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Terms in this set (29)
Thrombopoeitin effects on a megakaryocyte precursor
Begins the process of nuclear division without cell division. It first effects the small mononuclear precursor.
Cytokines of BFU-meg
Cytokines of CFU-meg
Describe a megakaryoblast
round with frayed edges, the N:C ratio is high, the cytoplasm is deeply basophilic but there is no granulation. The cytoplasm can be vacuolated. The chromatin pattern is finely organized and homogenous. There may be nucleoli. There may be multiple nucleus
Describe a promegakaryocyte
The edges are more irregular. The N:C ratio is decreased. The nucleus is irregular and lobulated. The chromatin is not organized and condensation is occuring. Nucleoli are rare. Cytoplasm is basophilic on edges. There is perinuclear granules (the granules do not extend to the edge of the cytoplasm)
What is the defining characteristic of a megakaryocyte
The granular megakaryocyte has granules fully filling the cytoplasm.
Defining characteristic of Mature megakaryocyte
N:C ratio is very low, the edges of the cytoplasm are spreading and demarcation zones are clearly visible in the cytoplasm\
Causes of thrombocytosis
physiologic, hemorrhage, splenectomy, myeloproliferative
Effects of EDTA on platelets with prolonged or excessive exposure
Causes of thrombocytopenia
Hereditary, immune destruction, malignancies, drugs
Characteristics of myeloproliferative disorders
proliferation of one or more myeloid lineage with relatively normal maturation of the cells. Splenomegaly and hepatomegaly are common. Commonly results in bone marrow failure due to myelofibrosis. The cells lines effected are granulocytic, erythroid or megakaryocytic
WHO Classification of Myeloproliferative Neoplasms
CML, Chronic neutrophilic leukemia, chronic eosinophil leukemia, polycythemia vera, primary myelofibrosis, essential thrombocythemia, chromic myeloproliferative disease unclassibfiable.
t(9;22)(q34;q11) translocation or BCR ABL fusion
Morphological findings of CML
neutrophilic leukocytosis with left shift without dysplasia, absolute basophilia (increased basophils)
Stages of CML
It is a bi- or tri- phase. Initial chronic phase, accelerated phase, blast phase
Incidence of CML
1-1.5/100,000. Most common in 40-50s
Body organs it effects
Chronic phase will affect hematopoeitic tissue such as the blood, marrow, spleen and liver. The blast phase will effect extramedullary sites including nodes, skin and soft tissue, CNS.
Symptoms of CML
fatigue, weight loss, anemia, night sweats, splenomegaly
Drug designed for CML
Gleevec, it blocks tyrosine kinase activity
Etiology of CML
The fusion of the ABL (c9) and BCR (C22) cause a constituitive tyrosine kinase activity.
The BCR gene
tyrosine kinase activity
signal transduction in regulating cell growth
PB of CML
mild anemia, shift left with median WBC 17 * 10E9. Absolute basophila. No significant dysplasia. Platelets normal or increased
BM of CML
Hypercellular, especially myeloid with decreased erythroid. < 5% blast. Increased megakaryocytes. Progressive increase in reticulin fibrosis
10-19% blasts in the blood or BM in the accelerated phase. 20% in the blast phase.
What % of blasts in CML indicates the blast phase
Diagnoses of the Accelerated phase of CML
Persistent WBC > 10, with splenomegaly unresponsive to therapy. Persistent thrombocytosis > 1000, persistent Thrommocytopenia < 100. Clonal cytogenetic evolution after initial diagnostic karyotype. 20% basophils in PB. 10-19% blasts in the PB or BM.
Diagnosis of CML Blast Phase
Blast equal to or greater 20% of PB or WBC. Extramedullary blast proliferation. Accumaltions of blasts occupy focal but significant areas of the bone marrow.
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