Pathophysiology - Inflammation and wound repair

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jaredseehawer
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141902
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Pathophysiology - Inflammation and wound repair
Updated:
2012-03-16 13:47:31
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pathophysiology
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Pathophysiology unit 5
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  1. What are the 4 cardinal signs of inflammation?
    - Heat

    - Redness

    - Tumor

    - Pain
  2. What are the goals of inflammation?
    Destroy injurious agents and remove them

    Wall off/confine these agents to limit their effects

    Stimulate/enhance immune response

    Promote healing
  3. What is the difference between acute and chronic inflammation?
    Acute inflammation has a short duration and is predominately neutrophils.

    Chronic inflammation lasts longer and is predominately lymphocytes and macrophages.
  4. What changes in circulation occur with acute inflammation?
    - Vasodilation

    - Increase in vessel wall permeability
  5. What percentage of one's total body weight is water?
    60%

    20% is extracellular, out of that 5% is plasma and 15% is interstitial
  6. What is edema?
    The abnormal accumulation of fluid in interstitial spaces or body cavities.
  7. What is ascites?
    Fluid accumulation in the abdoman.
  8. What is hydrothorax?
    Fluid accumulation in the thorax.
  9. What are the 6 mechanisms of edema?
    - Inflammatory

    - Hydrostatic

    - Osmotic/oncotic

    - Obstructive

    - Hypervolemic

    - Multifactorial
  10. What commonly causes obstrutive edema formation?
    - Tumor cells

    - Chronic inflammation

    - Lymphatic duct scarring

    - Filarial parasites
  11. What mechanism of edema is concerned with painful, red swelling?
    The inflammatory mechanism.
  12. What are exudates?
    Characteristic of swelling, the inflammatory mechanism of edema. Rich in protein and more cells.
  13. What are transudates?
    Characteristic of edema. Less protein and fewer cells.
  14. When the vessel wall becomes more permeable (acute inflammation), what happens to proteins in the vessel?
    Proteins can not escape normal vessels, but can leak out of inflamed vessels. Chemical mediators of inflammation are released.
  15. How does vascular flow change in inflamed vessels?
    Arterioles near site of injury constrict, vasodilation occurs.

    Capillaries become flooded with blood.

    Increased pressure forces plasma proteins through capillary walls.
  16. Explain the formation of inflammatory edema? (swelling)
    - Movement of protein rich fluid into interstitium

    - outflow of water/ions into extravascular tissue

    - Results in swelling
  17. What are the results of vasodilation?
    Blood flows slowly, plasma moves outward.

    Tissues become red/swollen (hyperemia causes redness).
  18. What are the results of increased vascular permeability?
    Chemical mediators of inflammation cause endothelium of capillaries and venules to retract.

    Creates spaces allowing proteins/WBCs to leave vessel.
  19. What are the 4 steps leukocytes take to leave a vessel?
    1) Margination: WBCs float to outer edges of slow vessel

    2) Rolling: WBCs roll along epithelial surface, briefly sticking

    3) Adhesion: WBCs firmly stick to endothelial surface

    4) Transmigration: WBCS cross endothelium and and basement membrane. (diapedesis)
  20. How do mast cells degranulate?
    Gegranulation is triggered by IgE, physical injury, or chemical agents.
  21. What are some chemicals mediators of inflammation?
    Histamine, seratonin, bradykinin

    Prostaglandins

    Platelet activating factor
  22. What are histamine's effects and how soon are they activated?
    Causes arteriolar dilation and increased vascular permeability.

    Immediate reaction.
  23. What are prostaglandins effects and what are "anti-prostanglandin" drugs?
    Cause pain and other roles of inflammation .

