exam 1 ch.2 dixon

  1. are the body’s response to injury
    inflammation and repair
  2. elininates injurious agents
    contains injuries
    heal defects
  3. alteration in the environment causing tissue damage
  4. examples of injury:
    physical, chemical, microoganisms, nutritional, deficiencies
  5. nonspecific response to injury & occurs in the same manner regardless of nature of injury
  6. Inflammation can be:
    • Local – one area
    • Systemic – throughout
    • Acute – minimal & brief
    • Chronic -continued inflammation & longer (weeks or months)
  7. suffix denoting inflammation (pulpitis, gingivitis, etc.)
  8. increase in numberof WBC's
  9. enlargement of lymph nodes
  10. small blood vessels, certain WBC’s, & chemical mediators
    Microscopic components
  11. constriction of microcirculation then dilation
    1st event
  12. increase blood flow flooding capillary beds – heat/erythema
    active hypermia
  13. plasma fluids & proteins that leave the blood vessels & enter the surrounding tissues. (Causes pain – sensory nerves in area)
  14. mainly plasma fluids/proteins (thin/clear)
  15. tissue debris/many WBC's and serous (thick/colored)
  16. clinical sign of edema (swelling)
  17. a formation of a natural drainage passage boring through tissue allowing drainage of exudates (Buccal Parulus)
  18. mechanical way of draining exudate
    incision and drainage (I/D)
  19. movement of WBC’s to periphery of vessel walls
  20. lining of vessel walls with WBC’s
  21. escape of WBC from vessels of plasma fluids that enter tissue
  22. what are the casues of emigration:
    • -inc bld flow casuing inc pressure
    • -opening of juntions of endothelial cells linning bld vessel
    • -inc mobility of WBC's
    • -chemical mediatiors causing directional movement of WBC's (chemotaxis)
  23. ingestion of foreign substances by WBC's
  24. what are the 6 types of WBC's:
    neutrophils, monocytes, lymphocytes, plasma cells, eosinophils, & mast cells
  25. also called PMN’s (polymorphonuclear leukocyte)
    1st cell to migrate and primary cell invoved in acute inflammation
  26. also called Macrophage
    2nd cell to emigrate
  27. involved in chronic inflammation and immune response
  28. macrophages, lyphocytes, & plasma cells become the predominantes
    chronic inflammation
  29. 60 – 70% of WBC pop.
    main funtion- phagocytosis then dies
  30. become macrophages after emigration
    3 – 8% of WBC pop.
    lysosomal enzymes to aide in destruction of foreign substances
  31. start or enhance the inflammatory response
    has 3 systems
    Chemical mediators
  32. what are the 3 systems of chemical mediators?
    • Kinin system
    • complement system
    • clotting mechanism
  33. Mediates inflammation by causing inc dilation of blood vessels at the site increasing permeability of blood vessels by widening gaps between endothelial
    Early phase of inflammation
    Kinn System
  34. Production of sequential cascade of plasma proteins that are present in the blood in an activated form
    Release of histamine (mast cells)
    Complement System
  35. clots bld and helps with repair
    Clotting Mechanism
  36. body temp regulated by?
    hypothalamic thermoregulatory center
  37. fever producing substances
  38. can reduce fever with medications
    acetaminophen (tylenol)
  39. inc of WBC'
    Norm #4 -10,000/mm (infection can casue this to rise to 10-30,000)
  40. enlargement of lymph nodes
    WILL be able to paplate-enlarged mass in area of inflammation
  41. primary cells of immune system
    production of lymphocytes in nodes
  42. inc number of cells
  43. inc size of cells
  44. distinctive form of chronic inflammation
    Granulomatous inflammation
  45. microscopic groupings of macrophages surrounded by lymphocytes & plasma cells – example: TB
    formation of granulomas
  46. large macrophages having multiple nuclei
    Multinucleated giant cells
  47. the bodies final defense mechanism in its attempt to restore injured tissue to its orgininal state
  48. occur in both epithelium and connective tissue
    repair usually is completed in 2 weeks
    microscopic events
  49. Day of injury-
    consist of fibrin, aggregated RBC's and platelets-clot formation (thrombocytes)
    -affected by:hereditary, drug extensive injury, certain diseases.
    clot forms
  50. One day after-
    acute inflammation takes place
  51. 2 days after-
    • monocytes emigrate
    • fibroblast inc in # and start producing new collagen fibers
    • the initial tissue formed in CT portion of injury called-granulation tissue
    • At end of day2-chronic inflm and immune response begins
  52. the initial tissue formed in CT portion of injury called
    granulation tissue
  53. 7 days after
    • fibrin is digested by tissue enzymes & sloughs off
    • initial repair is completed
  54. 2 wks after injury-
    • tissue has full strength-called scar tissue
    • paler in color at surface because of increased # of collagen fibers & decreased vascularity
  55. healing of an injury in which there is little loss of tissue
    surgical incision
    edges are joined by sutures
    less scar tissue
    Healing by primary intention
  56. injury whereby there is loss of tissue & the edges of the injury cannot be joined during healing
    inc scar tissue
    extraction site
    keloid formation – excessive scarring in skin
    Healing by secondary intentin
  57. excessive scarring in skin
    keloid formation
  58. infection occurs at site of surgical incision that is healing by 1° intention, and 2° intention may ensue
    * waiting to perform surgical tissue repair until infection is resolved
    Healing by 3rd intention
  59. occurs similar to tissue with exception of osteoblasts
    bone tissue repair
  60. interruption due to:removal of osteoblast-producing tissue
    inc movement of bone
    bone tissue repair
Card Set
exam 1 ch.2 dixon
Dixon exam 1 ch.2 oral path