1. Chapter 6, pg 38
    Immune systems basic division of labor: (4)
    • 1) innate and adaptative (aquired) immune response
    • 2) humoral and cell-mediated responses
    • 3) active and passive immunity
    • 4) natural and artificial immunity
  2. Chapter 6 pg 39
    Foriegn protiens are called________?
  3. Chapter 6 pg 39
    True or False, Polysaccarides and polypetides may also serve as antigens?
  4. Chapter 6, pg 39
    Inflamation is the process of ______ tissues?
  5. Chapter 6 pg 40
    True or False?
    ' lining the GI tract and other body orifices constitutes the first line of defense?'
  6. Chapter 6, pg 40
    Chemical barriers are part of the innate immunity?
    True or False?
  7. Chapter 6, pg 40
    Phlegmone definition?
    "the burning thing"
  8. Chapter 6, pg 41
    Cornelius Celsus described the four cardinal signs of inflamation as?
    rubor, tumor, calor and dolor (rednesss, swelling, heat, and pain).
  9. Chapter 6, pg 41

    Who noted in 1793 that, "inflamation is not the problem but a curative response"
    Scottish Surgeon, John Hunter
  10. Chapter 6, pg 41

    Who observed "the process of diapedesis, which refers to the manner in which red blood cells travers the endothelial lining of the microcirculation."
    Julius Cohnheim, pupil of Rudolph Virchow, in 1867
  11. Chapter 6, pg 41

    What did Russian Elie Metchnikoff in the 1880's discover?
    He discovered the process of phagocytosis in the larvae of starfish, demonstrating that both serum factors (antibodies and cellular factors (phagocytes) are involved in the immune response.
  12. Chapter 6, pg 41

    Waht did Sir Thomas Lewis demonstrate?
    He donstrated that chemical substances that are locally produced at the site of inflamation mediate the response
  13. .
  14. Chapter 6, pg 41

    An acute inflamation is of _______ onset and _______ duration?
    ........recent onset and short duration.
  15. Chapter 6, pg 41
    Process of acute inflamation? The key events that ensue when there is an acute injury are:
    • 1) Changes in vascular flow and in the diameter ofsmall blood vessels (hemodynamic changes)
    • 2) Changes in vascular permeability
    • 3) Stage of exudation: escape of fluid, protiens, and leukocytes frmo th eblood vessels into the extravascular environment, resulting in an increase in the fluid in this space (edema)and pus in the event fluid contains lots of cells and cellular debris.
  16. Chapter 6, pg 42
    Immediate response to injury is transient, vasodilation or vasoconstriction of the aterioles, usually for 3-5 seconds?
    vasoconstricion followed by more importantly ateriolar vasodilation.
  17. Chapter 6, pg 42

    Blood stasis puts back pressure on the ciruclation and further increases the rate of leakage, mostly from ______?
  18. Chapter 6, pg 42 changes in vascularity

    Blood vessels leak for two reasons:
    1. Passive leaking, due to vessel wall injury.

    2. Active process leaking, where non-injured vessels are affected by chemical mediators, (histamines, etc) that are liberated from the damaged tissue in such a way that their structure becomes leaky.
  19. Chapter 6, pg 42 Changes in vascular permeability

    Intravascular osmotic pressure generated by blood proteins that tends to move fluid into vessels, opposed by tissue osmotic pressure generated by its proteins and mucupolysaccharides that tends to extract fluid from the vessels. the net effect is a balance tipped in favor of _____?
    Extravasation or loss of fluid from th eblood into the tissue spaces.
  20. Chapter 6, pg 42

    Define Transudation.
    "Its the increase in hydrostatic pressure that drives a protein-por liquid outside the microcirculation."
  21. Chapter 6, pg 43

    Define Exudation.
    Soon after (transudation)   under the influence of various chemical mediators, there is a marked increase in the permeability of arterioles, capillaries, and especially the venules which allows for the protien-rich fluid. This process is called Exudation.
  22. Chapter 6, pg 43

    Define Margination.
    When statis occurs secondary to injury, white blood cells travel along the periphery of microvessels.
  23. Chapter 6 pg 43

    Define Pavementing.
     A process that by some mechanism adhesion occurs between the leukocytes and the walls of the capillaries and venules. (it is thought that there are complementary "adhesion molecules" on the leukocyte endothelial walls)
  24. Chapter 6 pg 44 Acute Inflamtion:

    During the first 6-24hrs the predominant emigrants are the ________. Followed by the ________ within 24-48 hours.
    Neutrophils followed by the monocytes.
  25. Chapter 6 pg 44

    Define Chemotaxis.
    Chemical attractants draw the leukocytes, which can "smell" these attractants, in a specific direction.

