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Yr 2 - EMS > Atheroma - Revision > Flashcards

Atheroma - Revision Flashcards

1
Q

What are the 3 layers of an arterial vessel?

A
  1. Intima
  2. Media
  3. Outer adventitia
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2
Q

Which layer of the arterial vessel is located closest to the arterial lumen?

A

Intima

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3
Q

What is the intima composed of?

A

A single layer of endothelial cells (endothelium)

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4
Q

Effect of NO and prostacyclin?

A

Relax blood vessels (vasodilation) and inhibit platelet activation (limit thrombosis)

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5
Q

What are NO and prostacyclin released by?

A

Endothelial cells

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6
Q

In normal endothelium, describe and explain the;

a) smooth muscle cells?
b) net coagulant or anticoagulation?
c) adhesion molecules?

A

a) relaxed - due to release of NO and prostacyclin
b) net anticoagulant properties
c) no expression of leucocyte adhesion molecule

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7
Q

How does the endothelium modulate contraction of smooth muscle cells in the media?

A

By releasing substances such as vasodilators and vasoconstrictors

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8
Q

Examples of vasodilators?

A

NO and prostacyclin

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9
Q

Example of vasoconstrictor?

A

Endothelin

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10
Q

What does ‘endothelial cell activation’ refer to? What could this be caused by?

A

Endothelium undergoes changes to allow it to contribute in the inflammatory response.

Caused by e.g: common stresses (e.g. shear stress and mild changes in temperature), transient infections and minor trauma.

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11
Q

What are the five core changes of endothelial cell activation?

A
  1. Loss of vascular integrity
  2. Expression of leucocyte adhesion molecules
  3. Change from antithrombotic to prothrombotic
  4. Cytokine production
  5. Vasoconstriction
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12
Q

What characterises the normal arterial endothelium?

A
  1. Net anticoagulant properties
  2. Net relaxation of smooth muscle cells
  3. Anti-inflammatory characteristics
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13
Q

What is the elasticity of a vessel regulated by?

A

The lamina elastica

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14
Q

Purpose of lamina elastica?

A

Provide elasticity and prevent the vascular wall from collapsing

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15
Q

Why is lamina elastica important in atherosclerosis

A

it prevents the weakening of the vessel wall that can prevail as a complication of atherosclerosis

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16
Q

Where is lamina elastica found?

A

Between intima and media

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17
Q

Normally, what do smooth muscle cells synthesise that contributes to connective tissue matrix of the vessel wall?

A

Collagen, elastin and proteoglycans

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18
Q

What inflammatory and vasoactive mediators do smooth muscle cells synthesis

A

E.g. IL-6 and TNF-a

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19
Q

Effect of IL-6 and TNF-a?

A

Stimulate leukocyte migration and induce the endothelial cells to express leukocyte adhesion molecules

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20
Q

What is an atheroma?

A

An abnormal accumulation of material in the intima

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21
Q

What are the 5 key stages of atheroma formation?

A
  1. Endothelial dysfunction
  2. Formation of lipid layer or fatty streak within theintima
  3. Migration of leukocytes and smooth muscle cells into the vessel wall
  4. Foam cell formation
  5. Degradation of extracellular matrix
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22
Q

What 3 main stages can the formation of the plaque be divided into?

A
  1. Fatty streak
  2. Plaque progression
  3. Plaque disruption
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23
Q

Does a fatty streak protrude substantially into the artery wall or impede blood flow?

A

No (people over 20 tend to have)

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24
Q

What allows circulating LDLs into the intima?

A

Disruption of endothelial barrier due to endothelial dysfunction

25
Q

What does entry of lipids into the intima stimulate?

A

Creates a proinflammatory environment and initiates the migration of leukocytes and formation of foam cells

26
Q

What are factors associated with endothelial dysfunction?

A 
Increased age
Male sex
Family history of CHD
Smoking
Elevated cholesterol
Low HDL-cholesterol
Diabetes mellitus
Hypertension
Obesity
High fat consumption
27
Q

How does NO function as an anti-atherosclerotic substance?

A
  1. Vasodilation
  2. Inhibition of platelet aggregation
  3. Anti-inflammatory effects
28
Q

Why are atheromas more likely to occur at sites of bifuraction?

A

Disturbed flow can impair protective functions

29
Q

How can smoking lead to atheromas?

A

Exposure to chemical irritants promotes endothelial dysfunction by increasing endothelial production of reactive oxygen species.

This leaves the endothelium become inclined to exhibit pro-inflammatory processes, such as secreting inflammatory cytokines.

30
Q

How do macrophages become foam cells?

A

Macrophages adhere to dysfunctional endothelial cells and transmigrate into the intima.

These macrophages are called ‘foam cells’ after they have taken up LDLs.

