Overview Inflamation

Mechanism
Causes:
• -1-Infection
• 2-Trauma
• 3-Physical injury (thermal, radiation)
• 4-Chemical injury
• 5-Immuological injury6-Tissue death…in viable tissue
adjacent to necrotic tissue

Types of inflammation
1-Acute inflammation : Of sudden onset and short duration
2-Chronic inflammation : Of gradual onset and long duration
 Cardinal Signs of acute inflammation
-Redness (rubor)
-Swelling (tumor)
-Heat (calor)
-Pain (dolor)
-Loss of function (functio laesa) (the fifth
cardinal sign added by Virchow)
 Major componentsof the acute
inflammatoryprocess
• 1. Vasoactive changes:
• Change in diameter. transient VC then
permanent VD of arterioles, capillaries and
post capillary venules.
• increase of the blood flow to the area which
is manifested clinically by local redness and
hotness of the affected area.
2. Increased capillary permeability:
• endothelial changes : Endothelial swelling
with widening of intra-endothelial gaps of
post capillary venules.
• endothelial damage involving arterioles,
capillaries and venules
• This results in leakage of protinacious fluid
(exudate) which causes inflammatory edema.
Exudate
• Due to increased vascular permeability.
• Rich in protein esp. fibrin(turbed)
• Coagulates on standing.
• High specific gravity ( more than 1018).
• Contains inflammatory cells.
Transudate
• Occurs late in inflammation
• Due to increased hydrostatic pressure.
• Low protein content.
• Does not coagulate on standing.
• Low specific gravity ( less than 1018).
• No inflammatory cells
• Can occur early in inflammation
Types of acute inflammatory exudate
• Serous: Clear fluid with few cells and fibrin
e.g in burns and common cold.
• Serofibrinous: Fluid rich in fibrin mainly in
seroussacs (pleura and pericardium).
• Pus: Thick,turbed fluid rich in cells (living and
dead neutrophils). Occurs in suppurative
inflammations
Oxygen dependent :
Activation of NADPH Oxidation  production superoxide radicals increased 
production H2O2 and hidroxyl free radicals  lipid peroxidation  cell death

Non dependent oxygent:

Lysosime, lactoferine, defensin and bacterial permeability protein
Less effective than oxygent dependent
 Reference
• Dr. Maha Abu Hasim, inflammation, 2013-
2014
• Sarah Beck,sbeck8@jhmi.edu