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CPR Exam 1 > Inflammation And CAD > Flashcards

Inflammation And CAD Flashcards

1
Q

Inflammation contributes to what heart disease

A

Atherosclerosis (Coronary, cerebral, Peripheral vascular disease)
5x higher risk when you reach 40yo-60yo

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2
Q

Atherosclerosis risk factors that are non changeable

A
  1. XY
  2. Genetics
  3. Age
  4. FH
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3
Q

Atherosclerosis risk factors that are changeable

A
  1. Hyperlipidemia
  2. HTN
  3. Diabetes
  4. Obesity
  5. Chronic inflammation
  6. Smoking
  7. VIT deficiency (B6)*
  8. Sedentary lifestyle
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4
Q

5 stages of Atherosclerosis happening

A
  1. Chronic endothelial injury (from any risk factor, toxins, virus)
  2. Endothelial Dysfunction: increased permeability of leukocytes
  3. Macrophages are activated (SM is recruited)
  4. M and SM trap lipids
  5. SM proliferates (ECM has lipids and grows)
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5
Q

What does the endothelial injury cause

Usually from risk factors

A

It causes chronic inflammation to repair the tissue

* most common from HTN and hyperlipidemia

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6
Q

Where does atherosclerosis happen most likely

A

Opening of exiting vessels, branch points, and posterior abd aorta
= these locations have flow disturbances (HEMODYNAMIC TURBULENCE)**

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7
Q

Endothelial Dysfunction is when

A

There is a chronic injury due to risk factor present
——> permanent permeability increased for leukocytes, monocytes
= inflammatory response

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8
Q

Stage 1 injury to endothelium causes what

A

Endothelium altered and expresses adhesion molecules, pro inflammatory cytokines, procoagulators
= initiates thrombus formation , atherosclerosis, vascular lesions

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9
Q

Basal endothelial cells

A

Non-thrombogenic, keeps blood fluid

Mediate SM to increase resistance

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10
Q

SM in vessels

A

Vascular repair and atherosclerosis
Can proliferate and make collagen, cytokines
Dilate and constrict vessels

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11
Q

What do IL-1 and TNF do

A

Increase P and E selectins on endothelium
Increase ligand on leukocytes
(Rolling of leukocytes)=slows them so they can attach, cluster and flatten to cross the endothelium
= large inflammation in ECM (IL-6 and IL1 and TNF, brings pro inflammatory)

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12
Q

Long term increase in IL 1 and TNF causes

A

Increased dilation = increased turbulence in the vessels

Brings proteins close to the damaged organs

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13
Q

Which proteins are brought to the sight of damaged organ

A
  1. Clotting protein
  2. Complement proteins
  3. Kinin cascade (dilation, increase permeability, pain receptors)
  4. Fibrinolytic protein (degrade clot when wound is healed)
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14
Q

What happens when the endothelium dysfunction has happened for a while

A

Macrophages enter the area causing SM thickening

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15
Q

Circulating lipids do what at these inflammed sites

A

They deposited in intima and phagocyted by M and modified
* modified to toxic LDL incident the M and SM cells
= stimulation of foam cells in these lesions ——> FATTY STREAK

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16
Q

Atheroma

A

Atheromatous ——> atherosclerotic plaques

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17
Q

What are CD36 scavenger receptors

A

M and monocytes have these to OXIDIZE LDL

Can also happen when binding to TLR4

18
Q

Oxidization of LDL has what types of cells

A

M1, IL1, IL6, CRP, Fibrinogen, Serum Amyloid A, C protein, plasminogen
M2 is in the plaques

19
Q

Inflammasome

A

Foam cells and cholesterol crystals form these when LDL is present and is oxidized
They make IL1, IL8 = INFLAMMATION

20
Q

Neutrophils NETosis

A

They release their NETs that provide platelets scaffolding, RBC activation, thrombosis
Also stimulates the M

21
Q

Inflammation at the foam cells and NETosis site causes what

A

SM cells recruitment and proliferation that make COLLAGEN (ECM)

22
Q

What stimulates SM proliferation

A

PDGF
FGF
TGF-a

23
Q

SM can also (lipids)

A

Phagocytosis LDL

24
Q

T cells effect on atherosclerosis

A

T cells are presented to the modified LDL by M and DCs

——> vascular inflammation

25
Q

INF-gamma does what

A

Activated Macrophages

26
Q

Mediators for adaptive immune system activated by the modified LDL and inflammation in vasculature

A

TH1, TH17, B cells
IFN-g, TNF-a , IL-17
(Adhesion molecules, cytokines, macrophage activation, uptake of oxLDL, HLAll presentation of Ag) = FATTY STREAKS

27
Q

Fatty streaks happen how

A

Foam cells, ECM Lipids, inflammation, SM cells

28
Q

Atherosclerotic plaque is what

A 
Dense collagen (FIBROUS CAP) over the fatty streak
Inside is SM and lipids, foam cells, thrombus, calcium  = necrotic*
29
Q

3 ways fatty streaks can become symptomatic

A
  1. Aneurysm and rupture of vessel
  2. Thrombus occlusion as plaque ruptures inside the vessel
  3. Plaque grows until critical stenosis of the vessel
30
Q

What are some things that can cause plaque rupture

A

Increased inflammation can degrade the fibrous collagen cap
Calcification
Physical stress (vasoconstriction and BP change)
Low amount of SM

31
Q

White thrombus

A

Erosion thrombosis
= goes away because BF
(thick fibrous cap, SM prominent, N NETs involved, high platelets)

32
Q

Red Thrombus

A

Thrombosis form rupture
= has lipid core
= thin cap, many M, remodeled a lot

33
Q

RISK FACTORS: Inflammatory markers

A

HSCRP (High sensitivity C-reactive Protein)
Serum Amyloid A
*not specific

34
Q

RISK FACTORS: Pro-coagulant markers

A

Plasma Homocysteine
Tissue plasminogen
Plasminogen activator inhibitor
*not specific

35
Q

RISK FACTORS: Process markers

A

Fibrinogen

36
Q

TX that you should do for Atherosclerosis

Non-specific

A

Steroids (increase adverse events)

NSAIDS (destabilize plaques)

37
Q

TX you should not fo for Atherosclerosis

Selective inhibitor

A

COX2 inhibitor (Vioxx)= increase in CVD mortality

38
Q

TX of Atherosclerosis

A

AB against IL-1B

  • IL-1B drives atherosclerosis (by making HSCRP)
  • ACZ885 canakinumab blocks this pathway
39
Q

STUDY on Canakinumab (anti-thrombosis)

A

Study showed that the drug in high and medium does decreased HSCRP, IL-6
No change in LDL
Decreases the mortality rate of each participant in these dosages

40
Q

CIRT study

A

Looking at Low dose METHOTREXATE
= no reduction in HSCRP, IL1, IL6 or mortality form CV event
*CANTOS study on IL-1B inhibitor had more of a significance

41
Q

Reason IL-1B inhibitor is not used

A

Not a significant difference in all mortality causes
And also expensive
Highly more risk of infection

42
Q

Future plan to help CVD

A

Vaccination against B-cells and T-cells for oxLDL

CRISPR technology

CPR Exam 1 (20 decks)

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