Morning Report 9/24/15 Bleedin’ and Clottin’

Teaching Pearls:

  • Hypercoagulable etiologies: Acquired vs inherited causes.
  • Inherited Hypercoagulable work-up: Protein C, Protein S, Factor V Leiden, Antithrombin 3, Prothrombin G2021A
  • Acquired causes: prolonged rest, high risk surgery, hospitalization, medications, age
  • In acute infection/acute clot, the Protein C, protein S and Antithrombin 3 levels may be decreased, giving a false positive result. The Factor 5 Leiden and Prothrombin Gene mutation are gene studies so they are not affected by acute illness.
  • You can see both arterial and venous clots in Anti-phospholipid syndrome and Paroxysmal Nocturnal Hematuria (think myelosuppression and thrombosis, intravascular hemolysis)
  • Thrombosis plus thrombocytopenia –> Think HIT, APS, PNH
  • Clinical Diagnosis of APS: Unexplained thrombocytopenia, spontaneous miscarriages, arterial/venous thrombosis
  • Laboratory Diagnosis of APS: aCL, B2GP, LA, timing requires positivity of markers even after three months due to false positive serologic studies

Inherited Thrombophilia

Conditions Epidemiology MOA Severity of Hypercoagulability
Factor V Leiden Most common cause, 5% of Caucasians Point mutation in one active site of protein C, decreased ability to inactivate factor V Moderate
Prothrombin Gene Mutation Second most common cause More stabilized prothrombin (harder to inactivate) Moderate
Protein C Less Common  Protein C inactivates factors Va and VIIIa. Severe
Protein S  Less Common  Protein S is a cofactor for protein C Severe
AT Deficiency  Less Common  Antithrombotic protein that inhibits factor II and X  Severe

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