ABPath Hematopathology key terms

Automated measurement of red cell, white cell, and platelet counts with indices and a leukocyte differential. Abnormal counts or indices prompt smear review and further testing.

Microscopic examination of a stained blood film to assess cell morphology, lineage distribution, platelet adequacy, and blood parasites. It confirms and explains abnormalities flagged by automated counts.

Paired procedure that obtains liquid marrow for cytology, flow cytometry, and genetic testing plus a core sample for architecture and cellularity. Used to evaluate cytopenias, neoplasms, and staging.

Laser-based method that measures surface or intracellular antigens on individual cells. Hematopathologists use it to immunophenotype leukemias and lymphomas, count blasts, and detect clonal populations.

Microscopic analysis of metaphase chromosomes from dividing cells to detect numeric and structural abnormalities. It provides prognostic information in acute leukemias, myelodysplastic syndromes, and multiple myeloma.

Multipotent bone marrow cell with self-renewal capacity that gives rise to all blood lineages. Its clonal transformation or failure underlies leukemia, marrow failure, and transplant strategies.

Regulated differentiation of stem cells into erythroid progenitors and mature red cells, driven mainly by erythropoietin. Ineffective erythropoiesis produces anemia with low reticulocyte counts despite marrow expansion.

Production of blood cells outside the bone marrow, usually in liver or spleen, when marrow fails or is infiltrated. It causes organomegaly and can partially compensate chronic anemia.

Reduction in hemoglobin concentration or red cell mass below age- and sex-specific reference limits. Symptoms include fatigue and pallor; classification uses MCV, reticulocyte count, and clinical context.

Anemia with mean corpuscular volume below the reference range, usually from iron deficiency, thalassemia, anemia of chronic disease, or sideroblastic defects. Iron studies and hemoglobin analysis identify the cause.

Panel of serum ferritin, iron, total iron-binding capacity, and transferrin saturation. It distinguishes iron deficiency from anemia of chronic disease and helps evaluate microcytic or unexplained anemia.

Anemia caused by premature red cell destruction, with reticulocytosis, indirect hyperbilirubinemia, and low haptoglobin. Causes include membrane defects, hemoglobinopathies, enzymes, antibodies, and microangiopathy.

Red cell destruction within blood vessels, releasing free hemoglobin and lactate dehydrogenase. It causes hemoglobinuria, haptoglobin depletion, and sometimes thrombosis, as seen in TTP or DIC.

Inherited hemoglobinopathy in which deoxygenated hemoglobin S polymerizes, stiffening red cells. This produces vaso-occlusion, painful crises, chronic hemolysis, and organ damage; diagnosis uses hemoglobin analysis.

Inherited disorders of reduced globin chain synthesis causing imbalanced hemoglobin production, microcytic anemia, and ineffective erythropoiesis. Severity ranges from trait to transfusion-dependent major disease.

Clonal bone marrow disorder marked by dysplasia, ineffective hematopoiesis, cytopenias, and increased risk of acute myeloid leukemia. Diagnosis combines morphology, blast percentage, cytogenetics, and molecular findings.

Neoplasm of myeloid blasts involving marrow or blood, typically with at least twenty percent blasts. Immunophenotype, cytogenetics, and molecular markers define subtypes and guide therapy.

Needle-shaped azurophilic cytoplasmic inclusion found in myeloid blasts, formed from fused primary granules. It supports a diagnosis of acute myeloid leukemia and is not seen in lymphoblasts.

Clonal stem cell disorders with overproduction of mature red cells, granulocytes, or platelets. Examples include polycythemia vera, essential thrombocythemia, primary myelofibrosis, and chronic myeloid leukemia; thrombosis and fibrosis are major risks.

Myeloproliferative neoplasm driven by BCR-ABL1 fusion. Blood shows marked granulocytosis with left shift and basophilia; tyrosine kinase inhibitors control the disease and require molecular monitoring.

