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Question
Answer
WBC count   Normal: 5-10 K/µL Leukopenia: <5 K/µL Leukocytosis: >10 K/µL  
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Causes of neutropenia   Drug toxicity (e.g. chemotherapy)//Severe infection (e.g. gram  
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Causes of lymphopenia   Immunodeficiency (e.g. DiGeorge syndrome [no thymus] or HIV)// High cortisol state (e.g. exogenous corticosteroids or Cushing syndrome)// Autoimmune destruction (e.g. SLE)// Whole body radiation  
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Causes of neutrophilic leukocytosis   Bacterial infection or tissue necrosis (release of marginated pool and recruitment of bone marrow neutrophils/ High cortisol state (release of marginated pool)  
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Marginated pool   leukocytes "hang" in lung vasculature//cortisol disrupts adhesion, releases marginated pool// causes leukocytosis  
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Fc receptors   Fc receptors help neutrophils recognize immunoglobulin (opsonin for phagocytosis)//lack of CD16 indicates lack of Fc receptors  
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Causes of monocytosis   chronic inflammatory states (autoimmune or infectious)// malignancy  
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Causes of eosinophilia due to increased IL   5 production//allergic reactions//parasitic infections//Hodgkin lymphoma  
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Causes of basophilia   classically seen in chronic myeloid leukemia  
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Causes of lymphocytic leukocytosis   viral infections//B. pertussis infection  
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Acute leukemia   accumulation of neoplastic blasts (>20% in the bone marrow)//blasts crowd out normal hematopoiesis// blasts enter blood, result in high WBC count with large appearance and "punched out" nucleoli  
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TdT   DNA polymerase in lymphoblasts, but not myeloblasts or mature lymphocytes// can stain for TdT to diagnose ALL  
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ALL   accumulation of >20% lymphoblasts in bone marrow// positive stain for TdT// most commonly arises in children// association with Down syndrome (usually >5yo)// subclassified into B  
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B- ALL   accumulation of TdT+ lymphoblasts expressing CD10, CD19, and CD20//excellent response to chemo// requires prophylaxis to scrotum and CSF// t(12,21) has good prognosis (usually in kids), t(9,22) has poor prognosis (usually in adults)  
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T-ALL   usually presents in teenagers as a thymic mass (called "lymphoma")// remember T's: T cells, teenagers, thymic mass  
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AML   accumulation of >20% myeloblasts in bone marrow// positive stain for myeloperoxidase// crystal aggregates of MPO: Auer rods// may arise from myelodysplastic syndromes  
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Acute promyelocytic leukemia   subtype of AML// has t(15;17): translation of retinoic acid receptor// RAR blocks maturation of promyelocytes// treatment = atra  
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Acute monocytic leukemia   subtype of AML//blasts usually lack MPO //characteristically infiltrate gums//  
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Acute megakaryoblastic   subtype of AML// blasts usually lack MPO //associated with Down syndrome (usually <5yo)  
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Chronic leukemia   accumulation of mature LYMPHOcytes, characterized by a high WBC count with blasts <20%// often insidious onset// usually seen in older adults  
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CLL   accumulation of naive B cells that co// most common type of leukemia// see increased lymphocytes and smudge cells// can involve lymph nodes  
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Complications of CLL   hypogammaglobulinemia (infection most common cause of death)// autoimmune hemolytic anemia//transformation to large B cell lymphoma (will see enlarging lymph nodes or spleen)  
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Hairy cell leukemia   accumulation of mature B cells with "hairy" cytoplasmic processes// TRAP+ // features: splenomegaly (hairy cells in red pulp), "dry" bone marrow tap (due to marrow fibrosis)// excellent response to cxtrpy  
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Adult T cell leukemia/lymphoma (ATLL)   accumulation of mature CD4+ T cells//associated with HTLV// presents with rash, generalized lymphadenopathy, hepatosplenomegaly, punched out bone lesions with hypercalcemia  
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Mycosis fungoides   accumulation of mature CD4+ T cells that infiltrate skin// presents with localized skin rash, plaques, nodules: called Pautrier microabscesses// cells can spread to the blood// characteristic lymphocytes with cerebriform nuclei (Sezary cells)  
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Myeloproliferative disorders   accumulation of mature myeloid cells// usually in late adulthood(50//high WBC count with hypercellular bone marrow// all myeloid cells are increased, but classified based on dominant myeloid cell producedall myeloid cells are increased, but classified bas  
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Complications of MPD   - increased risk for hyperuricemia and gout (high cell turnover) - progression to marrow fibrosis - transformation to acute leukem  
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CML   - type of MPD, granulocytes are predominant cell type - basophils characteristically increased - t(9;22): Philadelphia chromosome --> BCR-ABL fusion protein with increased tyrosine kinase activity  
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Treatment for CML   Imatinib// blocks tyrosine kinase activity of BCR  
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Outcomes of CML   can transform to AML (2/3) or ALL (1/3) because mutation is in the pluripotent stem cell  
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How to distinguish CML from leukemoid reaction CML will have:   negative LAP stain//increased basophils//t(9;22)  
