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LYMPHOMA
Dr. Saugat Chapagain
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
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
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
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
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)
Lab investigations
1. Peripheral Blood smear
– RBC
– WBC
– Platelet
2. Bone marrow examination
– Cellularity
– Myeloid cells
– Erythropoiesis
– Megakaryocytes
– Cytogenetics
3. Cytochemistry
Lymphoid
neoplasms
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
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
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
Hodgkin’s
disease
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
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.
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)
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
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
Investigations
Treatment
• Chemotherapy and/or radiation therapy
• Antiemetics/ antidiarrhoeal drugs, sedatives
• Bone marrow transplant
• Blood transfusion
• Immunotherapy
Non- hodgkin’s
lymphoma
Pathophysiology
• Pathophysiologically similar to HD
• No RS cells
• Most common lymphoma (62%)
• Mature/ immature B/T cell malignancies
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
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
Treatment
• Radiation – esp in early and localized lesions
• Total nodal irradiation
• Chemotherapy
• Bone marrow transplant
• Blood transfusion (supportive)
Lymphoma
Lymphoma

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Lymphoma

  • 2.
  • 3. 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
  • 4. 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
  • 5. 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
  • 6. 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
  • 7. 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)
  • 8. Lab investigations 1. Peripheral Blood smear – RBC – WBC – Platelet 2. Bone marrow examination – Cellularity – Myeloid cells – Erythropoiesis – Megakaryocytes – Cytogenetics 3. Cytochemistry
  • 10. 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
  • 11. 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
  • 12. 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
  • 14. 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
  • 15. 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.
  • 16. 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)
  • 17. 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
  • 18. 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
  • 20. Treatment • Chemotherapy and/or radiation therapy • Antiemetics/ antidiarrhoeal drugs, sedatives • Bone marrow transplant • Blood transfusion • Immunotherapy
  • 21.
  • 23. Pathophysiology • Pathophysiologically similar to HD • No RS cells • Most common lymphoma (62%) • Mature/ immature B/T cell malignancies
  • 24. 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
  • 25. 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
  • 26. Treatment • Radiation – esp in early and localized lesions • Total nodal irradiation • Chemotherapy • Bone marrow transplant • Blood transfusion (supportive)