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65 Cards in this Set
- Front
- Back
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Q: What do the preauricular nodes do?
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-drain scalp and skin of head
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Q: What is on the differential diagnosis with enlarged reauricular nodes?
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-scalp infections, mycobacterial infection
-malignancies include skin neoplasm, lymphomas, head and neck squamous cell carcinomas |
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Q: What do the posterior cervical nodes do?
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-drain scalp, neck, upper thoracic skin
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Q: What is on the differential with enlarged posterior cervical nodes?
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-same as preaurficlar nodes
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Q: What do the supraclavicular nodes do?
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-drain GI tract, genitourinary tract, pulmonary
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Q: What is on the differential for enlarged supraclavicular nodes?
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-abdominal/thoracic neoplasms, thyroid/laryngeal disease, mycobacterial/fungal infections
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Q: What do the submandibular nodes do?
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-drain oral cavity
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Q: What is on the differential for enlarged submandibular nodes?
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-mononuclosis, upper respiratory viral/bacterial infection, mycobacterial infection, toxoplasma, cytomegalovirus, dental disease, rubella
-malignancies include squamous cell carcinoma of the head and neck, lymphomas, leukemias |
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Q: What do the anterior cervical nodes do?
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-drain larynx, tongue, oropharynx, anterior neck, differential is the same as the submandibular nodes
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Q: What is acute nonspecific lymphadenitis?
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-lymph nodes undergo reactive changes whenever they are challenged by microbiologic agents, cell debris or foreign matter
-most often seen in the cervical region due to microbial drainage from infections of the teeth or tonsils and in the axillary or inguinal regions secondary to infections in the extremities |
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Q: Describe the morphology associated with acute nonspecific lymphadenitis.
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-nodes become swollen, gray-red and engorged
-histologically, prominence of lymphoid follicles, large germinal centers containing numerous mitotic figures, debris (bacterial) filled macrophages, centers may undergo necrosis -cells lining the sinuses become hypertrophied and cuboidal and often undergo hyperplasia |
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Q: Why are the nodes enlarged in acute lymphadenitis?
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-because of the cellular infiltration and edema, become tender to touch
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Q: What are some examples of benign reactive hyperplasia (chronic nonspecific lymphadenitis) in response to infection, inflammation or tumor?
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-follicular hyperplasia, interfollicular hyperplasia, mixed, sinus histio cytosis
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Q: Describe the morphology of follicular hyperplasia?
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-caused by stimuli that activate humoral immune responses, distinguished by the appearance of large, round or oblong B cell-rich germinal centers (secondary follicles) surrounded by a collar of small, resting naïve B lymphocytes (mantle zone)
-also present throughout the follicle are phagocytic macrophages containing nuclear debris and network of follicular dendritic cells |
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Q: What disease can lead to follicular hyperplasia?
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-rheumatoid arthiritis, toxoplasmosis, and early HIV infection
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Q: What else can be associated with follicular hyperplasia?
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-accompanied by marginal zone B-cell hyperplasia, marginal zone B cells accumulate in a rim external to the mantle zone of germinal centers
-these cell have moderately abundant pale cytoplasm and folded or reniform nuclei resembling those of monocytes, leading to the descriptive term monocytoid B cells |
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Q: Describe the morphology of interfollicular hyperplasia (paracortical lymphoid hyperplasia).
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-characterized by reactive changes within the T-cell regions of the lymph node that encroach on the B cell follicles, observe activated T cells (immunoblasts) that are 3-4X larger than resting lymphocytes, also have scattered macropahges
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Q: What disease cause interfollicular hyperplasia?
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-encountered in immunologic reactions induced by drugs (Dilantin), in acute viral infections (infectious mono), and following vaccination against certain viral diseases
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Q: Describe the morphology of sinus histiocytosis (Reticular hyperplasia).
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-distention and prominence of the lymphatic sinusoids, prominent in lymph nodes draining cancers such as carcinoma of the breast
-the lining endothelial cells are hyhpertrophied and macropahges are greatly INC in numbers resulting in expansion and distension of sinuses |
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Q: Describe the lymph nodes associated with chronic nonspecific lymphadenitis.
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-lymph nodes are not tender because their capsules are not under INC tension, common in inguinal and axillary nodes (which drain relatively large areas of the body
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Q: What are lymphomas?
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-malignant neoplasms of the lymphoid organs characterized by autonomous neoplastic growth of cells committed toward lymphoid differentiation
-tumors normally affect lymph nodes and spleen but may affect other lymphoreticular sites (liver, GI tract, lungs) -proliferations arising as discrete tissue masses |
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Q: Are lymphomas benign or malignant?
