Inflammation Lecture 1 Dr Ejaz WarisPresentation Transcript
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INFLAMMATI0N Dr. EJAZ WARIS , FCPS Assistant Professor Histopathology,FMHC
“ 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.
Lewis Triple Response:
Flush : capillary dilatation.
Flare : arteriolar dilatation.
Weal : exudation, edema.
Cardinal Signs of Inflammation
Rubor : Redness – Hyperaemia.
Calor : Warm – Hyperaemia.
Dolor : Pain – Nerve, Chemical med.
Tumor : Swelling – Exudation
Loss of Function :
The 5 Cardinal Signs of Heat Redness Swelling Pain Loss Of Func.
Two main components:
Two main types:
Cells of inflammation
Connective tissue matrix
Made up of :
Connective tissue cells
Acute Inflammation - Mechanism 1.Alterations in vascular calibre leading to increased blood flow 2.Microvasculature structural changes 3.Leukocyte emigration
A)vascular flow and calibre change
Inconstant transient vasoconstriction of arterioles for few seconds
slowing of circulation (increased permeability of the vasculature)
Vascular changes continued
B)increased vascular permeability
vascular leakage leading to escape of protein rich fluid into the interstitium is the hall mark of acute inflammation
How does endothelium becomes leaky in inflammation?
1)formation of endothelial gaps in venules
4)direct endothelial injury
5)leukocyte dependent injury
6)delayed prolonged leakage
7)leakage from new blood vessels
Sequence of events in the journey of leukocytes from the lumen to the interstitial tissue
Mechanism of Inflammation:
Play an important role in acute inflammation
Family no 1: Selectins
Family no 2:Ig-family adhesion proteins
Family no 3:Integrins
Family no 4:Mucin like glycoproteins
Pneumonia - Exudation
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