

vaso vasorum

nerves

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4
Q

What is the tunica media made of?

A

smooth muscle cells

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5
Q

what is the tunica Intimia made of?

A

Endothelium

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6
Q

Describe the structure of a capillary?

A

Made of endothelium supported by mural cells - pericytes and a basement membrane

Microvascular endothelium promoted homeostasis

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7
Q

What are the microvascular endothelium a source of?

A

Angiocrine factors required for the maintenace of tissue homeostasis and organ regeneration.

Not just a distribution system

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8
Q

What diseases may a dysfunctional endothelium cause?

A

Because it is so wide spread

ischaemia
cancer
diabetes
chronic inflammatory diseases

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9
Q

What is contact inhibition?

A

Process when the junction of two cells come together and this establishment of the junction stops the cells from growing more

So endothelial cells live a long life and have low proliferation rate unless angiogeness is needed

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10
Q

What blood related functions do endothelium have?

A
  • vascular tone
  • angiogensis
  • permeability
  • inflammation
  • haemostasis and thrombosis
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11
Q

What adhesion molecules do endothelial cells release? (inflammation)

A

ICAMs
VCAM

(both used for leukocyte adhesion during inflammation ^)

Selectins (type of lectin which starts the initial leukocyte adhesion)

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12
Q

What Inflammatory mediators do endothelial cells release? (inflammation)

A

IL-1 (promotes inflammatory cell recruitment)
IL-6
IL-8

Leukotrienes
MHC II

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13
Q

Which vasodilators do endothelial cells release? (vascular tone and permeability)

A

Nitric Oxide

Prostacyclin

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14
Q

What matrix products do endothelial cells release (angiogenesis)? (5)

A 
Fibronectin 
Laminin
Collagen
Proteoglycans
Proteases
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15
Q

What antithrombic factors do endothelial cells release? (thrombosis) (5)

A
  • Prostacyclin
  • Thrombomodulin
  • Antithrombin
  • Plasminogen activator
  • Heparin
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16
Q

Which procoagulant factors do endothelial cells release? (thrombosis)

A
  • VWF
  • Thomboxane A2
  • Factor V
  • Platelet activating factor
  • Plasminogen activator inhibitor
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17
Q

Which growth factors do endothelial cells release? (angiogenesis)?

A
  • Insulin like GF
  • Transforming GF
  • colony stimulating factor
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18
Q

Which pathways are switched on in resting endothelium?

A

anti inflammatory
anti thrombotic
anti rpoliferative

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19
Q

Which pathways are switched on when endothelium is active?

A

Pro inflammatory
Pro thrombotic
Pro angiogen

  • risk factors of atherosclerosis can cause chronic activation of the endothelium
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20
Q

What is the pathogenesis of atherosclerosis?

A

It is a response to injury:

initial injury caused by risk factor acitvated endothelium

  • > increased permeability
  • > increase the systems that increase leukocyte adhesion and migration
  • > leukocytes accumulate in subendothelial space
  • > forms ‘advances, complicated lesion of atheroscleroris’

Macrophages accumulate

21
Q

Which stimuli trigger endothelial cell dysfunction in atherogenesis?

A
  • Hypercholesterolaemia
  • Diabetes Mellitus/Metabolic syndrome
  • Hypertension
  • sex hormonal imbalance
  • Ageing
  • Oxidative stress
  • proinfammatory cytokines
  • infectious agents
  • environmental toxins
  • haemodynamic forces
22
Q

What is an example of hypercholesteraemia?

A

Oxidatively modified lipoproteins

risk factor for endothelial dysfunction

23
Q

Give an example of Sex hormonal imbalance?

A

Oestrogen deficiency and menopause

risk factor for endothelial dysfunction

24
Q

Give an example of environmental toxins?

A

cig smoke and air pollutants

risk factor for endothelial dysfunction

25
Q

Give an example of haemodynamic forces?

