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1. University of burao faculty of medicine Dr. Musa M. Abdi Baaxeer M.B.B.S( pak ) M.P.H (MAL)

2. Inflammation It is essential a protective response intended to eliminate both the initial cause of cell injury and necrotic cells and tissues arising a consequence of cell injury. The inflammatory process dilute , destroy or isolates the causative agent and set into motion the sequence of event that heals reconstitute the damaged tissue.

3. Inflammation During repair the injure tissue is replaced by regeneration of native parenchymal cells , by filling of the defect with fibroblast scar tissue,. Inflammation helps clear infection and along with repair, makes wound healing possible. Inflammation can cause potential harm for example inflammatory reaction underlie life threatening anaphylactic response insect bite, or drugs As well as chronic disease such us rheumatoid arthritis and atherosclerosis

4. Inflammation Inflammation in divided into two basic form. Acute inflammation : is relatively short duration, lasting from minutes to a few days and it is characterized by fluid plasma protein exudation and by predominantly neutrophil ic leukocyte accumulation. Chronic inflammation : is of longer duration (days to years) and is manifested histologically by Influx of lymphocyte and macrophages and by tissue destruction and repair.

5. Acute inflammation It is the immediate and early response to injury. The critical function of the response is to deliver leucocyte to the site of injury where they can help clear invading bacteria, as well as degrade necrotic tissue resulting from damage. Leukocytes themselves may prolong inflammation and induce tissue damage by releasing enzymes, chemical mediators, and toxic oxygen radicals.

6. Acute inflammation Acute inflammation has three major component. Alteration in vascular caliber that leads to a local increase in blood flow ( vasodilation ). Structural change in microvasculature that permits plasma protein to leave the circulation. Emigration of the leukocyte from the microcirculation and accumulation in focus of injury.

7. Acute inflammation These component accounts for three of the five classical local sign of acute inflammation Heat Redness Swelling Pain Loss of function

8. Acute inflammation Vascular change(change in vascular flow and caliber ). After an inconstant and transient(second) vasoconstriction of arterioles, vasodilatation occur, vasodilatation occur. Arterioles are involved first , resulting in the opening new microvascular bed in the area. The local increase blood is the cause of the redness ( erythema )and warmth characteristically seen in acute inflammation.

9. Acute inflammation Subsequently microvasculature become more permeable, resulting in the exudation of protein-rich fluid into the extravascular tissues. This causes the red blood cells to become effectively more concentration, thereby increasing blood viscosity and slowing the circulation. These changes are manifested microscopically by numerous dilated small vessels packed with erythrocytes a process called stasis

10. Acute inflammation As stasis develops leukocytes begin to settle out of the flowing blood and accumulate along the vascular endothelial surface, a process caller margination . after adhering to endothelial cells the leukocyte squeeze between them and migrite through the vascular wall into the intertitial tissue, a process called emigration.