10-14 - Acute Inflammation 2 (Levitt).txt

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10-14 - Acute Inflammation 2 (Levitt).txt
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2011-10-27 09:32:08
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  1. What are the major chemical mediators of inflammation?
    • "
      • vasoactive amines
      • complement system
      • kinin system
      • coagulation pathway
      • fibrinolytic pathway
      • arachodonic acid metabolites
      • PAF
      • cytokines
      • nitric oxide
      "
  2. What are the major categories of mediators?
    plasma-derived and cell-derived
  3. What are the major categories of cell-derived mediators?
    • "
      • : underline;"">Pre-formed - stored in granules and released upon stimulation (Histamine, Serotonin)
        • cause vasodilation
        • primary source is mast cells, platelets, basophils
      • : underline;"">Synthesized - under appropriate stimulation - Arachidonic acid derivatives (cyclooxygenase, lipoxygenase)
        • PAF
        • oxygen radicals
        • neutrophil products
        • macrophage products
      "
  4. What role does Hageman factor play in inflammation?
    • "
      • Hageman factor = Factor 12
      • activated by kinin, complement, clotting, and fibrinolytic systems
      • interact continuously in course of inflammation to localize area of destruction
      "
  5. Describe the kinin system.
    • "
      • kallikreins (proteases) generate kininogens (vasoactive peptides)
      • HMWK (high-molecular weight kininogen) + 12 --> 12a + Prekallikrein --> Kallikrein (activates F12 in loop feedback) + HMWK --> Bradykinin
      • most important product: bradykinin
        • causes arteriolar dilation
        • pain & contraction of smooth muscle
      • kallikrein is a potent activator of Hageman factor (F12)
        • converts C5--> C5a
        • chemotactic
      "
  6. Explain the kinin system in relation to pain.
    • "
      • protective mechanism with survival value (link to consciousness)
      • sensory nerves stimulated by
        • low pH
        • high extracellular [K+]
        • 5-HT
        • bradykinin
        • Net result: pain!
      • painless infectious are more dangerous (go undetected)
        • silent chlamydial salpingitis is more important cause of infertility and ectopic pregnancy (bc of tubul damage)
      "
  7. Describe the major components of the complement cascade system.
    • "
      • Classical & Alt. Pathways
        • C3 is critical control point (interacts with both pathways)
        • C3a & C5a = anaphylotoxins
          • release histamine from mast cells
          • C5a = chemotaxis
        • C3b & C5a = stimulate neutrophil degranulation
        • C3b, C2a, C4b = opsonins
        • MAC complex
          • C5-C9
          • cell lysis
        • C5-C7 = chemotactic for neutrophils
    •  

      "
  8. What activates the complement system?
    • "
      • release of enzymes from dying cells (tissue necrosis)
      • Ag-Ab complexes --> classical pathway
      • endotoxins of Gram(-) --> alternative pathway
      • products of kinin, coagulation, and fibrinolytic pathways
      "
  9. Describe the coagulation pathway and its relationships to fibrinolytic systems. What do these pathways have in common?
    • "
      • Intrinsic pathway
        • Hageman Factor (F12) is activated by surface contact
      • Extrinsic pathway
        • Tissue Factor released at sites of injury activates F7
      • Results in clotting & fibrinolysis balanced by 12a --> kallikrein --> plasmin
    • Commonalities

      • inducted by 12a (Hageman factor)
      • complement & counterbalance each other
      • important molecules: fibrinogen, fibrin, thrombin, plasminogen, plasmin
      "
  10. How is coagulation related to inflammation?
    • "
      • Thrombin splits fibrinogen to fibrinopeptides
        • induces vascular permeability
        • chemotactic
      • Thrombin increases leukocyte adhesion & fibroblast proliferation
      • Factor 10a increases vascular permeability & leukocyte exudation
      • Plasmin cleaves C3 & fibrin resulting in vascular permeability
      • Plasmin actives Hageman factor
      "
  11. What are ecosanoids? How are they formed? What can they form?
    • "

      Eicosanoids = Arachidonic acid metabolites

      • Synthesized from cell membrane phospholipids through phospholipase action (inhibited by corticosteroids)
      • Form leukotrienes via lipoxygena pathway (LOX)
      • Form prostaglandins & thromboxana (COX-1 & COX-2)
        • COX-1 inhibited by aspirin & indomethacin
      "
  12. What are the effects of arachidonic metabolites?
    • "
      • vasodilation
      • increased vascular permeability
      • pain
      • pyrogenesis (fever)
      • neutrophil activation
      "
  13. Describe the COX pathway.
    • "

