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lymphoma (presentation (Hodgkins (age <20 and >60, cells Reed…
lymphoma
presentation
Hodgkins
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symptomsfever, night sweats, weight loss
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additional symptoms hepatosplenomegaly, pleural effusion, bone pain, spinal/ nerve compression.
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anaemia, hypercalcaemia, eosinophilia, leykocytosis, hypoalbuminaemia. lymphocyte count.
Non hodgkins
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cells CD 19, 20, 22 positive
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Associated with EBV, HIV, SLE
extranodal involvement splenic, GIT , aseptic meningitis, skin, waldyers ring, hepatosplenomegaly
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classification
Hodgkin's
Reed sternberg cells. characterised by the hosts immune response. in order of the immune activation. 1.lymphocyte predominance = marked immune response, 2) mixed cellularity= moderate. nodular sclerosis = variable. 4) lymphocyte depleated = non-existent.
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mixed cellularity
older adults , usually present in stage 3 or 4, lymphnodes are replaced by infultrate by reed-sternberg cells, cellular response: lymphoid cells, esinophils, plasma cells, histiocytes.
nodular sclerosis
MOST COMMON: young males, mediastinal nodes, infiltrate is divided into nodules by bonds of collagen, grade 2 usually at diagnosis, pleomorphic reed-sternberg cells.
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Lymphocyte depleated
RARE: elderley, many pleomorphic Reed-sternberg cells and shows few reactive lymphoid cells stage 3 or 4 at Dx
Ann-Arbour staging system: 1) one lymph node or group, contiguious 2) several on the same side of the diaphragm 3) both sides of diaphragm 4) disseminated involvement of one or more extra nodal tissue like liver or bone marrow.
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Diagnosis: lymph node biopsy, CT, MRI, Spleen and liver biopsy andn bone marrow aspirate.
Non-Hodgkins
B cell
Small cell INDOLENT
small cell lymphomas are well differentiated, they look like normal B cells, and have a normal pattern of growth
follicular TYPICAL
small B cells, CD20+, proliferation of the follicles, 14-18 translocation, Bcl2 over expression blocks apoptosis, Bcl-2 is important to have becuase after somatic hypermutation the cells either recognise the antigen and proceed to the germinal centre or they go to apoptosis if they do not recognise it. blocking the Bcl-2 means the cells dont die
hyperplasia of follicles from infection histologically has same cortical architecture and will have macrophages there to eat up the B cells that failed somatic hypermutation.
lymphoma= the architecture is all fucked up, there are no macrophages in the germinal centers to eat up the should be apoptotic B cells so they overproliferate. there is also monoclonal K and lambda light chains.
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slowly and asymptomatic, means they are likely widespread at diagnosis , generalised lymphadenopathy
Similar to CLL but the CLL is the blood bourne one, lymphoma is the solid one
Dont treat untill symptomatic, survival is not better off if starting early. multiple nodes high bulky disease, B symptoms, end organ dysfunction, lung blocking pleural effusion. survival is 80% chemo and immunotherapy.
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mantle
late adult hood - painless lymphadenopathy, small B cells, expands region adjacent to follicle.
11:14 translocation. Cyclin D1, regulates G1 to S phase (cell cycle regulator (intracellular phosphorylator)
marginal
tumour cells expand into the marginal zone, CD20+, chronic inflammatory states, normal lymoh nodes do not have a marginal state only when they are active is the marginal zone produced.
caused by: hashimotos, sjogrens, H.Pylori MALT lymphoma.
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