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    Lymphoid Malignancies (1)

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    Reman A. Alingasa

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    Lymphoid Malignancies (1)

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    3 views30 pages

    Lymphoid Malignancies (1)

    Uploaded by

    Reman A. Alingasa

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    © All Rights Reserved
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    MLAB 1415-

    Hematology

    KeriLymphoid
    Brophy-Martinez
    Malignancies
    Hematological
    Malignancies
    “Monoclonal”
    Lymphoma
    Leukemia Myeloma

    Sezary Cell Multiple Myeloma


    CLL Hodgkins Lymphoma MGUS
    PL Non-Hodgkins
    HCL
    Introduction

    ■ Categories
    ❑ Leukemia
    ■ A malignant disease of hematopoietic tissue characterized by
    replacement of normal bone marrow elements with abnormal
    (neoplastic) blood cells.
    ■ Abnormal cells are also seen in peripheral blood
    ❑ Lymphoma
    ■ Abnormal proliferation of lymphoid cells within the lymphatic
    tissue or lymph nodes
    ■ Results in a solid tumor/mass
    ❑ Myeloma
    ■ Malignant disorders of B cells
    Normal Vs. Neoplastic

    Normal Neoplastic
    ■Polyclonal ■Monoclonal
    ■Regular ■Irregular
    ■Reversible ■Irreversible
    Pathogenesis/Risk Factors
    ■ Acquired genetic factors
    ❑ Proto-oncogenes
    ❑ Tumor suppressor genes
    ■ Inherited genetic factors
    ❑ Wiskott Aldrich
    ❑ Ataxia telangiectasia
    ■ Environmental factors
    ❑ Viral infections (EBV)
    ❑ Bacteria infections (Helicobacter pylori)
    ❑ Exposure to chemicals and/or herbicides
    ■ Misc
    ❑ Immunocompromised
    ❑ Auto-immune disorders
    Classification

    ■Factors to consider
    ❑ Morphological appearance of cells
    ■ Clonality
    ❑ Flow cytometry
    ❑ Chromosome analysis
    ■ Translocations present?
    ❑ Molecular analysis
    ❑ Clinical information & history
    Lymphoid Leukemias

    ● CLL- Chronic Lymphocytic Leukemia


    ● PL- Prolymphocytic Leukemia
    ● HCL- Hairy Cell Leukemia
    Chronic Lymphocytic
    Leukemia- CLL
    ■Clinical features
    ❑ Occurs in persons >50 years old
    ❑ Chronic fatigue, infection
    ■ Result of bone marrow replacement of normal cells with
    lymphocytes.
    ❑ Skin and organ infiltration and enlargement
    ❑ Median survival is 10 years
    Chronic Lymphocytic
    Leukemia(CLL)
    ■General requirements for diagnosis
    ❑ Peripheral blood and bone marrow
    lymphocytosis (>5 x 109/L)
    ❑ Lymphocytes are small with mature
    appearance
    ■ Nucleus is round, with block-type chromatin
    (soccer ball)
    ■ Cytoplasm scarce
    ❑ Smudge cells common
    ■ Occur due to the cell’s fragility in making a smear
    ❑ Prolymphocyte < 10%
    CLL Blood Picture
    Chronic Lymphocytic
    Leukemia
    ■ Treatment
    ❑ Usually treatment is not required until lymphocytosis
    causes other cells to be crowded out resulting in infections.
    ❑ Treatment depends on the stage at which the disease is
    diagnosed and is usually for the symptoms, not the
    disease.
    ■ Chemotherapy
    Prolymphocytic Leukemia

    ■Aggressive
    ■Non-responsive to treatment
    ❑ Poor prognosis
    ■Low incidence rate
    ■Origin can be B or T cell
    Prolymphocytic Blood Picture

    Punched
    out
    nucleolus
    Hairy cell leukemia
    (HCL)
    ❑ Presents in middle age

    ❑ Affects males 7:1 over females


    ❑ Splenomegaly

    ❑ Pancytopenia common
    ■ Increases opportunity for infections & bleeding

    ❑ Bone marrow aspirate can result in a “dry tap” due to


    marrow fibrosis.