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-all lymphomas are malignant
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Q: What are the classifications of lymphomas?
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-lymphomas are classified as either Hodgkins lymphomas or non-Hodgkin lymphomas (NHL), NHLs are further divided into B cell (80%) or T cell affected, the B and T cells affected can either be precursor or peripheral (mature)
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Q: What are the different groups of lymphoid neoplasms according to WHO classification?
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-precursor B-cell neoplasms, peripheral B-cell neoplasms, precursor T-cell neoplasms, peripheral T-cell and NK-cell neoplasms, Hodgkin lymphoma
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Q: What diseases are in the precursor B cell neoplasm classification?
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-precursor-B lymphoblastic leukemia/lymphoma
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Q: What diseases are in the peripheral B-cell neoplasms?
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-chronic lymphocytic leukemia/small lymphocytic lymphoma
-B-cell prolymphocytic leukemia -Lymphoplasmacytic lymphoma -Splenic and nodal marginal zone lymphomas -Extranodal marginal zone lymphoma -Mantle cell lymphoma -Follicular lymphoma -Marginal zone lymphoma -Hairy cell leukemia -Plasmacytoma/plasma cell myeloma -diffuse large B-cell lymphoma -Burkitt lymphoma |
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Q: What diseases are in the precursor T-cell neoplasms?
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-precursor-T lymphoblastic leukemia/lymphoma
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Q: What diseases are in the peripheral T-cell and NK-Cell neoplasms?
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-T cell prolymphocytic leukeamia
-Large granular lymphocytic leukemia -mycosis fungoides/Sezary syndrome -periphreal T-cell lymphoma, unspecified -anaplastic large cell lymphoma -angioimmunoblastic T-cell lymphoma -enteropathy-associated T-cell lymphoma -panniculitis-like T-cell lymphoma -hepatosplanic gammadelta T-cell lymphoma -adult T-cell leukemia/lymphoma -NK/T-cell lymphoma, nasal type -NK-cell leukemia |
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Q: What diseases are classified as Hodgkin lymphomas?
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-classical subtypes (nodular sclerosis, mixed cellularity, lymphocyte rich, lymphocyte depletion)
-lymphocyte predominance |
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Q: Describe the role of Fas in extrinsic (death receptor-initiated) pathway for apoptosis.
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-when fas is cross-linked by its ligand (FasL), three or more molecules or Fas come together and their cytoplasmic death domains form a binding site for an adapter protein (FADD Fas-assocaited death domain)
-FADD binds an inactive form of caspase-8 (procaspase-8) and cleaves it to form active caspase 8 -caspase 8 is pro apoptotic, cleave cytoskeletal and nuclear matrix proteins and thus disrupt the cytoskeleton and lead to breakdown of the nuclues |
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Q: What is the importance of Bcl-2?
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-family of proteins that are stimulated by growth factors and other survival signals, are anti-apoptotic, are oncogenes
-normally reside in mitochondrial membranes -when Bcl-2 levels are low, the permeability of the mito membrane INC and several proteins that can activate the caspase cascade leak out, Bcl-2 is replaced by Bax |
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Q: What does Bax do?
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-are pro-apoptotic proteins that stimulate apoptosis
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Q: Describe mantle cell lymphoma (MCL-1).
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-makes up about 3% of NHL, usually presents in the 5th to 6th decades of life and shows a male predominance, the tumor cells closely resemble the normal mantle zone B cells that surround germinal centers
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Q: What role does Bcl-1 have in MCL?
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-a translocation between chromosome 11 (cyclin D1) and 14 (IgH) occurs, juxtaposing the IgH to a region designated as B-cell lymphoma 1 (bcl-1)
-bcl-1 is the gene fro cyclin D1 (a G1 cell cycle regulator that promotes G1 to S phase progression), overexpression appears to overcome suppressor effect of retinoblastoma protein (Rb) |
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Q: Describe the morphology of MCL.
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-tumor cells may surround reactive germinal centers, producing a vaguely nodular appearance at low power, proliferation consists of a homogenous population of small lymphocytes with round to irregular to occasionally deeply clefted nuclear contours
-absent centroblasts and proliferation centers |
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Q: Describe the immunophenotyping used to diagnose MCL.
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-express CD19, CD20, high levels of IgM and IgD, CD5+ and CD23-, + for cyclin D1 protein
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Q: What are the clinical features of MCL?
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-painless lymphadenopathy, symptoms related to splenomegaly, poor prognosis, not curable with conventional chemotherapy, most patient succumb eventually to organ dysfunction caused by tumor infiltration
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Q: Describe diffuse large B-cell lymphoma (DLBCL).
