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236 Cards in this Set
- Front
- Back
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Bcl2
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Chromosome 18
On mitochondrial membrane Anti-apoptotic protein Bax homodimer can bind to it and promote apoptosis Promoter interacts with EBV LMP See in follicular lymphoma (except 50% of grade 3 and not in the primary cutaneous version). Can be useful for distinguishing reactive from neoplastic germinal centers. |
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Bcl6
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Chromosome 3
Expressed in germinal centers Expressed in some intrafollicular CD4 T cells Positive in 30-80% of large cell lymphomas |
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CD43
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Pan T cell marker
Use to diagnose granulocytic sarcoma, can be positive in anaplastic large cell lymphoma |
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Pax-5
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Marks pro-B cells to plasma cells
Stains 97% of reed-sternberg cells Positive in most B cell malignancies Also positive in lymphoplasmacytic lymphoma, Merkel carcinoma, and small cell carcinoma |
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Follicular lymphoma translocation/gene?
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t(14;18)
Bcl2 gene involvement? |
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Grading of follicular lymphoma?
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Based on proportion of centroblasts.
Grade 1: <6 per hpf Grade 2: 6-15 per hpf Grade 3: >15 per hpf Have to count 10 hpf in 10 follicles. |
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Grade of most follicular lymphomas?
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Grade 1 or 2 (80-90%)
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Grade of most pediatric follicular lymphomas?
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Low grade, but are more likely to be grade 3 than adults.
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Mum1?
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Post-germinal center transcription factor. Expressed by late centrocytes, but negative in follicular lymphoma.
Poor prognostic marker in DLBCL. |
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Antibodies used to detect follicular dendritic cells?
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CD21 and CD23
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What can normally express Bcl-2?
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T cells, primary follicles, and mantle zones.
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Bcl6 and Mum1 relationship
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Should be mutually exclusive in normal germinal centers. Co-expression can be seen in DLBCL.
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DLBCL and immunosuppression?
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Often EBV positive.
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Common chromosomal translocations in DLBCL?
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30% involve 3q27 (bcl-6). 20-30% involve bcl-2.
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Lymphomatoid granulomatosis, ke words:
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Angiocentric and angiodestructive.
EBV positive |
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Kimura disease?
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Reactive follicular hyperplasia, cortical and paracortical eosinophilia, and cortical and paracortical hypervascularity. Polykaryocytes.
IgE can cause nephortic syndrome, can see proteinaceous stuff in the germinal centers. |
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Angioimmunoblastic T-cell lymphoma
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Systemic.
Lymph nodes show a polymorphous infiltrate and proliferation of high endothelial venules. Constant association with EBV. In 75% of cases, EBV positive B cell expansion (immunoblasts in the paracortex) and FDCs (surrounding HEVs). Paracortical. Immuno: T cell markers, usually CD4. CD10, CXCL13, PD1. Trisomy 3, trisomy 5, additional X chromosome |
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Kikuchi Histiocytic Necrotizing Lymphadenitis
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Young asian women.
Excellent prognosis. Three phases: proliferative phase, with bizarre histiocytes eating apoptotic debris. necrotic phase. Resolution phase- foamy macrophages. |
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Rosai-Dorfman
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Sinus histiocytosis with massive lymphadenopathy. More common in black people. 40% of cases have extranodal involvement. S100 useful stain (very positive). Emperipolesis.
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Primary effusion lymphoma.
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Large B cell neoplasm.
Doesn't make a mass initially. Immunodeficient patients. HHV8 positive. Co-infection with EBV. CD45+, but lack pan-B cell markers (CD19, CD20, CD79a, IIg), other things can be positive (CD38, CD138, HLA-DR, CD30). May aberrantly express T cell markers (often causes problems immunophenotyping the cells). Bad prognosis- 6 months. |
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Plasmablastic lymphoma
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immunoblast lymphoma, but stains like plasma cells.
