Thrombocytopenia and Immune Thrombocytopenia

Platelets form the first plug at a damaged blood vessel. When their number is too low, bleeding usually occurs at the skin and mucous membranes rather than as deep tissue bleeding. The classic pattern is petechiae, purpura, easy bruising, epistaxis, gingival bleeding, prolonged menstrual bleeding, hematuria, or melena. Petechiae are pinpoint, nonblanching red-purple spots caused by blood leaking from small vessels into the skin. Purpura and ecchymoses are larger areas of the same process. Their presence supports a platelet problem, but the nurse must still determine whether bleeding is stable and superficial or progressing toward major hemorrhage. Immune thrombocytopenia (ITP) is an acquired autoimmune disorder. IgG autoantibodies bind platelet surface glycoproteins, especially GPIIb/IIIa and GPIb/IX. Splenic macrophages then recognize and remove the antibody-coated platelets. Autoimmunity can also impair megakaryocytes, reducing platelet production in the marrow. This dual mechanism explains an important treatment principle: thrombopoietin receptor agonists can help even though ITP is primarily a platelet-destruction disorder. They stimulate remaining megakaryocytes to produce more platelets, helping production outpace immune-mediated clearance. Primary ITP is defined as a platelet count below 100 ×...