A

Disturbed blood flow

risk factor for endothelial dysfunction

26
Q

What are the four mechanisms that contribute to the development of atheresclerosis plaque?

A

Leukocyte recruitment

Permeability

Sheer stress

Angiogenesis

27
Q

Describe the leukocyte adhesion cascade?

A

Endothelial cells capture the L

[Activation] = Rolling –> slow rolling –> becomes ‘arrested’

Paracellular and transcellular transmigration

28
Q

Which molecules are involved in the capture of Leukocytes on the endothelial cells?

A

Selectins
PSGL1
VLA4

29
Q

Which molecules activate leukocytes and leads to ‘arrest’?

A

Chemokines

ICAM

30
Q

Which molecules cause paracellular migration of leukocytes along endothelial?

A

PECAM
JAMs
ESAM

31
Q

Which molecules cause transcellular migration of leukocytes along endothelial?

A

ICAM1

PECAM1

32
Q

Where does leukocyte recruitment take place usually?

A

post capillary venules and transmigrate into tissues

  • post capillary venules are similar to capillaries but with mor epericytes
33
Q

What happens to leukocyte recruitment in atherosclerosis?

A

L adhere to the activated endothelial of LARGE ARTERIES and get stuck in subendothelial space

34
Q

How are foam cells formed?

A

monocytes migrate into subendothelial space, differentiate into macrophages and become foam cells

35
Q

What does increased permeability do?

A

Results in leakage of plasma proteins through the junctions into the subendothelial space

36
Q

WHy does atherosclerosis occur at branch points?

A

turbulent disturbed flow with nonuniform and irregular distribution of low wall shear stress. Where there are branches and curvatues

37
Q

What is the effect of of laminar blood flow on vascular endothelium?

A

Promotes:

anti thrombotic and antiflammtory factor (thrombomodulin)

endothelial survical

inhibition of SMC proliferation

NO production

38
Q

What does disturbed blood flow pormote in vascular endothelium?

A

thrombosis

inflammation - leukocyte adhesion

endothelial apoptosis

SMC proliferation

Los of NO productions

39
Q

What are the effects of NO on the vascular endothelium?

A

Dilates blood vessels

reduce platelet activation

inhibits monocyte adhesun

reduces proliferation and SMC in the vessel wall
Reduces release of superoixde radicals

Reduces ocidation of LDL cholesterol - major component of palque

40
Q

What is angiogenesis?

A

formation of new vessels by sprouting from existing vessels - triggered by the need for O2

41
Q

How does hypoxia lead to angiogenesis and hence vascular stablisation?

A

EC receptor binding

EC activation

EC proliferation

`Directional migration

ECM remodelling
tube reformation

Loop formation

vascular stabliation

42
Q

What is angiogenssi used for in the body?

A

Embryonic develoopment

Menustraul cyce
Wound healing

43
Q

What role does angiogensis play in cardiovascular disease?

A

promotes plaque growth

but also

therapeutic angiogenesis prevents post ischaemia

44
Q

What patterns of coagulopathy are seen in COVID 19 px?

A

venous and arterial thrombi frequent

increased coagulopathy correlates with pognosis

local thrombosis signs that it is due to a loss in endothelial homeostasis

45
Q

what is it called when both thrombotic factors and inflammatory functions are lost?

A

Thromboinflammation - both occuring due to activated endothelial cell

46
Q

when may thromboinflammation occur

A

sepsis

iichaemia reperfusion injury

47
Q

How does SARS CoV2 infection lead to procoagulant switch turning on?

A

Cytokine storm –> endothelial activation –> procoagulant switch

48
Q

Physiologically, in which vessels does leukocyte transmigration occur?

A

In post capillary venules

49
Q

Which of these processes promotes early development of atherosclerotic plaques?

A
  • Endothelial activation
  • Permeability
  • Leukocyte adhesion

CardioRespiratory 2 (12 decks)

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