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42 Cards in this Set
- Front
- Back
Where are auer rods found |
Myeloid lineage |
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Epidemiology of acute leukemia |
Presence of blasts in bone marrow and peripheral blood Anemia caused by bleeding and replacement of marrow components with leukemic blasts |
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Hallmark characterizations of acute leukemia |
Symptoms of short duration Mild to severe anemia low plts Many immature forms >20% Elevated leukocyte |
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Selecting appropriate treatment of leukemia relies on |
Accurate diagnosis |
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FAB divides acute leukemia into 2 major divisions |
Acute myeloid leukemia AML Acute lymphoblastic leukemia ALL |
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Acute myeloid leukemia is divided into |
M0 thru M7 Nine subtypes |
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Acute lymphoblastic leukemia is divided into |
3 categories L1 thru L3 |
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WHO categories emphasize |
Underlying common genetic characteristics as well as clinical signs and symptoms |
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Most common leukemia subtype |
Acute myeloid leukemia |
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AML is characterized by |
An increase in the number of immature cells in bone and arrest in their maturation |
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AML M0 |
Minimally differentiated Almost all blasts |
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AML M1 |
Most common leukemia in <18 mnth Typically occurs in middle age Majority blasts Auer rods |
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AML M2 |
Acute myeloblastic leukemia with maturation Blasts with maturation stages |
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AML M3 |
Promyelocytes predominant cell DIC risk is higher |
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AML M4 |
Proliferation of granulocytes and monocytes Early myelogenous cells are predominant but appx 20% of the cells are monocytes |
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AML M5 |
Pure monocytic leukemia 2 forms M5A and M5B Mostly monocytic Monoblast, promono, monocytes |
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AML M5A |
Most common in young adults 16 |
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AML M5B |
More common in middle age |
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Pure monocytic anemia constitutes less than what % of leukemia |
Less than 15% |
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AML M6 |
Erythroleukemia Erythroblasts and myeloblast and myeloblast Poik and aniso along with immature RBC |
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AML M7 |
Acute megakaryoblastic leukemia 50% or more of the blasts are from megakaryocyte lineage |
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Predominant type of leukemia in children 2-10 yrs old |
Acute lymphoblastic leukemia |
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ALL 3 categories |
L1: children L2: older children and adults L3: patients with leukemia secondary to burkitt lymphoma |
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WHO classification of ALL |
B cell neoplasm T cell neoplasm |
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B cell neoplasm |
Secrete monoclonal proteins (immunoglobulin) inappropriately causing increased blood viscosity |
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T cell neoplasm |
More aggressive Involveme extranodal/extramedullary sites like skin CNS |
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Signs and symptoms as ALL infiltrates tissue |
Joint and bone pain especially in extremities |
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Signs symptoms of ALL |
Hepatomegaly and lymphadenopathy Extramedullary hematopoiesis |
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Lab data of ALL |
25% have leukopenia 50%of cells are blast and the rest are mostly lymphs and smudge cells |
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Differentiate AML and ALL PBS |
AML: adults, >20% myeloblasts, auer rods ALL: children, >20% lymphoblasts |
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Cytochemistry of AML |
Positive peroxidase and SBB Negative TdT |
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Cytochemomistry of ALL |
Negative peroxidase and SBB Positive TdT |
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Almost 50% of all leukemia patients demonstrate |
Some form of chromosomal abnormality |
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Sudan black stain |
Myeloblast ID Detect cellular lipids Black staining is pos |
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Myeloperixidase stain |
Myeloblast ID Peroxidase activity present in primary granules of myeloid and monocytic cells |
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Periodic acid Schiff stain |
Lymphoblasts Stains glycogen stores in cells |
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Non specific Esterase |
differentiate myeloblast from monocyte Monocyte strongly positive Granules stain orange |
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Phosphatase stain |
Cells of hair cell leukemia are strongly positive |
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Surface markers |
Proteins on cell membrane that can be detected with immunologic reagents are extremely helpful in differentiating ALL |
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CALLA |
Common ALL antigen is found on surface of lymphoblasts in 70% of patients with ALL |
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Life threatening emergencies of acute leukemia |
Infections, bleeding, leukemic infiltration of organs, metabolic abnormalities, hyperleukocytosis |
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Treatment options of acute leukemia |
Chemo, stem cell transplant, vaccines?, immunotherapy |