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lecture 21 emmons-wright

instances where acute leukemia can be diagnosed without the presence of 20% blasts AML with following translocations: t(8;21) t(15;17) or inv(16)
general morphologic features of myeloblasts high N/C ratio, finely dispersed nuclear chromatin, 1 to multiple nucleoli, possible presence of fine granules or reddish-pink Auer rods; may be myeloperoxidase +
left shift granulocytes and rare blasts seen peripherally in blood, usually normal reaction to mod-severe infections especially in children
pathologic associations of AML exposure to radiation or chemo in the past, increased risk if prior CML, loose association with paroxysmal nocturnal hemoglobinuria
differences in cytogenetics of AML in groups younger than 40 y/o and those with median age of 65 those < 40 y/o: usually balanced translocation // those > 65 y/o usually have > 3 cytogenetic aberrations from accumulation of mutations, portends worse prognosis
how AML is diagnosed when > 20% myeloblasts are seen in the blood or bone marrow
AML with monoblastic differentiation cells with pale gray colored cytoplasm more abundant than myeloblast, fine & lacy chromatin with round or folded nucleus; nonspecific esterase + but MPO -, may express CD14, CD36, and/or CD6
markers of immature myelocytes (myeloblasts) CD34 is present on pluripotent hematopoietic stem cells and progenitor cells of many lineages; CD117 is hemato. stem cell growth-factor receptor
markers of any myeloblast CD13, 33
leukocyte common antigen CD45
AML with t(8;21) or RUNX1/RUNX1T1 occurs in younger pts, typically myeloblasts with spectrum of neutrophilic maturation, dysplastic features like abnl segmentation and hypogranulation, single Auer rods in blasts and mature neutrophils; favorable prognosis
markers of monoblastic lineage CD14, 36 and MAYBE 64
main cellular effect of t(8;21) or inv(16) in myeloblasts defect of core-binding factor & inhibition of normal myeloblast maturation
AML with inv(16) or CBFB/MYH11 mostly younger pts, typically mixture of myeloblasts and monoblasts with abnormal eosinophilic precurors, may have Auer rods, may be MPO (myelo) or non-specific esterase + (mono); fairly good prognosis
main cellular effect of t(15;17) in myeloblasts fusion of the PML gene on chromosome 15 and the retinoic acid receptor-α (RARα) gene on chromosome 17 resulting in the PML-RARα fusion gene
AML with t(15;17) aka APL or PML/RARA middle-aged adults, frequently presents as emergency DIC, typified by promyelocytes, "sliding plate" bi-lobed nuclei and dense purple granules, mult Auer rods, MPO+, microgranular variant, favorable prognosis when treated with all-trans retinoic acid
molecular markers for APL CD34- and CD117+
AMl with myelodysplasia-related changes up to 35% of all AMLs, older pts, arises from prev diagnosed myelodysplastic syndrome, demonstrates cytogenetic abnormalities associated with myelodysplasia and sig degree of multilineage dysplasia, poor prognosis
AML, therapy-related occurs as late complication of chemo or radiation for prior malignancy; implicated by drugs like alkylating agents, topo inhibitors, antimetabolites and antitubulin agents, often complex karytoype and poor prognosis
myelodysplastic syndromes causes ineffective hematopoiesis causing peripheral cytopenias and hyperplastic bone marrow, high risk of transformation into AML; associated with environmental exposures or prev chemo/radiation, which portends a poorer prognosis
histologic characteristics of myelodysplasia hypogranular and hypolobulated neutrophils, anisopoikilocytosis, basophilic stippling in nucleated RBCs, large and hypogranular plts, immature monocytes
pseudo-Pelger-Huët neutrophils cells typical of myelodysplastic syndromes
dyspoiesis seen in MDS = micromegakaryocytes and multinucleated forms with each nucleus having its own single lobe, multinucleated erythroid precursors, megaloblastoid changes or RBCs, nuclear fragmentation and apoptosis seen throughout
characteristics of chronic myeloproliferative neoplasms hypercellular bone marrow with intact maturation and minimally disturbed cytological appearance; pt presents with fatigue malaise weight loss gout extramedullary hematopoiesis BASOPHILIA
chronic myelogenous leukemia (CML type of CMPN, almost always typified by Philadelphia chr t(9;22) making bcr-abl fusion gene; neoplastic pluripotent BM stem cells causes marked leukocytic proliferation with wide array of maturational stages
phases of CML chronic phase - about nl blast count in BM of ~ 5% // accelerated phase - > 10% blasts // acute blastic or leukemic phase = more than 20% blasts
polycythemia vera (PV) CMPN with increased RBC production independent of nl erythropoiesis regulation; accompanied by increase in megakaryocytes and (maybe myeloid elements)
cytogenetic abnormality of PV mutation in exon 14 of JAK2 gene resulting in V617F substitution ///
clinical features of PV HTN and thrombotic episodes due to Hct being near or > 60%, WBCs from 12-50K, plts > 500K, low erythropoietin levels; pruritis, dizziness, paresthesias, erythromelalgia, visual disturbances
consequence of advanced PV severe bone marrow fibrosis and extramedullary hematopoiesis, called post-polycythemic stage. may also see absence of storage iron in BM due to sustained erythrocytosis
chronic myelofibrosis (CM) CMPD typified by increased in all myeloid cells but specifically megakaryocytes that drive abnormal reticular fiber and collagen deposition in the BM; half have the JAK2-V617F mutation
clinical features of CM pts usually asymptomatic until BM is fibrosed and signs of extramedullary hematopoiesis develop like splenomegaly. leukocytosis from 15-30K, occasional blasts, basophilia, circulating nucleated RBCs with L shift, megakaryocytic fragments, dry-tap BM
leukoerythoblastic rxn seen in chronic myelofibrosis = circulating nucleated RBCs with increased numbers of blastic leukocytes
essential thrombocythemia (ET) CMPD involving mainly megakaryocytes, dx'ed by sustained thromobcytosis of > 450K, half have JAK2-V617F
clinical features of ET multiple placental infarcts causing recurrent abortions, fetal growth retardation, transient cerebral ischemias, paresthesias, digital ischemia from microvascular occlusion
histological appearance of ET sizable clumps of plts on bone marrow aspirate, maybe be normocellular or mildly hypercellular, marked proliferation of enlarged megakaryocytes with nuclear hyperlobation
Created by: sirprakes