HIV+, often in oral cavity or other mucosal sites. EBV+. usually negative for CD45, CD20, pax5. CD56 + should make you think of underlying myeloma. EMA and CD30 often +. Ki67 is high. Bad prognosis. |
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Autoimmune disease in lymph nodes?
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Reactive follicular hyperplasia, plasma cell proliferation, and neutrophils in the sinuses.
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Toxoplasmosis in lymph node?
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Reactive follicular hyperplasia, small poorly formed granulomas within germinal centers is fairly specific, and monocytoid B cell hyperplasia.
Most common site is posterior cervical. The organism is rarely seen by exam or by genomic PCR. |
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Hyaline-vascular Castleman disase?
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Young people, asymptomatic. Mediastinal mass. Onion-skinning mantle zone around multiple germinal centers. Abnormal follicular dendritic cells.
Most common type. |
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Unicentric plasma cell Castleman disease?
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B symptoms. Elevated IL-6. Surgical excision is curative. Looks like: lots of plasma cells in the paracortex. Can be monotypic.
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Multicentric Castelman disease?
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Older people, HIV. POEMS syndrome (polyneuropathy, organomegaly, endocrinopathy, monocloncal gammopathy, skin). All patients with HIV have HHV8. Plasmablastic lymphoma can arise from.
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lymphoplasmacytic lymphoma.
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lymphoma of small B cells, plasmacytoid B cells, and plasma cells. Usually with waldenstroms. Can be HCV related. Usually involves BM, lymph node sinuses.
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Waldenstrom's =?
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lymphoplasmacytic lymphoma with bone marrow involvement, IgM paraprotein
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Dutcher body?
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PAS+ intranuclear inclusion in lymphoplasmacytic lymphoma.
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Poor prognosis in lymphoplasmacytic lymphoma?
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Old, cytopenias, high beta-2-microglobulin.
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Staining for Langerhan's giant cells?
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+ S100, CD1a
- CD68 |
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What kind of T cells in T-prolymphocytic leukemia?
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Post-thymic T cells.
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Leukemia with cytoplasmic blebs?
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Could be T-cell prolymphocytic leukemia.
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T-prolymphocytic leukemia in the skin?
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Perivascular or diffuse dermal infiltrates without epidermotropism.
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CD52 and T-prolymphocytic leukemia?
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Usually expressed at a high density and can be used as a target of therapy (monoclonal antibody)
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TCL-1?
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Onocgene overexpressed by T-cell prolymphocytic leukemia. Can do IH for. Can be a prognostic factor.
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Pro-lymphocytic leukemia: Cd4 or CD8?
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60% are CD4, 25% are double positive.
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Most common cytogenetic abnormality in T-PLL?
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inv(14), abnormalities of 8, deletions at 12
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What is T-LGL leukemia?
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Persistent increase in PB LGLs (2-20x10^9)
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In what other clinical scenarios can you see clonal expansion of T-LGLs?
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Post-stem cell tx, PTLD, low-grade B cell malignancies (hairy cell, CLL).
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Other disease associations for T-LGL leukemia?
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Rheumatoid arthritis, underlying malignancy (if CD34+)
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Helpful IH in T-LGL leukemia?
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TIA1, granzyme B
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Prognosis of T-LGL leukemia?
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indolent, but morbidity d/t NEUTROPENIA.
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CD3 in NK cells? CD5?
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Only cytoplasmic CD3, not surface. CD5 is negative.
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EBV and chronic lymphoproliferative disorder of NK cells? Course?
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Not related. Usually indolent course.
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Who gets aggressive NK-cell leukemias?
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Young asians
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Associated virus with aggressive NK-cell leukemia?
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EBV
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Oblique method to establish clonality in NK cell lesions?
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For females, pattern of X inactivation.
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Course of aggressive NK cell leukemia?
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Fulminant. Coagulopathy, hemophagocytic syndrome, multiorgan failure.
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Two major types of EBV-associated LPD or childhood?
