Acute Inflammation,Cell Derived and Plasma Protein Derived Mediators,Morphology
Transcript of Acute Inflammation,Cell Derived and Plasma Protein Derived Mediators,Morphology
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What is inflammation?
Inflammation
Inflammation is a complex reaction in tissues that
consists mainly of responses of blood vessels and
leukocytes
Protectiveresponse intended to eliminate the initial
cause of cell injury and the necrotic cells and tissues
arising from the injury
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Egyptian papyrus - 3000 B.C.
Celsus(Roman in 1st century A.D.)
Rubor - Tumor - Calor - Dolor
redness - swelling - heatpain
Rudolf Virchowadded loss of function later
Elie Metchnikoff -Phagocytosis
History
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Acute
Rapid in onset, lasting for min/hrs/days
Exudation of fluid and plasma proteins (edema)
Emigration of leukocytes predominantly
neutrophils
Chronic
Longer duration Lymphocytes and macrophages
Proliferation of blood vessels, fibrosis and tissue
necrosis
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Etiologies
Microbial infections: bacterial, viral, fungal,parasiticetc.-Toll like receptors
Physical agents: burns, trauma--like cuts, radiation
Chemicals: drugs, toxins, or caustic substances likebattery acids
Immunologic reactions: rheumatoid arthritis
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Microbial infections
One of the commonest causes of inflammation
Bacteria release specific exotoxins or endotoxins
In parasitic infections hypersensitivity plays an
important role
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Physical agents
Tissue damage leading to inflammation may occurthrough physical trauma, ultraviolet or other ionizingradiation, burns or excessive cooling
Irritant and corrosive chemicals
Corrosive chemicals (acids, alkalis, oxidizing agents)provoke inflammation through tissue damage
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Five classic local signs of acute
inflammation
Heat
Redness
Swelling
Pain
Loss of function
Calorvasodilatation
Ruborvasodilatation
Tumorvascular permeability
Dolormediator release
Functio laesa
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Components of Inflammation
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Acute inflammation is a rapid response to an injuriousagent that serves to deliver mediators of host defense-leukocytes and plasma proteins- to the site of injury
Alterations in vascular caliber
Structural changes in microvasculature
Emigration and activation of leukocytes
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Vascular changes
Transient vasoconstriction
Vasodilation
Exudation of protein rich fluid
Blood stasis
Margination
Transmigration
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LeukocyteAdhesionTransmigration
ChemotaxisPhagocytosis
Termination
Stasis
Vascular
permeability
Vasodilatation
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Vasodilation Earliest manifestation
First involves arterioles
Important mediators- Histamine and NO
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Histamine
Causes dilatation of arterioles first Increases the permeability of the venules
Principal mediator of the immediate transient phase
of increased vascular permeability, causing venulargaps
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Swelling (tumor)
Swelling result from edema, the accumulation of
fluid(exudate) in the extra vascular space
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Exudate Transudate
vascular permeability
High protein & cell
debris
Specific gravity >
1.020
Normal vascularpermeability
Low protein (mostly
albumin) Specific gravity