Abnormalities of White Blood Cells

Study Notes

White blood cell abnormalities are characterized by reactive changes in granulocytes and lymphocytes, as well as neoplastic changes.
Leukocyte, platelet, and red blood cell production originate from hematopoietic stem cells and colony-forming units.
Common malignancies affect lymphocyte precursors, more mature lymphocytes, and chronic leukemias.
Methods to identify hematopoietic cells rely on cell surface antigens.
Immunoglobulin production and multiple myeloma development are also critical aspects of this topic.

Reactive changes in granulocytes and lymph node morphology are contrasted with neoplastic alterations.
Leukocyte, platelet, and red blood cell production processes using hematopoietic stem cells and colony-forming units are reviewed.
Common malignancies affecting lymphocyte precursors, more mature lymphocytes, and chronic leukemias are identified.
Identifying methods for hematopoietic cell (surface antigen) identification are detailed.
Immunoglobulin production and multiple myeloma development are examined.

Hematopoietic stem cells differentiate into multipotent progenitors.
These progenitors further differentiate into early progenitors with either lymphoid or myeloid potential, leading to various mature blood cell types.
Lymphopoiesis, the development of lymphocytes, is detailed.
Myelopoiesis, the development of myeloid cells, is illustrated, showing different types of granulocytes and monocytes.

Various monoclonal antibodies (with associated designations like CD1, CD3, CD4, CD8, and others) target specific antigens and are used to identify different types of white blood cells or precursors.
Information on normal cellular distribution is provided using these markers associated with various cells and blood cell lineages.

Increased leukocytes (leukophilia) are often associated with inflammation, infection, TNF, IL-1, and decreased margination/extravasation of granulocytes.
Reduced leukocytes (leukopenia) are often linked to auto-immune diseases, drug toxicity, bone marrow diseases, ineffective erythropoiesis, and overwhelming viral infections like HIV.

Structure of the lymph node is examined, including the secondary and primary lymphoid follicles, paracortex, medullary cords, sinuses, and lymphatic vessels.

Various lymphoma types are categorized based on precursor B or T cells and other factors, including specific examples like B-cell acute lymphoblastic leukemia (B-ALL), different subtypes of chronic lymphocytic leukemia or lymphoma, and various T-cell pathologies.

Genetic mutations regulating cell differentiation (stem cell conversion), proliferation (MCY, RAS), and apoptosis prevention are key aspects of hematological malignancies.

Acute lymphoblastic leukemia (ALL) is often the most prevalent early childhood malignancy, typically presenting with symptoms like bleeding, infections, and organ involvement.
Chronic lymphocytic leukemia emphasizes the importance of chromosomal abnormalities as a crucial factor.
Lymphoma types (e.g., chronic lymphocytic leukemia, follicular lymphoma, diffuse large B-cell lymphoma) are described.

Morphology and immunophenotyping data are included, particularly related to CD22, CD19, and CD10 positive cells.

The different types of B-cell (e.g., follicular, diffuse large B-cell, mantle cell, Burkitt's) and T-cell malignancies are catalogued (e.g. large cell lymphoma, Mycosis Fungoides, Sezary syndrome, NK cell leukemia).

Distinct subtypes like nodular sclerosis, mixed cellularity, lymphocyte-rich, lymphocyte depletion, and lymphocyte predominance are identified based notably on the presence of Reed-Sternberg cells.

Immunoglobulin class (IgG, IgM, IgA, IgD, IgE) and subclasses (IgG1-4), levels, presence in secretions, activation and transfer properties are details. This also includes their structural complexity and function.

AML involves chromosomal aberrations, specifically those impacting differentiating genes and epigenetic modifications. Myelodysplasia, characterized by maturation defects and ineffective erythropoiesis, and the role of chromosomal defects, transcription factor issues, and p53 loss are detailed.