    A specific path or chemical gradient.
  26. Chapter 6 p 44

    Invading organisms are not recognized unless they are coated with_________?
    serum factors called opsonins, which are antibodies or blood complements that recognize and tag the foreign protein.
  27. Chapter 6 p44

    Hydrogen peroxide is utlized in oxygen dependent or oxygen independent phagocytosis?
    oxygen dependent.
  28. chapter 6 p 44

    Define Leukopenia.
    Decreased number of circulating leukocytes.
  29. Chapter 6, p44

    impaired adhesion can be a sign of
    acute alchohol poisoning
  30. Chapter 6 p 44

    impaired chemotaxis and migration .. can be a sign of ___?
  31. chapter 6 p44

    Defective phagocytosis can be a sign of _______ what disease?
  32. chapter 6 p44

    Impaired degradation ability can be a sign of _______?
    Chronic granulomatous disease in which there is diminished hydrogen peroxide formation.
  33. Chapter 6 p45

    Define Arthus Reaction.
    When neutrophils digest the walls of the venule.
  34. Chapter 6 p45

    Define Lymphangitis.

    as the exudate and the debris oftissue breakdown drain toward the lymph nodes, any surviving bacteria may produce infections elsewhere in the body via spread through the lymphatic system. Some of the bacteria may reach the blood stream itself and give rise to a dangerous systemic infection.
  35. Chapter 6 p 45

    Enzyme cascade mechanisms include the ______, _____, and ____________.
    complement, fibrinolytic, and kallikrein-kinin systems.
  36. Chapter 6 p46
    Histamine and serotonin (5-hydroxytryptamine) are chemicals which increase _________, of the _________ and allow local transudation of protein-poor fluid into extravascular space.
    permeability, of the venules
  37. Chapter 6 p46

    Histamines are stored?
    • 1) mast cells
    • 2) platelets
    • 3) basophils
  38. chapter 6 p46

    Agents that promote the release of these vasoactive amines include:
    • 1) physical agents (heat/cold)
    • 2) immunologic reactions
    • 3) anaphylatoxins (fragments of the complement proteins)
    • 4) histamine releasing faxtors derived from leukocytes and allergens.
  39. chapter 6 p 46
    Name three systems of Plasma Proteases:
    • 1. complement
    • 2. kinin
    • 3. clotting systems
  40. Chapter 6 p 46 Plasma Proteases

    Define Complements
    the complements number some 20 proteins. C3a increases vascular permeability. C5a increases permeability and enhances chemotactic behavior.  In typical complement sequence, an antigen interacts with host antibody producing an antigen-antibody complex  that goes onto bind complement;complement by-products then impel  histamine release and neutrophilic infiltration.
  41. Chapter 6 p46

    Define Kinins
    • * endogenous peptides produced by cascade
    • * factor XII of clotting system (Hageman Factor)
    • Activated Hageman factor -->plasma kallikrein->converts kiniogen -->variety of kinins.

    The most important of these is badykinin which is vasoactive nonapeptide (9 amino acids) inceses endothelial permeability & involved in pain perception.
  42. Chapter 6 p 46
    Describe, Clotting System Constituents.
    activated by Factor XII --> converts fibrinogen to fibrin, during conversino of which fibrinopeptides are produced. Induces great permeability and chemotaxis.
  43. Chapter 6 p 47
    Asperin, indomethacin and other non-steroidal anti-inflammatory drugs inhibit what enzyme____________?
  44. Chapter 6, p 47

    What does cylooxygenase do?
    it is the enzyme which transroms arachidonic acid into the prostaglandin PGG22, which itself is converted into PGH2 and fnially various vasoactive products.
  45. Chapter 6 p 47
    Which is a stronger inflamatory agent,
    leukotrienes or prostaglandins?
  46. chapter 6 p 47
    The enzyme 5-lipoxygenase (5-LO) helps convert arachidonic acid into______?
  47. chapter 6 p 47
    In treating colitis, hydorxy urea is used to block which one below?

    a) 5-LO
    b) Prostaglandin
    a) 5-LO
  48. Chapter 6 p47
    ECF-A is an abreviation for?
    Eosinophil Chemotractic factor of anaphylaxis
  49. Chapter 6 p47

    Describe/define Lymphokinines
    when a lymphocyte attacsk an antigen an array of mediator may be released called lymphokinines. They may induce and synthesize adhesion molecules, the modulation of platelet activity (including histmaine release etc)
  50. chapter 6 p48

    Does the elevation in body temperature aid in recovery.
    It is unknown if elevation of body temperature impedes or aids in recovery
  51. Chapter 6, p48
    Which is an acute phase reaction

    a) hypotension
    b) hypertension
  52. Chapter 6 p49

    Parasitic infections are associated with elevated levels of

    a) eosinophils
    a)  esoinophils
  53. chapter 6 p. 49
    Environmental allegens are associated with elevated levels of

    C) eosinophils
  54. Chapter 6 p 49

    In most infections ________ are elevated?

    C) neutrophils
  55. Chapter 6 p49

    Mumps, rubella and mononucleosis produce and elevation of
    a) neutrophils
    b) eosinophils
    c) lymphocytes
Card Set
Pathology Midterm II Review