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1) Hydroa vacciniforme: an indolent cutaneous malignancy.
2) Systemic EBV+ LPD: fulminant, preceded by a prodromal phase of polyclonal expanstion of EBV-infected T cells. |
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What ethnicity of children get EBV-associated LPD?
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Asian, native american.
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Etiology of hydroa vacciniforme?
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Neoplastic T (sometime NK) cells invade superficial dermis of sun-exposed areas. Angiocentric and angioinvasive. Epidermis shows pustules and ulceration
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Mosquite bite hypersensitivity?
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Associated with EBV-associated LPD of childhood, hydrao vacciniforme type.
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Systemic EBV+ T-cell LPD of childhood?
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Clinically similar to aggressive NK cell leukemia. But it's in the T cells. Marked hemophagocytosis. Liver failure, coagulopathy.
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Where do you see endemic ATLL?
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Japan, carribbean, and central Africa.
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What % of HTLV-a infected inviduals will develop ATLL?
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2.5%
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Most common extra-lymphatic site of involvement for ATLL?
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Skin (erythema, papule, nodule). It's a systemic disease.
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What is the most common clinical variant for ATLL?
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Acute (leukemia phase, lymphadenopathy, skin involvement).
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Clinical association with ATLL?
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Hypercalcemia, T cell immunodeficiency (can see opportunistic infections, like PCP and cryptococcal meningitis).
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Cytology of ATLL?
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A variety (small, medium, large cell, anaplastic, etc). Can look like other lymphomas, too (Hodgkins, angioimmunoblastic).
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Characteristic PB cell in ATLL?
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Plylobated nuclei of flower cell.
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CD4 or CD8 for ATLL? Other characteristic expression?
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Most cases are CD4+. Express like regulatory T cells: CD25 and FOXP3
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Gene of HTLV-a that is central leukemogenesis?
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Tax.
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A clever way to monitor disease in extranodal NK/T cell lymphoma, nasal type?
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Measure circulating EBV DNA.
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Histologic features of NK/T cell lymphoma? Cytology?
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Ulceration, necrosis. Can be angiodestructive. Glands are surrounded and show clear cell change.
Cytology is pretty variable, can see small, medium, large, or anaplastic cells. |
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CD56 and extranodal NK/T cell lymphoma?
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Not sensitive or specific. Need to see the EBV positivity to call. If EBV negative, then consider T-cell lymphoma, NOS
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What kind of enteropathy-associated T cell lymphoma can occur without celiac disease?
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Monomorphic variant (type II)
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Most common site(s) for enteropathy-associated T cell lymphoma?
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Jejunum or ileum
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HLAs associated with enteropathy-associated T cell lymphoma?
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HLA DQ2 and DQ8
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Immunophenotype of cells in enteropathy-associated T cell lymphoma?
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CD4 NEGATIVE, CD8 +/-, CD5-, CD3+
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Genotype of people with celiac disease?
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HLADQA1, HLADQB1
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Precursor lesion of enteropathy-associated T cell lymphoma?
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Refractory celiac disease with abnormal intraepithelial lymphocytes.
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Prognosis of enteropathy-associated T cell lymphoma?
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Not good- ulcerations, perforations, and the patient is already malnourished.
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Who gets hepatosplenic T cell lymphoma?
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Young (adolescent to early adult) males.
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Sites of involvement for hepatosplenic T cell lymphoma?
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Liver, spleen, bone marrow... not so much lymph nodes or skin.
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TCR associated with hepatosplenic T cell lymphoma?
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gammadelta.
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Disease association with subcutaneous panniculitis-like T cell lymphoma?
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20% have autoimmune disease (like lupus).
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Subcutaneous panniculitis-like T cell lymphoma vs. lupus panniculitis?
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Lupus panniculitis has plasma cells, and usually other inflammatory cells are absent with the lymphoma.
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Kind of T cells involved in subcutaneous panniculitis-like T cell lymphoma?
