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Lymphoma Slide 1 Lymphoma Slide 2 Lymphoma Slide 3 Lymphoma Slide 4 Lymphoma Slide 5 Lymphoma Slide 6 Lymphoma Slide 7 Lymphoma Slide 8 Lymphoma Slide 9 Lymphoma Slide 10 Lymphoma Slide 11 Lymphoma Slide 12 Lymphoma Slide 13 Lymphoma Slide 14 Lymphoma Slide 15 Lymphoma Slide 16 Lymphoma Slide 17 Lymphoma Slide 18 Lymphoma Slide 19 Lymphoma Slide 20 Lymphoma Slide 21 Lymphoma Slide 22 Lymphoma Slide 23 Lymphoma Slide 24 Lymphoma Slide 25 Lymphoma Slide 26 Lymphoma Slide 27 Lymphoma Slide 28
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Lymphoma

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introduction and differentiation between different forms of lymphoma
Hodgkins vs Non- Hodgkin's

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Lymphoma

  1. 1. LYMPHOMA Dr. Saugat Chapagain
  2. 2. Conceptual classification • Lukemia – based on cell type – Acute/ chronic – Myeloid/ lymphoid • Lymphoma – malignant tumor of lymphoreticular tissues: – Hodgkin’s lymphoma/ disease – Non Hodgkin’s lymphoma
  3. 3. Categories of haematopoeitic & lymphoid neoplasia 1. Myeloid neoplasms – Of myeloid cell lineage – RBC, platelets, granulocytes and monocytes 2. Lymphoid neoplams: – Of lymphoid cell lineage – Lukemias and lymphomas of B,T or NK origin 3. Histiocytic neoplasms – Proliferation of histiocytes – E.g. langerhans cell histicytosis
  4. 4. Etiology • Heridity – identical twins, family history, genetic disorders • Infections – HTLV-I, EBV, HCV, HIV, etc. • Environmental factors – radiation, carcionogen, etc. • Association with disease of immunity
  5. 5. Pathogenesis • Genetic damage to single clone of target cells – Proliferation of transformed clone • Chromosomal translocations – Lukemias have translocation of Philadelphia (Ph) chromosome in 70-90% cases with CML (long arm of chromosome 22 to chromosome 9) • Maturition defect – In acute lukemia – AML – maturition defect beyond the myeloblast/ promyelocytic level – ALL – lymphoblast level
  6. 6. Pathogenesis (Cntd…) • Myelosuppression – Accumulation of leukemic cells  suppression of normal hematopoeitic stem cells • Organ infiltration – Cells proliferate primarily in the bone marrow  infiltrate other sites • Cytokines – Reed sternberg cells secrete cytokines  reactive inflammation (in HL/ HD)
  7. 7. Lab investigations 1. Peripheral Blood smear – RBC – WBC – Platelet 2. Bone marrow examination – Cellularity – Myeloid cells – Erythropoiesis – Megakaryocytes – Cytogenetics 3. Cytochemistry
  8. 8. Lymphoid neoplasms
  9. 9. Introduction • Lymphoid cells constitute immune system of the body • Differentiation and maturation occurs in lymphoid tissues • Neoplasm of cells  leukemia • Neoplasm of tissues  lymphoma • ALL, CLL, NHL, HD
  10. 10. WHO classification (1999) 1. Hodgkin’s disease 2. Precursor (immature) B- cell malignancies 3. Peripheral (mature) B-cell malignancies 4. Precursor (immature) T-cell malignancies 5. Peripheral (mature) T-cell malignancies 2 & 4 – Blastic type; e.g. ALL 3 & 5 – CLL and other lymphomas
  11. 11. General comments • Incidence – – NHL (62%); HD (8%); plasma cell disorders (15%); CLL (9%, most common lymphoid leukemia) & ALL (4%) • Diagnosis – – Lymph node biopsy – Blood picture – Bone marrow Biopsy • Staging – Ann Arbor • Ancillary studies – CT scan, PET scan & gallium scan • Immune abnormalities
  12. 12. Hodgkin’s disease
  13. 13. Introduction • Primarily arises within LN • Extranodal secondaries • Peak incidence – between 15-35 and after 50s • Male> female • Proliferation of lymphocytes, histiocytes, eosinophils • Diagonistic feature  presence of (Dorothy) Reed Sternberg cells
  14. 14. Reed Sternberg Cell • Diagonistic of Hodgkin’s lymphoma/ disease • Classic RS cell – – Large, with bilobed nucleus (mirror image) / miltilobed sometimes. – Each nuclear lobe contains eosinophilic granular halo (owl eye appearance) • Lacunar type – – Smaller with pericellular space (lacuna) d/t cell shrinkage – Usu. In Nodulo sclerotic HD • Polyploid (popcorn) type – – Larger size with popcorn like lobulated nucleus • Pleomorphic – – Pleomorphic and atypical nuclei.
  15. 15. Classification of HD Rye classification (1966) 1. Lymphocyte predominance type 2. Nodular sclerosis type 3. Mixed cellularity type 4. Lymphocyte depletion type WHO classification – Nodular lymphocyte predominant HD – Classic HD (includes all 4 types in rye classification)
  16. 16. Pathophysiology • Proliferation of tumor with only a small proportion of cells are malignant • Mostly normal lymphocytes • RS cells – multinucleated giant cell mutations of T- lymphocytes • Infiltration leads to LN necrosis and fibrosis
  17. 17. Clinical Features • Painless swelling in one of lymph nodes (usu. Cervical region) with a h/o URTI • Persistent fever, night sweats, fatigue, weight loss • Malaise, pruritis, extreme pain, nerve irritation • Absence of pulse d/t rapid enlargement of the LN • Neck vein engorgement • Enlargement of reteroperitoneal nodes, spleen and liver
  18. 18. Investigations
  19. 19. Treatment • Chemotherapy and/or radiation therapy • Antiemetics/ antidiarrhoeal drugs, sedatives • Bone marrow transplant • Blood transfusion • Immunotherapy
  20. 20. Non- hodgkin’s lymphoma
  21. 21. Pathophysiology • Pathophysiologically similar to HD • No RS cells • Most common lymphoma (62%) • Mature/ immature B/T cell malignancies
  22. 22. Clinical features • Enlarged tonsils and adenoids • Painless rubbery enlargement of lymphatic tissue, usu. Cervical or supraclavicular nodes • In children – cervical nodes affected first with dyspnoea and coughing • An advancing disease • s/s specific to involved structure • Systemic c/c – fatigue, malaise, weight loss, fever, etc
  23. 23. Investigations • Blood count – anaemia • Uric acid level – elevated/ normal • Sr. calcium – elevated • Imaging – bone & CXR, lymphangiography, liver and spleen scans, CT abdomen  f/s/o metastasis • LN biopsy – cell type revealed • Biopsy of tonsil, bone marrow, liver or spleen  malignant cells
  24. 24. Treatment • Radiation – esp in early and localized lesions • Total nodal irradiation • Chemotherapy • Bone marrow transplant • Blood transfusion (supportive)
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introduction and differentiation between different forms of lymphoma Hodgkins vs Non- Hodgkin's

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