Vascular endothelium Flashcards

1
Q

What are the three structural layers of blood vessels?
Superficial to deep

A

Tunica adventitia - VAN
Tunica media - smooth muscle cells
Tunica intima - endothelium

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2
Q

What are pericytes?

A

Cells that wrap around capillaries for protection (act similar to astrocytes in blood brain barrier)

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3
Q

What is contact inhibition and why is it useful in endothelial cells?

A

Communication between cell-cell junctions to arrest growth when cells come into contact with each other - therefore a one-cell thick layer is created

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4
Q

What are the 6 functions of endothelium?
VIPATH

A

Vascular Tone
Inflammation
Permeability
Angiogenesis
Tissue Homeostasis
Haemostasis/Thrombosis

regulate vessel function

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5
Q

What is endothelial heterogeneity?

A

Endothelial cells have organotypic (tissue specific) structures and gene profiles to match the rq of the microenvironment

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6
Q

What are angiocrine factors?

A

Growth factors that result in the formation of tissue-specific endothelium

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7
Q

What is the most common way of forming new blood vessels?

A

Sprouting angiogenesis

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8
Q

What is the main trigger of angiogenesis?

A

Hypoxia

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9
Q

Mechanism of angiogenesis

A

Hypoxia
activation of pro-angiogenic factors (VEGF)
Bind to endothelium and trigger activation and proliferation towards region of hypoxia

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10
Q

Where is angiogenesis useful in the body?

A

Foetal Development,
Menstrual Cycle,
Wound Healing

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11
Q

Pathological causes of angiogenesis

A

Cancer
Retinopathy
Atherosclerosis
Ischaemic disease

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11
Q

Why is angiogenesis common in tumours?

A

As tumours get suddenly larger, certain areas become hypoxic - this triggers angiogenesis to supply blood to the larger parts of the tumour

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12
Q

What is the discrete step in tumour development where angiogenesis starts?

A

Angiogenic Switch

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13
Q

How is the structure of tumour blood vessels different to normal vessels?

A

Irregularly shaped, dilated, leaky

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14
Q

Complication of VWD

A

Angiodysplasia (vascular malformations) in the GI tract can cause severe intractable bleeding (no treatable by replacing VWF)

Shows that VWF affects platelet adhesion as well as endothelial angiogen

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15
Q

What are some risk factors for an activated endothelium?

A

Smoking, Mechanical Stress, High Blood Pressure, High Glucose

16
Q

What are the 4 mechanisms of endothelial dysfunction in atherosclerosis?

A

Leukocyte Recruitment,
Permeability,
Shear stress
Angiogenesis

Contribute to the development of atherosclerosis

17
Q

How does leukocyte recruitment occur?

A

Rolling
Adhesion
Transmigration into tissue

18
Q

When does leukocyte recruitment occur more frequently?

A

Inflammation - typically in post-capillary venules

19
Q

How does leukocyte recruitment contribute to atherosclerosis?

A

Leukocytes get stuck in sub-endothelial space,
monocytes -> macrophages -> foam cells
form plaque

20
Q

How does ^ permeability contribute to atherosclerosis?

A

Inflamm -> ^ permeability
LDL enters subendothelial space -> OxLDL
bind macrophages -> foam cells

21
Q

At what parts of the vascular tree do atherosclerotic plaques occur more commonly?

A

Bifurcations and curvatures
Formation of vortexes/turbulent flow
Leads to low shear stress

22
Q

Describe what laminar (high shear stress) blood flow promotes

A

Laminar :
anti-thrombotic, anti-inflammatory,
inhibition of smooth muscle cell proliferation
NO production

23
Q

What does disturbed, (low shear stress) flow promote

A

Thrombosis, inflammation
endothelial apoptosis
SMC proliferation
Red. NO prod.

24
Q

What are the protective effects of nitric oxide on vascular endothelium?

A

Vasodilator,
Antiplatelet,
reduces smc proliferation,
red. release of ROS

25
Q

What are the contradicting good and bad effects of angiogenesis?

A

Bad - angiogenesis promotes plaque growth
Good - therapeutic angiogenesis prevents damage post-ischaemia

26
Q

How does severe COVID-19 manifest in vasculature?

A

COVID-19 infection triggers cytokine storm activating endothelial cells and coagulation
-> ^ clot risk