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CD8 alphabeta T cells.
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Features of subcutaneous panniculitis-like T cell lymphoma?
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Nodules on trunk and extremities. No ulceration but frequent necrosis (can see foamy histiocytes of fat necrosis). Often neoplastic cells will rim individual adipocytes.
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Most common cutaneous T cell lymphoma?
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Mycosis fungoides
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Clinical stages of MF?
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Patch, plaque, tumor.
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Lymph node involvement of patients with MF?
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Enlarged LNs frequently show dermatopathic lymphadenopathy with paracortical expansion due to histiocytes. Increasing presence of cerebriform lymphocytes with increasing stage.
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MF and CD7?
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It is typically negative.
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Most important prognostic factor in MF?
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Clinical stage: the extent of cutaneous and extracutaneous disease.
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Prognosis of folliculotropic MF?
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Worse than regular.
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Triad of sezary syndrome?
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erythroderma, generalized lymphadenopathy, and clonally-related T cells with cerebriform nuclei in skin, lymph nodes, and peripheral blood.
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Additional requirements for Sezary syndrome with the triad?
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An absolute Sezary count of at least 1000 cells per mm3, CD4/CD8 ratio of more than 10, and loss of one or more T cell antigens.
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BM in Sezary syndrome?
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Often a remarkable sparing, despite disseminated disease.
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Granulomatous slack skin?
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An extremely rare subtype of cutaneous T cell lymphoma like MF
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Pagetoid reticulosis?
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An intraepidermal cutaneous T cell lymphoma like MF.
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Second most common group of cutaneous T cell lymphomas (after MF)? Second most common type?
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Primary cutaneous CD30-positive T cell lymphoproliferative disorders. Primary cutaneous anaplastic large cell lymphoma is second most common after MF.
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What is included in the CD30 positive T cell lymphoproliferative disorders?
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Cutaneous anaplastic large cell lymphomas and lymphomatoid papulosis, and borderline cases. A spectrum.
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Differential diagnosis of primary cutaneous large cell lymphoma?
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Systemic anaplastic large cell lymphoma with skin involvement, Transformed MF.
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Histology of primary cutaneous anaplastic large cell lymphoma?
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Usually non-epidermotropic infiltrates with cohesive sheets of large CD30 positive tumor cells.
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Prognosis of primary cutaneous anaplastic large cell lymphoma?
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Surprisingly good.
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Lymphomatoid papulosis?
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Chronic, recurrent, self-healing skin disease with large anaplastic (cerebriform or Hodgkin like cells) cells in the skin with a marked inflammatory background.
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3 types of histologic pictures of lymphomatoid papulosis?
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A, B, and C. A has the least atypical cells with mostly inflammation, and C is mostly atypical cells. B looks kind of like MF. Type B is CD30 negative!
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Peripheral T cell lymphomas, NOS?
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Account for 30% of peripheral T cell lymphomas in western countries in adults.
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Immunophenotype of peripheral T cell lymphoma, NOS?
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Usually CD4+, loss of CD5, 7, and/or 2.
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3 special variants of peripheral T cell lymphoma, NOS?
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1) Lymphoepithelioid variant (lots of epithelioid histiocytes), 2) follicular varaint (can look like follicular lymphoma), and 3) T-zone (can be mistake for benign paracortical expansion)
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Features of angioimmunoblastic T cell lymphoma?
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1) A peripheral T cell lymphoma with systemic disease, involving lymph nodes, and 2) a prominent proliferation of high endothelial venules and follicular dendritic cells.
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Viral association of angioimmunoblastic T cell lymphoma?
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EBV, but neoplastic T cells are EBV negative.
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Angioimmunoblastic T cell lymphoma and B cells?
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In 75% of cases, there is an expansion of EBV positive B cells.
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Cytology in angioimmunoblastic T cell lymphoma?
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Small to medium sized cells with cleared cytoplasm. Can see RS like cells
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B cell danger in angioimmunoblastic T cell lymphoma?