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-encompasses a heterogenous group of tumors that together constitute about 20% of NHL and 60-70% of aggressive lymphoid neoplasms
-slight male predominance with a median age of about 60 yo |
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Q: Describe the morphology of DLBCL.
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-tumor cells have large nuclei, open chromatin and prominent nucleoli
-the common morphologic features that unite this group of neoplasms are a relatively large cell size (usually four to five times the diameter of a small lymphocyte) and a diffuse pattern of growth -nucleoli may be two to three in number and located adjacent to the nuclear membrane or single and centrally placed |
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Q: Describe the immunophenotype of DLBCL.
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-mature B-cell tumor express the B-cell markers CD19 and CD20 and they show variable expression of germinal center markers such as CD10 and BCL6, most have surface Ig, negative for TdT
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Q: Describe the cytogenetics and molecular profile DLBCL.
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-heterogenous
-one frequent event is dysregulation of BCL6, a DNA-binding zinc-finger trancritptional regulator that is required for the formation of normal germinal centers -about 30% contain various translocations that have a common breakpoint at 3q27 within the BCL6 locus -also have mutations in c-MYC which are not seen in normal germinal center B cells |
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Q: Describe the c-myc protein.
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-this translocation places c-myc next to the highly expressed Ig heavy chain locus, C-myc participates in many cell processes including proliferation and apoptosis, probably releases the cell cycle from inhibition and rescues cells from apoptosis
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Q: Describe the clinical course and prognosis of DLBCL.
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-typically present with a rapidly enlarging, often symptomatic, mass at a single nodal or extranodal site
-aggressive tumors that are rapidly fatal if untreated, with intensive combination chemo, complete remission can be achieved in 60-80% of patients |
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Q: Describe marginal zone lymphomas.
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-originally reported in mucosal tissues, called mucosal associated lymphoid tissue or MALT lymphomas
-often in chronically inflamed tissue, like H. pylori gastritis -remain localized for long periods -sometimes respond if inciting agent removed such as Helicobacter |
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Q: What makes marginal zone lymphomas exceptional?
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-they often arise within tissues involved by chronic inflammatory disorders of autoimmune or infectious etiology
-they remain localized for prolonged periods, spreading systemically only late into their course -they may regress if the inciting agent (e.g. H. pylori) is eradicated |
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Q: Describe mycosis fungoides.
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-cutaneous T-cell lymphoma
-tumor of CD4+ helper T cells characterized by a market redilection to involve the skin, show three distinct stages |
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Q: Describe the morphology of mycosis fungoides.
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-irregular, convoluted nucleus, dense chromatin, indistinct nucleolus, scant cytoplasm
-there is appearance of extranodal marginal zone lymphomas in chronically inflamed tissues, this has led to the suggestion that this neoplasm lies on a continuum between reactive lymphoid hyperplasia and full-blown B-cell lymphoma |
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Q: What are the stages of Mycosis fungoides?
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-infection of skin with leasions that are scaly, red-brown patches, raised, scaling plaques that may even be confused with psoriasis and fungating nodules
-begins as eczema type lesions, raised indurated, irregularly outlined, erythematous plaques may then supervene, finally multiple, large red-brown nodules correlates with systemic spreading -disease progression is characterized by extracutaneous spread, most commonly to lymph nodes and bone marrow |
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Q: How does mycosis fungoides present?
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-presents with an inflammatory premycotic phase and pregresses through a plaque phase to a tumor phase
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Q: Describe the histology of mycosis fungoides.
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-there is infiltration of the epidermis and upper dermis by neoplastic T cells, which usually have nuclei with a cerebriform appearance due to marked infolding of the nuclear membrane
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Q: Describe Hodgkin lymphoma.
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-encompasses a group of lymphoid neoplasms that differ from NHL in several respects
-arises in a single node or chain of nodes and spreads first to the anatomically contiguous nodes |
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Q: What are the morphological characteristics of Hodgkin lymphoma?
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-presence of distinctive neoplastic giant cells called Reed-Sternberg cells that induce the accumulation of reactive lymphocytes, histiocytes (macrophages) and granulocytes
-Reed-Sternber cells are derived from germinal center or post-germinal center B cells, indicating that most HLs are unusual tumors of B-cell origin -the Reed-Sternberg cells make up 1-5% of the total tumor cell mass, making HL more difficult to study |
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Q: What is the epidemiology of HL?
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-accounts for 0.7% of all new cancer in the US, approx. 7400 new cases reported per year, average age of 32 years
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Q: Describe the morphology of Reed-Sternberg cells.
