Inflammation
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Shashi-Mar 2000 flammation-1 Introduction: “Inflame” – to set fire. Inflammation is “dynamic response of vascularised tissue to injury.” Is a protective response. Serves to bring defense & healing mechanisms to the site of injury.
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Transcript of Inflammation
Shashi-Mar 2000
Inflammation-1
Introduction:
“Inflame” – to set fire.
Inflammation is “dynamic response of vascularised tissue to injury.”
Is a protective response.
Serves to bring defense & healing mechanisms to the site of injury.
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Lewis Triple Response:
FlushFlush:: capillary dilatation.
FlareFlare:: arteriolar dilatation.
WealWeal:: exudation, edema.
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Red, Warm & Swollen(Flare, Flush & Weal – Lewis)
Triple response
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Inflammation - Mechanism
1. Vaso dilatation
2. Exudation - Edema
3. Emigration of cells
4. Chemotaxis
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Mechanism of Inflammation:
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Chemical Mediators:
Chemical substances synthesised or released which mediate the changes in inflammation.
Histamine by mast cells - vasodilatation.
Prostaglandins – Cause pain & fever.
Bradykinin - Causes pain.
Products of the complement system
Lymphokines released by sensitized T cells
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Acute Vs Chronic
Flush, Flare & Weal
Acute inflammatory cells - Neutrophils
Vascular damage
More exudation
Little or no fibrosis
Little signs - Fibrosis, Chronic inflammatory cells – LymphocytesNeo-vascularisationNo/less exudationProminent fibrosis
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Walling-off effect of inflammation
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Macrophage and neutrophil responses during
inflammation
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1. Tissue macrophage is a First line of defense against infection
2. Neutrophil invasion of the inflamed area is Second line of defense
3. Second macrophage invasion into the inflamed tissue is a Third line of defense
4. Increased production of granulocytes and monocytes by the bone marrow is a
Fourth line of defense
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Feedback control of the macrophages and neutrophil
response
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Formation of pus
Combination of necrotic tissue, dead neutrophils and macrophages and tissue fluid.
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Heat Redness Swelling Pain Loss Of Func.
The 5 Cardinal Signs of
