Ap 50 10-15 1 re system

Ap 50 10-15 1 re system

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  Related Terms aboutbody defense mechanisms  Immune system  Lymphoid system  Lymphoreticular system  Reticuloendothelial system (RES)  Mononuclear phagocyte system (MPS)
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  A complex systemof cellular and molecular components with functions including : -distinguishing self from not self -defense against foreign organism for substances Cellular components: lymphocytes and macrophages Molecular components: antibodies and lymphokines Immune System Definition
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  A group ofcells having the ability to take up and sequester inert particles and vital dyes: -Macrophages or macrophage precursors -Specialized endothelial cells lining sinusoids of the liver -Spleen -Bone marrow -Reticular cells of lymphatic system Reticuloendothelial System (RES) Mononuclear phagocyte system (MPS) or Macrophage system Definition
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  Pathology of thePathologyof the Definitions Lymphoreticular System Lymphoreticular System The system consisting of tissues of the lymphoid and tissues of the reticuloendothelial system
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  Pathology of thePathologyof the Lymphoid systemLymphoid system The lymphoid tissues in the body: Primary (central) lymphoid tissues i.e. thymus and bone marrow where lymphocytes differentiate from Secondary (peripheral) lymphoid tissues including lymph nodes, spleen, and gut (mucosal)-associated lymphoid tissues (MALT) Definitions Lymphoreticular System Lymphoid system
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  Scope of theSubject Organs: • Lymph nodes • Spleen • Thymus • Bone marrow Disease categories: • Developmenal disorders • Traumatic • Vascular (circulatory disorders) • Inflammatory disorders • Neoplasms and tumor- like conditions
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  Anatomy of alymph node
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  Methods for acquiringtissues  Fine needle aspiration cytology  Biopsy : Needle biopsy (core biopsy) Incisional biopsy (part of node) Excisional biopsy (whole node) Lymph node evaluation  Proper examination of a lymph node is a complicated task that may require a variety of specialized procedures depending on the nature of the CASE
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  Fine needle aspiration(biopsy) cytology FNA Definition: • Fine needle = 22 gauge or smaller • Useful for : • Reactive conditions e.g. infectious disease • Metastatic tumors • High grade lymphomas
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  ode aspiration, Papstain: -Adenocarcinoma, metastati
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  Lymph node biopsy •Core needle biopsy is adequate for the diagnosis of metastatic carcinoma , but for primary lymphoid disorders so far not recommended • Incisional biopsy is also not preferable in primary lymphoid disorders • Exicional biopsy of (whole) node with intact capsule by sharp dissection is highly useful for demonstration of nodal architecture, therefore most favorable
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  Lymph node biopsy Methodsused for evaluation • Histology / cytology • Microbiologic (Bacteriologic) study • Immunohistochemistry • Cytogenetics and molecular genetics • Electron microscopy
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  Reactive changes inlymph node, morphologic features • Follicular hyperplasia: • Caused by stimulation that activate humoral immunity • Increased and enlargement of large B cell rich germinal centres (secondary follicles) covered by a layer of resting B cell (the mantle zone) • Follicular center cells comprising the large proliferating lymphocytes (centroblasts), smaller cells having cleaved nuclear contour (so-called cleaved cells or centrocytes) and phagocytic macrophages (cells with pale staining cytoplasm and tingible bodies), some T cells and others • Paracortical (lymphoid) hyperplasia: • Caused by stimulation of cellular immunity • Widening of T cell regions of the node • Paracortical or interfollicular areas containing activated T cells (immunoblasts) and others • Sinus histiocytosis or Reticular hyperplasia: • Histiocytes = tissue cells, in this meaning includes macrophages and dendritic cells (Langerhans cells) along the sinusoids
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  tingible body
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  T cell areas)hyperplasia associated with proliferation
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  •histiocytes
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  •Cleaved cell lympho
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  Necrotizing lymphadenitis
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  Histoplasmosis
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  n in viralinfection sometime having features mimickin