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-large and have either multiple nuclei or a single nucleus with multiple neuclear lobes, each with a large inclusion-like nucleolus about the size of a small lymphocyte
-abundant cytoplasm -although Reed-Sternberg cells are requisite for the dianosis, they must be present in an appropriate background of non-neoplastic inflammatory cells (lymphocytes, plasma cells, eosinophils |
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Q: What are the clinical differences between Hodgkin and Non-Hodgkin lymphomas?
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-HL-more often localized to a single axial group of nodes (cervical, mediastinal, para-aortic), orderly spread by continiguity, mesenteric nodes and Waldeyer ring rarely involved, extranodal involvement uncommon
-NHL-more freq. involvement of multiple peripheral nodes, noncontiguous spread, Waldeyer ring and mesenteric nodes commonly involved, extranodal involvement common |
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Q: What is the clinical staging of HL and HNL?
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-stage I-involvement of a single lymph node region (I) or involvement of a single extralymphatic organ or site (IE)
-stage II-involvement of two or more lymph node regions on the same side of the diaphragm alone (II) or with involvement of limited contiguous extralymphatic organ or tissue (IIE) -stage III-involvement of lymph node regions on both sides of the diaphragm (III), which may include the spleen (IIIS) and/or limited contiguous extralymphatic organ or site (IIIE, IIIES) -stage IV-multiple or disseminated foci of involvement of one or more extralympathic organs or tissues with or without lymphatic involvement -all stages are further divided on the basis of the absence (A) or presence (B) of the following systemic symptoms (significant fever, night sweats, and/or unexplained weight loss of greater than 10% of normal body weight |
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Q: What is the morphology and immunophenotype and typical clinical features of nodular slcerosis HL?
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-frequent lacunar cells and occasional diagnostic R-S cells, background infiltrate composed of T lymphocytes, eosinophils, macrophages and plasma cells, fibrous bands dividing cellular areas into nodules. R-S cells CD15+, CD30+, EBV-
-stage 1 or 2 disease most common, frequent mediastinal involvement. F = M, most patients young adults |
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Q: What is the morphology and immunophenotype and typical clinical features of nodular sclerosis HL?
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-frequent mononuclear and diagnostic R-S cells. background infiltrate rich in T lymphocytes, eosinophils, macrophages, plasma cells. R-S cells CD15+, CD30+, 70% EBV+
-more than 50% present as stage 3 or 4 disease. M>F. biphasic incidence, peaking in young adults and agina in adults older than 55 |
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Q: What is the morphology and immunophenotype and typical clinical features of lymphocyte rich HL?
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-frequent mononuclear and diagnostic R-S cells. background infiltrate rich in T lymphocytes. R-S cells CD15+, CD30+. 40% EBV+
-uncommon. M>F. Tends to be seen in older adults |
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Q: What is the morphology and immunophenotype and typical clinical features of lymphocyte depletion HL?
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-reticular variant. frequent diagnostic R-S cells and variants with a paucity of background reactive cells. diffuse fibrosis variant. hypocellular fibrillar background with scattered diagnostic R-S cells and variants and few reactive cells. R-S cell CD15+, CD30+, most EBV+
-uncommon. more common in older males, HIV-infected individuals and in developing countries. more likely to present with advanced disease |
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Q: What is the morphology and immunophenotype and typical clinical features of lymphocyte predominance?
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-frequent L&H (popcorn cells) variants in a background of follicular dendritic cells and reactive B cells. R-S cells CD20+, CD15-, C30-, EBV-
-uncommon. young males with cervical or axillary lymphadenopathy. mediastinal involvement rare |
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Q: What is the origin of R-S cells?
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-they harbor identical rearranged Ig genes that show evidence of somatic hypermutation, establishing the cell of origin as a germinal center or post-germinal center B cells
-some (1-2%) have T-cell receptors rearrangements suggesting that HL arises in rare instances from transformed T cells |
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Q: What causes the characteristic accumulation of reactive cells in HL?
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-occurs in response to cytokines secreted by R-S cells, such as IL-5, IL-6, IL-13, TNF and GM-CSF
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Q: Describe the clinical course of HL.
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-presnets with a painless enlargement of lymph nodes, need lymph biopsy to diagnose
-night sweats and weight loss more common in stage III and IV -tumor stage is more important than histology for treatment |
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Q: What are the risks of HL treatment?
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-survivors of chemo have an INC risk of developing second cancer, MDS, AML and lung cancer lead the list of second malignancies
-non-neoplastic complications of radiotherapy include pulmonary fibrosis and accelerated atheroslcerosis |
