April 28th, 2009 
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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 fibroblastsdeposition 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.
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
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