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
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)