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2010-12-14 23:52:34

Robbins 4
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  1. Anasarca
    sever systemic edema
  2. Most common cause of systemic edema
    • CHF
    • Increased venous hydrostatic pressure
  3. most important cause of protein urea
    nephrotic syndrome
  4. lymphatic obstruction
    blocks removal of extra fluid
  5. hypoproteinurea
    • edema is worse
    • seen in periorbitals
  6. increased blood flow into a tissue
  7. impared outflow
  8. lung congestion
    with left heart failure
  9. liver congestion
    with right heart failure
  10. central lobular necrosis
    • last to receive blood
    • occurs with hypo perfusion
  11. hamatoma
    hemorrhage within a tissue
  12. petechia
  13. purpura
  14. ecchymoses
  15. permanent plug
    thrombin and fibrin
  16. Bernard soulier syndrome
    defective gp-Ib
  17. ADP on platelets
    changes gp IIIa/IIb to bind to fibrinogen
  18. Glanzmann thrombasthia
    • gp IIIb/IIa deficency
    • cant bind fibrin or other platelets
  19. primary vs secondary plug
    • primary only plts
    • secondary plts and fibrin
  20. AT3 inhibits
    2, ,9,10,11,12
  21. Thrombin induced t-PA
  22. Virchows triad
    • endothelial injury
    • alterations of normal blood flow
    • hypercoagulability
  23. turbulent blood flow
    brings platelets into contact with the endothelium
  24. oral contraceptives and pregnancy
    hypercoagulable because of increase in factor production
  25. Antiphospholipid syndrom
    patients have antibodies against phospholipids that can activate platelets or inactivate protein C
  26. mural
    non occlusive thrombi
  27. sites of arterial thrombi formation
    athroscletotic plaques and turbulent areas of vessel bifurcation
  28. extension of plaques
    • arterial grom retrograde
    • venous grow antegragede
  29. pre death vs post death thrombus
    lines of zahn layers of pale thrombin and fibrin with lines of dark blood cells
  30. thrombus on a heart valve
  31. verrucous endocarditis
    • aka libman sacks
    • patients with lupus erythematosus
    • circulating immune complexes
  32. Fate of a thrombus
    • propagation, causing obstruction
    • embolism
    • dissolution
    • organazation and recanalization
  33. superficial venous thrombi
    saphanous vein
  34. deep venous thrombi
    femoral vein
  35. most venous emboli
    are asymptomatic and not found till after the embolize
  36. Trousseau syndrome
    embolism form molignancy
  37. systemic thromboembolism
    usually form a mural clot in the left heart, on a valve or aorta
  38. fat embolus
    • second leading cause behind thromboembolis
    • 1-3 days after injury
    • fatty release is toxic to endothelium
  39. caisson disease
    more chronic decompression sickness
  40. Infarction
    • area of ischemic necrosis caused by occlusion of either arterial 97% or venous
    • venous is usually congestion
  41. Red infarts
    • venous occlusion
    • loose tissue; lungs
    • duel circulations
    • preveous congestion
    • site of repercussion
  42. white infarct
    end arterial circulation
  43. histological characteristic of infarction
    • coagulative necrosis
    • exception os the brain; liquefaction necrosis
  44. septic infarts usually become and abscess
  45. slow developing occlusions
    • are less likely to infarct
    • more time to develop alternative circulation
  46. septic shock
    • increased cadiac output due to arterial dilation
    • mostly gram negative bacteria; endotoxins
    • all effects from LPS
  47. Shock lung
  48. hypovelemic vs septic shock
    • hypovolemic; cold skin
    • septic; warm skin