Dr Rezaur Rahman

Dr Rezaur Rahman

INFLAMMATION

Definition of Inflammation:Inflammation is a complex reaction in

living vascularized tissue to injurious agents leading to the exudation and accumulation of protein rich fluid and leucocytes in extravascular tissue, provided the injury does not destroy the tissue.

Reaction of vascularized tissue to injury

Accumulation of protein rich fluid and leucocytes in extravascular tissue

Purposes:A protective response to-1. to dilute, localize and destroy the

injurious agent2. to limit tissue injury3. to restore the tissue towards

normalityHarmful effect: eg, hypersensitivity

reaction

Acute Inflammation:Rapid local response of living tissue to

injuryLasts for minutes to a few daysExtravascular accumulation of protein

rich fluid and leucocytes, predominantly Neutrophils, ie, Exudative lesion

Stereotype,ie, wide variety of agents share the same basic features

Chronic Inflammation:Persists for weeks to monthsExtravascular accumulation of

Lymphocytes and MacrophagesTissue destruction and attempts to

healing by proliferation runs simultaneously, ie, Proliferative lesion

Not stereotype

Cardinal signs of Acute Inflammation

Rubor or rednessCalor or heatTumor or swellingDolor or painLoss of function(functio laesa)

Aetiology of Acute Inflammation1. Infectious agent: Bacteria, virus, fungi,

protozoa2. Immune reaction: Hypersensitivity reaction3. Trauma: blunt/penetrating4. Physical agent: eg, burn, ionizing radiation5. Foreign bodies: eg, sutures, dirt6. Chemical agent: acids, alkalies, bile7. Tissue necrosis: eg, infarcts

Events in Acute Inflammation:1.Vascular changes:• Changes in vascular flow & caliber• Increased vascular permeability(Vascular

leakage)2.Exudation of blood constituents:• Fluid Exudate• Cellular Exudate3.Changes in tissue tissue components

Vascular changes(Flow & Caliber)Vasodilation, due to-a)Histamineb)Nitric oxide,etcIncreased permeability of

microvasculatureSlowing of circulation/ Stasis, due to-a)Exudationb)Microcirculation packed with red cellc)Increased viscosity of blood

Accounts for warmth and redness

Opens microvascular beds

Increased intravascular pressure causes an early transudate (protein-poor filtrate of plasma) into interstitium (vascular permeability still not increased yet)

Movie- Vasodilation

Vascular changes(Vascular Leakage)

Vascular changes(Vascular Leakage)

Vascular changes(Vascular Leakage)

Cellular events:A) Leucocyte Extravasation1 In the limen-a)Marginationb)Rollingc)Adhesion to endothelium2 Transmigration or diapedesis across

endothelum3 ChemotaxisB) Phagocytosis

leukocytes first roll, then become activated and adhere to endothelium, thentransmigrate across the endothelium, pierce the basement membrane, and migrate

toward chemoattractants

Movie- Leucocyte Rolling

Chemotaxis:Following extravasations, leukocytes emigrate in

tissues toward the site of injury by a process called chemotaxis.

Exogenous chemo attractants:Exogenous chemo attractants: bacterial products, etc.

Endogenous chemo attractants:Endogenous chemo attractants: components of the (LTB4), cytokines, etc.

PhagocytosisRecognition and attachmentEngulfment

PhagosomePhagolysosome

killing and degradationOxydent dependent mechanism:I.H2O2-MPO-Halide systemII.Reactive Oxygen intermediates-O2- ,H2O2,

OH- Oxydent independent mechanism: killing

occur by substances of lysosomal granules- Lysozyme, Lactoferrin, BPI, Defensin

Morphological Variants:1. Suppurative or Purulent inflammation2. Fibrinous inflammation3. Serous inflammation4. Serofibrinous inflammation5. Catarrhal inflammation6. Pseudomembranous inflammation7. Acute inflammatory ulcer8. Haemorrhagic inflammation9. Necrotizing inflammation

Movie- Inflammation

Thank You