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<3 > Inflammation And Coronary Artery Disease > Flashcards

Inflammation And Coronary Artery Disease Flashcards

1
Q

What diseases can atherosclerosis underly?

A

Coronary, cerebral and peripheral vascular diseases

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2
Q

What are some constituational risk factors for CAD?

A

Genetic abnormalities
Family hx
Increasing age
Male

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3
Q

What is an important emerging risk factor for CAD?

A

High sensitivity c reactive protein (HSCRP)f

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4
Q

What is HSCRP?

A

An acute phase protein that triggers the oxidation of LDL

Perpetuates CVD

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5
Q

What can cause CHRONIC endothelial injury?

A

Hyperlipidemia
Hypertnesion
Smoking

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6
Q

What are some exmpales of Endothelial DYSfucntion?

A

Increased permeability

Leukocyte adhesion

Monocyte adhesion

Emigration

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7
Q

What are the 5 steps that arterial walls will take in response to injury?

A
  1. Chronic endothelial injury
  2. Endothelial dysfunction
  3. Macrophage activation
  4. Macrophage and SM. M. Engulf LIPIDS
  5. Sm. M. Proliferation, Extracellular lipid
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8
Q

Where is atherosclerosis more commonly seen in vessels?

Why here?

A

At opening of exiting vessels, branch point, posterio abdominal aorta

Bc normally more flow disturbances seen here

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9
Q

What arteries most frequently get atherosclerosis?

A
  1. Abdominal aorta
  2. Coronary
  3. Popliteal
  4. Int. Carotid a.
  5. Circle of willis
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10
Q

What is the surface of endothelial cells?

What does this allow for?

A

Nonthrombogenic surface - maintains blood in a fluid state

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11
Q

What happens if there a dysfunction occurs in endothelial cells?

A

Pro-inflamm. And Pro-thrombogenic response

Initiated thrombus formation, atherosclerosis and vascular lesion of HTN

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12
Q

What is the basal state of endothelial cells?

Vs. activated due to injury?

A

Non-adhesive, non-thrombogenic surface

Active:

  • turbulent flow
  • hypertension
  • cytokine entry
  • increased expr. Of PRO-coagulatns and PRO-inflamm. Fxs
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13
Q

What is the role of vascular smooth msucle cells?

A

Can proliferate and repair

  • synthesize collagen, elastin and proteoglycans
  • GFs and cytokines
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14
Q

How can lipids initiate endothelial dysfunction?

A

Lipids in plaques = chol.

Deposition and accumulation of cholesterol in INTIMA

Macrophages take up and oxidize

OxLDL further accumulates in macrophages and sm.M. —> foam cells —> fatty streak

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15
Q

What will be stimulated in reponse to accumulation of toxic LDL?

A

Inflammatory response - recruitment of leukocytes via IL-1 and TNF 6

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16
Q

What will IL-1 and TNF-6 do for the injured endothelium?

A

Will increase expression of P and E selectins

=slows down leukocytes so they can bind chemokines

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17
Q

What will leukocytes do once attached to chemokines?

A

Will flatten and migrate thru endothelium

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18
Q

What is the first leukocyte to respond?

Spec.?

A

Neutrophils (hours)

LFA1-ICAM1

IL-8/IL-8L

19
Q

What leukocyte will appear over a matter of days?

Spec.?

A

Macrophages

VLA4-VCAM1

20
Q

What will the cytokine and leukocytes due to the injured endohteliuM?

A

Increase vascularity —> edema

21
Q

Why is edema good in injured endotheiuM?

A

Brings plasma proteins into contact w/ damaged area

22
Q

What are the proteins in the Edema exudate caused by the cytokines and leukocytes?

A
  1. Clotting proteins
  2. Complement proteins
  3. Kinin cascade
  4. Fibrinolytic protein
23
Q

What is the function of the Kinin cascade protein in the inflamm. Exudate?

A

Vasodilation

-increase permeability of blood vessels and stimulate pain Rs.

24
Q

What R. Will oxidize lipids?

A

Scavenger R. CD36

25
Q

Upon macrophage activation, what will they differentiate into?

A

To M1 tissue macrophages = pro-inflamm. Response macrophages

26
Q

What will the M1 macrophages transform into?

A

Foam cells

27
Q

What do the cholesterol crystals w/in foam cells promote?

A

Activation of Inflammasome

28
Q

What is the inflammasome?

A

Signaling system for detection of pathogens and stressors

-results in production of IL-1 and IL-18 (both potent inflammatory cytokines)

29
Q

What does Neutrophils NETosis do?

A

Creates a scaffolding for platelet/RBC activation, aggregation and thrombosis

30
Q

What GFs are needed for Smooth muscle cell proliferation?

What will SM. M. Cell proliferation do?

A

PDGF
Fibroblast GF
Transforming GF = Alpha TGF

Will increase thickness of intima

31
Q

What will activate macrophages?

A

IFN-gamma

32
Q

Why are T cells initially unresponsive to plaques?

A

Bc of peripheral tolerance

33
Q

How are T cell clones made reactive to lipids?

A

Presentation of self-epitopes bc of macrophages

T cells cause inflammation causing atherosclerosis

34
Q

What is the fatty streak?

A

Streak of foam cells and extracellular lipid formed in intima when it is expanding (due to sm. M. Cell proliferation)

35
Q

How does an atherosclerotic plaque form?

A

Soft fatty streak covered w/ fibrous cap over time

36
Q

What is the center of the Fatty Streak like?

What will it contain?

A

Necrotic

-contains lipid, debris, foam cells and thrombus

37
Q

What is the center of the fatty streak surrounded by?

A

Surrounded by a zone of inflammatory
And
sm. M. Cells

38
Q

What is the fibrous cap covering the fatty streak made up of?

A

Dense collagen fibers

39
Q

What will accelerate the degradation of the fibrous cap and inhibit its re-synthesis?

A

Increased inflammation in plaque

40
Q

How is a thrombosis due to EROSION caused?

What kind of thrombus will this be?

A

When the fibrous cap is thick and intact

-sessile, non-occlusive thrombus

41
Q

How is a thrombosis due to RUPTURE caused?

What kind of thrombus will this be?

A

Thin fibrous cap w/ fissure

-occlusive thrombus

42
Q

If the atherosclerosis is an inflamm. Response,

How can you tx (non-specifically)?

A

Steroids

NSAIDs (destabilize plaque)

43
Q

What is a selective inhibitor that can tx atherosclerosis?

A

COX2 inhibitor

44
Q

What did the CANTOS study propose for Atherosclerosis tx?

A

IL-1Beta inhibitor

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