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    Add as FriendAcute Inflammation

    by: arun

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    1 : Acute Inflammation Reaction of a tissue & its microcirculation to a pathogenic insult. A complex reaction in vascularized connective tissue. Characterized by movement of fluid and leucocytes from blood into extra vascular tissues by generation of chemical mediators
    2 : Elements Vascular Cellular Chemical mediators
    3 : Aetiologic Agents Physical Chemical Biologic/Infectious Immunologic
    4 : Signs of inflammation Inflammatio-Latin word Phlogosis-Greek Celsus Rubor-redness Calor-heat Tumour –swelling Dolor-pain
    5 : Types of inflammation Acute Exudation of fluid + plasma proteins Polymorphs Mins - hrs-days Chronic Lymphocytes + Macrophages Proliferation of BV + CT + necrosis Longer
    6 : Aims Eliminate pathologic insult Remove injured tissue components Protective response Hand in hand with repair Steps: Initiation-stimulus Amplification: activation of cellular inflammation Termination: Elimination
    7 : The components of acute and chronic inflammatory responses: circulating cells and proteins, cells of blood vessels, and cells and proteins of the extracellular matrix. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    8 : Vascular events Haemodynamic Changes Vasoconstriction followed by vasodilatation Alteration in vascular caliber & flow Increase hydrostatic pressure Slowing of circulation- Viscosity & stasis Leucocytic margination
    9 : Vascular events Increased vascular permeability Escape of protein rich fluid into interstitium Oedema-excess of fluid in interstitium or serous cavities Imbalance of hydrostatic pressure Transudate-low protein, sp gr-< 1.012 Permeability not altered Exudate-high protein, sp gr > 1.020 Permeability altered Pus –rich in polymorphs
    10 : The major local manifestations of acute inflammation, compared to normal. (1) Vascular dilation and increased blood flow (causing erythema and warmth), (2) extravasation and deposition of plasma fluid and proteins (edema), and (3) leukocyte emigration and accumulation in the site of injury. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    11 : Blood pressure and plasma colloid osmotic forces in normal and inflamed microcirculation. A, Normal hydrostatic pressure (red arrows) is about 32 mm Hg at the arterial end of a capillary bed and 12 mm Hg at the venous end; the mean colloid osmotic pressure of tissues is approximately 25 mm Hg (green arrows), which is equal to the mean capillary pressure. Although fluid tends to leave the precapillary arteriole, it is returned in equal amounts via the postcapillary venule, so that the net flow (black arrows) in or out is zero. B, Acute inflammation. Arteriole pressure is increased to 50 mm Hg, the mean capillary pressure is increased because of arteriolar dilation, and the venous pressure increases to approximately 30 mm Hg. At the same time, osmotic pressure is reduced (averaging 20 mm Hg) because of protein leakage across the venule. The net result is an excess of extravasated fluid. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    12 : Increased vascular permeability Endothelial cell contraction- Immediate transient response- only venules-chem mediators Cytoskeletal & junctional re-organization Direct endothelial injury-Immediate sustained response-cell necrosis & detachment-All levels Leucocyte mediated injury Leakage from regenerating capillaries-Angiogenesis
    13 : Diagrammatic representation of five mechanisms of increased vascular permeability in inflammation Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    14 : Cellular events-Aims Delivery of leucocytes to the site of injury Ingest & kill bacteria & microbes Degrade necrotic tissues & foreign antigens May prolong inflammation Rarely induce tissue damage by releasing enzymes & chem mediators, toxic radicals
    15 : Cellular events-Steps Extravasation-Journey of the leucocytes from lumen to interstitial tissue Margination, Rolling Adhesion Transmigration/ Diapedesis Chemotaxis - Migration in interstitial tissue towards a chemical stimulus Leucocyte activation Phagocytosis Release of Leucocyte products
    16 : Extravasation Margination-Stasis of blood-Peripheral margination, roll along, adhere transiently- Pavementing Insert pseudopods b/w cell junctions Traverse the basement membrane Escape into extravascular space