Clonal proliferation of small mature B lymphocytes, usually CD5-positive and CD23-positive with dim surface immunoglobulin. It often presents as asymptomatic lymphocytosis and may require therapy for progression or cytopenias.

Neoplasm of lymphoid blasts in marrow and blood, most common in children. Immunophenotype, cytogenetics, and minimal residual disease testing determine risk and treatment.

B-cell lymphoma characterized by Reed-Sternberg cells in an inflammatory background. It usually involves lymph nodes, spreads contiguously, and is classified as classic or nodular lymphocyte-predominant types.

Large neoplastic cell with binucleation or multilobation and prominent nucleoli, often with a perinucleolar halo. It is the diagnostic hallmark of classic Hodgkin lymphoma and derives from germinal-center B cells.

Plasma cell neoplasm causing lytic bone lesions, anemia, renal insufficiency, and hypercalcemia. Marrow shows clonal plasma cells, and serum or urine monoclonal protein is usually present.

Simultaneous reduction of red cells, white cells, and platelets in blood. Causes include marrow failure, infiltration, chemotherapy, megaloblastic disease, and peripheral destruction; marrow examination is often needed.

Replacement of bone marrow space by fibrosis, tumor, or granulomatous disease, impairing blood cell production. It causes cytopenias, teardrop red cells, and often a dry marrow aspirate.

Platelet count below the reference limit, usually less than 150,000 per microliter. It results from decreased production, immune destruction, consumption, or sequestration and increases bleeding risk when severe.

Autoimmune disorder in which antibodies destroy platelets, producing isolated thrombocytopenia without another apparent cause. Treatment includes observation, corticosteroids, intravenous immunoglobulin, or thrombopoietin receptor agonists.

Thrombotic microangiopathy from severe ADAMTS13 deficiency, causing platelet-rich microthrombi, microangiopathic hemolysis, thrombocytopenia, and organ ischemia. Plasma exchange is urgent and life-saving.

Immune reaction to heparin-platelet factor 4 complexes that activates platelets, causing thrombocytopenia and paradoxical thrombosis. Heparin must stop, and a non-heparin anticoagulant is started.

Clotting assay that measures the extrinsic and common coagulation pathways after tissue factor addition. It is prolonged in warfarin therapy, liver disease, vitamin K deficiency, and disseminated intravascular coagulation.

Clotting assay that measures the intrinsic and common pathways. It screens for hemophilia, monitors unfractionated heparin, and may be prolonged by lupus anticoagulant or factor inhibitors.

Patient plasma is mixed with normal plasma and the prolonged clotting time is repeated. Correction indicates factor deficiency; failure to correct suggests an inhibitor such as lupus anticoagulant or a specific factor antibody.

Fibrin degradation product released when cross-linked fibrin is broken down. It is sensitive for thrombosis and disseminated intravascular coagulation but nonspecific because inflammation, surgery, and pregnancy also raise it.

Systemic activation of coagulation consumes platelets and clotting factors, causing bleeding and thrombosis. Laboratory findings include prolonged PT and aPTT, low fibrinogen, thrombocytopenia, and elevated D-dimer.

Inherited or acquired deficiency or dysfunction of von Willebrand factor, which impairs platelet adhesion and stabilizes factor VIII. It causes mucocutaneous bleeding and is diagnosed with von Willebrand factor antigen and activity tests.

Pretransfusion testing that determines ABO and Rh type and screens serum for unexpected antibodies. A negative screen permits rapid crossmatching when blood is urgently needed.

Adverse response to blood component transfusion, including acute hemolytic, febrile nonhemolytic, allergic, septic, and pulmonary reactions. Management begins by stopping the transfusion and evaluating the patient.

Prompt, documented communication of laboratory results that may be life-threatening, such as severe thrombocytopenia, marked leukocytosis, or circulating blasts. It supports immediate clinical action and patient safety.