Heme Part 2

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  1. What is the most common congenital bleeding disorder?
    von willebrands disease
  2. What 2 components make up factor 8?
    VWF and factor 8c
  3. The majority of cases of VWD are due to a qualitative or quantitative issue?  Is it AD or AR?
    • 80% are due to a quantitative issue, this is type 1 VWD
    • AD
  4. Treatment for type 1 VWD
  5. Is DDAVP effective for VWD types 2 and 3?
    • Variable effect for type 2
    • Ineffective for type 3
  6. What is DDAVP?  How does it work?
    • Synthetic analogue of ADH
    • IV administration stimulates VWF from endothelial cells to immediately increase VWF and factor 8 activity
  7. T or F, VWD may contraindicate neuraxial anesthesia?
  8. What diseases can cause an acquired hemophilia?
    Diseases that produce autoantibodies (SLE or RA) or lymphoproliferative d/o (leukemia or lymphoma)

    Acquired hemophilia is the most common
  9. What is the most common cause of non-immune-mediated factor deficiencies?
    abnormal production due to coumadin treatment
  10. What are major causes of thrombocytopenia?
    • decreased BM production
    • -xrt and chemo
    • -drugs
    • -infections
    • -chronic dz
    • -infiltration by cancer cells
    • increased non-immune mediated consumption
    • -tissue trauma
    • -vascular grafts
    • -toxemia
    • -DIC
    • immune-mediated consumption
    • -drugs
    • -autoimmune disorders
    • dilution
    • sequestration
  11. Disseminated intravascular coagulation
    • widespread activation of the clotting mechanism
    • fibrin deposited throughout the vascular tree
    • simultaneous depression of normal inhibitory mechanisms to prevent coagulation
  12. What can trigger DIC?
    TF (released from traumatized or dying tissue)
  13. What conditions are associated with DIC?
    sepsis, viremias, OB issues, extensive tissue damage, liver failure, extensive head injury, extensive vascular endothelial damage, hemolytic transfusion rxn, metastatic cancer, leukemia, snake venom
  14. How can sepsis contribute to DIC?
    Either the bacteria itself or the toxics released from the bacteria activate the clotting mechanism
  15. TTP, ITP, and HIT can lead to _____.
  16. What's the difference between type 1 and type 2 HIT?
    • type 1- non-immune mediated
    • -transient and clinically insignificant Plt decrease that occurs during 1st full day of full dose UF heparin
    • type 2- immune mediated
    • occurs in pts receiving heparin for > 5 days
    • heparin must be d/c
    • significant risk of thromboembolic event if heparin is continued
  17. What is the patho of HIT type 2
    • -antibodies induce Plt activation and aggregation and so thrombi form
    • -since Plts are being used to form thrombi, there's decreased Plt activity
  18. What drugs can cause thrombocytopenia?
    Decreased BM production- thiazide diuretics, sulfonamides, phenytoin, ETOH

    Immune mediated consumption- heparin, quinidine, cephalosporins, vanco
  19. How do cyclooxygenase (COX) inhibitors affect coagulation?
    • Block thromboxane A2 generation
    • Inhibit Plt granule release and Plt aggregation
  20. What's an example of a COX inhibitor?
    ASA and NSAIDs
  21. How do phosphodiesterase inhibitors affect coagulation?
    Decrease Plt aggregation
  22. What are examples of phosphodiesterase inhibitors?
    persantine and dipyridamole
  23. How do glycoprotein 2b/ 3a inhibitors affect coagulation?
    Bind to the 2b / 3a Plt receptor and prevent binding of fibrinogen
  24. What are examples of 2b/ 3a inhibitors?
  25. How do ADP receptor pathway inhibitors affect coagulation?
    Prevent receptor signaling and irreversibly inhibit the ADP Plt activation pathway
  26. What are examples of ADP receptor pathway inhibitors?
    Plavix and ticlid
  27. Warfarin MOA
    Vitamin K antagonist
  28. Vitamin K is needed for synthesis of what factors?
    2, 7, 9, and 10
  29. What lab value is used to monitor coumadin levels?
    PT or INR
  30. Heparin MOA
    Inhibits secondary hemostasis
  31. What lab value is used to monitor heparin levels?
  32. What is the reversal agent for selective Xa inhibitors?
    There isn't one, even giving FFP won't reverse the anti-coagulation
  33. Direct thrombin inhibitors MOA
    Binds directly to thrombin to inhibit secondary hemostasis
  34. What is the reversal agent for direct thrombin inhibitors?
    There isn't one
  35. What are examples of classes of anti-Plt meds?
    COX inhibitors, phosphodiesterase inhibitors, GP 2b/ 3a inhibitors, ADP receptor pathway inhibitors
  36. What are examples of anti-coagulant mediations?
    warfarin, heparin, selective factor Xa inhibitors, direct thrombin inhibitors
  37. Which 2 anti-coagulant meds are least selective?
    Heparin and warfarin
  38. What drugs are examples of anti-coagulation and fibrinolysis inhibitors (i.e. cause clotting)?
    • Protamine
    • Aprotonin
    • Lysine analogues
  39. Virchow's triad
    • 3 factors that predispose to clot formation:
    • abnormal blood flow
    • endothelial injury
    • hypercoagulability
  40. What factors can contribute to abnormal blood flow?
    Turbulence (atherosclerotic plaques) or stasis
  41. In the heart and arterial circulation, what is the primary factor contributing to thrombus formation?
    endothelial injury
  42. What can cause endothelial injury?
    Stress from HTN, turbulent blood flow, HL, hyperglycemia, vascular injury or infection
  43. Thrombophilia
    Form of inherited hyper coagulable disorder
  44. What are examples of acquired hyper coagulable disorders?
    • myeloproliferative d/o (polycythemia)
    • malignancies
    • pregnancy
    • nephrotic syndrome
    • lupus anti-coagulant
Card Set:
Heme Part 2
2013-12-13 20:23:35
BC Nurse Anesthesia
heme part 2
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