1. A young patient is diagnosed with a pulmonary embolism, and is found to have a large DVT. No acquired risk factors for hypercoagability are found, and genetic etiologies are suspected. The patient is still in the ER and has not yet received anticoagulation. Which of the following tests can be performed to evaluate possible hypercoaguable states:

2. An acquired inhibitor to factor X can be caused by which of the following?

3. Of extracellular matrix constituents, which is the most important pro-thrombotic component?

4. The diagram shown for this question illustrates initial platelet adhesion and aggregation. The substance highlighted by the red box best represents?

5. All of the following may result in a prolonged thrombin clotting time (TCT) EXCEPT:

6. Heparin induced thrombocytopenia is caused by heparin interacting with:

7. The diagram shown for this case represents a platelet control and the patient's platelets is tested for aggregation in the presence of low dose and high-dose ristocetin. In addition, electrophoresis showed decreased large molecular weight von Willebrand's multimers. Mixing the patient's plasma with random donor platelets resulted in the same platelet arrogation findings with high and low dose ristocetin. Based on this information, the best diagnosis is:

8. All of the following are symptoms of type 1 von Willebrand’s disease EXCEPT:

9. A 46 y/o woman is found to have a prolonged aPTT with a normal PT. A mixing study was performed, and the aPTT corrected into the high normal range. Clinically, the patient does not have any evidence of bleeding or bleeding tendencies. Further questioning reveals the patient has been noted to have a prolonged aPTT during a routine physical exam 5 years ago. He was referred to a hematologist at that time who told him he was fine and not to worry. Based on these findings, which of the following is the most likely etiology of the patients prolonged aPTT?

10. Which of the following has the greatest effect in inhibiting both factors V and VIII?