inflammation
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| what are the goals of inflammation? | respond, remove, restore
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| what are stimulators/ initiators of inflammation | infections, trauma, physical or chemical agents, tissue necrosis, foreign bodies, hypersensitivity immune reactions
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| what are the five cardinal signs of inflammation? | redness, pain, heat, loss of function,
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| general responses to inflammation: processes | vascular, activation of chemical mediators (plasma and cell derived) migration and activation of cells termination/resolution
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| in an acute inflammatory response, describe the timing, specificity, predominant cell type, vascular response, and tissue response | immediate response, mostly innate immunity, neutrophils, prominent edema, and structure and function may be restored
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| in a chronic inflammatory response, describe the timing, specificity, predominant cell type, vascular response, and tissue response, | slower activation, cell mediated immunity, lymphocytes/macrophages/plasma cells, less prominent edema, typically a loss of function
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| what are the components of the inflammation process | vasculature (fluid, chemicals, cells), connective tissue (matrix, cells) parenchyma
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| describe what vascular changes take place during inflammation | altered hemodynamics (vasoconstriction, vasodilation), altered vascular structure (contraction of endothelial cells, increased vascular permeability, increased interstitial fluid and cells that exit vessels)
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| what are the two types of edema | transudate and exudate
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| describe the transudate fluid in terms of hydrostatic and colloid osmotic pressure | its more watery, less cellular components present. hydrostatic pressure is increased and colloid osmotic pressure is decreased significantly..it is noninflammatory
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| describe exudate fluid | the fluid is leaving with a lot of protein and cells because they leak out of the vasculature...it is inflammatory. there is increased vascular permeability
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| describe the source of chemical mediators of inflammation | plasma derived, cell derived, extracellular matrix
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| list preformed chemical mediators of inflammation in secretory granules of cells(cell derived) | histamine, seratonin. the source is from mast cells, basophils, platelets
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| list several newly synthesized chemical mediators of inflammation (cell derived) | prostaglandins, leukotrienes, platelet activating factor, reactive oxygen species, nitric oxide, cytokines, neuropeptides
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| list chemical mediators that are plasma derived (come from liver) | complement activation proteins: C3a, C5a, C3b, C5b-9, bradykinin, coagulation, fibronolysis system
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| describe some functions of the complement system | phagosytosis/destruction (opsonization: coating bacteria for phagocytosis), vascular inflammatory effects (anaphylotoxins: increase vascular permeability/vasodilation), cellular inflammatory effects (wbc adhesion, activaiton, chemotaxis)
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| what are the vasoactive amine chemical mediators | histamine and seratonin (preformed and released from storage vacuoles within mast cells)
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| these chemical mediators are generated from cell membrane phospholipids and consist of prostaglandins, leukotrienes, and lipoxins | arachidonic acid metabolites
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| these chemical mediators are generated from membrane phospholipids and have broad range effects on inflammation | platelet activating factor (PAF)
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| these chemical mediators are proteins produced by many cell types and consist of TNF and IL | cytokines
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| these chemical mediators are small proteins that function in chemotaxis | chemokines
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| this chemical mediator is a soluble gas, is a potent vasodilator, and a toxic free radical | NO-nitrous oxide
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| these chemical mediators are acid and neutral proteases that degrade cellular and ECM proteins and result in cell death and slow tissue destruction, also allow for migration of inflammatory cells into tissues: one example is alpha 1 antitrypsin, | lysosomal molecules.
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| in this disease, there is an imbalance of lysosomal molecules. the imbalance between protease and antiprotease results in destruction of the alveolar wall | emphysema
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| this chemical mediator is involved in NADPH oxidative system within RBC's | ROS
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| this chemical mediator is involved with pain (substance P) | neuropeptides
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| what are the chemical mediators which are potent vasodilators? | NO, prostaglandins, histamine
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| what are the chemical mediators involved with fever? | IL1, TNF, prostaglandins
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| what are the chemical mediators involved with pain? | prostaglandins, bradykinin
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| what are the chemical mediators involved with tissue damage? | lysosomal enzymes of leukocytes, ROS, NO
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| what are the chemical mediators involved with chemotaxis, and leukocyte recruitment and activation | TNF, IL1, chemochines, C3a, C5a, leukotriene, bacterial products
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| what are the chemical mediators involved with increased vascular permeability? | histamine and seratonin, C3a and C5a, bradykinin, leukotrienes, PAF, substance P
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| what cell is involved with acute inflammation? | neutrophils
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| what cells are involved with chronic inflammation? | lymphocytes, macrophages, plasma cells
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| what are the possible outcomes of inflammation | resolution, healing by fibrosis, or ongoing chronic inflammation
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| what is one example of an acute inflammation? | gastric ulcer
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| what are three possible causes of chronic inflammation? | persistent infection or injurious stimulus, prolonged exposure to injurious stimulus, autoimmunity
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| in chronic inflammation, what disease is an example of persistent infection or injurious stimulus | tuberculosis
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| in chronic inflammation, what is an example of prolonged exposure to an injurious stimulus | silicosis, athersclerosis
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| in a chronic inflammation, what are examples of autoimmunity | rheumatoid arthritis, hashimotos, lupus
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| what are the processes of chronic inflammation | tissue infiltration by mononuclear cells (macrophages, lymphocytes, plasma cells), tissue destruction, tissue repair (angiogenesis, fibrosis)
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| longstanding resident of macrophages in tissues are called this | histiocytes
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| this is a distinctive pattern of chronic inflammation that forms aggregates of activated macrophages that assume and epitheliod appearance. some macrophages coalesce to form a syncytium: multinucleated giant cell that surround mononuclear inflammatorycell | granulomatous inflammation
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| this is a granulomatous inflammation with necrosis | caseating granuloma
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| this is a granulomatous inflammaiton with no necrosis | noncaseating granuloma
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| this disease is an example of caseating granuloma | tuberculosis
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| this disease is an example of noncaseating granuloma | sarcoidosis
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| what are some systemic effects of inflammation | fever, elevated plasma, elevated WBC's
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| when blood cells stack because of increased plasma cell concentration, it's called this | rouleaux
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| what does increased sed rate mean | there is increased cells in the plasma
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