BOD Exam 2

  1. an increase in the amount of blood in the vasculature in a given part of the body due to local vascular dilation
    Hyperemia & Congestion
  2. Congestion is either _____ or ______.
    • acute - leading to anoxic injury
    • chronic - leading to hypoxic injury
  3. Congestion may result in (5)
    • hemorrhage
    • edema
    • thrombosis
    • necrosis
    • fibrosis
  4. Secondary effects of hemorrhage (4)
    • resorption of fluid
    • erythrocytes lysed & phagocytosed
    • fibrinolysis - breakdown of clots
    • potential scarring - ingrowth of granulation tissue from hematoma
  5. local arteriolar dilation leading to an increase in the amount of blood in the vasculature
  6. venous engorgement is called
  7. During liver congestion, hypoxic injury occurs where? It results in what?
    • Periphery of the acinus (connecting central veins)
    • loss of hepatocytes and fibrosis
  8. Lung congestion is caused by
    interference with blood flow through left heart
  9. Pulmonary congestion leads to (2)
    edema & fibrosis
  10. What is hemosiderosis
    macrophages in lungs eat RBCs and iron builds up
  11. When does hypostatic congestion occur?
    • Post mortem gravity
    • ante mortem recumbent animals
  12. Edema may be classified as (3)
    • effusions
    • transudates
    • exudates
  13. Edema fluid that contains both serum and blood is called
  14. Causes of generalized edema (3)
    • cardiac edema
    • renal failure
    • hepatic failure or malnutrition/malabsorption
  15. Cardiac edema occurs when
    there is venous congestion resulting in increased blood volume and increased hydrostatic pressure (blood is forced out into the tissues)
  16. renal failure causes generalized edema by
    urinary protein loss & decreased oncotic pressure
  17. Why does hepatic failure or malabsorption cause generalized edema?
    Decreased plasma oncotic pressure - fluid goes out and doesn't come back in
  18. What is ansarca?
    generalized edema over entire body
  19. Three causes of localized edema
    • venous obstruction
    • lymphatic obstruction
    • inflammatory edema or vascular injury
  20. Termination of blood loss from the vasculature is called
  21. Hemostasis is maintained by
    pro and anti-coagulant mechanisms
  22. formation of a solid adherent blood clot within the lumen of a vessel or the heart
  23. Three types of blood clots
    • Normal (hemostasis)
    • Thrombi (excessive clot formation)
    • post-mortem blood clotting (chicken fat clot)
  24. Three events in hemostasis
    • vasoconstriction
    • platelet plug - platelets adhere to damaged endothelial cells and each other
    • coagulation - enzymatic cascade involving pre-formed clotting factors in blood
  25. Three steps of platelet activation
    • adhesion and shape change
    • aggregation
    • secretion (release reaction)
  26. What promotes platelet adhesion?
    von Willebrand's factor binds subendothelial collagen and platelets bind to that
  27. What causes platelet aggregation?
    • ADP and Thromboxane A2 promote formation of primary plug
    • Thrombin promotes further aggregation and polymerizes fibrin producing definitive plug
  28. Platelet aggregators (6)
    • ADP and Thromboxane A2
    • thrombin
    • collagen
    • epinephrine
    • immune complexes
    • platelet activating factor
  29. Important coagulation cofactor
  30. Anticoagulant factors of endothelial cells
    • NO & PGI2 inhibit platelet aggregation
    • produce antithrombins
    • modulate fibrinolysis via plasminogen activators & inhibitors
  31. Plasminogen is present where?
    plasma and platelet membranes
  32. Plasminogen binds
  33. Plasminogen active form
  34. Plasmin digests
    polymerized fibrin
  35. Two plasminogen activators
    • tissue type - produced by endothelial cells
    • urokinase like - present in plasma
  36. DIC stands for
    Disseminated Intravascular Coagulation
  37. DIC is characterized by (4)
    • widespread activation of clotting mechanisms
    • consumption of platelets and clotting factors
    • activation of fibrinolysis
    • widespread hemorrhage
  38. Causes of DIC
    infection, trauma, neoplastic disease
  39. Pathogenesis of DIC
    massive release of tissue factor or thromboplastic substances into the circulation
  40. In Gram negative sepsis, what is the first step in the DIC mechanism?
    Endotoxin induces expression of tissue factor, IL-1, TNF in monocytes & macrophages
  41. What do IL-1 and TNF do?
    induce tissue factor expression from endothelial cells and upregulate WBC binding
  42. During gram negative sepsis, endotoxin ultimately causes what?
    widespread activation of clotting and fibrinolysis in microvasculature
  43. Gram negative sepsis ultimately causes DIC by doing what?
    using up platelets and clotting factors and causing microvascular hemorrhage
  44. Is thrombosis a normal component of hemostasis?
  45. Local control of clotting cascade (3)
    • antithrombins
    • proteins C & S
    • plasminogen-plasmin system
  46. Virchow’s Triad for thrombosis pathogenesis:
    • Damage to vessel
    • increased coagulability of blood
    • changes in flow
Card Set
BOD Exam 2
Biology of disease exam 2