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  Malignant proliferative diseasesof leucocytes categorization • Lymphoid neoplasms: being a diverse group of entities with there phenotypes closely resemble to particular stage of normal lymphocyte differentiation, a feature used for diagnosis and classification • Myeloid neoplasms: arising from hematopoietic stem cells (that give rise to erythroid, myeloid and thrombocytic lineages) and leading to peripheral blood count implying the term leukemia • Histiocytoses: meaning proliferative lesions of macrophages and dendritic cells, including entities of malignant histiocytoses, Langerhans cell histiocytoses
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  Lymphoma VS Leukemia •Lymphoma is used to describe proliferation arising as discrete tissue masses, mainly in lymph nodes and occasionally in extra-nodal organs / tissues • Leukemia is used to for neoplastic proliferation of neoplasms presenting with widespread involvement of the bone marrow and usually accompanied by the presence of tumor cells in peripheral blood Definition: Lymphoma = Any neoplasm of lymphoid tissue Leukemia = Neoplastic/progressive proliferation of cells in hematopoietic tissues At time of clinical presentation
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  Lymphoma (malignant lymphoma) •Hodgkin Lymphoma (HL) or Hodgkin Disease (HD) : almost all cases arise in a single node / chain of nodes of neck region then spreading to contiguous nodes and regions with rather predictable fashion : presence of neoplastic cells called Reed-Sternberg cells among background of reactive cells • Non-Hodgkin Lymphoma (NHL) : about 2/3 of cases arising in nodes and the rest in other tissues/organs (extranodal) with sometimes unpredictable systemic spreading : tumor cells = lymphocytes (T-cell, B-cell, & NK-cell) Definition: Any neoplasm (all as malignant) of lymphoid tissue
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  Case of Hodgkinlymphoma in present textbook Section of tissue preserved by Dr.Hodgkin
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  Hodgkin Disease =Hodgkin Lymphoma  Reed-Sternberg cells (R-S cells) are found that in most cases of HL, derived from B cell, so HL now considered as unusual B-cell neoplasm  R-S cells are aneuploidae  EBV episomes are found in R-S cells, an evidence that EBV infection involve in the disease formation  Background cells (reactive cells) accumulation occur as response to cytokines secreted by the R-S cells Definition: -A group of lymphoid malignancy having morphological characteristic as presence of Reed-Sternberg cells among reactive lymphocytes, histiocytes and granulocytes. - Arises in single node or chain of nodes with predictable pattern of spreading.
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  a of lymphnode showing Reed-Sternberg cells among
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  A Reed-Sternberg cell showing owl’seyes features with larg e inclusion-like nucleoli among background cells
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  R-S cell: nowconsidered as tumor cell in HD that elaborates substances causing mixed cellularity in the lesion D30 positive reaction of R-S cell
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  Hodgkin lymphoma, mixedcellular
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  Nodular sclerosis Hodgkinlymphoma
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  gkin lymphoma, lymphocyte-richwith pop-corn R-S c
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  •R-S cell variants•Mummified cell
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  Classification of HodgkinLymphoma, WHO • Nodular sclerosis • Mixed cellularity • Lymphocyte-rich • Lymphocytic depletion • Lymphocytic predominance
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  Some important principlesin lymphoid neoplasms particularly NHL • Monoclonal :-each developing lymphocyte has a single/unique antigen receptor, therefore the daughter cells derived from malignant progenitor share the same antigen receptor gene, e.g. production of the same immunoglobulin resulting in monoclonal gammopathy in myeloma • Neoplastic B and T cells tend to behave like their normal (original) cells, leading to characteristic pattern of involvement, e.g. follicular lymphoma, mantle cell lymphoma • Recirculation of lymphoid cells (both the normal and the neoplastic) through the lymphatics and peripheral blood: dissemination of NHL always considered since the time of diagnosis • Majority of lymphoid neoplasm are of B cell origin • Disruption of the normal architecture and function of immune system: evident as susceptibility to infection and manifestation of autoimmunitity in some cases