    ❑ Hairy cell leukemia can be treated with a one-time


    chemotherapy regimen with a good prognosis of long-term
    survival.
    Hairy cell

    TRAP stain
    Lymphoma
    Sezary’s Syndrome

    ■Leukemic phase of the most common


    cutaneous T-cell lymphoma, mycosis
    fungoides
    ■Lymphadenopathy
    ■Red skin due to lesions that progress to
    tumor stage
    Sezary Cell
    Hodgkin’s Lymphoma

    — Cause is unknown, but has been linked to Epstein-Barr


    virus.
    — Bimodal distribution
    ■ Diagnosed between 15 and 35 years of age
    ■ Over 50 population
    — Males have higher incidence rates
    ■ Lymph nodes are involved
    ❑ Regional, contiguous sites
    Hodgkin’s Lymphoma

    —Characteristic cell is the Reed-Sternberg


    ❑ Giant size (up to 45µm in diameter)
    ❑ Abundant acidophilic cytoplasm
    ❑ Multinucleated or polylobated nucleus
    ❑ Gigantic nucleoli
    Treatment & Prognosis

    ■ Treatment and prognosis


    ❑ Radiation of localized involvement
    ❑ Chemotherapy
    ❑ Combination of above
    ❑ With early diagnosis, long-term disease-free survival
    is seen in about 75% of cases.
    Non-Hodgkin’s Lymphoma:
    Burkitt Lymphoma
    ■ Endemic to Africa
    ■ Found in immunocompromised
    patients, particularly AIDS
    patients
    ■ Rapid growth and tumor cell
    death results in “starry sky”
    appearance of the biopsy
    caused by macrophages
    cleaning up the dead cells.
    ■ Characteristic overgrowth of
    facial bones in the African
    variety and abdominal mass in
    the non-endemic variety.
    Myeloma
    Plasma Cell Disorders

    • Disorders that do not involve lymph nodes


    • Secrete monoclonal immunoglobulin into
    the serum and /or urine
    • Disorders
    • Plasma Cell Myeloma
    ■ Multiple myeloma
    ■ Waldenstroms macroglobulinemia
    • Monoclonal gammopathy of undetermined
    significance (MGUS)
    Plasma Cell Myelomas

    ■ Overproduction of abnormal plasma cells which are the final


    stage in the development of B lymphocytes.
    ■ These cells secrete immunoglobulin, resulting in lytic bone
    lesions
    ■ Risk increases with age- rare under 40
    ❑ Median age 70 years old
    ■ Suspected cause is chronic stimulation of the immune
    system from environmental sources.
    ❑ Ionizing radiation
    ❑ Viruses
    Features
    ❑ Increased production of immunoglobulin heavy and light chains
    (monoclonal gammopathy)
    ■ Heavy chains: IgG, IgA, IgD, IgE, IgM
    ■ Light chains: kappa, lambda
    ■ Most common type of plasma cell myeloma is increased
    production of IgG.
    ❑ Bence-Jones protein
    ■ Light chains spill into the urine and can be detected by lab
    test
    ■ Causes kidney damage

    ❑ Hyperviscosity syndrome
    ■ Excess immunoglobulin causes viscous blood which sludges
    and causes fluid congestion.

    ❑ Normal Immunoglobulin production decreased


    ■ Results in infections
    Lab Findings

    ■ CBC and peripheral smear


    ❑ Red cells form characteristic rouleaux formation (resemble stacked
    coins)
    ❑ Plasma cells may be seen in peripheral blood
    ■ Bone marrow
    ❑ Increased number of plasma cells which form “sheets”

    ■ ESR
    ❑ Increased - serum protein causes red cells to stick together and fall faster

    ■ Chemistry studies
    ❑ Increased BUN and creatinine (kidney tests)
    ❑ Increased calcium
    ❑ Increased LDH
    Plasma Cell Myeloma

    C: hyperCalcemia
    R: Renal insufficiency
    A: Anemia
    B: lytic Bone lesions
    Plasma Cell Myeloma

    ■Treatment
    ❑ Chemotherapy
    ❑ Radiation for localized areas
    ❑ Bone marrow/stem cell transplant for
    younger patients
    ❑ Poor prognosis for individuals that are
    symptomatic
    References
    ■ http://www.itriagehealth.com/wl/disease/burkitt-lymphoma-%2
    8lymph-node-tumor%29#wrapperTop
    ■ http://www.med-ed.virginia.edu/courses/path/innes/wcd/
    lympleuk.cfm
    ■ McKenzie, S. B., & Williams, J. L. (2010). Clinical Laboratory
    Hematology . Upper Saddle River: Pearson Education, Inc.

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