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Pathology 2-2
Duke PA pathology
| Question | Answer |
|---|---|
| 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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