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Polycythemia vera   - type of MPD, RBCs are predominant cell type - assoc with JAK2 kinase mutation - blood becomes hyperviscous, requires phlebotomy (without, death usually within a year)  
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S/sx of polycythemia vera   - splenomegaly (extramedullary hematopoiesis) - leukoerythroblastic smear (teardrop RBCs, nucleated RBCs, immature granulocytes) - increased risk of infection, thrombosis, bleeding  
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How to distinguish polycythemia vera from reactive polycythemia In polycythemia vera:   EPO levels are decreased// oxygen saturation is normal  
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Essential thrombocythemia   type of MPD, platelets are particularly increased// assoc with JAK2 kinase mutation //symptoms related to increased risk of bleeding AND/OR thrombosis (platelets either working really well or not at all)//rarely progresses to marrow fibrosis or acute leuk  
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Myelofibrosis   - type of MPD, megakaryocytes are particularly increased - assoc w/ JAK2 kinase mutation (50% of cases) - megakaryocytes produce excess PDGF --> marrow fibrosis  
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Causes of painful vs. painless lymphadenopathy   lymphadenopathy Painful: usually draining region of acute infection// Painless: seen w/ chronic inflammation, metastatic carcinoma, or lymphoma  
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Follicular lymphoma   - NHL of small CD20+ B cells that form follicle-like nodules - typically late adulthood - can progress to diffuse large B-cell lymphoma  
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Pathophys of follicular lymphoma   - Bcl2 normally inhibits apoptosis in peripheral cells - follicular cells generally lack Bcl2 so they can undergo testing - t(14;19) --> overexpression of Bcl2 --> cells that fail testing no longer die --> neoplasm  
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Treatment of follicular lymphoma   reserved for symptomatic pts//involves low  
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How to distinguish follicular lymphoma from reactive follicular hyperplasia Follicular lymphoma shows:   disruption of LN architecture// lack of tingible body macrophages (white spaces in follicle indicate macrophages are gobbling up apoptotic B cells)// Bcl2 expression //monoclonality  
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Mantle cell lymphoma   NHL of small CD20+ B cells that expand mantle zone around follicle //typically late adulthood  
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Pathophys of mantle cell lymphoma   t(11;14) --> overexpression of cyclin D1 --> promotes G1/S transition in cell cycle --> neoplasm  
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Marginal zone lymphoma   - NHL of small CD20+ B cells that expand the marginal zone around the mantle/follicle - assoc with chronic inflammatory states (e.g. Hashimoto thyroiditis, Sjogren syndrome, H. pylori gastritis)... marginal zone typically only present with chronic inflam  
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Burkitt lymphoma   - NHL of intermediate-sized CD20+ B cells - associated with EBV - translocations of c-myc (nuclear regulator) --> cell growth - high mitotic index and "starry sky" appearance under microscope  
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Classic presentation of Burkitt lymphoma extranodal mass in a child or young adult   extranodal mass in a child or young adult - African form: jaw - Sporadic form: abdomen  
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Diffuse large B   - most common form of NHL - large CD20+ B cells grow diffusely in sheets - clinically aggressive - arises sporadically or from transformation of lower-grade lymphoma - presents in late adulthood  
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Hodgkin lymphoma overview   - proliferation of Reed-Sternberg cells - cytokine release attracts other inflammatory cells, may lead to fibrosis and "B" symptoms (night sweats, fever, chills) - reactive cells are the bulk of the tumor - nodular sclerosis is most common subtype  
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Reed Sternberg cells   - large B cells with multilobed nuclei & prominent nucleoli ("owl eye" appearance) - neoplastic in Hodgkin lymphoma - classically CD15 and CD30+ with NO CD20 expression - secrete cytokines that attract lymphos, plasma cells, macrophages and eosinophils  
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Nodular sclerosis   - most common subtype of Hodgkin lymphoma - classically presents with enlarging cervical or mediastinal lymph node in young adult, usually female - lymph node divided by bands of sclerosis - Reed Sternberg cells present in lake-like spaces (aka lacunar  
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Best/worst prognosis for Hodgkin lymphoma   - lymphocyte-rich subtype has best prognosis - lymphocyte-deprived has worst prognosis (usually in elderly and HIV+)  
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Multiple myeloma   malignant proliferation of plasma cells in marrow// high serum IL //plasma cells overproduce osteoclast activating factor, Igs, light chain  
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S/sx of multiple myeloma   osteoclast activating factor// IgA & IgG// = bence jones protiens  
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Monoclonal gammopathy of undetermined significance (MGUS)   increased serum protein with M spike// other features of multiple myeloma are ABSENT// common in elderly, some will develop multiple myeloma  
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Waldenstrom macroglobulinemia   B cell lymphoma with monoclonal IgM production// similar to multiple myeloma but: no lytic bone lesions// visual and neurologic deficits (due to serum hyperviscosity)// bleeding (defective platelet aggregation)// treat with plasmapheresis  
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Langerhans cell histiocytosis   neoplastic proliferation of Langerhans cells// characteristic Birbeck (tennis racket) granules seen on EM// cells are CD1a+ and S100+//  
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data source   clarebp on quizlet(dot)com  
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