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Year 2 > Fundamentals of Atherogenesis > Flashcards

Fundamentals of Atherogenesis Flashcards

1
Q

What are the three long-term results of atherosclerosis on the body

A
  1. Heart Attack
  2. Stroke
  3. Gangrene
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2
Q

What are the risk factors for atherosclerosis

A
  1. Age
  2. Smoking
  3. High serum cholesterol
  4. Obesity
  5. Diabetes
  6. Hypertension
  7. Family History
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3
Q

Where are atherosclerotic Plaques found

A

Peripheral and coronary arteries

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4
Q

What causes neointima

A

Scar tissue that forms within the blood vessels due to proliferation of smooth muscle cells in the MEDIA giving the appearance of fused intima and media layers

Wall Thickness changes generally lead to this

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5
Q

Define the term ‘atherogenesis’

A

The developmental process of atheromatous plaques

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6
Q

What is stenosis

A

Abnormal narrowing in a blood vessel caused by a lesion

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7
Q

What is the early atherogenesis characterised by

A

LPL in blood plasma INVADE endothelium and become oxidised and glycated

Monocytes in the blood adhering to the endothelium and migrating into sub-endothelial space

Monocytes -> Macrophages in subendothelial space

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8
Q

What happens after the endothelium has been initially damaged by the LPL

A
  1. Inflammatory response

2. Monocytes differentiate into macrophages and enter artery wall with platelets

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9
Q

Describe the role of Monocytes at the site of endothelial damage

A

Monocytes -> Macrophages

Macrophages ingest oxidised LDL and turn into FOAM CELLS - forms fatty streak

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10
Q

What are foam cells

A

Macrophages that have many vesicles containing lots of LDL

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11
Q

What happens to the foam cells

A

They dies and encourage further inflammation

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12
Q

What happens to the smooth muscle cells during plaque formation

A

They proliferate and migrate from media to intimate in response to cytokine released by damaged endothelial cells

  1. Forms fibrous capsule covering fatty streak
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13
Q

How is fibrosis of fatty streak prevented by the undamaged neighbouring endothelial cells

A

Release Nitric Oxide to prevent proliferation of smooth muscles

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14
Q

Describe the structure of an atherosclerotic plaque

A
  1. Lipid
  2. Necrotic Core
  3. Connective Tissue
  4. Fibrous ‘cap’
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15
Q

Define the calcification process of atherogenesis

A
  1. Calcification forms among vascular smooth muscle adjacent to atheroma
  2. As cells die, extracellular calcium deposits between muscular wall and outer portion of atheromatous plaques
  3. Atheromatous plaque interferes with calcium regulation causing it to accumulate and crystallise
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16
Q

Describe how the lipid part of the plaque forms

A
  1. LDL moves into vessel wall
  2. Cholesterol released from LDL and oxidised (causes inflammation)
  3. Foam cells and platelets cause smooth muscle proliferation and migration
  4. Smooth muscle cells during this process ingest lipids which gets replaced by collagen and transform into foam cells
  5. Lipid deposits (atheroma) produce enzymes that cause artery to enlarge over time
17
Q

Why is LDL essential in inflammation of the arterial wall and not HDL, VLDL etc

A

LDL can pass in and out of there arterial wall in excess as it is small enough

18
Q

What is the injury hypothesis of atherosclerosis

A

Injury to endothelial cells leads to endothelial dysfunction

Signals sent to monocytes which accumulate in the vessel wall

19
Q

What inflammatory cytokines are found in plaques

A 
IL-1
IL-6
IL-8
IFN-gamma
TGF-beta
MCP-1
C reactive protein
20
Q

Describe the process of leukocyte (monocyte) migration in response to chemoattraction to the site of plaque formation

A
  1. Chemoattraction
  2. Carbohydrate ligans on circulating leukocytes bind to SELECTIN on inner vessel walls with only marginal affinity
  3. Leukocytes slow down and roll along inner wall
  4. Chemokines released by macrophages activate rolling leukocytes and cause surface intern molecules to go from low to high affinity
  5. Integrins bind tightly to receptors on endothelium
  6. Transmigration - leukocyte extend pseudopodia and pass through gaps between endothelial cells
21
Q

At what age can fatty streaks begin to appear at

A

10

22
Q

What do fatty streaks consist of

A

Lipid-Maiden Macrophages
T-Lymphocytes

Both in the intima

23
Q

What do fatty streaks progress to

A

intermediate lesions

24
Q

Structure of an intermediate lesion

A
  1. Foam Cells lipid-maiden macrophages)
  2. Smooth muscle cells
  3. T Cells
  4. Adhesion and aggregation of platelets
  5. Extracellular lipids
25
Q

What do intermediate lesions progress to

A

Fibrous plaques

26
Q

Problems caused by fibrous plaques

A
  1. Impeded blood flow

2. Prone to rupture

27
Q

Structure of Fibrous Plaques

A
  1. Covered by dense fibrous cap
  2. Smooth muscle cell layer that overlies lipid and necrotic core
  3. Calcified

(SMC, Macrophages, Foam cells, T cells)

28
Q

What is the progression from fibrous plaques

A

Plaque rupture

29
Q

Describe the growth behaviour of a plaque

A
  1. Plaques are constantly growing and receding
30
Q

How is the fibrous cap of a plaque maintained

A
  1. Fibrous cap has tone resorbed and redeposited to be maintained
31
Q

How does plaque rupture occur

A
  1. If balance has shifted in favour of inflammatory conditions (increased enzyme activity), the cap weakens and ruptures
32
Q

What is plaque rupture

A

Basement membrane, collagen and necrotic tissue is exposed and vessels undergo haemorrhage within the plaque

Thrombus forms and vessel occludes

33
Q

What occurs after plaque rupture

A

Plaque Erosion

34
Q

What is Plaque Erosion

A
  1. Fibrous cap does not disrupt
  2. Luminal surface underneath the clot may not have endothelium present but is SMC rich
  3. May be a prominent lipid core
35
Q

What is PCI

A

Non-surgical procedure used to treat stenosis of coronary arteries via coronary catheterisation

36
Q

Limitation of PCI

A

Restenosis

37
Q

What is a drug-eluting stent

A

A peripheral coronary stent that releases a drug to block cell proliferation - prevents fibrosis

38
Q

Two commonly used agents in Drug Elution

A

Taxol

Sirolimus

Year 2 (155 decks)

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