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Can progress to EBV positive diffuse large B cell lymphoma.
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Phenotype of T cells in angioimmunoblastic T cell lymphoma?
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Like follicular helper T cells: positive for CD3, CD10, and CXCL13
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Prognosis of angioimmunoblastic T cell lymphoma?
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Not good. Most die within 3 years.
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Most ALCL, ALK+ happens in?
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Young people.
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ALCL, ALK+ accounts for what percentage of childhood lymphomas?
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10-20%
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Most patients with ALCL, ALK+ present in?
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High stage disease (lymphadenopathy, extranodal site involvement)
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Hallmark cell in ALCL, ALK+?
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Large with horseshoe or kidney shaped nucleus with an eosinophilic aread next to the nucleus.
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Patterns of ALCL, ALK+?
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Common (can see anaplastic cells in the sinuses, like a metastatic tumor), lymphohistiocytic, small cell (can look signet or fried egg), Hodgkin-like (can look like nodular sclerosis), mixed.
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ALK is on what chromosome? Where is it normally expressed in the body?
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Chr 2. Not expressed in any postnatal tissue, except for rare cells in the brain.
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Staining pattern of CD30 in ALCL, ALK+?
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Cell membrane and golgi regions.
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Immunohistochemical features of ALCL, ALK+?
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Negative for CD3 (!).
ALK+, CD30+, EMA+. Strongly positive for CD25. Also for cytotoxic markers, TIA and granzymeB |
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Cytoplasmic granular ALK staining?
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Diffuse large B cell lymphoma with immunoblastic/plasmablastic features.
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Most frequent genetic aberration in ALCL, ALK+?
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t(2;5) nucleophosphmin-ALK
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Overall 5-year survival of ALCL, ALK+? ALK-?
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80%,
48% |
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Clinical differences between ALK- and ALK+ ALCL?
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ALK- peeps are older and worse prognosis. Cells are uglier.
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Hodgkin lymphoma accounts for what % of all lymphoma?
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30
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Staging for Hodgkin lymphoma?
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I one site (LN or lymphatic tissue)
II. More sites, same side of diaphragm III. Both sides of diaphragm (III2, vessel nodes) IV. Extranodal site |
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2 main types of Hodgkin lymphoma?
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Nodular lymphocyte predominant and classical Hodgkin lymphoma
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4 types of Classical Hodgkin lymphoma?
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Nodular sclerosis, mixed cellulariy, lymphocyte depleted, and lymphocyte rich
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"popcorn" cells?
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L and H cells, nodular lymphocyte predominant hodgkin lymphoma?
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What does nodular lymphocyte predominant Hodgkin lymphoma look like?
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Nodules in the lymph node of small lymphocytes, histiocytes, and L&H cells.
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Popcorn cells stain...
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+cd20, cd79a, oct2, bob1.
Negatvie for cd15 and cd30 |
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Ring of t lymphocytes around a bigger cell?
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Hodgkin lymphoma
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architectural pattern of nlphl?
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Large spherical networks of dendritic cells.
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Who gets nlphl and prognosis?
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Young men, and good prognosis
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Percentage of hodgkin's lymphomas that are classical type?
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95%
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Who gets Classical Hodgkin lymphoma?
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bimodal peak (15-35) and later in life
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EBV is linked to what kinds of hodgkin lymphoma?
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mixed cellularity type and lyphocyte depleted
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Anatomic site most frequently involved by classic Hodgkin lymphoma?
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Cervical lymph nodes (75%) of cases
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Splenic involvement by classic Hodgkin lymphoma is associated with what?
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An increased risk of extranodal dissemination.
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Subtype of Hodgkin lymphoma most likely to be found in the mediastinum?
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Nodular sclerosis
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Mummified cell?
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A Reed-Sternberg cell that has condensed cytoplams and pyknotic reddish nuclei.
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Lacunar cell?
