ASCP SH key terms

A self-renewing bone marrow cell that can divide to produce more stem cells or commit to any blood lineage. Its descendants mature along myeloid or lymphoid pathways under the influence of cytokines and the marrow microenvironment.

A glycoprotein hormone made mainly by peritubular kidney cells in response to tissue hypoxia. It drives erythroid progenitors to survive, proliferate, and mature, and its level rises when hemoglobin falls.

An immature red cell that has extruded its nucleus but still contains residual ribosomal RNA. Supravital stains such as new methylene blue make the RNA visible as a mesh, and a raised count signals increased marrow output.

A reticulocyte percentage adjusted for anemia severity by multiplying the raw percentage by the patient hematocrit divided by a normal hematocrit, roughly 45 percent. It better estimates whether the marrow response is adequate.

An intermediate of red cell glycolysis that binds deoxyhemoglobin and stabilizes the tense state, lowering oxygen affinity so more oxygen is released to tissues. Its concentration rises in chronic hypoxia and anemia.

Calculated values derived from the red cell count, hemoglobin, and hematocrit: mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration. They classify anemia as microcytic, normocytic, or macrocytic and direct further testing.

A small peptide hormone from the liver that blocks iron export from enterocytes and macrophages by degrading ferroportin. Inflammation raises hepcidin, restricting iron delivery to erythroid precursors and contributing to anemia of chronic inflammation.

Anemia with a mean corpuscular volume below about 80 femtoliters, usually reflecting defective hemoglobin synthesis. Common causes are iron deficiency, thalassemia, anemia of chronic inflammation, and less often lead poisoning or sideroblastic defects.

A ratio of mean corpuscular volume to red cell count used to separate thalassemia trait from iron deficiency. Values under about 13 favor thalassemia; higher values favor iron deficiency.

A microcytic anemia from depleted iron stores, most often from chronic blood loss. Low ferritin with high iron-binding capacity and low transferrin saturation confirm it; marrow iron is absent and platelets are often increased.

A macrocytic anemia caused by impaired DNA synthesis, typically from vitamin B12 or folate deficiency. Marrow shows nuclear-cytoplasmic asynchrony and blood shows hypersegmented neutrophils; B12 deficiency may also cause neurologic damage.

An inherited membrane protein defect, often in spectrin, ankyrin, or band 3, that makes red cells spherical and fragile. Cells are trapped in the spleen, producing hemolysis, splenomegaly, and increased osmotic fragility.

An inherited hemoglobinopathy in which a glutamic acid to valine substitution at position six of beta globin produces hemoglobin S. Deoxygenated hemoglobin S polymerizes, deforming cells into sickle shapes that cause hemolysis and vaso-occlusion.

A technique that separates hemoglobin variants by charge on cellulose acetate or agarose gel, often with an alkaline and an acid run used together. It detects and quantifies hemoglobins S, C, E, F, and A2.

An X-linked enzyme deficiency that leaves red cells unable to regenerate NADPH, so they cannot withstand oxidative stress. Certain drugs, fava beans, or infection trigger intravascular hemolysis with bite cells and Heinz bodies.

A group of inherited disorders with reduced or absent synthesis of alpha or beta globin chains, causing imbalance and precipitation of the unaffected chain. The result is ineffective erythropoiesis, microcytosis disproportionate to anemia, and variable hemolysis.

A clonal stem cell disorder with loss of glycosylphosphatidylinositol-anchored proteins, including CD55 and CD59, that normally protect cells from complement. Red cells are lysed by complement, causing hemoglobinuria, thrombosis, and marrow failure.

Marrow failure with hypocellularity and pancytopenia in the absence of infiltration or fibrosis. Most cases are immune-mediated against stem cells, and patients present with anemia, bleeding, and infection.

A neoplasm of clonal plasma cells that fills the marrow and usually secretes a monoclonal immunoglobulin. Features include lytic bone lesions, renal failure, hypercalcemia, anemia, and rouleaux formation on the blood film.

A clonal stem cell disorder producing ineffective hematopoiesis, cytopenias, and dysplastic morphology in one or more lineages. Blasts are increased but remain under twenty percent, and the risk of progression to acute leukemia is substantial.

The product of the Philadelphia chromosome translocation, t(9;22), which creates a constitutively active tyrosine kinase driving chronic myeloid leukemia. Detection by PCR or FISH confirms the diagnosis and monitors response to tyrosine kinase inhibitors.

A myeloid leukemia with t(15;17) fusing PML and RARA, blocking differentiation at the promyelocyte stage. It carries a high risk of disseminated intravascular coagulation and responds to all-trans retinoic acid and arsenic trioxide.

A method that labels cells with fluorescent antibodies against surface or intracellular markers and measures them one cell at a time. It establishes lineage, maturation stage, and clonality in leukemia and lymphoma.

The presence of increased band neutrophils and less mature granulocytes in peripheral blood, reflecting a marrow response to infection, inflammation, or marrow stress. Extreme forms containing blasts are called a leukemoid reaction.

Complementary marrow specimens: an aspirate provides liquid particles for morphology, flow cytometry, and cytogenetics, while a core biopsy preserves architecture and cellularity. Both are needed to judge cellularity, infiltration, and fibrosis.

The initial response to vessel injury in which platelets adhere to exposed collagen through von Willebrand factor, become activated, and aggregate into a plug. It is assessed by platelet count and platelet function tests.

A large multimeric plasma protein that mediates platelet adhesion to subendothelial collagen and also carries and stabilizes factor VIII. Deficiency causes mucocutaneous bleeding with prolonged bleeding time or closure time.

A clotting test that recalcifies citrated plasma with a surface activator and phospholipid, measuring the intrinsic and common pathways. It monitors unfractionated heparin and detects deficiencies of factors VIII, IX, XI, and XII.

The prothrombin time measures clot formation after adding tissue factor and calcium, testing the extrinsic and common pathways. The international normalized ratio standardizes results across reagent lots for warfarin monitoring.

A procedure in which patient plasma is combined with normal plasma and the prolonged clotting time is remeasured. Correction indicates a factor deficiency; failure to correct suggests an inhibitor such as a lupus anticoagulant or specific antibody.

A fragment released when cross-linked fibrin is degraded by plasmin, reflecting active coagulation and fibrinolysis. It is highly sensitive for venous thromboembolism but nonspecific, rising in infection, pregnancy, surgery, and malignancy.

An immune reaction in which antibodies against heparin-platelet factor 4 complexes activate platelets, causing thrombocytopenia and paradoxical thrombosis. It typically appears five to ten days after heparin exposure and requires stopping heparin.

An automated rule that compares a current result with the patient's previous value and flags differences exceeding a set limit. It catches specimen mix-ups, wrong labels, and true acute changes before results are reported.

A set of statistical quality control rules applied to plotted control values that decide whether an analytical run is accepted or rejected. Rules such as 1-3s and 2-2s balance error detection against false rejection.

The range containing the central ninety-five percent of values from a defined healthy population, usually estimated as the mean plus or minus two standard deviations. Results outside it are flagged but do not by themselves prove disease.

A method that counts and sizes cells by detecting changes in electrical resistance as they pass through a small aperture. The resulting volume histograms for red cells, white cells, and platelets generate flags for manual review.

The rate at which red cells fall in a vertical tube in one hour, increased by rouleaux-forming proteins such as fibrinogen and immunoglobulins. It is a nonspecific inflammation marker affected by anemia and red cell shape.