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CPR Exam 1 > 28. Inflammation & CAD > Flashcards

28. Inflammation & CAD Flashcards

1
Q

what are the non-modifiable risk factors for athersclerosis

A

genetic abnormalities

FHx

age

male

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2
Q

what are the modifiable risk factors for athresclerosis

A

lifestyle changes

inflam

hyperlipidemia, HTN, DM

vit B6 deficiency

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3
Q

what are the procoagulant markers

A

plasma homocysteine

tPA

plasminogen activator inhibitor

lipoprotein A

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4
Q

what are the inflam markers that increase risk for athresclerosis

A

HSCRP

acute phase ILs (IL-1, IL-6, TNF)

serum amyloid A

possible chronic infection

prgenancy associated plasma protein A

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5
Q

where do most athresclerosis lesions occur

A

at openings of exiting vessels

branching poinds

post abd aorta

-bc increased risk of hemodynamic turbulence

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6
Q

rate the vessels impacted by athresclerosis in severity

A

worst - abd aorta

coronary As

popliteal As

ICA

least severe- circle of willis

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7
Q

what is an activated endothelial state & when does it happen

A

endothelial tissue injury ==> become procoagulant with the following phenotypes:

pro inflam

prothromnogenic

–> lead to initiation of thromobus formation, athresclerosis & vascular lesions in HTN

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8
Q

what increases the expression of P & E selectin on the endothelium

A

IL-1 & TNF (secreted by macrophages)

-slow leukocytes down & responde to chemokines (IL-8)

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9
Q

what is the role of circulating macrophages in arthersclerosis

A

cholesterol & cholesterol esters (lipids) form plaque in intima

–> macrophages take up the oxLDL –> accumulate and turn into foam cells –> create fatty streaks –> stimulate inflam response

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10
Q

what causes the recruitment of leukocytes in endothelial damage

A

tissue macrophases release IL-1, IL-6, IL-8 & TNF

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11
Q

which complement pathway is active in inflammation

A

alternative pathway

C3BbP –> C5a & C3a - recruit more neturophils & monocytes

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12
Q

what is the fxn of the kinin cascade during inflam

A

vasodilation, increase permeability of blood vessels and stimulate pain receptors

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13
Q

which receptor is specific for oxLDL on macrophages &

what happens onces they bind?

A

scavenger receptor CD36 (lipid can also bind TLR-4)

activate/differntiate M1 tissue macrophages –> proinflam response

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14
Q

what does the activation & differentiation to M1 tissue macrophages cuase in inflam

A

production & relase of acute phase cytokines

transformation to foam cells

cholesterol crystals with foam cells –> promote inflammasome activity

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15
Q

what is the result of activating the NLRP3 inflammasome from the cholesterol crystals?

A

produce and secrete IL-1beta & IL-18

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16
Q

what do cholesterol crystals & IL-1 induce in neutrophils

A

release of NETs and DAMPs

nets = prothombogenic

-lay down scaffold for platelet/RBC activation, aggregation & thrombosis

17
Q

what are the effects of elastase released by neutrophils

A

decreased elascticity in vessels

18
Q

which adaptive immune cells are most involved in arthresclerosis

A

Th1

Th17

B-cells

19
Q

why do T & B cells react to our own cells during atherosclerosis

A

oxLDL isnt the same molecule thats present during development

20
Q

what causes the atherosclerotic plaque

A

soft fatty streaks become covered w/ fibrous caps

center is necrotic w/ lipids, debris, foam cells & thrombus

surrounded by zone of inflammatory & Sm. M

21
Q

what is the most significant inflam marker for CV risk

A

HSCRP

22
Q

what levels of HSCRP is considered high risk for CV disease

A

> 3 mg/L

23
Q

what was the outcome of the anti-inflam canakinumab trial

A

not significant enough decrease in risk for CV disease

24
Q

what happens when endothelium is injured and taken out of its basal state

A

-upregulation of procoagulants,

adhesion molecules & proinflam factors

  • altered expression of chemokine, cytokines & growth factores
25
Q

what happens after activation of adaptive immunity

A

increased

  1. adhesion molecule expression
  2. release of cytokines/chemokines
  3. increase MHC/HLA II expression
  4. increased oxLDL uptake
  5. increase macrophage activaiton

ACC-MHOM

26
Q

what happens if you have a a thick fibrous cap

A

thrombosis erosion

27
Q

how can a fibrous cap become thin/weak

A

increase inflam –> accelerate fibrous cap degradation & inhibit resynthesis –> decrease collagen –> weaken

28
Q

what can happen if a fibrous cap is thin

A

rupture

CPR Exam 1 (27 decks)

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