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Nodular sclerosing Hodgkin lymphoma.
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Interesting staining pattern of RS cells? Best B cell marker for RS cells?
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CD30+, CD15 usually +, CD45 negative. Mum1 intensely +. Pax5 is best B cell marker.
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Oct2 and Bob1 in RS cells?
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Usually both are absent
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What % of Classical Hodgkin lymphoma is curable?
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85
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How many nodules do you need to call it nodular sclerosis CHL?
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Just one
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Mixed cellularity CHL?
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Looks like nodular sclerosis, except no sclerosis. Cases that dont fit the other types are put in this category.
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Rarest CHL subtype?
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lymphocyte-depleted
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Common cytogenetic abnormalities seen in CLL?
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trisomy 12, del 11q23(bad prognosis), del 13q14
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Bad prognosis things in CLL?
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High CD38, p53, unmutated IgH, deletions of 17p and 11 q.
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Things that affect the red pulp of the spleen?
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Hairy cell leukemia, T-LGL, hepatosplenic T cell lymphoma. Also, histiocytoses, extramedullary hematopoiesis,
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Translocations in Burkitt lymphoma?
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t(8;14)
t(2;8) t(8;22) |
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How do you tell the difference between T-cell rich large B cell lymphoma and nodular lymphocyte predominant HL?
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You only hae to find one nodule- NLPHL can have a very diffuse architecture, so do a follicular dendritic cell marker to find the nodules.
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L&H cells tend to be ringed by what?
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CD3 positive T cells.
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Oct2/Bob1?
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Positive in LH cells, but negative in most RS cells.
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What percent of nodular sclerosing HOdgkin lymphomas involve the mediastinum?
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80%
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Where does lymphocyte-depleted Hodgkin's lymphoma like to be?
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In the retroperitoneal lymph nodes or abdominal organs.
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Which Hodgkin's lymphoma could be mistaken for DLBCL?
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Classical, lymphocyte depleted. It has mostly large Reed-Sternberg cells.
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Common clinical for hairy cell leukemia?
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Older (50ish) white male with pancytopenia.
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CD25?
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For hairy cell and systemic mastocytosis. Also adult T cell leukemia/lymphoma is usually positive.
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Hematologic malignancy with the highest familial predisposition?
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CLL
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What does Zap-70 tell you?
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It is a surrogate for the mutational status of CLL. Zap70 positive is associated with unmutated (worse prognosis).
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Danger of CLL?
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10% develop DLBCL
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How does B-prolymphocytic leukemia present?
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B symptoms, massive splenomegaly, and a rapidly rising white count.
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Circulating villous lymphocytes?
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splenic marginal zone lymphoma
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What does splenic marginal zone lymphoma look like?
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Nodules in the white pulp surrounding germinal centers with marginal zones of larger pinker cells surrounding the nodules.
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Cytogenetics in splenic marginal zone lymphoma?
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Not t(11;18). Loss of 7q more common.
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Monocytopenia?
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Characteristic of hairy cell leukemia.
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Morphology of hairy cell leukemia in the spleen?
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Fried egg appearance.
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Characteristic cytochemistry for hairy cell leukemia?
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Tartrate-resistant acid phosphatase (TRAP) positivity
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Most specific marker for hairy cell leukemia?
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Annexin A1- not expressed by any other B cell lymphomas, but is expressed by T cells and myeloids.
CD103 Also express CD11c, CD25 CD19, CD22 |
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Viral association of LPL?
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HCV in some places (with type II cryoglobulinemia)
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Most common antibody in MGUS?
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IgG (70%)
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Things with MGUS that make it more likely to progress?
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IgM or IgA (vs. IgG) and higher amount of plasma M protein.
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Where do most extraosseous plasmacytomas occur?
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In the upper respiratory tract.
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Renal diseases associated with myeloma?
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Cast nephropathy (myeloma kidney), amyloid, and light chain deposition disease (which is not amyloid)
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Curious fact about antibiotic treatment for H. pylori?
