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CPR > Inflammation and CAD > Flashcards

Inflammation and CAD Flashcards

1
Q

What are risk factors for atherosclerosis?

A
  • Genetics
  • FHx
  • Increasing age
  • XY chromosomes
  • Hyperlipidemia
  • Htn
  • Smoking
  • Diabetes
  • Vitamin deficiencies
  • Obesity/ Sedentary lifestyle
  • Chronic inflammation
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2
Q

What is the most common chronic injury to endothelium?

A
  • Htn & Hyperlipiemia
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3
Q

Where does atherosclerosis occur?

A
  • Most lesions occur at openings of vessels. branch points, or posterior abdominal aorta
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4
Q

What does the endothelial dystunction stage lead to?

A
  • Increased permeability leukocyte adhesion, monocyte ahesion and emigration
  • Acute Inflammatory Response
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5
Q

What are the characteristics of an activated endothelium ?

A
  • Increased expression of procoagulants, adhesion molecules and proinflammatory factors
  • Altered expression of chemokines cytokines and growth factors
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6
Q

What are the characteristics of an endothelium in a basal state?

A
  • Non adhesive
  • Non thrombogenic surface
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7
Q

With endothelial dysfunction what does the altered phenotype lead to?

A
  • Proinflammatory andp rothormbogenic
  • Initates thrombus formation, atherosclerosis and vascular lesions
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8
Q

Why is edema important?

A
  • Brings plasma proteins into intimate contact with damaged area
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9
Q

What proteins are found in the inflammatory exudate (seen with edema)?

A
  • Clotting proteins
  • Complement
  • Kinin casscade:
    • vasocilation, increase permeability, stimulate pain receptors
  • Fibrinolytic protein:
    • degrades clot
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10
Q

Describe the circulating lipids in response to endothelial injury.

A
  • Lipids in atheromatous plaques are cholesterol and cholesterol esters
  • LDL gets deposited into the intima and retained and gets phagocytsed by macrophages and then oxidized
  • Modified LDL accumultates within the macrophages and smooth muscle cells called uptake
  • Uptake stimulates an inflammatory response to the toxic form of LDL (Foam Cells)
  • Foam cells collect in lesions called fatty streak
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11
Q

What is the receptor for oxLDL?

A

Scavenger receptor on monocytes CD36

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12
Q

What promotes infalmmasome activation within a foam cell?

A

Cholesterol crystals

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13
Q

What is an inflammasome?

A
  • Signaling system for detection of pathogens and stressors
  • Recruitment and assembly of inflammasome proteins results in production of Il-1 and IL-18 (potent inflammatory cytokines)
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14
Q

What is NeTosis?

A
  • Scaffolding for platelet RBC activation aggregation nd thrombosis
  • Stimulates macrophage to have inflammatory response
  • Comes from Neutrophil
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15
Q

What stimulates Sm mm growth?

A
  • PDGF released by adherent platelets macrophages and endothelial cells and sm mm cells
  • Fibroblast growth factor
  • TGF-alpha
    • sm mm chemokine
  • Proliferating sm mm cells synthesize ECM including collagen
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16
Q

Mediators of adaptive immunity with CAD and Atherosclerosis? What do they result in?

A
  • IFN-y
  • TNF-a
  • IL-17

Increased:

  • adhesion moleculs
  • cytokine release
  • HLA II expression and Ag persentation
  • OxLDL uptake
  • Macrophage activation

Results in fatty streaks

17
Q

Describe the atherosclerotic plaque.

A
  • Fatty streak gets covered with a fibrous cap of dense collagen fibers
  • Center of plaque is necrotic with lipid, debris, foam cells and thrombus
  • Surrounded by zone of inflammatory cells and sm mm cells
18
Q

Compare thrombosis due to erosion vs rupture.

A

Thrombosis: (White thrombus)

  • Fibrous cap is thick and intact
  • Sm mm cells prominent
  • Neutrophil extracellulr traps (NETs) involved
  • More frequent in Non-STEMI

Rupture: Red thrombus

  • Thin fibrous cap with fissure
  • Macrophages prominent
  • Usually expansively remodeled
  • More frequent in STEMI
19
Q

What are the inflammatory marker emerging risk factors?

A
  • High sensitivity C-reactive protein (HSCRP)
  • Serum amyloid A
20
Q

What are the pro coagulant marker risk factors?

A
  • Plasma homocysteine
  • Tissue Plasminogen activator
  • Plasminogen activator inhibitor
21
Q

How do you treat atherosclerosis?

A

Non specific agents:

  • Steroid: increase in CV adverse events and mortality
  • NSAIDs: increase because they destabilize plaques

Selective inhibitor:

  • COX2 inhibitor: increases CVD mortality
22
Q

How can you block IL-1Beta inflammatory path?

A
  • ACZ885 canakinumab selectively blocks it
  • IL-1B is crucial in driving atherosclerosis
23
Q

What is the CANTOS study?

A
  • high and medium dose decreased percent of HSCRP and IL-6
  • no change in LDL
  • Decreased HSCRP decreased all cause mortality rate and cadriovascular mortality over the 5 years
24
Q

CANTOS/CIRT study?

A
  • Cardiovasuclar inflammation reduction trial
  • Low dose methotrexate , all patients were post MI with T2DM
  • No reduction in IL-1b IL-6 or HSCRP or CV events

CPR (18 decks)

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