Inflammation and Wound Healing

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Author:
Aleksbaron
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261016
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Inflammation and Wound Healing
Updated:
2014-02-09 13:41:06
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OBMP 8004
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Exam 1
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  1. Cardinal signs of inflammation by Celsus?
    • Rubor: red
    • Tumor: swelling
    • Calor: Heat
    • Dolor: Pain
    • Functio Laesa: loss of function
  2. Acute inflammation is characterized by what cells?
    Plasma proteins, leukocytes (neutrophils)
  3. Chronic inflammation is characterized by which cells?
    Lymphocytes, macrophages, fibrosis, tissue necrosis
  4. Three major components of acute inflammation?
    • 1. Vasodilation
    • 2. Endothelial cell contraction
    • 3. Emigration of leukocytes to site of injury
  5. When do neutrophils assume a peripheral orientation (margination) along endothelium?
    In acute inflammation during the stasis of blood flow due to inc concentration of RBCs
  6. What is the hallmark of acute inflammation?
    Exudate: protein rich fluid in to intersititium
  7. The most common mechanism of vascular leakage?
    formation of gaps in endothelium in VENULES!!

    reversible and short lived (15-30mins)

    Histamine, Bradykinin, Leukotrienes, subst P

    endothelial cell contraction
  8. Endothelial cell retraction is caused by? (Different than contraction)
    Cellular reorganization (delayed response and lasts longer that cell contraction)

    induced by IL-1, TNF, INF-gamma, hypoxia, sublethal injury to cells

    Mostly venules, but also capillaries.
  9. Direct endothelial injury?
    Another form of vascular leakage, immediate and sustained. Affects all levels of vasculature.
  10. Increased transcytosis?
    Another mechanism of endothelial leakage (mostly venules)

    Vesiculovascular organelles are used near the intercellular junctions
  11. Leukocyte-Mediated Endothelial Injury?
    Another mech for endotehlial cell leakage (mostly venules)

    Neutrophils attempt to engulf endothelial cells but cannot and release ROIs that irreversibly injure cell

    Caused by immune complex adherence to the endothelial cells (Igm and Igg)
  12. Sequence of events of leukocyte extravasation?
    • 1. Margination
    • 2. Rolling
    • 3. Adhesion
    • 4. Diapedesis

    Chemotactic stimulus
  13. What mediators play a role in endothelial activation?
    Selectins E and P (inc expression)
  14. What mediators play a role in rolling of leukocytes?
    Initial rapid loose adhesion, selectins binding to Sialyl Lewis X ligand (carbohydrate)
  15. What mediators play a role in leukocyte adhesion?
    Chemokines activate LFA-1 (conformational change) which now binds to ICAM on endothelial cells
  16. What mediators play a role in leukocyte transmigration?
    Endothelial cells have ICAM and PECAM (both cells) binding to LFA-1

    Collagenases are used to break down BM
  17. Neutrophils are involved in acute inflammaiton for the first 6-24 hours and then monotcytes replace from  24-48 hours
  18. Examples of exogenous chemoattractants?
    bacterial peptides with N-formyl methionine, lipids
  19. Examples of endogenous chemoattractants?
    Complement components (C5a), leukotrienes, cytokines
  20. Phagocytosis and the three distinct steps?
    • 1. Recognition of particle to be ingested
    • 2. Engulfmenet into a vacuole
    • 3. Killing followed by degradation
  21. What are the macrophages recognizing for attachment in phagocytosis?
    Mannose carbs, LPS, have receptors for opsonins like C3b, C3Bi, C1q, Fc portion of IgG and IgM when bound
  22. Describe the killing and degradation process of phagocytosis?
    Activation of NADPH oxidase converts oxygen to superoxide anion converted to hydrogen peroxide (MPO) in prescense of Cl converts to HOCL.

    Lactoferrin is an oxygen independent pathway for killing.
  23. How are the inflammation and kinin system connected?
    Kallikrein makes Bradykinin that leads to vasodilation, vascular permeability, smooth muscle contraction

    Kallijrein has chemotactic activity and converts c5 to c5a an opsonin
  24. Inflammation and the clotting system relation?
    Hageman factor begins the clotting cascade.

    Thrombin causes leukocyte adhesion, fibrblast prolif

    Factor XIIa inc vascular permeability and leukocyte extravasation
  25. Il-1 and TNF cause acute phase reactions in inflammation like?
    Fever, inc sleep, dec appetite, inc acute-phase proteins, shock, neutrophilia
  26. How is NO made?
    Regularly by eNOS requiring inc of calcium in cell

    Can be induced (iNOS) in activated macrophages by TNF-alpha and INF-gamma (no Ca required)
  27. Functions of NO?
    • 1. vasodilator (potent)
    • 2. dec platelet aggregation
    • 3. block neutrophil rolling and adhesion on venules
    • 4. reduces neutrophil recruitment
    • 5. antimicrobial producing different ROIs
  28. When does connective tissue replacement commonly occur in acute inflammation?
    In pyogenic infections
  29. Some predisposing factors for chronic inflammation?
    • 1. persistent infecitons
    • 2. prolonged exposure to exo or endogenous toxic agents
    • 3. autoimmunity
  30. Repair in chronic inflammation is caused by?
    Angiogenesis and fibrosis
  31. What is the half life of a monocyte?
    1 day compared to

    activated macrophages that life months to years
  32. What mediators activate macrophages?
    IFN-gamma secreted by T cells and NK cells

    Bacterial LPS
  33. Macrophages can proliferate locally....
    in atheromatous plaques
  34. What mediators promote lymphocyte recruitment?
    IL-1, IFN, and chemokines
  35. Granulamotous inflammation consists of?
    macrophages transformed into epithelium like cells, surrounded by a collar of lymphocytes and plasma cells
  36. Two types of granulomas:
    • 1. Foreign body
    • 2. Immune: TB
  37. Epithelioid cells fuse to form?
    Giant cells (20 or more small nuclei)

    If peripherally arragned: Langhans-type giant cell

    If haphazardly placed: Foreign body-type giant cells
  38. True or false, foreign body granuloma have specific immune response?
    False
  39. What do pyrogens do?
    Increase temp (acute phase) LPS stimulates Il-1 and TNF release upregulating COX which increases prostaglandins.

    PGE2 stim cAMP in hypothalamus reseting temp set point

    leads to heat shock proteins which enhance lymphocyte response to antigens
  40. What are some acute phase proteins?
    C reactive protein, fibrinogen, serum amyloid protein A

    CRP and fibrinogen induced by IL-6

    SAA induced by IL-1 and TNF
  41. What is the role of acute phase proteins?
    Act as opsonins

    Bind to chromatin to clear necrotic nuclei

    Inc fibrinogen causes rouleaux in erythrocytes (stacking due to discoid shape)
  42. Long term effects of acute phase proteins?
    SAA causes amyloidosis

    CRP sustained inc causes MI
  43. What causes DIC?
    High levels of LPS and subsequent levels of IL-1 and TNF.

    TNF and LPS combo induce TF expression which intiates coagulation

    this also inhibits tissue factor pathway inhibitor
  44. How do we have cardiac failure in inflammation?
    Too much inflammatory mediators cause inc NO production leads to loss of perfusion pressure resulting in heodynamic shock
  45. How do inflammatory cytokines affect glucose levels in blood?
    impair function of liver to move glycogen ro glucose, impaired gluconeogenesis
  46. What causes SEPSIS or septic shock?
    Triad: DIC, hypoglycemia, and cardiac failure

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