Guest guest Posted April 20, 2009 Report Share Posted April 20, 2009 Pathobiology of Inflammation and Repair Part 3: Chronic Inflammation and Repair go over chart on p. 74 Chronic Inflammation Basic Features prolonged, actively inflammed, tissue destruction, and attempts at healing Setting for chronic inflammation persistent infections- granulomatous formation prolonged exposure to toxic agents autoimmune diseases Characterized by: infiltration with mononuclear cells- macs, lymphs, and plasma cells tissue destruction angiogenesis and fibrogenesis Mononuclear infiltration major player is tissue macrophage Mononuclear phagocyte system (RE system) monocytes begin to migrate early in acute inflammation, and are predominant cell type in 48 hours. macs are activated by cytokines Products of these macrophages are involved in tissue injury and fibrosis Three mechanisms of macrophage accumulation continued recruitment of monocytes from the circulation by continued expression of adhesion molecules and chemotactic factors C5a, IL-8, etc. local proliferation of macrophages immobilization of macs at target site other cells involved include lymphs, plasma cells, eosinophils, and mast cells Fibrosis (repair by connective tissue) attempts at repair lead to scarring and fibrosis Four components of process angiogenesis migration and proliferation of fibroblasts deposition of extracellular matrix remodeling Granulation tissue is angiogenesis and fibrosis Granulomatous inflammation distinctive pattern of chronic inflammatory response in which the predominant cell type is an activated macrophage with a modified (epitheloid) appearance Granulomas are small round collections of macrophages surrounded by a rim of lymphocytes Two types: Foreign body granulomas and immune granulomas Granulomatous inflammation occurs with: TB, sarcoidosis, leprosy, cat scratch fever, schistosomiasis, syphilis, deep fungal diseases, inorganic metals and dusts Can be caseating or non-caseating Inability to digest inciting agent + CMI Repair Two distinct processes may be involved: Regeneration- replacement of dead tissue by parenchymal cells of the same type Replacement- connective tissue stroma (scar formation) Chronology of the Repair process Removal of the inflammatory exudate 36 hrs to 3-4 weeks begins with migration of macrophages Regeneration by parenchyma or fibrous proliferation type of replacement depends on the type of tissue injured begins within a few hours Factors influencing the repair process Types of cells Labile cells- continue to multiply throughout life Stabile cells- contain a latent capacity to regenerate, but under normal conditions do not undergo mitotic activity Permanent Cells- no regenerative capacity (ex. cardiac myocytes and neurons) Repair by connective tissue Sequence of scar formation fibroblasts and endothelial proliferation begins as early as 24 hours and migration along fibrin strands begins within a few days Collagen is detectable in 4 days increase in collagen leads to increased wound strength progressive devascularization ( weeks to months ) Integration of Parenchymal and Connective Tissue Healing Wound Healing Healing by first intention (primary union) ideal healing occurs in a clean wound when the edges have been approximated Healing by second intention (secondary union) extensive tissue loss dead tissue must be removed before healing can occur contraction of collagen after healing has occurred causes depression at the scar site Stimulation of Cell Proliferation No one knows how cell proliferation is initiated. see areas of research on p 71-2 Wound Strength Collagen is the ultimate source of strength of the healed wound Factors which modify the Inflammatory-Reparative Response age is not a factor A severe protein depletion impairs wound healing Vit C is important in formation of collagen hydrocortisones inhibit inflammatory reaction the better the blood supply, the more resistant to infection immobilization is important in healing of bone and excessive hemorrage Quote Link to comment Share on other sites More sharing options...
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