Imflammation Flashcards
Inflammation is the
host response to injury
It can occur due to infection, trauma, exposure to noxious chemicals or allergens
Inflammation can occur due to certain conditions
meningitis, arthritis,
Inducers of inflammation can include:
cell lysis during viral replication, virulence factors - LPS (endotoxin), exotoxins, helminth-derived proteases, PAMP’S,
Cellular necrosis and release of intracellular contents, degredation of basement membrane, loss of epithelial or endothelial integrity - leakage of plasma proteins
Point of inflammation
- Deliver effector molecules, drugs and cells to the site of infection or injury
- Induce local blood clotting
- Stimulate adaptive immune response
- Promote repair of injured tissue
Outcome of acute inflammation
when stitches are applied due to surgery, by 6 months for example, the signs of any inflammation can clear
Outcome of inflammation
Complete elimination of pathogen (in the case of acute inflammation)
Inflammatory disease
Infections where inflammation causes damage: hepatitis c, Sepsis, tuberculosis,
Post inflammatory fibrosis: Hepatic Cirrhosis, chronic rejection
Cardinal signs of inflammation
Redness, swelling, heat, pain, loss of function, lethargy, apathy, loss of appetite, increased sensitivity to pain
Characteristic features
:
Vasodilation, vascular permeability, leukocyte extravasation,
Stimulation of immune response - drainage to lymph nodes,
Extravasation,
selectin mediated adhesion to leukocyte is weak, and allows leukocytes to roll along the vascular endothelial surface. During extravasation, the number of binding molecules increases
Main components of inflammatory response
Mast cells, granulocytes (neutrophils and eosinophils), mononuclear phagocytes (monocytes and macrophages), T lymphocytes, platelets, NK cells, Fibroblasts,
Vasoactive mediators include
histamine and kinins,
Lipid mediators include
eicosinoids
Different cells produce different
cytokines and mediators
Histamine
Causes degranulation also through c3a and c5a, cytokines, mechanical damage, has receptors H1 TO H4, on vascular smooth muscle it causes vasodilation, binds to endothelial cell receptors,
Kinins
activate cascades (|clotting),
Prostaglandins and Leukotrienes
prostaglandins generated from cox 1 and 2,
these are powerful vasodilators, potentiate vasoactive mediators, pryogenic, short half life.
Leukotrienes are generated from arachidonic acid by 5- lipoxygenase,
TNF
cytokine which induces chemokine production, and adhesion of molecules on endothelial cells, activates phagocytes, increases proteins triggering local clotting,
Development of Inflammation
dilation of small blood vessels (via histamine, prostaglandins e.t.c.)
Increased vascular permeability - passage of fluid and small proteins endothelial cell activation, repair and resolution
Pain and fever
Pain can be caused by inflammatory mediators, badykinin causes pain, Exudation of plasma increases tissue pressure
Fever causes an increase in temperature, defences work better, faster lymphocyte division, increases cell migration,
stimulated macrophages release IL-1 stimulating PGE2 synthesis. Acts on Hypothalamus.
When inflammation occurs,
activity of edema rises, then of neutrophils (pmn), the macrophages
Neutrophils are
phagocytes, they engulf pathogenic material. They can phagocytose a bacteria for example. If the pathogen is too big, they can release materials to degranulate the pathogen,
People who lack neutrophils would be
immunodeficient
The neutrophil response has to be turned off after it is not necessary
for the resolution of inflammation. The neutrophils are programmed to die via apoptosis, and certain changes to the neutrophil promote the uptake via phagocytosis.