      Mediated by COX1 & COX 2 - leads to formation of prostaglandins. Results in a variety of mediators:

      • Prostaglandins - PGD2 causes vasodilation, PGE2 causes pain & fever
      • Prostacyclin (PG12) - formed in vascular endothelium to cause vasodilation & inhibit platelet aggregation
      • Thromboxane (TXA2) - formed in platelets to cause vasoconstriction & promote platelet aggregation
    • Blocked by:

      • NSAIDS
      • Steroids - blocks at cell membrane level; regulation of lipocortin-1 inhibits release of arachidonic acids from membrane phospholipid
    • COX-3 recently discovered; plenty in brain; ? site of action for tylenol ?

    •  

    •  

    •  

      "
  14. Describe the LOX pathway.
    • "
      • leads to formation of leukotrienes, which cause
        • chemotaxis (eosinophils, PMNs)
        • vasoconstriction
        • bronchospasm
        • increased vascular permeability
      • act late in inflammation
      • Inhibitors of leukotriens are used in asthmatics
      "
  15. Describe lipoxins.
    • "
      • Formed by platelets with LTA4 from leukocytes
      • Inhibits neutrophil chemotaxis & adhesion
      • Stimulates monocyte adhesion
      • Stimulates vasodilation
      • Inhibits action of LTC4 (vasoconstriction)
      • May be negative regulator of leukotrienes
      • Collaborative productoin: PMNs / platelets
      • Inhibit PMN activities
      "
  16. What are the major vasoactive amines released from mast cells and platelets? What are their functions?
    • "
      • Histamine - abundant in mast cell granules which are abundant arond blood vessels
      • Serotonin - action similar to histamine; found in platelets & released after platelet aggregation or PAF influence
      • PAF - numerous effects which are 100-100,000x more effective than histamine including vasodilation & increased vascular permeability
      "
  17. Describe the general characteristics of cytokines.
    • "
      • Produced by lymphocytes or macrophages after stimulation by toxins, injury, or inflammatory mediators
        • Biggest influences: LPS (Gram-) & IFNg (viruses, etc.)
      • Include: lymphokines, monokines, chemokines, colony stimulating factors, interleukins, & growth factors
      • Categorized by actions
        • Autocrine
        • Paracrine - activation of neighboring cells including neutrophiles & fibroblasts
        • Endocrine - acts systemically (acute phase rxns) including: fever, fatigue, lower appetite, increased WBC
      "
  18. What functions do the cytokines provide?
    • "
      • Regulate lymphocytes - IL2, 4, 10 & TGF-b
      • Natural immunity - TNF-a, IL1b, IL6, IFNg, & IFNb
      • Activate macrophages - IFNg, TNFa&b, IL5, 10, 12
      • Chemokines - IL8 (leukocytes), lymphotaxin, eotaxin
      • Stimulate hematopoiesis - IL3, 7, c-kit, CSF, & stem cell factor
      "
  19. Which cytokines are considered most important?
    • "

      IL-1: endothelial cell activation

    • IL-2: T-cell growth factor

    • TNF-a: a.k.a. cachectin

    •  

    • IL-1 & TNFa are the most important

      • endothelial cell activation
      • acute phase response
      • fibroblast stimulation
      • stimulate leukocytes to secrete cytokines
      "
  20. Describe the general characteristics of nitric oxide.
    • "
      • Formed by NO synthase (NOS)
        • constitutively expressed
        • expression increased with Ca influx
        • NOS induced in macrophages by TNF-a or IFN-g
      • Potent vasodilator
      • Involved in pathogenesis of septic shock
      • Actions: short-lived; depend on [NO]
        • small amounts in endothelial cells cause smooth muscle relaxation & vasodilation; anti-thrombogenic to platelets
        • small amouns in neurons --> neurotransmitter
        • large amounts in macrophages --> cytotoxic free radical; kill bacteria / tumors
        • inappropriate release --> shock
      "
  21. What are the possible outcomes of acute inflammation?
    • "


      • Resolution - when process is limited to tissues capable of regeneration



      • Scarring - tissue fixed by fibrosis; extensive process or tissues unable to regenerate



      • Abcess formation - invading organism cannot be eradicated or drained; accumulation of pus



      • Chronic inflammation - irritant persists; evolution to mononuclear infiltrate



      • "

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