Duke PA pathology
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| exposure to toxic agents - exogenous | silica (silicosis)
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| exposure to toxic agents - endogenous | toxic plasma lipid components (atherosclerosis)
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| autoimmunity | rheumatoid arthritis, systemic lupus, erythematosus
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| histological features of chronic inflammation | infiltration, tissue destruction, healing
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| infiltration with mononuclear cells in chronic inflammation | macrophages, lymphocytes, and plasma cells
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| tissue destruction in chronic inflammation | induced by the inflammatory cells
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| How does healing occur in chronic inflammation? | fibrosis and angiogenesis
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| Fibrosis | replacement of damaged tissue by connective tissue
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| Angiogenesis | new blood vessel formation
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| Monocytes emigrate into tissue early in inflammation and transofrm into what cell? | macrophage - a larger phagocytic cell
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| When do macrophages predominate in chronic inflammation? | 48 hours - recruitment, division, immobilization
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| What does the activation of macrophages result in? | secretion of biologically active products
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| When do monocytes begin to emigrate into tissues? | early in inflammation where they transform into the larger phagocytic cell known as the macrophage
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| What do lymphocytes produce in chronic inflammation? | inflammatory mediators
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| What do lymphocytes participate in in chronic inflammation? | cell-mediated immune reactions
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| What do lymphocyte plasma cells produce in chronic inflammation? | antibody
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| How do lymphocytes and macrophages interact in chronic inflammation? | a bi-directional fashioni
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| What are eosinophils involved in? | immune reactions mediated by IgE, parasitic infections (contain protein toxic to parasites)
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| How do eosinophils fight against parasitic infections? | eosinophil granules contain a protein that is toxic to parasites
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| Mast Cells | release mediators (histamine) and cytokines
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| granulomatous inflammation pattern of inflammation | predominant cell type is an activated macrophage with a modified epithelial-like appearance. Giant cells may or may not be present
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| granuloma | focal area of granulomatous inflammation
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| foreign body granulomas | form when foreign material is too large to be engulfed by a single macrophage
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| immune granulomas | insoluble or poorly soluble particles elicit a cell-mediated immune response
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| sarcoidosis | poorly soluble antigen-antibody complexes
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| How is liver involved in inflammation? | secretion of acute phase proteins
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| What glucocorticoid response occurs in inflammation? | increased production (stress response)
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| What happens to vasopressin in inflammation? | decreased secretion leading to reduced volume of body fluid to be warmed
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| What does fever do in inflammation? | improves efficiency of leukocyte killing, impairs replication of many offending organisms
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| What autonomic responses occur in inflammation? | redirection of blood flow to minimize heat loss, increase pulse, bp, decreased sweating
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| What behavioral responses occur in inflammation? | shivering, chills, anorexia, somnolence, malaise
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| leukocytosis | increased leukocyte count in the blood
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| neutrophilia occurs in what cases? | bacterial infections
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| lymphocytosis occurs in what cases? | infections mono, mumps, measles
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| eosinophilia occurs in what cases? | parasites, asthma, hay fever
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| leukopenia | reduced leukocyte count, in typhoid fever, some viruses, rickettsiae, protozoa
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| What are prediosposing factors for orbital mucormycosis? | diabetic ketoacidosis, leukemia
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| Where may chemical mediators of inflammation be derived from? | plasma or cells
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| Where do chemical mediators of inflammation bind? | to specific receptors on target cells
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| What do chemical mediators of inflammation cause in target cells? | release of mediators, which may amplify or ameliorate inflam. Response
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| How many cells do chemical mediators of inflammation work on? | one or a few, have widespread targets and may have differing effects depending on cell and tissue types
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| How long is the response of chemical mediators of inflammation? | usually short lived
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| What do chemical mediators of inflammation have the potential to cause? | harmful effects
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| Review vasoactive vs. chemotactic mediators | slide #62
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| Histamine | released from mast cells (also basophils and platelets)
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| What does binding of antigen (allergen) to IgE on mast cells cause? | release of histamine contained granules
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| What other mechanisms cause release of histamine? | nonimmune mechanisms (cold, trauma), release by other mediators
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| What does histamine do? | dilates arterioles and increases permeability of venules (wheal and flare reaction)
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| Bradykinin | small peptide release from plasma precursors
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| What does bradykinin do? | increases vascular permeability, dilates blood vessels, causes pain, rapid activation
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