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CMBM 3 > Mechanism of Inflation > Flashcards

Mechanism of Inflation Flashcards

1
Q

What is inflammation?

A

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

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2
Q

What is inflammation usually linked to ?

A

elimination of microbial cause and repair of damaged tissue

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3
Q

What are three different categories of inflammation?

A

acute

chronic

allergic

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4
Q

What is acute inflammation?

A
  • initial response to tissue damage regardless of cause - recruit neutrophils (infiltrate)
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5
Q

What is chronic inflammation?

A

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

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6
Q

What is allergic inflammation?

A

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

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7
Q

What are some autoimmune diseases?

A

RA

systemic lupus

erythematosus

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8
Q

What are the components of inflammatory response?

A

endothelium

platelets

clotting factors

complement components

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

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9
Q

Where are mast cells commonly found?

A

mucosal subepithelial skin

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10
Q

What are the common processes in inflammation?

A
  • 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
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11
Q

What are the cardinal signs of inflammation?

A

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

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12
Q

What are the causes of the cardinal signs of inflammation?

A

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

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13
Q

What are inflammatory stimuli?

A

infection

trauma

physical and chemical agents

tissue necrosis

foreign bodies

immune hypersensitivities (fight against own body)

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14
Q

What about the stimulus leads to the response?

A

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)

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15
Q

What interaction releases inflammatory mediators??

A

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.

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16
Q

What happens in a capillary when inflammation is occurring?

A

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

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17
Q

What are some vasoactive mediators?

A

eicosanoids (PG, TX)

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18
Q

The upregulation of adhesion molecules will result in ?

A

*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

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19
Q

Where does Sialyl-Lewis x-modified glycoprotein attach?

A

P-selectin

E-selectin

20
Q

What are chemo attractant substances?

A

chemokine

complement components

21
Q

What is diapedesis?

A

outward passage of blood cells through intact vessel walls

22
Q

What are the cellular sources of inflammatory mediators?

A

tissue macrophages and dendritic cells

mast cells

leukocytes

endothelial cells

liver

epithelial cells

fibroblasts

keratinocytes

23
Q

What inflammatory mediators are produced by the liver?

A

Factor XII activation

  • Kinin
  • coagulation

Complement activation

  • C3a - anaphylatoxins
  • C5a - anaphylatoxins
  • C5b-9 - MAC
24
Q

Review 3 complement activation pathways.

A

Alternate - microbe

Classical - antibody

Lectin - mannose binding lectin

25
Q

Plasma protein system interacts between?

A

clotting cascade

kinan cascade

complement sytem

26
Q

What pathways does the Hagemna factor activate?

A

clotting cascade

kinan cascade

complement sytem

27
Q

Actions of eicosanoids

A

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
Q

What are the roles of cytokines in inflammation?

A

****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
Q

Which cytokines are pro-inflammatory?

A

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
Q

What is IFN- gamma responsible for?

A

activation of macrophages

31
Q

What does IL-17 lead to?

A

ultimately leads to neutrophil production from bone marrow and neutrophil activation

32
Q

What does IL-2 activate?

A

T cells (not needed in acute response)

33
Q

What does IL-6 induce?

A

induces release of acute phase proteins from liver

34
Q

What do CC chemokines recruit?

A

mononuclear cells and eosinophils

  • MIP
  • MCP
  • RANTES
  • eotactin
35
Q

CXC chemokines

A

IL-8

-neutrophil recruitment

36
Q

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

A

Acute:

fever

increase sleep

decreased appetite

****acute-phase proteins

***Hemodynamic effect (shock)

**neutrophilia

37
Q

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

A

increased leukocyte adherence

increased PGI synthesis

increased procoagulate acivity

decreased anticoagulative activity

Increased IL1, IL8, IL6 PDGF

38
Q

Compare Acute, Chronic, and allergic inflammation

A

Duration short longer

Time frame fast response slower

Type of infiltrating cell neutrophil monocyte/lymphocyt

chemotactic stimuli

use of ICAM vs. VCAM

39
Q

What are the stages of inflammation pathologically?

A

edema

neutrophils

monocytes/macrophages

40
Q

Look at slide for granuloma formation

A

slide -round in appearance

multinucleated cells

41
Q

What happens in chronic inflammation?

A
  1. Acute inflammation with upregulation of chemokine, adhesion molecules
  2. TH1 cells release IFN, TNF, IL-2, RANTESq
42
Q

What attracts mononuclear cells?

A

CC Chemokines -CCL2 - CCl3 - CCL4 -CCL5

43
Q

What is an allergic inflammation?

A

reaction to harmless proteins (grass, cockroach crap)

44
Q

Which cell is harmless protein presented to?

A

Th2

45
Q

Which IL causes change in B cell?

A

IL4 (check)

46
Q

What happens when the mast cell degranulates?

A

histamine released

cytokine breaks down arachanodonic acid

47
Q

Table 2–1 Features of Acute and Chronic Inflammation

A

First curve - edema

Second curve - neutrophils (acute)

Third curve - macrophages (chronic)

CMBM 3 (28 decks)

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