    17 : The multistep process of leukocyte migration through blood vessels, shown here for neutrophils. The leukocytes first roll, then become activated and adhere to endothelium, then transmigrate across the endothelium, pierce the basement membrane, and migrate toward chemoattractants emanating from the source of injury. Different molecules play predominant roles in different steps of this process-selectins in rolling; chemokines in activating the neutrophils to increase avidity of integrins (in green); integrins in firm adhesion; and CD31 (PECAM-1) in transmigration. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    18 : Transmigration-Diapedesis Along IC junction-PECAM-1 Leucocyte diapedesis-vennules Collagenases degrade basement membrane 6-24 hrs-Polys 24-48hrs-mono
    19 : Chemotaxis Definition: Locomotion oriented along a chemical gradient by leucocytes to the site of injury Varying rates Chemo-attractants Exogenous-Bacterial products Endogenous-C5a, LTB4, IL-8
    20 : Schematic and histologic sequence of events following acute injury. The photomicrographs are representative of the early (neutrophilic) (left) and later (mononuclear) cellular infiltrates (right) of infarcted myocardium. The kinetics of edema and cellular infiltration are approximations. For sake of simplicity, edema is shown as an acute transient response, although secondary waves of delayed edema and neutrophil infiltration can also occur. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    21 : Leucocyte activation Production of Arachidonic acid metabolites by DAG & increased Ca De-granulation & secretion of lyso enzymes & activation of oxidative burst Modulation of leucocyte adhesion molecules Priming-Increased rate & extent of leucocyte activation
    22 : Phagocytosis Recognition & attachment Particle is coated by opsonins-bind to WBC Engulfment-pseudopods flow around & enclose it Limiting membrane of the phagocytic vacuole & that of lysosomal granule fuse Discharge of granule contents into phagolysosome Neutrophils & monocytes are degranulated
    23 : Phagocytosis Killing -Oxygen dependant-HMP shunt-halogenation or lipid peroxidation Microbes, fungi, virus, protozoa & helminths Chronic granulomatous disease Oxygen independent-BPI protein- Platelet activation & degradation Lysozyme Lactoferrin Major basic protein Degradation- Acid hydrolases-azurophil granules-drop in pH
    24 :
    25 : Release of leukocyte products Membrane protuberance Release of products into phagolysosome & EC space Lysosyme enzymes- neutrophils Oxygen derived active metabolites AA metabolites- PG & leukotreines Amplify effect of initial stimulus
    26 : Chemical mediators of inflammation Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    27 : Major effects of interleukin-1 (IL-1) and tumor necrosis factor (TNF) in inflammation. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    28 : Functions of nitric oxide (NO) in blood vessels and macrophages, produced by two NO synthase enzymes. NO causes vasodilation, and NO free radicals are toxic to microbial and mammalian cells. NOS, nitric oxide synthase. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    29 : Regulation of Inflammation Acute Phase Reactants Anti-trypsin, antochymotrypsin, PAI Fibrinogen, plasminogen Tpt proteins Corticosteroids Free cytokine receptors Suppressor T cells Anti inflammatory chemical mediators
    30 : Factors determining variation of response Factors involving organisms Type of infection Virulence Dose Portal of entry Factors involving hosts General health Immune state / leucopenia Site or type of tissue involved Local host factors
    31 : Type of exudation Serous Fibrinous Purulent or suppurative Haemorrhagic Catarrhal
    32 : Serous inflammation. Low-power view of a cross-section of a skin blister showing the epidermis separated from the dermis by a focal collection of serous effusion. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    33 : Fibrinous pericarditis. A, Deposits of fibrin on the pericardium. B, A pink meshwork of fibrin exudate (F) overlies the pericardial surface (P). Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    34 : Suppurative inflammation. A, A subcutaneous bacterial abscess with collections of pus. B, The abscess contains neutrophils, edema fluid, and cellular debris. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier
    35 : Outcomes of acute inflammation: resolution, healing by fibrosis, or chronic inflammation Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 21 February 2006 05:24 AM) © 2005 Elsevier

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