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DR EJAZ WARIS
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"Opportunities are usually disguised by hard work, so most people don't recognize
them."
- Ann Landers
Shashi-Mar 2000
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INFLAMMATI0N
Dr. SHAHILA JALEELHistopathologySZH,Lahore
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.
INTROD……….
Injurious stimuli cause a protective vascular connective tissue reaction called “inflammation”• Dilute• Destroy• Isolate• Initiate repair
Acute and chronic forms
Lewis Triple Response:
Flush: capillary dilatation. Flare: arteriolar dilatation. Weal: exudation, edema.
Gastric Ulcer:
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Laryngitis:
Acute Enteritis:
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Pneumonia
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Cardinal Signs of Inflammation
Rubor : Redness – Hyperaemia. Calor : Warm – Hyperaemia. Dolor : Pain – Nerve, Chemical
med. Tumor: Swelling – Exudation Loss of Function:
Heat Redness Swelling Pain Loss Of Func.
The 5 Cardinal Signs of
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Inflammation
Two main components:vascular reactioncellular reaction
Two main types: acute chronic
Chemical mediators
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Cells of inflammation
Circulating cells
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Connective tissue matrix
Made up of :
A)collagen fibers B)elastic fibers C)glycoproteins D)proteoglycans
Connective tissue cells
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Acute Inflammation - Mechanism
1.Alterations in vascular calibre leading to increased blood flow
2.Microvasculature structural changes
3.Leukocyte emigration
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Vascular changes
A Inconstant transient vasoconstriction of arterioles for few seconds followed by vasodilationAccounts for warmth and rednessOpens microvascular beds
Increased intravascular pressure causes an early transudate (protein-poor filtrate of plasma) into interstitium (vascular permeability still not increased yet)
Vascular permeability (leakiness) commencesTransudate gives way to exudate
(protein-rich)Increases interstitial osmotic pressure
contributing to edema (water and ions) slowing of circulation (increased
permeability of the vasculature) stasis Leukocyte migration
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Vascular changes continued
B)increased vascular permeabilityvascular leakage leading to escape of protein rich fluid into the interstitium is the hall mark of acute inflammation
exudatetransudateedemapus
An exudate is an extravascular fluid that has a
high protein concentration cellular debris high specific gravity. Its presence implies an increase in the normal
permeability of small blood vessels in an area of injury .
A transudate is a fluid with low protein content (most of which is albumin) little or no cellular material low specific gravity It is essentially an ultrafiltrate of blood plasma that
results from osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability
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Edema denotes an excess of fluid in the interstitial tissue or serous cavities; it can be either an exudate or a transudate.
Pus, a purulent exudate, is an inflammatory exudate rich in leukocytes (mostly neutrophils), the debris of dead cells and, in many cases, microbes.
IMMEDIATE TRANSIENT RESPONSE – RESPONSE TO
MINOR INJURY
IMMEDIATE SUSTAINED RESPONSE – RESPONSE
TO
MORE SERIOUS INJURY, CONTINUES FOR SEVERAL
DAYS, DAMAGE TO VESSELS
DELAYED RESPONSE – INCREASES IN CAPILLARY
PERMEABILITY, DELAYED 4-24 HR, RADIATION
INJURIES, SUNBURN
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1)formation of endothelial gaps in venules
2)cytoskeletal reorganization 3)increased transcytosis 4)direct endothelial injury 5)leukocyte dependent injury 6)delayed prolonged leakage 7)leakage from new blood vessels
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Mechanism of Inflammation:
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Leukocyte emigration/extravasation
Sequence of events in the journey of leukocytes from the lumen to the interstitial tissue
Margination Pavementing Rolling Adhesion Transmigration/diapedesis
Adhesion molecules
Play an important role in acute inflammation
4 families Family no 1: Selectins
E-selectin,P-selectin,L-selectinFamily no 2:Ig-family adhesion proteins
ICAM-I,ICAM-II,PECAM-I,VCAM-I
Adhesion molecules
Family no 3:IntegrinsLFAMAC-1VLA-4
Family no 4:Mucin like glycoproteinsCD-34Glycam-1
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Neutrophil Margination
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Vascular changes
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Pneumonia - Exudation
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