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The process of acute inflammation


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The process of acute inflammation

  1. 1. Objectives:1. Understand the sequence of vascular and cellular events in thehistological evolution of acute inflammation2. Learn the roles of various chemical mediators of acute inflammation3. Know the three possible outcomes of acute inflammation4. Visualize the three morphologic patterns of acute inflammation A.Y.2012-2013 1 @CBBitangcor Presentations
  2. 2. Sequence of Events• Normal Histology• Vasodilation• Increased Vascular Permeability• Leakage of Exudate• Margination, Rolling and Adhesion• Transmigration (Diapedesis)• Chemotaxis• PMN Activation• Phagocytosis: Recognition, Attachment, Engulfment, Killing (degradation or digestion)• Termination• 100% Resolution, Scar, or Chronic Inflammation as the three possible outcomesA.Y.2012-2013 @CBBitangcor Presentations 2
  3. 3. Vascular Changes • Changes in Vascular Flow and Caliber • Increased Vascular Permeability Dilation Endothelial gaps Direct Injury Leukocyte Injury Transocytosis (endo/exo) New Vessels Leakage of Proteinaceous A.Y.2012-2013 EXUDATE, not TRANSUDATE @CBBitangcor Presentations 3
  4. 4. Extravasation of PMNs• Margination (PMNs go toward the wall)• Rolling (Tumbling and heaping)• Adhesion• Transmigration (Diapedesis)Adhesion Molecules(glycoproteins)affecting Adhesion andTransmigration • Secretins (from endothelial cells) • Integrins (from many cells) A.Y.2012-2013 @CBBitangcor Presentations 4
  5. 5. Chemotaxis PMNs going to the site of injury AFTER TransmigrationLeukocyte Activation triggered by the offending stimuli for PMNs to: -Produce eicosanoids (arachidonic acid derivatives) Prostaglandins (and thromboxanes) Leukotrienes Lipoxins -undergo DEGRANULATION -secrete CYTOKINESPhagocytosis Recognition Engulfment Killing (Degradation/Digestion)Chemical Mediators From plasma or cells Have "triggering" stimuli Usually have specific targets Can cause a "cascade"A.Y.2012-2013 Are shortlived @CBBitangcor Presentations 5
  6. 6. Sources of Chemical Mediators• The chemical mediators of inflammation can be derived from plasma or cells.Plasma-derived mediators:i) Complement activation• increases vascular permeability (C3a,C5a)• activates chemotaxis (C5a)• opsoninization (C3b,C3bi)ii) Factor XII (Hegman factor) activation• Its activation results in recruitment of four systems: the kinin, the clotting, the• fibrinolytic and the compliment systems.A.Y.2012-2013 @CBBitangcor Presentations 6
  7. 7. Cellular mediators Cells of origin FunctionsHistamine Mast cells, basophiles Vascular leakage & plateletsSerotonine Platelets Vascular leakageLysosomal enzymes Neutrophiles Bacterial & tissue destruction, macrophagesProstaglandines All leukocytes Vasodilatation, pain, feverLeukotriens All leukocytes LB4 Chemoattractant LC4, Broncho and LCD4, & LE4 vasoconstrictionPlatlete activating factor All leukocytes Bronchoconstriction and WBC primingActivated oxygen species All leukocytes Endothelial and tissue damageNitric oxide Macrophages Leukocyte activationCytokines A.Y.2012-2013 Lymphocytes, @CBBitangcor Presentations Leukocyte activation 7 macrophages
  8. 8. 3 Outcomes of Acute Inflammation • 100% Resolution • Scar • Chronic Inflammation Morphologic Patterns of Acute Inflammation • Serous (watery) • Fibrinous (hemorrhagic, rich in Fibrin) • Suppurative (PUS) • UlcerativeA.Y.2012-2013 @CBBitangcor Presentations 8
  9. 9. Serous (watery)A.Y.2012-2013 @CBBitangcor Presentations 9
  10. 10. Fibrinous (hemorrhagic, rich in Fibrin)A.Y.2012-2013 @CBBitangcor Presentations 10
  11. 11. Suppurative (PUS)A.Y.2012-2013 @CBBitangcor Presentations 11
  12. 12. UlcerativeA.Y.2012-2013 @CBBitangcor Presentations 12