AIM Step 10
3rd Year MBBS
Blood & Immunology
3rd Year MBBS
Blood & Immunology
Student Memory Support
Lymphoid Neoplasms, Lymphomas and Plasma Cell Disorders
High-yield memory reinforcement for rapid KMU examination revision.
1. High-Yield Flashcards
Tap each question to reveal the answer.
What is the basic WHO principle for classifying lymphoid neoplasms?
Cell lineage and stage of differentiation, supported by morphology, immunophenotype and genetics.
What is the central pathogenic defect in acute lymphoblastic leukemia?
Impaired lymphoid differentiation with increased survival and proliferation of lymphoblasts.
Why do anemia and thrombocytopenia develop in ALL?
Expanding lymphoblasts replace normal bone marrow and suppress normal hematopoiesis.
Which marker supports an immature lymphoid precursor phenotype in ALL?
Terminal deoxynucleotidyl transferase, or TdT.
Which morphological finding favors AML rather than ALL?
Auer rods, which are needle-shaped cytoplasmic inclusions of myeloid blasts.
What is the basic pathogenic pattern in CLL?
Abnormal survival and gradual accumulation of a clonal population of mature B lymphocytes.
What produces smudge cells in chronic lymphocytic leukemia?
Fragile neoplastic lymphocytes rupture during peripheral blood smear preparation.
Which immunophenotypic pattern strongly supports CLL?
B-cell markers with co-expression of CD5 and CD23, with relatively weak CD20 and surface immunoglobulin.
What is the fundamental neoplastic cell in multiple myeloma?
A clonal plasma cell producing a monoclonal immunoglobulin or immunoglobulin component.
Why does multiple myeloma cause destructive bone lesions?
The malignant plasma-cell clone promotes osteoclast activity while normal bone formation is suppressed.
Which morphological features characterize a typical plasma cell?
Eccentric nucleus, clock-face chromatin, basophilic cytoplasm and a pale perinuclear hof.
What causes rouleaux formation in multiple myeloma?
Increased circulating proteins reduce repulsive forces between red cells, causing coin-like stacking.
What is the characteristic malignant cell of classical Hodgkin lymphoma?
The Reed-Sternberg cell, typically expressing CD30 and commonly CD15.
Which Hodgkin lymphoma subtype shows broad collagen bands and lacunar cells?
Nodular sclerosis classical Hodgkin lymphoma.
Which three molecular associations help distinguish follicular, mantle cell and Burkitt lymphoma?
Follicular → BCL2; mantle cell → cyclin D1; Burkitt → MYC.
What combination forms the basis of modern lymphoma diagnosis?
Tissue architecture, cell morphology, immunophenotype and selected genetic studies.
2. Mnemonics
Mnemonic Title: Multiple Myeloma Major Clinical Effects
Mnemonic Word: CRAB
Meaning: Calcium elevation, Renal impairment, Anemia, Bone destruction.
Mnemonic Title: Classical Hodgkin Lymphoma Subtypes
Mnemonic Word: NMLL
Meaning: Nodular sclerosis, Mixed cellularity, Lymphocyte-rich, Lymphocyte-depleted.
Mnemonic Title: Important Infection–Lymphoma Links
Mnemonic Word: E-H-H-H
Meaning: EBV → Burkitt/extranodal NK-T; H. pylori → gastric MALT; HTLV-1 → adult T-cell leukemia/lymphoma; HHV-8 → primary effusion lymphoma.
3. Memory Tables
ALL vs CLL
| Feature | ALL | CLL |
|---|---|---|
| Cell | Immature lymphoblast | Mature clonal B lymphocyte |
| Core mechanism | Blocked differentiation with blast expansion | Abnormal survival and accumulation |
| Morphology | High N:C ratio, scant cytoplasm | Small cells, clumped chromatin |
| Useful clue | TdT-positive precursor phenotype | CD5/CD23-positive B-cell phenotype |
| Important effect | Marrow failure | Impaired humoral immunity |
Hodgkin vs Non-Hodgkin Lymphoma
| Feature | Hodgkin Lymphoma | Non-Hodgkin Lymphoma |
|---|---|---|
| Tumor cell | Reed-Sternberg cell in classical disease | Varies with lymphoma subtype |
| Background | Prominent reactive inflammatory cells | Often neoplastic lymphoid population dominates |
| Spread | Relatively orderly between adjacent nodes | May be less predictable |
| Classification | Classical subtypes + NLPHL | Multiple precursor, B-cell, T-cell and NK-cell entities |
4. Rapid Revision Points — Last-Minute Revision
Must Remember:
- Lymphoid tumors are classified by lineage and maturation stage, not simply by the site of enlargement.
- ALL is a precursor-cell neoplasm; accumulation of blasts suppresses normal bone-marrow function.
- T-ALL may involve the thymus and therefore may present with a mediastinal mass.
- CLL cells are mature-appearing but function poorly, explaining recurrent infections despite lymphocytosis.
- Deletion involving 17p affects the TP53 pathway and may indicate aggressive CLL biology.
- Myeloma bone destruction links bone pain, pathological fractures and hypercalcemia to one pathological process.
- Free monoclonal light chains may damage the kidneys and may appear in urine as Bence Jones proteins.
- Classical Hodgkin lymphoma contains relatively few malignant cells within a much larger reactive inflammatory background.
- Nodular sclerosis Hodgkin lymphoma is identified by collagen bands and lacunar-type tumor cells.
- Lymphoma diagnosis integrates tissue architecture, morphology, immunophenotyping and relevant genetic testing.
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KMU Exam Trap: A characteristic smear or cell finding may strongly suggest a diagnosis, but morphology alone does not reliably classify every lymphoid neoplasm.
5. Clinical Memory Hooks
Child with pallor + bruising + circulating blasts
→
Think marrow replacement by lymphoblasts in ALL.
→
Think marrow replacement by lymphoblasts in ALL.
Older patient + persistent lymphocytosis + recurrent infections
→
Think dysfunctional mature B-cell accumulation in CLL.
→
Think dysfunctional mature B-cell accumulation in CLL.
Bone pain + anemia + renal impairment + hypercalcemia
→
Connect the findings to clonal plasma-cell myeloma.
→
Connect the findings to clonal plasma-cell myeloma.
Painless lymphadenopathy + Reed-Sternberg-type cells in inflammatory background
→
Think classical Hodgkin lymphoma and confirm with the tissue pattern and immunophenotype.
→
Think classical Hodgkin lymphoma and confirm with the tissue pattern and immunophenotype.
6. Starred High-Yield Exam Points
- ⭐ TdT supports an immature lymphoid precursor phenotype in ALL.
- ⭐ CLL characteristically combines a mature B-cell phenotype with CD5 and CD23 expression.
- ⭐ Multiple myeloma: monoclonal plasma cells → bone destruction, anemia, renal injury and hypercalcemia.
- ⭐ Classical Reed-Sternberg cells characteristically express CD30 and commonly CD15.
- ⭐ Follicular lymphoma → t(14;18) → increased BCL2-mediated cell survival.
- ⭐ Mantle cell lymphoma → t(11;14) → cyclin D1 overexpression.
- ⭐ Burkitt lymphoma → MYC dysregulation → very rapid proliferation and starry-sky morphology.