Dr. Nguyen

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  1. P-selectin
    • Sialyl-Lewis X-modified proteins
    • roles--rolling
  2. E-selectin
    • Sialyl-Lewis X-modified proteins
    • roles--rolling and adhesion
  3. GlyCam-1, CD34
    • L-selectin
    • roles: Rolling (neutrophils, monocytes)
  4. ICAM-1 (immunoglobulin family)
    • CD11/CD18 integrins (LFA-1, Mac-1)
    • roles: firm adhesion, arest, transmigration
  5. VCAM-1 (immunoglobulin family)
    • VLA-4 integrin
    • roles: Adhesion
  6. CD31
    • CD31 (homotypic interaction)
    • roles: Transmigration of leukocytes through endothelium.
  7. Sources of chemical mediators
    • cells (histamine, serotonin, prostglandins, leukotrienes, platelet-activating factor, ROS, NO, cytokines [TNF, IL-1, IL-6], chemokines)
    • plasma: synthesized in liver (complement, kinins, and proteases activated during coagulation)
  8. Cell-derived mediators
    • preformed mediators in secretory granules: histamine, serotonin (from mast cells, basophils, platelets)
    • newly synthesized: prostglandins, leukotrienes, platelet-activating factor, ROS, NO, cytokines, neuropeptides (from leukocytes, mast cells, EC, macrophages, lymphocytes, nerve fibers)
  9. Plasma protein-derived mediators
    • complement activation: C3a and C5a (anaphylatoxins), C3b, C5b-9 (membrane attack complex)
    • Factor XII (Hageman factor) activation: Kinin system (bradykinin), coagulation/fibrinolysis ystem
  10. Histamine
    • From mast cells, basophils, platelets
    • vasodilation, increased vascular permeability, endothelial activation
  11. Serotonin
    • from platelets
    • vasoconstriction
  12. Prostaglandins
    • from mast cells and leukocytes
    • vasodilation, pain, and fever
  13. leukotrienes
    • from mast cells and leukocytes
    • increased vascular permeability, chemotaxis, leukocyte adhesion and activation
  14. Platelet-activating factor
    • from leukocytes and mast cells
    • vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst, bronchoconstriction
  15. ROS
    • from leukocytes
    • killing of microbes, tissue damage
  16. Nitric Oxide (NO)
    • from endothelium and macrophages.  
    • vascular smooth muscle relaxation, killing of microbes.
  17. Cytokines (TNF, IL-1, IL-6)
    • from macrophages, endothelial cells, and mast cells
    • local: endothelial activation (expression of adhesion molecules).  Systemic: fever, metabolic abnormalities, hypotension (shock). They are proteins that modulate the function of other cell types. They bind to specific receptors on target cells.
  18. chemokines
    • from leukocytes and activated macrophages
    • chemotaxis and leukocyte activation
  19. complement
    • from plasma
    • leukocyte chemotaxis and activation, direct target killing (MAC), vasodilation (mast cell stimulation)
  20. Kinins
    • from plasma
    • increased vascular permeability, smooth muscle contraction, vasodilation, pain
  21. Two pathways that arachidonic acid undergoes
    • Cyclooxygenase pathway
    • lipoxygenase pathway
  22. Proteases activated during coagulation
    • from plasma
    • endothelial activation, leukocyte recruitment
  23. Cyclooxygenases
    prostglandins and thromboxanes
  24. Lipoxygenases
    leukotrienes and lipoxins
  25. Prostaglandins
    • Vasodilation
    • potentiates inflammation
    • inhibits platelets
    • pain
    • fever
  26. Thromboxanes
    • vasoconstriction
    • platelet aggregation
  27. Leukotrienes
    • vasoconstriction
    • bronchospasm
    • increase vascular permeability
  28. Lipoxins
    • inhibit inflammation
    • decrease leukocyte chemotaxis
  29. What inhibits Phospholipase A2?
  30. What inhibits cyclooxygenase pathway?
  31. Three interrelated plasma-derived mediators that play a key role in inflammatory response
    • complement system
    • kinin system
    • clotting factor system
  32. Complement System
    • Assembly of the MAC (membrane attack complex) with lysis of offending agent.  Two mechanisms:
    • -classical pathway (cytokines and endotoxins...NO and ROS kills ingested organisms, stimulates inflammation)
    • -alternate complement pathway (not actively microbicidal, involved in tissue repair, promote angiogenesis, activate fibroblasts, collagen synthesis)
  33. C3b
  34. C3a
    • Anaphylatoxin
    • mast cell degranulation
    • increase in vascular permeability
  35. C5a
    • Anaphylatoxin
    • mast cell degranulation
    • increase vascular permeability
  36. Clotting system's two divisions
    • Intrinsic pathway-consists of plasma proenzymes which can be activated by Hageman factor, results in activation of thrombin, cleavage of fibrin and generation of fibrin clot
    • Extrinsic pathway
  37. Chronic Inflammation
    • Tissue infiltration by mononuclear cells--macrophages, lymphocytes, plasma cells
    • Tissue destruction--induced by products of inflammatory cells
    • attempts at repair--CT replacement, angiogenesis, fibrosis
  38. Phagocytes in Liver
    Kupffer cells
  39. Phagocytes in spleen and lymph nodes
    sinus histiocytes
  40. Phagocytes in CNS/retina
    microglial cells
  41. Classically activated macrophage (M1)
    • ROS, NO, Lysosomal enzymes-->leads to microbicidal actions, phagocytosis and killing of many bacteria and fungi
    • IL-1, IL-12, IL-23, and chemokines-->inflammation
  42. Alternatively activated macrophage (M2)
    • Growth factors, TGF-beta-->Tissue repair and fibrosis
    • IL-10 and TGF-beta-->Anti-inflammatory effects
  43. Outcome of chronic inflammation
    • resolution/regeneration/restitution of normal structure
    • repair/organization/healing by CT/fibrosis/scarring
    • It can continue indefinitely...i.e. rheumatoid arthritis
  44. Diagnostic tests for inflammation
    • CRP: C reactive protein
    • SAA: Serum amyloid A
    • ESR: Erythrocyte Sedimentation rate
    • Leukocyte count:neutrophilia, eosinophilia, lymphocytosis, lymphopenia
  45. Cachexia
    loss of weight, muscle atrophy, fatigue, weakness, and significantloss of appetite in someone who is not actively trying to lose weight. The formal definition of cachexia is the loss of body mass that cannot be reversed nutritionally: Even if the affected patient eats more calories, lean body mass will be lost, indicating a primary pathology is in place.
    cyclosporin A emulsion
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Dr. Nguyen
2013-09-03 00:55:00
Dr Nguyen

Dr. Nguyen cells
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