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MALT-associated with h. pylori has been known to go into remission with antibiotic treatment.
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Most common site of MALT lymphoma?
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Stomach
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How does follicular lymphoma typically present?
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With widespread disease.
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Most common B cell lymphoma in the skin?
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Primary cutaneous follicle center lymphoma
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Difference between blastoid and pleomorphic mantle cell lymphoma?
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Blastoid has blasty looking cells (open chromatin, prominent nucleoli) and a high mitotic rate. Pleomorphic cells are big and ugly and often polylobated.
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Vessels seen in mantle cell lymphoma?
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Pale, hyalnized vessels.
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B cell lymphomas that are positive for CD10 and bcl-6?
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Germinal center phenotype: follicular lymphoma and Burkitt lymphoma.
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Common morphologic variants of DLBCL, NOS?
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Centroblastic, immunoblastic, and anaplastic.
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Commonest translocation in DLBCL, NOS?
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Involves the bcl-6 gene on chr 3. DLBCL, NOS is usually bcl-6 positive.
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How do you tell the difference between nodular lymphocyte predominent hodgkins and T-cell/histiocyte rich large B cell lymphoma?
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T-cell rich B will have a lot of histiocytes.
T-cell rich B doesn't have T cells rosetting around the big cells. T-cell rich B doesn't have the follicular dendritic cell framework. |
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IHC difference between primary cutaneous follicle center lymphoma and primary cutaneous DLBCL, leg type?
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DLBCL leg type is often bcl-2 positive and the follicle center one is usually bcl-2 negative.
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Other sites involved by lymphomatoid granulomatosis?
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Lung and also brain, kidney, liver, and skin.
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A large B cell lymphoma that is in the thymus only and no other lymph nodes or bone marrow?
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Primary thymic (mediastinal) large B cell lymphoma.
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Typical location for plasmablastic lymphoma?
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Oral cavity, mucosal sites.
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Gender predilection for Burkitt?
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Males (2-3:1)
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Types of Burkitt, clinically?
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Endemic, sporadic, and immunodeficiency-associated.
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EBV and Burkitt?
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Usually seen in cases of endemic BL (along with malaria infection), less commonly in sporadic.
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Burkitt and HIV?
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Usually HIV+ patients develop BL with CD4 counts are still high, suggesting that it is not just immunosuppression alone.
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Burkitt leukemia?
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Rarely presents with predominantly PB invovlement, but may.
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Lymphoma with medium-sized cells with squared-off borders?
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Burkitt
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What do the circulating prolymphocytes look like in T-prolymphocytic leukemia?
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Medium with basophilic nongranular cytoplasm and chromatin that is coarse with a nucleolus. Cytoplasmic blebs are characteristic.
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Prognosis for T-prolymphocytic leukemia?
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Not good.
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Prognosis of T cell large granular lymphocytic leukemia?
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An indolent disease- morbidity comes from the anemia and neutropenia.
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Type of T cell in MF?
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CD4
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Pattern of ALK staining in ALCL?
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If they have the t(2;5) then nuclear AND cytoplasmic. Other translocations may show other patterns.
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Most common cause of chronic benign lymphadenopathy in the US?
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Cat scratch disease.
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Cat scratch disease in the lymph node?
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Subcapsular granulomas to stellate necrotic abscesses surrounded by palisading histiocytes.
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Cells you may see in EBV lymphadenopathy?
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Many immunoblasts that can have Reed-sternberg like features.
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Who is prone to H. influenza infection in lymph nodes?
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People who are susceptible to infections with encapsulated organisms (also, strep and staph), so agammaglobulinemia.
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Associations of HHV8?
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Kaposi's, primary effusion lymphoma, some multicentric castleman's. (8 the CKE)
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Things that can cause a suppurative lymphadenitis?
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Staph, cat scratch disease, and LGV
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Things that can cause a necrotizing lymphadenitis?
