3rd Year MBBS
Blood & Immunology
Lymphoid Neoplasms, Lymphomas and Plasma Cell Disorders
Connect the cell of origin, mechanism, morphology, clinical presentation and diagnostic clues for rapid revision.
1. THE TOPIC IN ONE CONNECTED FLOW
Lymphoid neoplasms arise when a precursor lymphocyte, mature lymphocyte or plasma cell develops genetic abnormalities that allow abnormal survival or proliferation. The resulting clone retains features of its normal cellular counterpart, so the cell of origin helps explain whether the disease appears as ALL, CLL, lymphoma or plasma-cell myeloma and guides its pathological diagnosis.
Mature B/T/NK cell
Plasma cell
Immature lymphoid precursor → blocked maturation and blast accumulation → ALL;
mature dysfunctional B cell → prolonged survival and gradual accumulation → CLL/SLL;
terminally differentiated B cell → clonal plasma cells and monoclonal protein → multiple myeloma;
lymphoid clone within tissue → altered nodal architecture → Hodgkin or non-Hodgkin lymphoma.
2. KEY CLINICAL CONNECTIONS
ALL: lymphoid precursor abnormality
→ lymphoblast accumulation
→ marrow replacement
→ anemia, thrombocytopenia and infection.
CLL: prolonged survival of mature B cells
→ persistent clonal accumulation
→ lymphocytosis, lymph-node involvement and impaired humoral immunity.
Clonal plasma cells
→ monoclonal immunoglobulin/light-chain production
→ renal injury and reduced normal antibody function.
Marrow infiltration + increased osteoclastic bone destruction
→ anemia + bone pain/fractures + hypercalcemia.
Reed-Sternberg cells in a reactive inflammatory background
→ consider classical Hodgkin lymphoma.
Monomorphic lymphoid population with nodular or diffuse architectural effacement
→ consider non-Hodgkin lymphoma
→ confirm lineage with immunophenotyping and selected genetic testing.
3. AIM HIGH-YIELD INTEGRATION REVIEW
→ precursor B/T, mature B, mature T/NK, Hodgkin and plasma-cell neoplasms
→ morphology and immunophenotype identify the individual entity.
→ lymphoblast accumulation
→ marrow failure; TdT supports precursor phenotype, while B- or T-cell markers establish lineage.
→ small lymphocytes in blood/tissue
→ impaired effective antibody function; tissue involvement may show proliferation centers.
→ monoclonal protein + marrow involvement + altered bone remodeling
→ renal impairment, anemia, recurrent infection, bone destruction and hypercalcemia.
→ cytokine-mediated recruitment of reactive inflammatory cells
→ characteristic tissue background and relatively orderly spread between adjacent lymph-node groups.
mantle cell lymphoma → cyclin D1-driven cell cycling;
Burkitt lymphoma → MYC-driven proliferation.
HTLV-1 → adult T-cell leukemia/lymphoma;
EBV → Burkitt and extranodal NK/T-cell lymphoma;
HHV-8 → primary effusion lymphoma.