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CARDIORESPIRATORY 2 > VASCULAR ENDOTHELIUM > Flashcards

VASCULAR ENDOTHELIUM Flashcards

1
Q

What are the 3 layers of blood vessels?

Excluding capillaries and venules

A

Tunica adventitia - vasa vasorum, nerves
Tunica media - smooth muscle cells
Tunica intima - endothelium

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2
Q

What is the structure of a capillary?

A

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

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3
Q

Why is microvascular endothelium so important?

A

Source of angiocrine factors needed for tissue homeostasis and organ regeneration

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4
Q

Where is non-fenestrated microvasculature seen?

A

muscle, lung, skin, BBB

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5
Q

Where is fenestrated microvasculature seen?

A

Kidney gomerulus

GI tracy

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6
Q

Where is discontinuous microvasculature seen?

A

Liver

Marrow sinus

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7
Q

What are the dimensions of an endothelial cell?

A

1-2 um thick

10-20 um in diameter

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8
Q

How do endothelial cells form a flat monolayer?

A

Via contact inhibition where endothelial cell-cell junctions are formed. Once formed this signals the cells to stop growing

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9
Q

What functions of the blood vessels and tissues does the endothelium control?

A 
Vascular tone
Angiogenesis
Permeability
Inflammation
Haemostasis and thrombosis
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10
Q

How do the endothelial cells control thrombosis and haemostasis?

A 
Procoagulant factors (VWF, thromboxane A2...)
Antithrombotic factors (prostacyclin, antithrombin...)
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11
Q

How do the endothelial cells control angiogenesis?

A 
Matrix products (fibronectin, laminin, collagen...)
Growth factors (IGF, TGF, colony stimulating factor)
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12
Q

How do the endothelial cells control inflammation?

A 
Inflammatory mediators (IL 1/6/8, leukotrienes, MHC II)
Adhesion molecules (ICAMs, VCAM, selectins)
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13
Q

How do the endothelial cells control vascular tone and permeability?

A 
Vasoconstricting factors (ACE, thromboxane A2...)
Vasodilating factors (nitric oxide, prostacyclin)
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14
Q

What are the two sides of endothelial homeostasis?

A

Resting endothelium:

  • anti-inflammatory
  • anti-thrombotic
  • anti-proliferative

Activated endothelium:

  • pro-inflammatory
  • pro-thrombotic
  • pro-angiogenic
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15
Q

List the factors which can cause activation of the endothelium

A 
Mechanical stress
Inflammation
High blood pressure
OxLDL
Highe glucose
Viruses
Smoking
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16
Q

What does chronic activation of the endothelium lead to?

A

Atherosclerosis

17
Q

What does activated endothelium cause?

A

Thrombosis
Senesence
Leukocyte recruitment
Permeability

18
Q

Outline the pathogenesis of atherosclerosis

A
  1. Endothelial dysfunction causing leukocyte migration and adhesion into the sub-endothelial spaces
  2. Fatty streak/foam cell formation
  3. Formation of advanced, complicated lesion of atherosclerosis
19
Q

What are the stimuli and risk factors for atherogenesis?

A

Hypercholesterolaemia
Diabetes mellitus/metabolic syndrome
Hypertension
Sex hormonal imbalance (oestrogen def, menopause)
Ageing (endothelial cell senescence and inflammation)
Oxidative stress
Pro inflammatory cytokines
Infectious agents
Environmental toxins
Haemodynamic forces (disturbed blood flow)

20
Q

What are the mechanisms in the pathogenesis of atherosclerosis?

A

Leukocyte recruitment
Permeability
Shear stress
Angiogenesis

21
Q

Where does leukocyte adhesion and migration usually occur?

A

Post-capillary venule and transmigrated into tissues

22
Q

What are post-capillary venules?

A

Structure similar to capillaries but have more pericytes

23
Q

What normally occurs in the transmigration of leukocytes into tissues compared to what occurs in atherosclerosis?

A

Transmigration via paracellular or transcellular in post capillary venules then chews up basement membrane to get to tissue

In atherosclerosis, leukocytes adhere to activated endothelium which are expressing markers in LARGE ARTERIES. When they squeeze through the endothelium they are instead presented with the thick walls of the artery and become stuck in subendothelial space

24
Q

How are foam cells in atherosclerosis formed and what does this promote?

A

Monocytes migrate into the subendothelial space and differentiate into macrophages and become foam cells promoting the formation of plaque

25
Q

What is the role of vascular permeability in the pathogenesis of atherosclerosis?

A

Increased permeability causing leakage of plasma proteins especially lipoproteins through the junctions into the subendothelial space.

The lipoproteins are trapped by proteoglycans in the subendothelial space and then are oxidised. The macrophages accumulated in the space then phagocytose the oxidised lipoproteins to form the foam cell

26
Q

Where does atherosclerosis occur predominately and why?

A

Bifurcations and curvatures in the vascular tree because low/disturbed blood flow occurs here. This causes low wall shear stress

27
Q

What effect does laminar blood flow have on vascular endothelium?

A

Promotes:

  • Anti-thrombotic factors
  • Anti-inflammatory factors
  • Inhibition of SMC proliferation
  • Nitric oxide production
28
Q

What effect does disturbed blood flow have on vascular endothelium?

A

Promotes:

  • Thrombosis
  • Inflammation
  • SMC proliferation
  • Loss of nitric oxide production
29
Q

What are the effects of nitric oxide on the cardiovascular system?

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 (major component of plaque)

30
Q

What is angiogenesis?

A

The formation of new vessels by sprouting from existing vessels generally triggered by need for oxygen

31
Q

What processes is angiogenesis essential for?

A

Embryonic development
Menstrual cycle
Wound healing

32
Q

What is the relationship between angiogenesis and CVD?

A

2 faced:

  • Promotes plaque growth causing blocks
  • Used therapeutically preventing damage post
    ischaemia. Stimulated to revascularise heart tissue
33
Q

What is the link between thrombosis and coagulopathy in COVID19 patients?

A

Both venous and arterial thrombi frequent in COVID19 patients
Coagulopathy correlates with poor prognosis
Anti-thrombotic therapy is recommended to all hospitalised patients

34
Q

What is thromboinflammation?

A

Loss of normal antithrombotic and anti-inflammatory functions of endothelial cells

Occurs in many disorders e.g. sepsis

35
Q

What is the mechanism for endothelial activation and damage in COVID19 disease?

A

2 possible mechanisms:

  • Cytokine storm secondary to infections
  • COVID enters endothelial cells causing direct damage (no published evidence that COVID binds to endothelial)

CARDIORESPIRATORY 2 (8 decks)

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