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Kikuchi, cat scratch, tularemia, anthrax, yersinia pestis (bubonic plague), typhoid fever.
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Eosinophils in the lymph node, along with granulomas?
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Allergic granulomatosis in lymph nodes.
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Angiolymphoid hyperplasia with eosinophils?
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Epithelioid hemangioma.
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Symptoms of hyaline-vascular Castelman's disease?
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Usually asymptomatic.
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Treatment for solitary Castelman's disease?
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Surgical excision.
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Dermatopathic lymphadenitits?
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Nodular, interfollicular/paracortical histiocytic expansions with some pigment.
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Kawasaki disease, aka?
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Mucocutaneous lymph node syndrome. Pharyngitis, lymphadenopathy, arthritis, skin rash, and coronary arteritis.
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Where does Kimura disease affect?
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Subcutaneous in the head and neck, salivary glands, and lymph nodes.
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A systemic histiocytic disease that is CD1a negative?
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Erdheim-chester disease.
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Hallmark cells of ALPS?
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CD45RO-, CD4/8- T cells.
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What does the lymph node look like in Hyper-IgM syndrome?
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There are primary follicles but no germinal centers.
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Most important risk factor for EBV-drive PTLD?
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EBV seronegativity at the time of transplant.
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Organs with the highest incidence of PTLD?
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Lung- high
Heart and liver- intermediate Kidney- low. |
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When does EBV-positive PTLD tend to present?
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In the era of cyclosporine, usually within the first year (EBV- tends to present later).
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LPD associated with patients who have Crohn's disease taking infliximab?
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Hepatosplenic T cell lymphoma.
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Gender predilection in LCH?
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Males (3.5:1)
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Leukemia associated with LCH?
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T lymphoblastic leukemia- the T cell receptor gene rearrangement is present in LCH cells.
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Most specific feature for Castelman in LN?
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Double germinal center. (also onion skinning and lollipop- vessels diving into germinal center).
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Characteristic pattern of dermatopathic lymphadenitis?
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Interfollicular expansion.
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Funny thing about cells in Kikuchi?
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Histiocytes: are crescentic and express MPO.
Neutrophils: excpetional in their absence (compared to the amount of necrosis) |
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Cells you can see in ALPS?
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T cells: CD4/8 negative and are naive (CD45+), yet cytotoxic (perforin, TIA).
B cells: CD5+ |
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Syphillis in the lymph node?
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Capsular fibrosis with infiltration by plasma cells and lymphocytes.
Rememember the obliterative endarteritis |
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Stain that differentiates between interdigitating and follicular dendritic cells?
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CD21
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Angiolymphoid hyperplasia with eosinophilia vs. Kimura?
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Kmura has LAD, peripheral hypereosinophilia, and increased IgE (and affects asian men) and ALH with E does not (and affects women usually).
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Cells that are positive for naphthyl- ASD chloroacetate are?
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Myeloids, mast cells, and macrophages.
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Hairy cell leukemia often presents with?
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Infections due to pancytopenia
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Mechanism of resistance to Gleeved in CML?
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May happen by mutations, overexpression of ABL/BCR, or reduced cellular uptake of drug.
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Hodgkin's lymphoma most likely to transform to DLBCL?
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Nodular lymphocyte predominant.
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Hairy cell leukemia can be positive for which marker, commonly associated with another lymphoma?
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Cyclin D1
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Which feature is not seen in HIV lymphadenopathy?
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I think it's capsular fibrosis (that's syphilis)- reactive follicular hyperplasia with serpentine follicles, plasma cells/mixed infiltrate with hypervascularity in the interfollicular zones, mantle cell invagination into the germinal centers, dermatopathic lymphadenitis.
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M v F in follicular lymphoma?
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1:1.7 (female predominance)
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Pattern of LCH in the lymph node?
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Sinusoidal pattern.
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Status of T cell receptor in NK/T cell lymphoma?
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Usually nonmutated, not rearranged.
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