31
Q

What hypothesis can explain the recruitment of inflammatory cells after injury?

A

Response to injury hypothesis

32
Q

How do foam cells encourage the plaque progression?

A

Serving as a source of proinflammatory cytokines.

33
Q

What are the 2 features of an atherosclerotic plaque?

A
  1. Lipid-rich necrotic core

2. Fibrous cap

34
Q

What does the fibrous cap contain?

A

Dead foam cells, macrophages, smooth muscle cells, lymphocytes and extracellular matrix

35
Q

How can the vessel compensate during the early stages of the atherosclerotic plaque?

A

a compensatory outward remodeling of the plaque wall (preserves the diameter of the vessel lumen)

36
Q

Progressive vessel narrowing may result in ischaemia. What are some ischemic symptoms?

A

angina pectoris or intermittent claudication

37
Q

During the phase of transition from fatty streak to plaque formation, where do the smooth muscle cells migrate from/to?

A

From the media to the intima

38
Q

Once in the intima, what do smooth muscle cells do?

A

proliferate within the intima and secrete extracellular matrix molecules

39
Q

What do foam cells release that directly contribute to the migration and proliferation process of SMCs?

A

platelet derived growth factor (PDGF), cytokines and growth factors

40
Q

What predisposes a plaque to rupture? What influences this process?

A

Metabolic processes in extracellular matrix weaken the fibrous cap.

This process is influenced by the balance of matrix deposition synthesis by smooth muscle cells and degradation by matrix metalloproteinases (MMP)

41
Q

What is MMP secreted by?

A

Foam cells that are stimulated by inflammatory cytokines

42
Q

How does MMP weaken the fibrous cap?

A

degrades collagen and elastin of the fibrous cap

43
Q

What causes the lipid core to grow?

A

Cell death leads to release of cellular contents, whereby more lipids and cellular debris is absorbed to the dynamic lipid core

44
Q

What is released when the fibrous cap is ruptured? What does this lead to?

A

The highly thrombogenic components of the necrotic core are in direct contact with the circulating monocytes in the blood

Will lead to the formation of thrombus at the rupture site.

45
Q

What does inflammatory stimuli in the plaque environment iniciate?

A

smooth muscle cells, endothelial cells, and foam cells to release tissue factor that initiates the extrinsic coagulation pathway

also stimulate expression of antifibrinolytics

46
Q

How can activated endothelial cells contribute to thrombosis?

A

depositing fibrin at the vascular wall

47
Q

What are the most common locations of atherosclerosis?

A
  1. Dorsal section of the abdominal aorta
  2. Proximal coronary arteries
  3. Popliteal arteries
  4. Descending thoracic aorta
  5. Internal carotid arteries
    6, Renal arteries
48
Q

What is angina pectoris?

A

chest pain or discomfort due to coronary heart disease –> when the heart muscle doesn’t get as much blood as it needs

49
Q

What are the 2 ways in which atherosclerosis can cause occlusion?

A
  1. Growing plaque/thrombus occluding vessel

2. Embolisation

50
Q

What are the 4 major clinical consequences of atherosclerosis?

A
  1. Acute narrowing of vessel lumen
  2. Chronic occlusion
  3. Embolism
  4. Aneurysm
51
Q

If the thrombus formed after plaque rupture causes a complete occlusion, what can it result in? What can this manifest as?

A

results in ischemic necrosis (infarction) of the tissue

manifested as stroke, MI, gangrene of several possible organs such as intestine, spleen or lower extremities

52
Q

What characterises chronic occlusion?

A

When the occlusion is gradual and incomplete, it may chronically disturb the blood supply to tissues

53
Q

What can chronic occlusion lead to? What are the clinical manifestations?

A

This can result in chronic ischemia of those tissues

Manifestations:

  • angina pectoris
  • intermittent claudication
  • organ atrophy (atrophy due to impairment of blood flow )
54
Q

What is embolisation?

A

The transfer of the fragments of disrupted atheroma to distal vascular sites, which results into occlusion of those sites.

55
Q

Fragments of thrombi in abdominal aorta may transfer to the popliteal artery.

What may this result in?

A

Gangrene of the leg

56
Q

How can a plaque lead to an aneurysm?

A

Atherosclerotic lesion may extend into the medial layer, resulting into atrophy and loss of elastic tissue. This can subsequently cause dilatation and weakness of the artery, forming aneurysm.

57
Q

What are dangers of aneurysms?

A

may suddenly rupture

58
Q

Purpose of expression of leucocyte adhesion molecules in endothelial activation?

A

Facilitates the recruitment and attachment of circulating leukocytes to the vessel wall.

59
Q

What is endothelial cell activation typically induced by?

A

Endothelial cell activation is typically induced by proinflammatory cytokines, such as TNF-α and IL-6

Yr 2 - EMS (60 decks)

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