Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
Pathology Associates Of Lexington, P.A.
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Hematopathology Topics
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  • CBC (complete blood count test) topics:
  • Thymic/thoracic
  • Bone marrow findings
  • spleen findings:
    1. siderosis: implies hemolytic anemia or hemochromatosis [L07-6908].
    2. increased foamy macropahges: implies platelett consumption by spleen as in ITP.
    3. increased red pulp polys: implies sepsis..."septic splenitis" (or prolonged operative manipulation).
    4. enlarged & inflammed spleen (acute, subacute, or chronic splenitis [likely related to some systemic infection...FA08-32]; acute or chronic splenic tumor or pseudotumor; septic spleen): is enlargement primarily congestion?...if so, would not use the tumor or pseudotumor term.
    5. increased red pulp fibrosis: implies increased portal forward or back pressure.
  • benign pathological lymph nodes:
    1. infectious
      • suppurating stellate granulomatous adenitis:
        1. cat scratch (Bartonella): whole node often destroyed [L07-2437].
        2. LGV (Chlamydia).
        3. tularemia: likely quite ill.
        4. always check for mycobacterial.
      • casseating granulomatous lymphadenitis: AFB or fungal infections.
      • hyperplasia with prominent & serpigenous germinal centers: think viral.
    2. noninfectious (at least no organism demonstrated):
      • stellate granulomatous, nonsuppurative: think of rheumatoid problems.
      • foreign material: silicone adenopathy [L07-8846].
      • suppurating stellate granulomatous splenitis:
        • infectious, as above, but incompletely worked up
        • idiopathic necrotizing granulomatous lymphadenitis (intense study is negative for organisms known to cause this reaction) [L08-4147].
  • Pseudolymphoma (vs. not-as-yet-diagnosable lymphoma):
    1. skin: [MMM, S-05-6780; HAB, S-06-16018...use of CD3, CD20, & CD23 to show a benign, non-monotypic pattern].
    2. nodes:
      • in a case of "common variable immunodeficiency (compensatory increase in T-cell component) [LMC-05-6145].
    3. lung:
      • in a case of "common variable immunodeficiency (compensatory increase in T-cell component) [LMC-05-6145].
    4. other:
  • Malignant lymphoma:
    1. Hodgkin's disease:
      • lymphocyte predominant can be very subtle, even failing to show atypical histiocytes or R-S cells [___].
    2. non-Hodgkin's lymphoma
  • Leukemia:
    1. acute: hypercellular marrow
      • lymphoid
      • monocytoid: spectrum of with or without "differentiation" [S-04-5214].
      • granulocytic (AML...blast count >30%)
      • mixed: AMML
      • other (mast cells, plasma cells, megakaryocytes, lymphoma cells)
    2. hypoplastic acute: hypocellular marrow with increased blasts; peripheral blood may or may not be blastic. If thought benign & given GCSF and Procrit, will dump increased blasts into PB because these agents cannot make leukemic blasts mature5.
    3. smoldering: hypercellular marrow
      • lymphoid
      • monocytoid
      • granulocytic [S-03-4109 ].
      • other (mast cells, plasma cells, megakaryocytes, lymphoma cells).
    4. subacute: hypercellular marrow
      • lymphoid
      • monocytoid
      • granulocytic
      • other (mast cells, plasma cells, megakaryocytes, lymphoma cells)
    5. chronic: hypercellular marrow
      • lymphoid: adult T-cell lymphoma/leukemia [S07-2516]
      • monocytoid
      • granulocytic
      • other (mast cells, plasma cells, megakaryocytes, lymphoma cells)
  • Myeloproliferative syndromes (MPS or CMPD): hypercellular marrow with some effectiveness in raising counts of one or more peripheral blood elements ; the JAK2 gene related to tyrosine kinase is altered as a point mutation into an oncogene & is strongly specific for MPS [S08-3992] (JAK2V617F mutations are present in almost all patients with polycythemia vera, and in approximately half of those with essential thrombocytosis and myelofibrosis).
    1. polycythemia vera (Osler–Vaquez disease).
    2. essential thrombocythemia (thrombocytosis)
    3. chronic idiopathic myelofibrosis/myelosclerosis (agnogenic myeloid metaplasia)
    4. chronic myelogenous (myeloid) leukemia
    5. atypical chronic myelogenous (myeloid) leukemia
    6. chronic neutrophilic leukemia
    7. chronic myelomonocytic leukemia, myeloproliferative variant
    8. juvenile chronic myeloid leukemia
    9. chronic eosinophilic leukemia (and the hypereosinophilic syndrome)
    10. MPS/CMPD, unclassifiable
  • Myelodysplastic syndromes (MDS): hypercellular marrow with some ineffectiveness in one or more peripheral blood elements so that there are usually -cytopenias at presentation
    1. primary (the blast % is based on morphology because N/C asynchrony shows elevated blast markers sooner than blastic nuclear change2 [S-03-12958]):
      • refractory anemia (RA) [S-04-3702].
      • refractory anemia with ringed sideroblasts (RARS)
      • refractory anemia with excess of blasts (RAEB)...blasts <20%
      • refractory anemia with excess of blasts in transformation (RAEB-T)...blasts 20-30%; new WHO advocates dropping this acronym and calling this "AML >20%".
      • chronic myelomonocytic leukemia (CMML)
      • chronic myelomonocytic leukemia in transformation (CMML-T)
      • myelodysplastic syndrome, unclassified (MDS-U)
        1. megakaryocytic type [S-03-15566] (meg-only dysplasia)
      • "5Q- syndrome": predominantly in elderly women and consists of macrocytic anemia, thrombocytosis (50% of patients), erythroblastopenia and megakaryocyte dyspoietic hyperplasia with nuclear hypolobation & chromosome 5q deletion.
    2. secondary (therapy/toxic related)
  • MPS/MDS overlap cases: [S-03-12900]
  • Other:
    1. cytokine effect in bone marrow [LMC-03-7297].
    2. interleukin-6 syndrome [S-03-16214].
  • Monoclonal cell populations & marrow may be histologically normal: molecular monoclonality before morphologic or clinical criteria are met for a malignant process (we'd categorize sort of like we do small monoclonal proteins as MGUS). In marrows for MGUS workups, we are trying to (1) see if we can demonstrate morphological evidence of increased plasma cells; and, (2) do we see any concerning cytological features; or (3) are there frankly malignant features. It often takes the IHC marker for CD138 to help one discern a too-great concentration of plasma cells. Failure to discern an abnormal morphological population in these tiny samples DOES NOT rule out dyscrasia.
References:
  1. Brunning RD & McKenna RW, Atlas of Tumor Pathology: Tumors of the Bone Marrow, AFIP 3rd series fascicle #9, 1994.
  2. Am. J. Heme, Sept. 2003.
  3. Tumors of Haematopoietic and Lymphoid Tissue, WHO, 2001.
  4. Dr. Armstrong's Jan. 2005 memo (ref. AJCP [Dr. R. W. McKenna] Oct. 2004, p. 588).
  5. Our hemepath's or consultant's tips & comments.
  6. Goldman, John M., "A Unifying Mutation in Chronic Myeloproliferative Disorders", NEJM 352(17):1744-1746 April 28, 2005.
(posted 2002; additions 19 April 2003; latest addn 26 July 2008)
 
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