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Lymphoreticular .pptx
This document provides an overview of the lymphatic system and lymphadenopathy. It discusses the primary and secondary lymphoid organs, causes of lymphadenopathy including infections, immune diseases, and malignancies. Hodgkin's lymphoma and non-Hodgkin's lymphoma are described as neoplastic proliferations of white blood cells that can cause generalized lymphadenopathy. The classification, clinical features, etiology, diagnosis, and prognosis of Hodgkin's and non-Hodgkin's lymphoma are summarized. Causes of splenomegaly including infections, hematologic malignancies, and connective tissue diseases are also reviewed.
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Lymphoreticular .pptx
- 1. LYMPHORETICULAR SYSTEM Dr. Umme KulsumMunmun Assistant Professor Department of Pathology Chandpur Medical College
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- 6. Bone marrow- B cells Thymus– T cells Circulate through blood Secondary lymphoid organs eg. Lymph node, spleen, tonsil , Peyer’s patches
- 7. LYMPHADENOPATHY Antigenic stimulation Activation of resident immune cells Primarylymphoid follicles enlarge (germinal center) Enlargement of Lymph node
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- 9. LYMPHADENITIS Inflammation of lymphnode: Secondary lymphoid follicles with reactive germinal centers
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- 11. CAUSES OF LYMPHEDENOPATHY •Viral (EBV, CMV, HIV etc) • Bacterial (Streptococcus, Staphylococcus, Mycobacterium, Cat- scratch disease etc) • Fungal • Parasitic Infectious Diseases • Castleman disease • Sarcoidosis etc Immune Diseases
- 12. CAUSES OF LYMPHEDENOPATHY •Lymphoma • Leukemia • Metastatic cancers Malignancies • Rheumatoid arthritis • SLE • Drug reactions Others
- 13. GENERALIZED LYMHADENOPATHY More thantwo non – contiguous group of lymph nodes
- 14. CAUSES OF GENERALIZED LYMPHADENOPATHY Infections •TB • HIV • Infectious mononucleosis • Toxoplasmosis Malignancy Autoimmune disease Storage diseases Histiocytoses Drug reactions
- 15. NEOPLASTIC PROLIFERATIONS OF WHITEBLOOD CELLS • Present with widespread involvement of bone marrow peripheral blood • Liquid malignancy of either lymphoid or myeloid series Leukemia • Proliferations that arise as discrete mass • Solid malignancy of lymphoid series • Begins as malignant transformation of lymphocytes in lymphatic system Lymphoma
- 16. NEOPLASTIC PROLIFERATIONS OF WHITEBLOOD CELLS Lymphoid neoplasm B cell, T –cell or NK cell origin Phenotypes of neoplastic cell closely resembles that of a particular stage of normal lymphocyte maturation
- 17. NEOPLASTIC PROLIFERATIONS OF WHITEBLOOD CELLS Myeloid neoplas Arise from haemopoietic progenitors
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- 20. WHO CLASSIFICATIONS OF LYMPHOIDNEOPLASMS Precursor B-cell Neoplasm Peripheral B – cell Neoplasm Precursor T – cell Neoplasm Peripheral T – cell /NK – cell Neoplasm Hodgkin Lymphoma
- 21. WHO CLASSIFICATIONS OF LYMPHOIDNEOPLASMS • B – cell acute lymphoblastic leukaemia/lymphoma ( ALL) Precursor B-Cell Neoplasm • Follicular Lymphoma • Diffuse large B cell lymphoma • Marginal zone Lymphoma • Burkitt lymphoma • Extranodal Marginal zone lymphoma Peripheral B-Cell Neoplasm
- 22. WHO CLASSIFICATIONS OF LYMPHOIDNEOPLASMS • T –Cell acute lymphoblastic leukaemia/lymphoma ( ALL) Precursor T-Cell Neoplasm • Peripheral T-Cell Lymphoma • Anaplastic Large cell lymphoma • Mycosis fungoides • Extranodal NK/Tcell lymphoma • Angioimmunoblastic T Cell lymphoma Peripheral Cell Neoplasm
- 23. WHO CLASSIFICATIONS OF LYMPHOIDNEOPLASMS • Classical subtypes • i. Nodular Sclerosis • ii. Mixed cellularity • iii. Lymphocyte rich • iv. Lymphocyte depletion • Lymphocyte predominance Hodgkin Lymphom
- 24. WORKING FORMULATION • Anobsolete classification of non-Hodgkin lymphomas, first proposed in 1982. Low Grade Intermediate grade High grade
