ABIM Hematology key terms

A normocytic or mildly microcytic anemia driven by inflammatory cytokines that raise hepcidin, trapping iron in macrophages and reducing erythropoietin response. Ferritin is typically normal or high despite low serum iron.

A liver-derived peptide hormone that degrades ferroportin, blocking intestinal iron absorption and macrophage iron release. It rises with inflammation and iron overload and falls with iron deficiency and hypoxia.

Patterns of serum iron, total iron-binding capacity, transferrin saturation, and ferritin used to distinguish iron deficiency (low ferritin, low saturation) from inflammation and overload, with soluble transferrin receptor helping when ferritin is ambiguous.

A corrected reticulocyte percentage that adjusts for anemia severity and, when prolonged, for marrow shift time. It estimates whether the marrow response to anemia is adequate or blunted.

A stepwise evaluation using reticulocyte count, lactate dehydrogenase, haptoglobin, indirect bilirubin, and direct antiglobulin testing to confirm red cell destruction and classify it as immune or non-immune.

A test that detects antibody or complement coating red cells. A positive result supports immune hemolysis, with the pattern of IgG and complement helping separate warm, cold, and drug-related causes.

An IgG-mediated hemolysis with positive IgG direct antiglobulin test, active at body temperature. First-line therapy is glucocorticoids, with rituximab used for relapse or steroid dependence.

A complement-mediated hemolysis caused by IgM antibodies that bind red cells in cool peripheral blood. It is often clonal and treated with avoidance of cold, rituximab, or complement inhibition.

An X-linked enzyme deficiency that impairs protection from oxidative stress, causing episodic hemolysis after infection, certain drugs, or fava beans. Diagnosis is confirmed by enzyme assay, ideally when not acutely hemolyzing.

A clonal stem cell disorder lacking glycosylphosphatidylinositol anchors, leaving red cells vulnerable to complement. It causes intravascular hemolysis, thrombosis, and cytopenias and is treated with complement inhibitors.

A technique using surface and intracellular markers to identify cell lineages, clonality, and abnormal populations. It is central to diagnosing leukemia, lymphoma, paroxysmal nocturnal hemoglobinuria, and minimal residual disease.

Red cell fragmentation from small-vessel thrombosis or shear stress, producing schistocytes, elevated lactate dehydrogenase, and low haptoglobin. Causes include thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, and disseminated intravascular coagulation.

A metalloprotease that cleaves von Willebrand factor multimers. Severe deficiency allows platelet-rich microthrombi and defines thrombotic thrombocytopenic purpura, which is treated urgently with plasma exchange.

An urgent assessment combining complete blood count with smear review, lactate dehydrogenase, haptoglobin, creatinine, coagulation studies, and ADAMTS13 activity to separate thrombotic thrombocytopenic purpura from other microangiopathies.

A hemoglobinopathy caused by hemoglobin S that polymerizes on deoxygenation, producing vaso-occlusion, hemolysis, and organ damage. Care includes hydroxyurea, vaccination, and prompt treatment of acute complications.

A separation technique that quantifies hemoglobin variants and is used to diagnose thalassemia and hemoglobinopathies. High-performance liquid chromatography is a common alternative method.

Grouping of inherited globin-chain synthesis defects by the affected chain and severity. Beta thalassemia major requires chronic transfusion, while trait states are microcytic with normal or near-normal hemoglobin.

A sickle cell complication of fever, respiratory symptoms, and a new pulmonary infiltrate, often with hypoxemia. It requires antibiotics, oxygen, hydration, and often simple or exchange transfusion.

Removal of patient red cells with replacement by donor units to rapidly lower the fraction of abnormal hemoglobin. It is used for severe sickle complications, including acute chest syndrome and stroke.

Bedside and laboratory assessment of fever, chills, dyspnea, urticaria, or hypotension during transfusion. It distinguishes hemolytic, febrile, allergic, and circulatory overload reactions and guides immediate stopping of the transfusion.

Evidence-based thresholds and clinical triggers for red cell, platelet, plasma, and cryoprecipitate transfusion. Restrictive strategies reduce exposure, and single-unit red cell dosing is preferred in stable patients.

An inadequate platelet count increment after transfusion, commonly from alloimmunization to HLA antigens. Management includes HLA-matched or crossmatched platelets and treating non-immune causes such as sepsis or splenomegaly.

Laboratory identification of human leukocyte antigens used to select compatible platelets, assess transplant donor compatibility, and interpret drug hypersensitivity associations. High-resolution typing improves matching for alloimmunized patients.