    NSAIDs
  24. What is chemotaxis?
    WBCs move toward the site of injury following along a chemical gradient.
  25. What are some chemotactic factors for leukocytes?
    Bacterial products

    Components of the complement system

    Various chemical mediators
  26. What are the 3 plasma protein systems that mediate inflammation?
    - Complement system

    - Clotting system

    - Kinin system
  27. What is the Complement System?
    A plasma protein system that consists of 30 different proteins that work in a cascade to enhance inflammation.
  28. What is the Clotting System?
    A plasma protein system that forms a fibrinous meshwork at the site of inflammation that traps exudates and other inflammatory shiz.
  29. What is the function of thrombin?
    Thrombin converts finbrinogen to fibrin and enhances WBS adhesion to the endothelium.
  30. What is the Kinin System?
    A plama protein system that leads to the formation of bradykinin which causes increased vascular permeability and vasodilation. (similar to hisamine but activates @ slower pace)
  31. What are the 4 steps of phagocytosis?
    1) Adherence (opsonization)

    2) Engulfement

    3) Fusion of lysosome with phagosome

    4) Destruction of target by lysosomal enzymes
  32. What are some possible outcomes of acute inflammation?
    Complete resolution

    Scarring/fibrosis

    Abscess formation

    Progression to chronic inflammation
  33. What characterizes chronic inflammation?
    Active inflammation, tissue injury, and healing all taking place simultaneously.
  34. What are common causes of chronic inflammation?
    Injurious agents persist

    Interference in normal healing process
  35. What are the 2 possible outcomes of wound healing?
    - Resolution: good as new

    - Repair: connective tissue restores strength but not function

    Both begin early in inflammatory process.
  36. What are labile cells and some examples?
    Continually dividing cells that proliferate throughout life.

    Skin, bone marrow, GI tract lining
  37. What are quiescent cells and some examples?
    Stable cells that demonstrate low level of replication.

    Bone, kidney, fibroblasts, liver
  38. What are nondividing cells and some examples?
    Permanent cells that stop divinding during prenatal life.

    Nerve cells, cardiac m., skeletal m.
  39. What 3 factors are important in skeletal m. fiber repair?
    - Multinucleated: provide multiple copies of genes that speeds stuff up.

    - Myoblasts: fuse to create m. fibers

    - Satellite cells: repair damaged fibers
  40. What are some factors that affect wound healing in general?
    Site of wound, mechanincal factors, wound size, infection, circulatory status, nutritional/metabolic factors, age.
  41. What are tension lines?
    Parallel bundles of collagen and elastic fibers that align with te stress placed on skin during normal movement.
  42. What is the clinical significance of tension lines?
    When one excises a wound, a long, thin incision along a tension line will heal better than if the surgeon were to simply cut around the outline of the tumor.
  43. What is debridement?
    First, absolutely essential step in would healing.

    Clean up of particulate matter by phagocytosis.

    Clot break up by fibrinolytic enzymes.

    Natural is slow while surgical debridement is quicker.
  44. What is first intention healing?
    Primary union. Wounds with minimal tissue loss (surgical wound). Preferred.
  45. What is second intention healing?
    Large, open defects and infected wounds that involve formation of granulation bed.
  46. Describe the entire process of wound healing (7 steps)
    1) Injury causing acute inflammatory response

    2) Debridement

    3) Formation of granulation bed

    4) Angiogenesis by fibroplasia

    5) Epithelialization

    6) Contraction

    7) Maturation
  47. What two overlapping phases occur with wound repair?
    Reconstruction phase

    Maturation phase (fine-tuning of new connective tissue)
  48. What is epithelialization?
    When healthy epithelial cells migrate into the wound.

    Causes scab to get loose. ew.

    Contact inhibition (sealing the wound)

    Can be aided by keeping wound moist.
  49. What does the reconstructive phase of wound healing consist of?
    Blood clotting seals of wound.

    Debridement.

    Promotion of angioblasts and fibroblasts.

    Granulation tissue formation within 3 to 5 days.
  50. What is angiogenesis?
    New endothelial cells (angioblasts) migrate into wound "scaffolding" and organize into vessels.
  51. What is fibrosis?
    When fibroblasts enter the area and begin to proliferate, they produce collagen which develops strength.
  52. What cells are responsible for wound contraction?
    Myofibroblasts which have features of both fibroblasts and smooth m. cells and they exert pull on neighboring cells.
  53. What is the maturation phase of wound healing?
    Scar tissue is remodeled and gains maximum strength which can take months.

    Type 3 collagen is replaced by stronger Type 1.
  54. Describe the differences between steroids and NSAIDs.
    Steroids are stronger glococorticoids and inhibit mast cells/phagocytes and can suppress immunity.

    NSAIDs are weaker such as ibuprofen and advil and inhibit protaglandins. Result in decreased production of stomach mucus.

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