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- 26. CINICAL PRESENTATIONS Enlarged non-tenderlymph nodes (often > 2 cm) Symotoms related to involvement of extranodal sites (skin, stomach, brain etc) Systemic symptoms (“B symptoms”) Fever, night sweats, weight loss Symptoms related to hepatosplenomegaly Symptoms related to complications of bone marrow infiltration (Infections, anaemia, bleeding and coagulopathies)
- 27. ETIOLOGY • Exposure toradiation and certain chemicals (benzene etc) • Infections (EBV in HL, H. pylori in gastric MALToma) • Immunodeficiency • Autoimmune disease • Older age group
- 28. HODGKIN LYMPHOMA • Firstdescribed by Thomas Hodgkin in 1832 • Characteristic features: Arises in a single node or chain of nodes (esp. cervical) Contains rare neoplastic distinctive giant cells (“Reed Sternberg cells”), in a background of abundant reactive inflammatory cells One of the most common cancers in young adults
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- 30. VARIANTS OF RSCELL
- 31. CLASSIFICATION • Nodular lymphocytepredominant Hodgkin lymphoma • Classical Hodgkin lymphoma Nodular sclerosis Hodgkin lymphoma Mixed cellularity Hodgkin lymphoma Lymphocyte-rich Hodgkin lymphoma Lymphocyte-depleted Hodgkin lymphoma
- 32. CLASSICAL HODGKIN LYMPHOMA NodularSclerosis (66%) -Fibrous bands and nodules -“Lacunar cell” variant of cell Mixed Cellularity (25%) - Abundant RS cells - Background of lymphocytes, eosinophils, plasma cells, neutrophils Lymphocyte Rich (5%) - Scattered RS cells in lymphocyte rich Lymphocyte Depleted - Abundant RS cells and mononuclear variants - Only few background lymphocytes
- 33. NODULAR LP HODGKIN LYMPHOMA •5% of all Hodgkin lymphoma • “Popcorn cells” / “L&H cells” rather than RS cells • Background of small B-lymphocyte
- 34. • Distinction betweenClassical HL and Nodular LP HL is based partly on immunophenotype Classical: CD15+ CD30+ CD45- CD20- NLPHL: CD15- CD30- CD45+ CD20+
- 35. ANN ARBOR STAGINGSYSTEM • I – Involvement of a single lymph node region or lymphoid structure • II – Involvement of two or more lymph node regions on the same side of the diaphragm • III – Involvement of lymph node regions or structures on both sides of diaphragm • IV – Involvement of extranodal sites
- 36. Prognosis of HodgkinLymphoma • Generally better than non-Hodgkin lymphomas • Depends greatly on stage (more so than histological subtype) • 90-100% of Stage IA and IIA curable
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- 38. NON - HODGKINLYMPHOMA • Very diverse group of disorders • Unimodal age distribution, with increasnig incidence with age • Many arise in extranodal sites (although the majority are nodal)
- 39. Divided clinically into Low grade - Indolent, slow-growing, but resistant to therapy and rarely curable - Often present with painless generalized lymphadenopathy High grade - Aggressive, rapidly progressive, but sensitive to treatment and potentially curable - Often present with solitary rapidly enlarging mass
- 40. CAUSES OF SPLENOMEGALY •Liver disease (cirrhosis, hepatitis, portal hypertension) • Haematologic malignancy (lymphoma, leukaemia, myeloproliferative disorders) • Portal or hepatic vein thrombosis • Congestive cardiac failure • ITP, haemolytic anaemia, thalassemia
- 41. DIAGNOSTIC APPROACH FOR LYMPHADENOPATHY •History and evaluation (Size, site, duration, tenderness, localized/generalized, ‘B’ symptoms) • CBC • Mantoux test • Microbiological test • Serology: CMV, HIV, toxoplasmosis • ANA, Rheumatoid factor
- 42. DIAGNOSTIC APPROACH FOR LYMPHADENOPATHY •LDH • Imaging test • FNA • Biopsy and histopathology (to confirm malignancy) • Immunohistochemistry to categorize Hodgkin/ Non- Hodgkin lymphoma B/T cell lymphoma etc • Flowcytometry
- 43. CAUSES OF SPLENOMEGALY •Infections ( malaria, TB, HIV, infectious mononucleosis etc) • Connective tissue disease (SLE, rheumatoid arthritis etc) • Infiltrative disorders (sarcoidosis, amyloidosis, glycogen storage diseases). • Focal lesions (hemangiomas, abscess, cysts, metastasis).
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