Chapter 23: Alterations of Hematologic Function

Anemia, characterized by insufficient red blood cell count or hemoglobin concentration, encompasses multiple classification systems based on etiology, cell size, and hemoglobin content. Macrocytic anemias result from vitamin B12 deficiency due to intrinsic factor loss or folate depletion, producing enlarged fragile cells alongside neurologic and gastrointestinal manifestations. Microcytic hypochromic anemias include iron-deficiency states from hemorrhage or nutritional inadequacy, sideroblastic anemia involving defective heme synthesis with mitochondrial iron accumulation, and thalassemias reflecting globin chain synthesis defects. Normocytic normochromic anemias encompass bone marrow failure conditions, acute blood loss, hemolytic processes from autoimmune mechanisms or hereditary membrane abnormalities like spherocytosis and sickle cell disease, plus chronic disease-related anemia. Polycythemia conditions feature excessive erythrocyte production; primary polycythemia vera arises as a clonal myeloproliferative disorder with thrombotic complications, while secondary forms develop from tissue hypoxia or pathologic erythropoietin production. Leukocyte disorders include quantitative abnormalities such as infection-related leukocytosis and neutropenia-induced immunosuppression, as well as qualitative dysfunctions. Leukemias represent malignant hematopoietic transformations classified by lineage and developmental stage, with distinct genetic markers such as the Philadelphia chromosome in chronic myeloid leukemia. Lymphoid neoplasms encompass Hodgkin lymphoma characterized by Reed-Sternberg cells and non-Hodgkin lymphomas arising from B, T, or natural killer cell populations, alongside plasma cell dyscrasias like multiple myeloma producing monoclonal immunoglobulin and osteolytic bone damage. Platelet and coagulation disorders span quantitative thrombocytopenia from immune destruction or production failure, qualitative aggregation defects, and inherited or acquired coagulation factor deficiencies including hemophilias, von Willebrand disease, and disseminated intravascular coagulation representing pathologic systemic fibrin deposition and consumption.