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Pathology 2-2

Duke PA pathology

exposure to toxic agents - exogenous silica (silicosis)
exposure to toxic agents - endogenous toxic plasma lipid components (atherosclerosis)
autoimmunity rheumatoid arthritis, systemic lupus, erythematosus
histological features of chronic inflammation infiltration, tissue destruction, healing
infiltration with mononuclear cells in chronic inflammation macrophages, lymphocytes, and plasma cells
tissue destruction in chronic inflammation induced by the inflammatory cells
How does healing occur in chronic inflammation? fibrosis and angiogenesis
Fibrosis replacement of damaged tissue by connective tissue
Angiogenesis new blood vessel formation
Monocytes emigrate into tissue early in inflammation and transofrm into what cell? macrophage - a larger phagocytic cell
When do macrophages predominate in chronic inflammation? 48 hours - recruitment, division, immobilization
What does the activation of macrophages result in? secretion of biologically active products
When do monocytes begin to emigrate into tissues? early in inflammation where they transform into the larger phagocytic cell known as the macrophage
What do lymphocytes produce in chronic inflammation? inflammatory mediators
What do lymphocytes participate in in chronic inflammation? cell-mediated immune reactions
What do lymphocyte plasma cells produce in chronic inflammation? antibody
How do lymphocytes and macrophages interact in chronic inflammation? a bi-directional fashioni
What are eosinophils involved in? immune reactions mediated by IgE, parasitic infections (contain protein toxic to parasites)
How do eosinophils fight against parasitic infections? eosinophil granules contain a protein that is toxic to parasites
Mast Cells release mediators (histamine) and cytokines
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
granuloma focal area of granulomatous inflammation
foreign body granulomas form when foreign material is too large to be engulfed by a single macrophage
immune granulomas insoluble or poorly soluble particles elicit a cell-mediated immune response
sarcoidosis poorly soluble antigen-antibody complexes
How is liver involved in inflammation? secretion of acute phase proteins
What glucocorticoid response occurs in inflammation? increased production (stress response)
What happens to vasopressin in inflammation? decreased secretion leading to reduced volume of body fluid to be warmed
What does fever do in inflammation? improves efficiency of leukocyte killing, impairs replication of many offending organisms
What autonomic responses occur in inflammation? redirection of blood flow to minimize heat loss, increase pulse, bp, decreased sweating
What behavioral responses occur in inflammation? shivering, chills, anorexia, somnolence, malaise
leukocytosis increased leukocyte count in the blood
neutrophilia occurs in what cases? bacterial infections
lymphocytosis occurs in what cases? infections mono, mumps, measles
eosinophilia occurs in what cases? parasites, asthma, hay fever
leukopenia reduced leukocyte count, in typhoid fever, some viruses, rickettsiae, protozoa
What are prediosposing factors for orbital mucormycosis? diabetic ketoacidosis, leukemia
Where may chemical mediators of inflammation be derived from? plasma or cells
Where do chemical mediators of inflammation bind? to specific receptors on target cells
What do chemical mediators of inflammation cause in target cells? release of mediators, which may amplify or ameliorate inflam. Response
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
How long is the response of chemical mediators of inflammation? usually short lived
What do chemical mediators of inflammation have the potential to cause? harmful effects
Review vasoactive vs. chemotactic mediators slide #62
Histamine released from mast cells (also basophils and platelets)
What does binding of antigen (allergen) to IgE on mast cells cause? release of histamine contained granules
What other mechanisms cause release of histamine? nonimmune mechanisms (cold, trauma), release by other mediators
What does histamine do? dilates arterioles and increases permeability of venules (wheal and flare reaction)
Bradykinin small peptide release from plasma precursors
What does bradykinin do? increases vascular permeability, dilates blood vessels, causes pain, rapid activation
Created by: ges13
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