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• Heparin-Induced Thrombocytopenia

  Is the consequence of an immune response to UFH (standard

  IV heparin), and LMWH that is reflected in a reduced platelet

  count

   HIT antibodies are specific for platelet factor 4 (PF4) complexed

  with heparin

   H:PF4 is a hapten that triggers immune production of IgG

  isotype anti-H:PF4 antibodies that now bind the H:PF4
• Treatment of DIC

   Diagnosis and treatment of underlying disorder

   Surgery, antiinflammatory agents, antibiotics, or obstetric

  procedures

   Supportive therapy

   UFH

   Plasma

   Platelet transfusions
• Antiphospholipid Antibodies

  Transient alloimmune APLAs

  oMost APLAs arise in response to a bacterial, viral, fungal,

  or parasitic infection or to treatment with one of a

  variety of drugs

  Autoimmune APLAs

  oPart of the autoantibodies that arise in collagen vascular

  diseases, SLE, RA, scleroderma, and Sjogren's syndrome
• Antiphospholipid Antibodies

  Comprise a family of immunoglobulins that bind

  protein-phospholipid complexes

  APLAs arise as IgM or IgG

  Are sometimes called nonspecific inhibitors

  B2

  -GPI: the plasma protein most often bound to APLAs
• Thrombosis Double Hit

  Thrombosis is often associated with a combination of

  genetic defect, disease, and lifestyle influences

  Many heterozygotes experience no thrombotic event

  during their lifetimes, whereas others experience clotting

  only when two or more risk factors converge
• Congenital Thrombosis Risk Factors

   FVL gene mutation

  omost common inherited thrombosis risk factor

   Prothrombin G20210A gene mutation

  osecond most common inherited thrombophilia in patients

  with a personal and family history of deep vein thrombosis
• Congenital Thrombosis Risk Factors

  Occurs in young adults

  Occurs in unusual sites

  omesenteric, renal, or axillary veins

  Is recurrent

  Occurs in a patient with a family history of thrombosis
• Thrombosis Risk Factors Associated with

  Systemic Diseases

   Myeloproliferative neoplasms

  A cardinal sign of APML is DIC secondary to the release of

  procoagulant granule contents from malignant promyelocytes

   PNH

  oCaused by stem cell mutation that modifies membrane-anchored

  platelet activation suppressors

   Chronic inflammatory diseases

   Nephrotic Syndrome
• Thrombosis Risk Factors Associated with

  Systemic Diseases

   Chronic antiphospholipid antibodies (APLAs)

  oConfer a risk of venous/arterial thrombosis (a condition called

  antiphospholipid syndrome or APS)

  oOften accompany autoimmune connective tissue disorders

   Malignancies

  oOften implicated in venous thrombosis

  oTumor production of tissue factor analaogues
• Thrombophilia

   Or hypercoagulability

  Is the predisposition to thrombosis secondary to a congenital

  or acquired condition

   Known causes are:

  oPhysical, chemical, or biological events

  oUncontrolled platelet activation and blood coagulation system activation

  o Blood coagulation control protein deficiencies

  oUncontrolled suppression of fibrinolysis
• Thrombosis

  Is the inappropriate formation of a platelet or fibrin clot that

  obstructs a blood vessel

  Is a multifaceted disorder resulting from circulatory stasis and

  abnormalities in the coagulation system, coagulation control

  mechanisms, platelet function, the blood vessel wall, or

  leukocyte activation molecules

   Causes ischemia and necrosis