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Inflammation reza2003 e video

Inflammation reza2003 e video



Class1: Acute Inflammation

Class1: Acute Inflammation



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    Inflammation reza2003 e video Inflammation reza2003 e video Presentation Transcript

    • Dr Rezaur Rahman
      • Dr Rezaur Rahman
    • 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-
      • to dilute, localize and destroy the injurious agent
      • to limit tissue injury
      • to restore the tissue towards normality
      • Harmful effect: eg, hypersensitivity reaction
    • Acute Inflammation:
      • Rapid local response of living tissue to injury
      • Lasts for minutes to a few days
      • Extravascular 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 months
      • Extravascular accumulation of Lymphocytes and Macrophages
      • Tissue destruction and attempts to healing by proliferation runs simultaneously, ie, Proliferative lesion
      • Not stereotype
    • Cardinal signs of Acute Inflammation
      • Rubor or redness
      • Calor or heat
      • Tumor or swelling
      • Dolor or pain
      • Loss of function(functio laesa)
    • Aetiology of Acute Inflammation
      • Infectious agent: Bacteria, virus, fungi, protozoa
      • Immune reaction: Hypersensitivity reaction
      • Trauma: blunt/penetrating
      • Physical agent: eg, burn, ionizing radiation
      • Foreign bodies: eg, sutures, dirt
      • Chemical agent: acids, alkalies, bile
      • 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 Exudate
      • 3.Changes in tissue tissue components
    • Vascular changes(Flow & Caliber)
      • Vasodilation , due to-
      • Histamine
      • Nitric oxide,etc
      • Increased permeability of microvasculature
      • Slowing of circulation/ Stasis , due to-
      • Exudation
      • Microcirculation packed with red cell
      • 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 Extravasation
      • 1 In the limen-
      • Margination
      • Rolling
      • Adhesion to endothelium
      • 2 Transmigration or diapedesis across endothelum
      • 3 Chemotaxis
      • B) Phagocytosis
    • leukocytes first roll, then become activated and adhere to endothelium, then transmigrate 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: bacterial products, etc.
      • Endogenous chemo attractants: components of the (LTB4), cytokines, etc.
    • Phagocytosis
      • Recognition and attachment
      • Engulfment
      • Phagosome
      • Phagolysosome
      • killing and degradation
      • Oxydent dependent mechanism:
      • H2O2-MPO-Halide system
      • Reactive Oxygen intermediates-O2 - ,H2O2, OH -
      • Oxydent independent mechanism: killing occur by substances of lysosomal granules- Lysozyme, Lactoferrin, BPI, Defensin
    • Morphological Variants:
      • Suppurative or Purulent inflammation
      • Fibrinous inflammation
      • Serous inflammation
      • Serofibrinous inflammation
      • Catarrhal inflammation
      • Pseudomembranous inflammation
      • Acute inflammatory ulcer
      • Haemorrhagic inflammation
      • Necrotizing inflammation
      • Movie- Inflammation
    • Thank You