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CPR Midterm > Inflammation and CAD > Flashcards

Inflammation and CAD Flashcards

1
Q

what contributes to the development of atherosclerosis?

A

inflammation

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2
Q

what are the big 3 modifiable risk factors for atherosclerosis?

A

hyperlipidemia, hypertension, and diabetes (all synergistic)

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3
Q

What is the first stage in the development of atherosclerosis?

A

chronic endothelial injury

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4
Q

what is the second stage in the development of atherosclerosis?

A

endothelial dysfunction

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5
Q

what is the third stage in the development of atherosclerosis?

A

macrophage activation and smooth muscle recruitment

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6
Q

what is the fourth stage in the development of atherosclerosis?

A

macrophages and smooth muscle cells engulf lipid

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7
Q

what is the 5th and final stage of development of atherosclerosis?

A

smooth muscle proliferation, collagen and other extracellular matrix deposition

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8
Q

what are the most common causes of chronic injury and or dysfunction of endothelium?

A

hypertension and hyperlipidemia

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9
Q

where do most lesions of atherosclerosis tend to occur at?

A

openings of exiting vessels, branch points, posterior abdominal aorta

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10
Q

what does chronic endothelial injury lead to?

A

an acute inflammatory response

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11
Q

what occurs during the endothelial dysfunction phase (stage 2)?

A

there is increased permeability, leukocyte adhesion, monocyte adhesion, and emigration into the intima

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12
Q

what are some characteristics of endothelial cells in the basal state?

A

they are non-adhesive and they have a non-thrombogenic surface

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13
Q

what are some characteristics of endothelial cells in the activated state?

A

they have increased expression of procoagulants, adhesion molecules, and pro-inflammatory factors

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14
Q

what molecules increase expression of P&E selectins on endothelium and ligands on leukocytes?

A

IL-1 and TNF

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15
Q

what is the long term effects of IL-1 and TNF increasing the expression of P&E selectins on endothelium and ligands on leukocytes?

A

there will be changes in the hemodynamics in the microenvironment

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16
Q

what do the macrophages begin secreting when they begin phagocytosing debris?

A

TNF, IL-1, and IL-6

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17
Q

what effect does edema have on the tissue?

A

it brings plasma proteins into the intimate contact with the damaged area

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18
Q

what are the proteins that are in the inflammatory exudate?

A

clotting proteins, complement, kinin cascade, and fibrinolytic protein

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19
Q

what does the kinin cascade cause?

A

vasodilation, increase in permeability of blood vessels

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20
Q

what does fibrinolytic protein cause?

A

degrades the clot when the wound has healed

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21
Q

what happens once the macrophages start moving into the area that has suffered endothelial dysfunction?

A

it starts to thicken and increase the amount of cells

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22
Q

what are the lipids in atheromatous plaques?

A

cholesterol and cholesterol esters

23
Q

what happens to the cholesterol and cholesterol esters that are deposited in the intima and retained there?

A

they are phagocytosed by the macrophages and then partially oxidized (aka modification)

24
Q

what is uptake?

A

when the modified LDL starts to accumulate within the macrophages and smooth muscle cells

25
Q

what does the process of retention, modification, and uptake of LDL stimulate?

A

an inflammatory response

26
Q

what are the macrophages that being to accumulate the partially oxidized LDL now known as?

A

foam cells

27
Q

foam cells collect in lesions known as what?

A

fatty streaks

28
Q

what can sense oxidized lipids?

A

scavenger receptor CD36 on monocytes or TLR-4

29
Q

what happens when monocytes recognize oxidized lipids through their scavenger receptor CD36?

A

they differentiate to M1 (classical) tissue macrophages; then produce and release acute phase cytokines, transform to foam cells

30
Q

what is the inflammasome?

A

a signaling system for detection of pathogens and stressors

31
Q

what does the recruitment and assembly of inflammasome proteins result in?

A

the production of large quantities of both IL-1 and IL-18 which are potent inflammatory cytokines

32
Q

What effect do cholesterol crystals have on neutrophils?

A

they cause the neutrophils to deploy their NETs

33
Q

what is the role of the neutrophil’s NETs?

A

they provide scaffolding for platelet and RBC activation-; netosis will stimulate the macrophages to have an inflammatory response

34
Q

several growth factors are implicated in smooth muscle proliferation. What are these growth factors?

A

PDGF, Fibroblast growth factor, TGF-alpha

35
Q

What is PDGF released by?

A

locally adherent platelet macrophages, endothelial cells, and smooth muscle cells

36
Q

what acts as a smooth muscle chemokine?

A

TGF-alpha

37
Q

when does the adaptive immune system start responding?

A

stage 4

38
Q

What can the modified LDL lead to?

A

events leading to APC activation and subsequent loss of tolerance to ApoB of LDL- autoreactive Ts and Bs- they lose their tolerance

39
Q

What are the mediators of the adaptive immunity?

A

IFN-gamma, TNF-alpha, and IL-17

40
Q

what cells are responsible for the adaptive immunity?

A

Th1, Th17, and b cells

41
Q

over time a soft fatty streak becomes covered with what?

A

a fibrous cap

42
Q

what does the center of the plaque contain?

A

it is necrotic and it contains lipids, debris, foam cells and thrombus

43
Q

some plaques are more prone to rupture than others. What plaque type is more likely to rupture?

A

thin fibrous caps- the red thrombus

44
Q

which type of plaque is more stable and more likely to erode?

A

the white thrombus- thick fibrous cap

45
Q

which plaque more frequently causes STEMI?

A

the red thrombus

46
Q

what is the prominent cell type in a red thrombus?

A

macrophages

47
Q

what is the prominent cell type in a white thrombus?

A

smooth muscle cells

48
Q

what is a major inflammatory marker?

A

high sensitivity C-reactive protein

49
Q

what effect do steroids have on CAD?

A

they increase cardio vascular adverse events and mortality

50
Q

what effect do NSAIDs have on CAD?

A

they increase cardio vascular events due to destabilizing the plaque

51
Q

what effect does the COX2 inhibitor have on CAD?

A

it increases CVD mortality

52
Q

what is instrumental in driving atherosclerosis and comes off the inflammasome?

A

IL-1 beta

53
Q

what is ACZ885 (canakinumab)?

A

it was a human mAb, that selectively blocked the IL-1beta inflammatory pathway

CPR Midterm (21 decks)

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