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My LSS- CVS > CVS 17: Vascular Endothelium > Flashcards

CVS 17: Vascular Endothelium Flashcards

1
Q

What is atherosclerosis and which arteries does it particularly affect?

A
  • Build up of fibrous and fatty material inside the arteries and is the underlying condition that causes CHD
  • those which supply the head, brain and legs
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2
Q

What sort of disease is atherosclerosis?

A

A chronic inflammatory disease

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3
Q

What are the steps causing atherosclerosis?

A
  1. Endothelial dysfunction in atherosclerosis leads to increased permeability, leukocytes migration and adhesion under the endothelium
  2. Fatty-streak formation and foam cell formation
  3. Formation of an advanced and complicated lesion where a necrotic core and fibrous cap is formed with macrophage accumulation
  4. Angiogenesis to supply the new mass
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4
Q

What are the three layers of blood vessels? Which vessels are exceptions to the three layer structures

A
  1. Tunica intima- endothelium
  2. Tunica media- smooth muscle cells
  3. Tunica adventitia- vasa vasorum, nerves

**capillaries and venules

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5
Q

What is contact inhibition?

A

Formation of a monolayer by the endothelial cells

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6
Q

what is heterogeneity in terms of endothelial cells?

A

Not all endothelial cells are the same

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7
Q

Describe the structure of endothelial cells

A

Very flat

1-2μm which and 10-20μm in diameter

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8
Q

Name the four critical functions of endothelial cells

A
  • inflammation
  • vascular tone and permeability
  • angiogenesis
  • thrombosis and haemostasis
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9
Q

What state are healthy endothelial cells in?

A
  • anti-inflammatory
  • anti- thrombotic
  • anti- proliferative
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10
Q

What state are endothelial cells in during inflammation?

A
  • pro-inflammatory
  • pro-thrombotic
  • pro-angiogenic
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11
Q

What do leukocytes normally adhere to during inflammation?

A
  • leukocytes adhere to the endothelium of post-capillary venules and transmigrate into tissues
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12
Q

What goes wrong with leukocyte recruitment during atherosclerosis?

A
  • leukocytes adhere to the activated endothelium of large arteries
  • they get stuck in the sub endothelial space
  • newly formed post-capillary venues at the base of lesions = further entry
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13
Q

Summarise the process of transmigration, diapedesis and chemotaxis

A
  1. Rolling- weak selectin binding
  2. Activation- activate integrin binding
  3. Firm adhesion- integrin binding with ICAM-1 on endothelial cells
  4. Diapedesis- paracellular–> transcellular transmigration
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14
Q

What is the function of VE-cadherins for transmigration of leukocytes across the endothelium?

A
  • VE-cadherin (vascular endothelial cadherins) acts as a zipper
  • allow cell membranes to bind in a homophilic way
  • leukocytes has to unzip the cadherins to get through
  • allows substances to get through without monolayer falling apart
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15
Q

What happens if you have a mutation in VE-caderins?

A

Not compatible with life

Can’t fight off infections

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16
Q

What is the difference between the transmigration process between venues and arteries?

A
  1. Capillary- endothelial cells surrounded by basement membrane and pericytes (TM is possible) just uses enzymes to get through BM
  2. Post-capillary venues- similar to capillary but with more pericytes
  3. Artery: three thick layers, so can get through endothelium but can’t go through other layers –> atherosclerosis
17
Q

What is the consequence of increased vascular permeability?

A
  • Leakage of plasma protein through endothelial junctions into sub-endothelial space
18
Q

What is found right below the endothelium?

A
  • sticky molecules

= collagens and proteoglycans

19
Q

How are foam cells formed?

A
  • LDLs go under the endothelial layer when endothelium is activated
  • stuck in sub endothelium because of sticky proteins
  • oxidised in oxidative environment
  • macrophages phagocytose oxidised LDLs
  • forms foam cells
20
Q

What is the significance of foam cells?

A

Source of chronic inflammation

21
Q

What are the two different types of flow? Briefly describe them

A
  1. Laminar flow
    - streamlined
    - outermost layer moves slowest, innermost moves fastest
    - platelets carried in centre
  2. Turbulent flow
    • Interrupted
    • Rate of flow exceeds critical velocity
    • when fluid passes a contraction, sharp turn or rough surface
22
Q

Why does atherosclerosis occur at branch points?

A

You get turbulent flow at branch points

Laminar flow= detected by endothelium as +ve protective signal but turbulent = opposite

23
Q

What does laminar flow promote?

A
  • anti- thrombotic, anti- inflammatory factors
  • endothelial survival
  • NO production
  • Inhibition of SMC proliferation
24
Q

What does turbulent blood flow promote?

A
  • coagulation
  • leukocyte adhesion
  • SMC proliferation
  • endothelial apoptosis
  • loss of NO production
25
Q

What are the beneficial effects of NO? (6 effects)

A
  • dilates blood vessels
  • reduces platelet activation
  • inhibits monocyte adhesion
  • reduces proliferation of SMC in vessel wall
  • reduces release of superoxide radicals
  • reduces oxidation of LDL cholesterol
26
Q

What are epigenetic?

A
  • functionally relevant, inheritable changes to gene expression which do not involve a change in the nucleotide sequence
27
Q

Name three key epigenetic mechanisms

A
  • DNA methylation
  • histone modification
  • miRNa
28
Q

What is angiogenesis?

A

Formation of new blood vessels by sprouting from pre-existing vessels

29
Q

When do you get angiogenesis and what happens to trigger it?

A
  • when a tissue become hypoxic
  • releases chemicals
  • activates existing blood vessels
  • triggers change in cell –> tip cell
  • tip cell takes over and controls formation of blood vessel
30
Q

What is the disadvantage of angiogenesis in CVD?

A

PROMOTES GROWTH OF ATHEROSCLEROTIC PLAQUES
- advanced plaque -> necroticdebris-> hypoxia-> angiogenesis from vasa vasorum -> more leukocytes come in -> plaque grows

31
Q

What are the potential benefits of angiogenesis in CVD?

A
  • tissue which suffered from MI becomes fibrotic –> heart failure
  • can reoxygenate myocardium through therapeutic angiogenesis
32
Q

What is cellular senescence?

A

Growth arrest that halts the proliferation of ageing and/ or damaged cells

33
Q

What are the advantages of senescence?

A

Prevents transmission of damage to daughter cells so that they don’t take over. Protective against cancer

34
Q

What are the disadvantages of senescence?

A

Pro-inflammatory and pro-thrombotic and contribute to diseases. Found in atherosclerotic lesions.

35
Q

What can trigger endothelial cell senescence?

A

CV risk factors such as oxidative stress

36
Q

What does red wine contain which could be beneficial? How is it beneficial?

A

RESVERATROL

- has anti-inflammatory properties on the endothelium

37
Q

What is the red wine paradox?

A

HORMETIC ACTION

  • beneficial low dose
  • cytotoxic at higher doses

My LSS- CVS (21 decks)

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