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  Aetiological Factors inLymphomas • Genetic factors: – Inherited genetic factors – Chromosomal aberrations e.g. translocations – Oncogenes • Infections: – Viruses: Epstein-Barr virus (EBV) and Burkitt lymphoma Kaposi Sarcoma herpesvirus (KSHV) and B-cell lyphoma HTLV-1 and adult T-cell leukemia/lymphoma – Helicobacter infection: gastric B-cell lymphoma • Environments: contamination of radioactive substances from nuclear power plants and nuclear weapons • Iatrogenic factors: radiotherapy and certain kind of chemotherapeutic agents
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  Clinical manifestations oflymphomas
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  Manifestations of Lymphomas
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  Lymphoma, small bowelextra-nodal manifestation •Monotonus growth of neoplastic lymphocytes
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  features of lymphnode lymphoma oscopic features in H&E stain notonus growth pattern
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  Follicular lymphoma inmicroscopic sec oss features of follicular NHL cut section
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  Tumor cells inthe follicular structu
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  Neoplastic follicleymphoid follicleswith the mantle zone
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  •Small cell •Largecell •Anaplastic / blast c
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  Diffuse lymphoma
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  itt lymphoma: sectionshowing starry sky feature
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  Non-Hodgkin Lymphoma classification •Rappaport’s classification • WHO classification • Working (international) formulation classification • Revised European-American Classification of Lymphoid Neoplasms (REAL) Controversy and Confusion in classification of NHL and related lymphoid neoplasms are long-time well known for learners in pathology
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  Categorization based onmorphologic features • Diffuse lymphoma – Small cell – Mixed small and large cell – Large cell – Lymphoblastic • Follicular lymphoma – Small cell – Mixed small and large cell – Large cell • Burkitt lymphoma • Anaplastic large cell lymphoma
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  Classification of lymphoidmalignancy based on cell origin • Precursor B-cell neoplasms =neoplasms of immature B cells • Peripheral B-cell neoplasms = neoplasms of mature B cells • Precursor T-cell neoplasms =neoplasms of immature T cells • Peripheral T-cell and NK-cell neoplasms = neoplasms of mature T cells and natural killer cells • Hodgkin lymphoma =neoplasm of Reed-Sternberg cells and variants (now believed as transformed B cells in most cases)
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  Hairy Cell Leukemia
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  Burkitt’s lymphoma
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  Treatment of Lymphomas •Surgery: Not as definite treatment for disease but resection of the hollow organ with transmural involvement insisted to prevent perforation • Radiation therapy: in a large mass lesion and for some specific type particularly HL • Chemotherapy: with multiple drugs • Immunotherapy • Bone marrow transplantation • Multimodality By a long-time-development in treatments, several types of lymphomas can now be well controlled and/or cured.
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  Lymphoma in immunodeficiencystates • Primary immunodeficiency • Organ transplant recipients • Patients with HIV infection • Other acquired disease of immunosystem, e.g. rheumatoid arthritis, Sjogren syndrome, Hashimoto thyroiditis etc.
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  Langerhans cell histiocytosis Langerhanscell histiocytosis presents as three clinicopathologic entities: 1.Multifocal multisystem Langerhans cell histiocytosis (Letterer-Siwe disease) 2.Multifocal unisystem Langerhans cell histiocytosis (Hand-Schuller-Christian disease) 3.Eosinophilic granuloma: usually unifocal lesion involving bone, but sometimes multifocal and involvement in other organs Definition: Proliferative disorders of dendritic cells, the Langerhans cells or antigen presenting cells (APC)
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  Eosinophilic granuloma
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  Eosinophils Langerhans cells
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  so-called Malignant Histiocytosis -Rappaport, 1966: proposed the term malignant histiocytosis for disease systemic neoplastic proliferation of cells histologically identified as histiocytes with fever and fatal outcome. - Scott & Robb-Smith, 1939: described the same entity as Histiocytic Medullary Reticulosis (HMR). - Several cases found as virus-associated hemophagocytic syndrome, having the same clinico-pathologic features. - Familial hemophagocytic reticulosis, also found as viral infection in a family with immune defect. - Cell marker and molecular analysis studies showins most cases as high grade NHL, usually anaplastic large cell (Ki-1).
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  End of theSession