Patho- Circulation Part 2.txt

  1. What is the vascular response to a breach in small vessels? (3)
    vasoconstriction, hemostasis and fibrin/platelet plug
  2. What is the vascular response to a breach in a medium sized vessel? (3)
    hemostasis, contraction and retraction of vessels, external compression by tissue and BP
  3. What is the vascular response to a breach in a large vessel? (4)
    hemostasis, contract/retraction of vessel, external compression, and the tendency to form hematomas w/ a fibrous connective tissue capsule
  4. Hemostasis is based on the interplay b/w... (4)
    endothelia, basement membrane, circulating blood elements, and plasma proteins.
  5. Process whereby flowing blood is converted into a solid coagulum.
  6. ____________ may occur post-mortem.
  7. The intrinsic coagulation pathway is ___________ in origin, occurs ___________, and is activated by ________________.
    intravascular; slowly; contact with foreign substances
  8. The extrinsic coagulation pathway is activated by ______________ and ___________ and occurs ________.
    extravascular tissue; blood vessel damage; quickly
  9. Coagulation enzyme activation occurs on ________________.
    damaged vascular and platelet surfaces
  10. Intrinsic and extrinsic coagulation pathways converge at ___________, which is a ___________enzyme.
    factor X; vit K dependent pro-
  11. Cleavage by factor X of _________ to make ________act at the site of vessel damage to... (3)
    prothrombin; thrombin; enhance the intrinsic clotting cascade (activating factors V, VIII, XI), makes fibrin, help stabilize the clot (activating factor V)
  12. Inactivation of the intrinsic clotting cascade occurs with the interaction of thrombin with ___________.
  13. De-bulking clots occurs by _________, mainly by the enzyme _________.
    fibrinolysis; plasmin
  14. ____________ inhibit platelet aggregation.
  15. 3 mechanical factors that manage the gradients of coagulation-anticoagulation cascade proteins.
    blood flow, turbulence, and plasma proteins levels
  16. An area of hemostasis is also a(n) _________________.
    pro-inflammatory stimulus
  17. The process of inappropriate intravascular blood coagulation during life.
  18. By definition, thrombi are ____________.
    attached to vessel walls
  19. Thrombi on a wall.
  20. Thrombus on the heart or great vessels.
  21. Thrombus causing vascular obstruction.
  22. Thrombus with a tail that extends in the direction of blood flow.
  23. Thrombus that occurs at a bifurcation of vessels.
  24. Thrombus that incorporates an infectious agent.
  25. Thrombus that is a sterile lesion.
  26. What is the consistency of thrombi? (5)
    dry, rough, granular surface, brittle (friable), laminated
  27. Thrombi are more commonly located in _________.
  28. Acute thrombi contain _________, have alternating layers of _________ and ________.
    all blood elements; fibrin; erythrocytes
  29. Chronic thrombi have been repaired by __________; there is evidence of ____________.
    fibrosis; acute and chronic inflammation
  30. Endothelial damage releases ______________ and exposes the ______________; released platelet proteases and tissue thromboplastin from damaged endothelia simultaneously activate the __________.
    platelet activating factor; basement membrane; extrinsic system
  31. Vascular events often seen with thrombosis. (5)
    congestion and/or edema, hemorrhage, infarction, aneurysms
  32. When a thrombus occludes an artery, there is _____________ and high probability of ___________.
    peripheral ischemia; infarction
  33. When a thrombus occludes a vein, there is _________ and ____________ on surrounding tissue.
    local hypoxia; pressure effects
  34. Inflammation develops with thrombosis because...
    of the initial tissue/vessel insult and a blood clot in vivo is a "foreign" object
  35. The resolution of thrombi includes ____________ and ____________.
    liquefaction; absorption
  36. Process whereby intravascular foreign particulate matter is mechanically transported by the vascular system to lodge at a site distant to its point of origin.
  37. Most emboli arise in the ____________from ________; their major effects are on the ____________.
    venous side; thrombi; arterial side
  38. A solid embolism that is a detached intravascular fragment of a thrombus.
  39. Solid emboli can be caused by... (4)
    parasites, neoplastic cells, bacteria, or clumps of erythrocytes due to incompatible blood transfusion
  40. Clumps of erythrocytes due to incompatible blood transfusions.
    spodogenous emboli
  41. Liquid emboli are made of _______.
  42. Gas emboli occur due to ______________.
    injections of air
  43. Emboli are mostly found in the.... [organs]
    lungs, liver, and CNS
  44. Emboli may cause... (3)
    ischemia, infarction, gangrene
  45. A localized area of ischemia-induced coagulation necrosis produced by a rapid mechanical blockage of the arterial blood supply following obstruction from within or vessel compression from without.
  46. ___________ results from deprivation of adequate blood (oxygen) supply to a tissue.
  47. The size of the infarct is greater in tissues with _____________, such as__(2)__, or in tissues with a ___________, such as ___________.
    poor collateral circulation; cardiac muscle, kidney; high metabolic rate; brain
  48. Venous infarction often occurs in the _____________ and is followed by invasion of ___________ and an onset of ___________.
    intestine; saprophytic bacteria; moist gangrene
  49. A red infarct is filled with __________and commonly occurs in the... (3)
    blood; intestine, lungs, spleen (due to many collaterals)
  50. A pale infarct is ___________ poor; it commonly occurs in the... (3)
    erythrocyte; kidney, heart, and skeletal muscle (due to poor collateral circulation)
  51. Microscopically, infarctions have a sharply demarcated area of _____________ adjacent to ____________ outlined with blood and lekocytic infiltrates.
    ischemic coagulation necrosis; viable tissue
  52. Chronic infarction lesions are ___(3)___ microscopically and show ________ and ________.
    shrunken, pitted, and distorted; scar tissue; mineralization
  53. A rapid onset systemic condition characterized by uncontrolled activation of the intrinsic and/or extrinsic coagulation systems leading to production of intravascular fibrin thrombi and emboli.
  54. DIC is often associated with... (5)
    septicemia, endotoxemia, extensive trauma, cancer, and endotheliotropic viruses
  55. DIC begins with _________________, causing release of __________ and initiation of _________; this causes generation of _________, and hydrolysis of clotting factors and platelets leads to ________ and ________.
    massive endothelial damage; platelet factor 3; intravascular coagulation; plasmin; fibrin split products (FSPs); fibrin degeneration products (FDPs)
  56. With DIC, the pathologic findings include...(4)
    excessive capillary bleeding w/ petechiae and ecchymoses, longer clotting times, intravascular hemolysis, thrombocytopenia
  57. What are the clinical features of circulatory distress associated with DIC? (3)
    hypotension, weak pulse, tachycardia
  58. What are the clinical features of pulmonary distress associated with DIC? (1)
  59. What are the clinical features of renal failure associated with DIC? (1)
  60. What are the clinical features of homeostatic failure associated with DIC? (1)
  61. Intravascular coagulation following somatic death is mediated by...
    uncontrolled release of tissue and endothelial-origin thromboplastins
  62. Post-mortem blood coagulation is facilitated by...
    slowed or absent blood flow.
  63. Lack of post-mortem clots suggests...
    the presence of pre-mortem coagulation defects or in vivo depletion of coagulation proteins
  64. Post-mortem coagulation is not _________; clots are morphologically...(3)
    attached to vessel wall; moist,smooth,flexible
Card Set
Patho- Circulation Part 2.txt