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  1. This is the formation of excessive amount of clot (fibrin and/or platelet derived) within the vessel lumen causing vessel occlusion.
  2. A very high FVIII concentration can induce what?
  3. What helps to maintain the balance in hemostasis (between coagulation and fibrinolysis)?
    Regulatory Mechanisms
  4. Which type of thrombosis (veinous or arterial) is coagulation based? WHich is platelet-derived?
    • Venous
    • Arterial
  5. How does Arterial Thromboemobolic Disease primarily manifest? What are the two clincial symptoms? What are the two treatments?
    • MI & Stroke
    • "Cold Extremities" & Gangrene of Extremity
    • Anti-Platelet Drugs & Heparin
  6. What color is a thrombus in an artery? In a vein?
    • White
    • Red (has trapped RBCs and platelets)
  7. Deep Vein Thrombosis in more common than _____ and _______ combined.
    • MI
    • Stroke
  8. What is the leading cause of childbirth death in North America, as well as the most common preventable hospital death?
    Pulmonary Embolism
  9. Coagulation generates VTE and then breakdown of fibrin clot forms ________. These become elevated in blood after the formation of a VTE, and are usually lower in patients without VTE. Therefore, we use this assay to rule out VTE.
    • D-dimers
    • D-dimer Assay
  10. This is a set of genetic abnormalities and/or acquired conditions which predisposes the individual to an increased risk of thromboembolic disease. This presents with mainly venous thrombosis, and usually manifests in young adults (20-50 years). The cause of the thrombotic presentation is usually spontaneous and an inciting event. This is a complex genetic disease -- there is no single cause. There is a standard treatment for all causes.
  11. The two molecular causes of Thrombosis are a loss of function, caused by a deficit in ______________, and a gain in function, caused by an increase in ___________.
    • Protein C
    • FVIII
  12. This is caused by an inability of patient's plasma to be inhibited by Activated Protein C (APC). There is a mutation of the APC cleavage site in what factor, and what is this known as?
    Factor VLeiden
  13. The highest prevalence of abnormalities in patients with VTE is caused by what?
    Unknown Cause
  14. This mutation increases Prothrombin levels. The mechanism is longer surviving mRNA. This is a genetic abnormality.
    Prothrombin-UT 20210 Mutation
  15. In this syndrome, there is a heterogeneous family of auto-antibodies (lupus anticoagulant) against the PL-Protein Complex. The majority are asymptomatic, but about 30% of patients develop thrombosis. This can be transient or long term. Thrombosis and obstetrical complications can arise, including a.rterial, venous, and recurrent fetal loss
    Anti-Phospholipid Syndrome or Lupus Anticoagulant
  16. Most of the transient cases of Anti-Phospholipid Syndrome, or Lupus Anticoagulant, is due to what? What are the long-term cases due to?
    • Viral Infection
    • Auto-immune or unknown
  17. What lab test is done for Anti-Phospholipid Syndrome, or Lupus Anticoagulant?
    LA Panel -- do three tests, need at least one positive; must be present on 2 occassions at least 12 weeks apart to be long-term
  18. When is the optimum time to do a work-up on a Thrombophilia patient?
    When they are asymptomatic and are not on any therapy
  19. Heparin-induced thrombocytopenia is an immune-mediated activation of platelets. It results in ___________ due to platelet and coagulation activations.
  20. How is Heparin-Induced Thrombocytopenia tested in the lab?
    • Detection of Antibody: ELISA
    • Functional Antibody Tests: Serotonin (14C) Release Assay
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