Mechanism of Inflation Flashcards Preview

CMBM 3 > Mechanism of Inflation > Flashcards

Flashcards in Mechanism of Inflation Deck (47)
1

What is inflammation?

complex reaction to tissue injury -involves alteration to epithelial cells - recruits WBC -always lead to at least some tissue damage

2

What is inflammation usually linked to ?

elimination of microbial cause and repair of damaged tissue

3

What are three different categories of inflammation?

acute

chronic

allergic

4

What is acute inflammation?

- initial response to tissue damage regardless of cause - recruit neutrophils (infiltrate)

5

What is chronic inflammation?

if acute cannot clear infection - more mononuclear (lymphocyte or monocyte)cells will infiltrate

6

What is allergic inflammation?

kind of response associated with allergies (hay fever, allergic rhinitis) -mucosal tissue - eosinophils (and mononuclear cells)

7

What are some autoimmune diseases?

RA

systemic lupus

erythematosus

8

What are the components of inflammatory response?

endothelium

platelets

clotting factors

complement components

Connective tissue cells: - mast cells - macrophages - everywhere connective tissue matrix - elastic fibers, collagen fiber proteoglycan

9

Where are mast cells commonly found?

mucosal subepithelial skin

10

What are the common processes in inflammation?

-stimulus

-release of inflammatory mediators

-vasodilation

-increased vascular permeability

- up-regulation of adhesion molecules on endothelial cells and leukocytes

-diapedesis, chemotaxis, and acivation of leukocytes

11

What are the cardinal signs of inflammation?

Rubor (redness) Tumor (swelling) Calor (heat) Dolor (pain) Functio (loss of function)

12

What are the causes of the cardinal signs of inflammation?

redness , warmth >>> erythema due to vascular dilation, increased blood flow

swelling >>> extravasation of plasma

-leukocyte accumulation at site of injury

 

pain >>> kinin stimulation of nerve fibers

13

What are inflammatory stimuli?

infection

trauma

physical and chemical agents

tissue necrosis

foreign bodies

immune hypersensitivities (fight against own body)

14

What about the stimulus leads to the response?

microorganisms have PAMPs that are detected by PRR(pathogen recognition receptors on every cell) - once recognized, damaged cells release DAMPS (damage-associated molecular pathogens) which are recognized by DRR (damage recognition receptors)

15

What interaction releases inflammatory mediators??

DAMPS also interact with PRR or DRRs to release inflammatory mediators

 

interaction of PAMPS with PRRS leads to the production of mediators by variety of cells.

16

What happens in a capillary when inflammation is occurring?

stimulus causes the endothelial cells to constrict to cause a gap (vasodilation) to release antibodies, complement components, platelets

17

What are some vasoactive mediators?

eicosanoids (PG, TX)

18

 

The upregulation of adhesion molecules will result in ?

*P-selectin - rolling (neutrophils, monocytes, lymphocytes)

*E-selectin - rolling & adhesion (neutrophils,monocytes, Tcell)

*ICAM-1 - (intercellular adhesion molecule for leukocytes) - attaches to LFA-1 *VCAM - adhesion of eosinophils, monocytes, lymphocytes -attaches to VLA4

*PCAM - expressed on both leukocyte and endothelium

19

Where does Sialyl-Lewis x-modified glycoprotein attach?

P-selectin

E-selectin

20

What are chemo attractant substances?

chemokine

complement components

21

What is diapedesis?

outward passage of blood cells through intact vessel walls

22

What are the cellular sources of inflammatory mediators?

tissue macrophages and dendritic cells

mast cells

leukocytes

endothelial cells

liver

epithelial cells

fibroblasts

keratinocytes

23

What inflammatory mediators are produced by the liver?

Factor XII activation

- Kinin

- coagulation

 

Complement activation

-C3a - anaphylatoxins

-C5a - anaphylatoxins

-C5b-9 - MAC

24

Review 3 complement activation pathways.

Alternate - microbe

Classical - antibody

Lectin - mannose binding lectin

25

Plasma protein system interacts between?

clotting cascade

kinan cascade

complement sytem

26

What pathways does the Hagemna factor activate?

clotting cascade

kinan cascade

complement sytem

27

Actions of eicosanoids

Vasoconstriction - Thromboxine A2

                                leukotrienes C4, D4, E4

 

Vasodilation - PGI1, PGE1, PGE2, PGD2

 

Increased vascular permeability - leukotrienes C4, D4, E4

 

Chemotaxis, leukocyte adhesion - leukotriene B4, HETE, lipoxins

28

What are the roles of cytokines in inflammation?

****Learn!!!****

Pro-inflammatory

IL1 - numerous

TNF-a  - numerous

IL-6 induces release of acute phase proteins from liver

IL-17 - leads to neutrophil production from bone marrow and neutrophil act.

IL2 - activation of Tcells

IFN-gamma - activation of macrophages

 

Recruitment of mononuclear cells and eosinophils -CC Chemokines

neutrophil recruitment - CXC chemokines

29

Which cytokines are pro-inflammatory?

IL-1 - numerous; activates endothelial, upregulates expression of adhesion molecules

TNF-alpha - numerous; activates endothelial, upregulates expression of adhesion molecules

IL-6 - induces release of acute phase proteins from liver

IL-17 - (TH17) ultimately leads to neutrophil production from bone marrow and neutrophil activation

IL-2 - activation of Tcells

IFN-gamma - (TH1) activation of macrophages

30

What is IFN- gamma responsible for?

activation of macrophages

31

What does IL-17 lead to?

ultimately leads to neutrophil production from bone marrow and neutrophil activation

32

What does IL-2 activate?

T cells (not needed in acute response)

33

What does IL-6 induce?

induces release of acute phase proteins from liver

34

What do CC chemokines recruit?

mononuclear cells and eosinophils

-MIP

-MCP

-RANTES

-eotactin

35

CXC chemokines

IL-8

-neutrophil recruitment

36

What are the acute phase effects of IL-1 and TNF?

Acute:

fever

increase sleep

decreased appetite

****acute-phase proteins

***Hemodynamic effect (shock)

**neutrophilia

37

What are the endothelial effects of IL-1 and TNF?

increased leukocyte adherence

 

increased PGI synthesis

increased procoagulate acivity

decreased anticoagulative activity

Increased IL1, IL8, IL6 PDGF

38

Compare Acute, Chronic, and allergic inflammation

Duration   short                       longer

Time frame  fast response      slower

Type of infiltrating cell  neutrophil         monocyte/lymphocyt

chemotactic stimuli

use of ICAM vs. VCAM

39

What are the stages of inflammation pathologically?

edema

neutrophils

monocytes/macrophages

40

Look at slide for granuloma formation

slide -round in appearance

multinucleated cells

41

What happens in chronic inflammation?

1. Acute inflammation with upregulation of chemokine, adhesion molecules

2. TH1 cells release IFN, TNF, IL-2, RANTESq

42

What attracts mononuclear cells?

CC Chemokines -CCL2 - CCl3 - CCL4 -CCL5

43

What is an allergic inflammation?

reaction to harmless proteins (grass, cockroach crap)

44

Which cell is harmless protein presented to?

Th2

45

Which IL causes change in B cell?

IL4 (check)

46

What happens when the mast cell degranulates?

histamine released

cytokine breaks down arachanodonic acid

47

Table 2–1 Features of Acute and Chronic Inflammation

First curve - edema

Second curve - neutrophils (acute)

Third curve - macrophages (chronic)