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CPR > Inflammation and Coronary Artery Disease > Flashcards

Inflammation and Coronary Artery Disease Flashcards

1
Q

Atherosclerosis

A

Deposition of plaques of fatty materials on the inner walls of arteries

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2
Q

What underlies the pathogenesis of coronary, cerebral and peripheral vascular disease?

A

Atherosclerosis

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3
Q

What is a major contributor to the development of atherosclerosis?

A

INFLAMMATION

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4
Q

What are a few non-modifiable risk factors for atherosclerosis?

A

Genetics - higher for males (XY)
Family History
Increasing age

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5
Q

What are a few modifiable risk factors for atherosclerosis?

A 
Hyperlipidemia
Hypertension
Smoking
Obesity
Chronic inflammation
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6
Q

What are the 5 main steps to the development of atherosclerosis?

A
  1. Chronic Endothelial Injury
  2. Endothelial Dysfunction
  3. Macrophage activation and Smooth muscle recruitment
  4. Macrophage and Smooth muscle cells engulf lipids
  5. Smooth muscle cell proliferation and deposition of collagen and ECM
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7
Q

What are the layers of the blood vessel from superficial to deep?

A

Endothelium
Intima
Media
Adventitia

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8
Q

What layer of the blood vessel houses the smooth muscle cells?

A

Media

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9
Q

What causes a chronic endothelial injury?

A

Risk factors such as hyperlipidemia, hypertension, smoking that induce chronic inflammation that try to repair the damage

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10
Q

Where are the most common areas for development of atherosclerosis and why?

A

Openings of exiting vessels
Branch points
Posterior abdominal aorta
– Due to flow disturbances (turbulence)

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11
Q

What is the response to the chronic endothelial injury?

A

Endothelial dysfunction - acute inflammatory response activated
== Increased leukocyte and monocyte adhesion

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12
Q

What immune factors are important in recruiting leukocytes during endothelial dysfunction?

A

IL-1, IL-6 and TNF

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13
Q

Describe what IL-1 and TNF do in the recruitment of leukocytes?

A
  • Increase expression of P and E selectins on endothelium and the ligands on leukocytes
    = Leukocyte ROLLING (bind,detach,bind)
    == Leukocyte SLOWS DOWN
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14
Q

What does slowing down of a leukocyte allow?

A

Allows them to respond to chemokines in the area

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15
Q

What do chemokines do for leukocyte adhesion?

A
  • INCREASE affinity of integrins on the leukocyte for binding
  • Leukocytes then attach to the endothelium, flatten and migrate through to the intima
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16
Q

Long term effect of the recruitment of leukocytes?

A

Changes in hemodynamics in microenvironment

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17
Q

What 4 types of plasma proteins does the inflammatory exudate during endothelial dysfunction bring into contact with the injured area?

A
  1. Clotting proteins - clot formation
  2. Complement proteins - destroy bacteria
  3. Kinin cascade - increase permeability of blood vessels
  4. Fibrinolytic proteins - degrade clots
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18
Q

The Endothelial Dysfunction phase activates the Acute inflammatory response. What does this increase the expression of?

A

Procoagulants
Adhesion molecules
Proinflammatory factors

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19
Q

What are the most common circulating lipids?

A

Cholesterol and Cholesterol Esters

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20
Q

Describe how Foam Cells are are stimulated via an inflammatory response?

A
  1. Circulating lipids (cholesterol and cholesterol esters) deposit and accumulate in the Intima
  2. Lipids are phagocytosed and modified by macrophages
  3. Modified LDL accumulated in macrophages and smooth muscle cells
    == Stimulates Foam Cell inflammatory response
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21
Q

3 steps to stimulation of inflammatory Foam Cell response?

A
  1. Retention (of cholesterols in Intima)
  2. Modification (oxidation and phagocytosis by macrophages)
  3. Uptake (of modified LDL by macrophages and smooth muscle cells)
22
Q

What accumulates in macrophages and smooth muscle cells to cause foam cell stimulation?

A

Modified LDL

23
Q

When Foam Cells collect in lesions it is known as?

A

Fatty streaks

24
Q

Describe how Foam Cells are created?

A
  • Oxidized lipids bind scavenger receptor CD36 on monocytes
  • Activates them and differentiate into M1 macrophages
  • Release IL-1, IL-6, TNF to transform into Foam Cells
25
Q

What within Foam cells promotes inflammasome activation?

A

Cholesterol Crystals

26
Q

What inflammatory factors do inflammasomes produce?

A

IL-1 and IL-18

27
Q

What forms an important scaffolding for platelet and RBC aggregation and thrombosis?

A

Neutrophil NETs between Neutrophils and Macrophages

28
Q

What important cytokine do macrophages release for more inflammation?

A

IL-1beta

29
Q

What 3 things can cause proliferation of smooth muscle cells?

A
  1. PDGF
  2. Fibroblast Growth Factor
  3. TGF-alpha
30
Q

When smooth muscle cells are caused to proliferate, then what happens?

A

They migrate from the Media to the Intima and then synthesize collagen and ECM

31
Q

Once smooth muscle cells proliferate and migrate, what do they produce?

A

Collagen and ECM (extracellular matrix)

32
Q

Once macrophages and smooth muscle cells engulf lipids, what become active?

A

T and B cells

33
Q

After modified LDL is uptaken by macrophages and dendritic cells, then what happens?

A

Presentation to and activation of T cells (Th1, Th17, B cells)
- Vascular inflammation and atherosclerosis

34
Q

List some of the components of a fatty streak in the endothelium of a vessel?

A

Foam cells
Lipids
Inflammatory and smooth muscle cells
ECM

35
Q

Over time, what covers a fatty streak?

A

Fibrous cap

36
Q

What is a fibrous cap made of?

A

Dense Collagen

37
Q

What is in the center of a plaque?

A

Necrotic, cell debris and foam cells

38
Q

Atherosclerosis starts at a young age. Plaque formation is usually _____

A

Asymptomatic

pre-clinical phase

39
Q

Once atherosclerosis progesses to middle age/elderly individuals, it usually becomes ______

A

Symptomatic

clinical phase

40
Q

Thrombosis due to erosion

A

White thrombus

41
Q

Thrombosis due to rupture

A

Red thrombus

42
Q

Fibrous cap differences in a thrombosis due to erosion and due to rupture?

A

Erosion: Fibrous cap thick and intact
Rupture: Thin fibrous cap with fissure

43
Q

What cell types are prominent in a thrombosis due to erosion and due to rupture?

A

Erosion: Smooth muscle cells
Rupture: Macrophages

44
Q

Thrombosis due to erosion has more ____ than a thrombosis due to rupture

A

NETs

45
Q

Thrombosis due to rupture has a more expansively _____ fibrous cap than a thrombosis due to erosion

A

Remodeled

46
Q

Some plaques are more prone to rupture than others, true or false?

A

TRUE

47
Q

Can physical stresses also cause plaques to rupture?

A

Yes

48
Q

What is an emerging risk factor for atherosclerosis?

A

High Sensitivity C - reactive protein

49
Q

Are there any break through treatments yet for atherosclerosis?

A

NO

- vaccination and CRISPR?

50
Q

Has treating with anti-inflammatory agents of blocking IL-1beta worked for treated atherosclerosis?

A

No

51
Q

In what layer of a blood vessel is the plaque forming?

A

Intima

52
Q

What surrounds the center of a plaque (cell debris, foam cells)?

A

Inflammatory and smooth muscle cells

CPR (48 decks)

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