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SPR2015_WEEK4 > inflammation and atherogenesis > Flashcards

inflammation and atherogenesis Flashcards

1
Q

step 1 of atherogenesis

endothelial activation

A

1) LDL enters intima

2) oxidized and stim endothelial cell to express adhesion molec

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2
Q

step 2 of atherogenesis

monocyte localization

A

3) monocytes adhere to endothelial cells expression VCAM-1

4) monocytes respond to chemokines (MCP-1) and migrate into intima

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3
Q

step 3 of atherogensis

macrophage activation

A

5) monocytes –> foam cell via mCSF
6) macrophages express scavenger receptor for uptake of oxid LDL

7) foam cells interact with inflammatory molec
- further macrophage apoptosis
- pro-inflamm mediators

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4
Q

why is inflammation involved with atherogenesis

A

host response to bacterial infection –> incr risk of sterile inflammation (no bacteria in subintima)

oxidized LDL and cholesterol are DAMPs recog by innate immune system assoc with potential infection –> sterile inflamm

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5
Q

role of dendritic cells in ather

A

present antigens –> activ T cells

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6
Q

what if you have no monocytes

A

no atherosclerosis (b/c nothing to respond to oxid LDL)

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7
Q

monocytes are ___ leukocytes

A

innate immune system leukocytes

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8
Q

___ accumulation in mouse atherogenesis proportional to extent of disease

A

monocyte accumulation

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9
Q

monocyte adhesion to activated endothelium is ___ in atherogenesis

A

obligate step

monocytes interact with VCAM-1 via integrins (VLA-4)
arrests monocyte against endothelium
so monocytes can diapadese into subendothelial space

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10
Q

____ is an obligate step in atherogenesis

A

monocyte adhesion

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11
Q

what happens when you inhib monocyte adhesion

A

decr atherosclerosis initiation

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12
Q

what are key molec that when knocked out decr atherosclerosis initiation?

A

adhesion molecules –> nothing for monocytes to stick to endothelium

1) VLA-4 (monocyte tight adhesion to VCAM-1)
2) B2 integrins (all 4 CD18) and CD11c

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13
Q

atherosclerosis is a ___ type response

A

Th1 response with IL-1 and IL-6

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14
Q

role of adaptive immunity in atherogensis

A

1) after dendritic cell presents antigen, activ T cells
2) incr IFN-gamma nd atherosclerosis
3) Th17 –> promote plaque instability and neoangiogenesis

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15
Q

blockage of what Th17 component decr atheroslcerosis

A

block IL-17, decr atherosclerosis

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16
Q

Th1 response in atherogenesis

A

1) T cells patrol endothelium
2) T cells interact with APC (presenting oxidized LDL) to initiate T cell response for atherogenesis
3) Th1 response

4) further endothelial activ, foam cells
incr lesion formation/plaque vulnerability

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17
Q

Treg response in atherogenesis

A

Treg incr collagen formation, decr plaque vulnerability and lesion formation

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18
Q

overall role of inflammation in atherogenesis

*******KNOW

A

1) immune response to injury initiate atherogenesis
2) innate immune cell interact with endothelium –> initial plaque formation
3) T cells promote further expansion of lesion and plaque vulnerability

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19
Q

after establishing fatty streak, ___ drives additional plaque expansion to form unstable plaque

A

inflammatory mediators

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20
Q

after establishing fatty streak, inflammatory mediators ___

A

drive additional plaque expansion

21
Q

plaque expansion is a ___ process

A

Th1 process with macrophage apoptosis

22
Q

5 steps in inflammation driving plaque instability

A

1) basal inflammation
2) endothelial activation
3) oxid stress
4) neoangiogenesis
5) plaque instability

23
Q

step 1
inflammatory cells in

basal inflammation

A

cytokines

acute phase reactants

24
Q

step 2
inflammatory cells in

endothelial activ

A

monocyte adhesion

leukocyte diapadesis

25
Q

step 3
inflammatory cells in

oxid stress

A

LDL oxid

foam cells

26
Q

step 4
inflammatory cells in

neoangiogenesis

A

blood vessel form
intraplaque hemorrhage
activ MMP

27
Q

step 5
inflammatory cells in

plaque instability

A

rupture/erosis

platelet activ

28
Q

what are major drivers of plaque instability (3)

A

1) macrophage apoptosis + necrosis –> “necrotic core”
2) MMP degrade fibrous cap
3) intraplaque hemorrhage weaken core

29
Q

role of MMPs in atherosclerosis

A

MMPs destablize plaque

Breakdown of type 1 collagen

30
Q

what is necessary for atherosclerotic plaque to become MI

A

1) lesion expansion
2) macrophage apoptosis/necrosis
3) weaken fibrotic cap
4) plaque rupture

31
Q

how is CRP produced?

A

by hepatocytes

and macrophages and smooth muscle cell

32
Q

what does CRP bind to?

A

1) modified membranes
2) apoptotic cells
3) lipoproteins

33
Q

what pathway is CRP in?

A

classical complement

34
Q

fxn of CRP in therapy

A

1) CRP predict incr CV risk

2) statin lower cholest and CRP

35
Q

JUPITER trial

pt either receive placebo or statin

A

after 4 yrs, patients with elev CRP and normal LDL had benefit with taking statin, support inflamm in CV disease

36
Q

why would statins be used in people with normal cholesterol

A

because can also lower inflammatory biomarkers (CRP)

37
Q

why does autoimmune disease have accelerated atherogenesis

A

1) incr monocyte/macrophage activ
2) decr endothelial vasodilator fxn (in RA)
3) proinflamm HDL –> incr LDL oxid (RA, psoriasis)
4) plaque instability (RA)

38
Q

how does inflammation affect HDL fxn

A

1) endotoxemia/inflamm changes HDL size, decr reverse cholesterol transport
2) HDL becomes pro-atherogenic

39
Q

HDL cholesterol efflux inversely assoc with (2)

A

1) carotid intima-media thickness (plaque thickness)

2) risk of CAD

40
Q

impaired HDL efflux assoc with ____

A

more severe psoriasis

41
Q

____ assoc with more severe psoriasis

A

impaired HDL efflux

42
Q

what happens if you treat psoriasis? how does that affect HDL

A

incr macrophage efflux capacity and incr HDL FUNCTION!!!

TREATING DID NOT CHANGE HDL LVL

43
Q

how does plaque morphology change in RA?

A

RA patient had more vulnerable plaque in LAD

44
Q

confounding factors when looking at psoriasis with CV events

A

obesity, HTN, smoking, diabetes which are also assoc with CV disease

45
Q

if you have RA at younger age, then you have ____ CV disease

A

more severe and earlier

46
Q

treatment of ___ may lower risk of CV events

A

autoimmune disease

47
Q

what is currently being done to control CV risk in RA and psoriasis patients?

A

using TNF alpha inhibitors

48
Q

effect of prednisone on CV risk

A

prednisone incr CV risks despite being an anti-inflamm drug

HTN
incr salt retention

SPR2015_WEEK4 (14 decks)

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