Replacement or rescue of marrow function with donor or autologous stem cells after conditioning. Key issues include graft source, engraftment, graft-versus-host disease, and infection prophylaxis.

Donor immune cells attacking recipient tissues, typically skin, gut, and liver. Acute and chronic forms differ in timing and features and are managed with immunosuppression while preserving graft-versus-tumor effect.

Infections and toxicities arising from weakened immunity after transplant or therapy. Prevention includes prophylaxis, vaccination, and monitoring for opportunistic organisms and secondary malignancies.

Rapid evaluation and empiric broad-spectrum antibiotics for fever in a patient with severe neutropenia. Risk stratification, cultures, and antifungal escalation guide care.

Use of clinical scores and disease factors to decide between inpatient intravenous therapy and outpatient oral therapy for febrile neutropenia. It also guides duration and antifungal prophylaxis.

A myeloproliferative neoplasm defined by BCR-ABL1 fusion, causing marked granulocytosis and splenomegaly. Tyrosine kinase inhibitors achieve durable remissions, monitored by quantitative transcript levels.

Serial quantitative polymerase chain reaction measurement of BCR-ABL1 transcript levels to track response and detect loss of response in chronic myeloid leukemia. Rising levels prompt resistance testing and therapy change.

Clonal marrow disorders with overproduction of one or more lineages, often with splenomegaly and thrombosis risk. Driver mutations such as JAK2, CALR, and MPL help classify polycythemia vera, essential thrombocythemia, and myelofibrosis.

Use of karyotype and molecular abnormalities to assign prognosis and guide therapy in myeloid and lymphoid cancers. Risk groups influence transplant decisions and intensity of treatment.

Low-level cancer cells detectable by sensitive methods such as flow cytometry or sequencing after treatment. Its presence predicts relapse and guides decisions in leukemia and other hematologic malignancies.

Clonal plasma cell disease with myeloma-defining events such as hypercalcemia, renal insufficiency, anemia, bone lesions, or high-risk biomarkers. Treatment combines proteasome inhibitors, immunomodulators, and steroids.

Assessment of serum and urine protein electrophoresis with immunofixation, free light chains, and bone marrow to distinguish benign monoclonal gammopathy from myeloma and related disorders.

Volume repletion, bisphosphonates or denosumab, and treatment of the underlying cause for malignancy-associated hypercalcemia. Calcitonin provides rapid but transient control.

Proactive hydration, urate-lowering therapy, and electrolyte monitoring in patients at risk of rapid tumor breakdown. It prevents hyperkalemia, hyperphosphatemia, hyperuricemia, and acute kidney injury.

Cancer-associated hypercoagulability that increases risk of deep vein thrombosis and pulmonary embolism. Anticoagulation choice depends on bleeding risk, drug interactions, and renal function.

An immune reaction to heparin causing platelet activation, thrombocytopenia, and thrombosis. Management requires stopping heparin and starting a non-heparin anticoagulant.

Selection, dosing, and monitoring of anticoagulants with attention to renal function, bleeding risk, and reversal. It includes perioperative planning and recognition of drug interactions.

A collaborative process in which clinicians and patients weigh benefits, harms, and personal goals, especially for transplant, intensive chemotherapy, and goals-of-care discussions.

Eliciting patient values and preferences to align treatment intensity with what matters most. It supports advance care planning and timely transitions to comfort-focused care.

A structured, empathic conversation delivering serious diagnoses or prognoses while checking understanding and responding to emotion. It preserves trust and supports subsequent decision-making.

Confirming that a patient understands a proposed treatment, its alternatives, and its risks, and can reason about the decision. When capacity is impaired, surrogate decision-making and advance directives guide care.

Identifying and reducing disparities in access, diagnosis, and outcomes across populations, such as differences in sickle cell care, transplant referral, and clinical trial enrollment.

Structured handoffs and multidisciplinary teamwork across inpatient, outpatient, and home settings. It reduces errors, prevents readmissions, and supports safe medication and anticoagulation management.

Systematic use of data, process measures, and plan-do-study-act cycles to improve outcomes such as transfusion safety, time to antibiotics in neutropenic fever, and anticoagulation reliability.

Documenting errors and near misses to identify system failures and drive prevention. It complements root cause analysis and supports a culture of transparency and learning.

Critically assessing study design, bias, and applicability to decide whether new evidence should change practice. It supports lifelong learning and incorporation of guidelines into patient care.