Flashcards in 3.24.14* Goorha - Acute and Chronic Leukemias Deck (20):
three types of acute leukemia
aplastic anemia clinical features
a. blood cell -penia
b. common infections of mouth/throat
c. bruising, excessive bleeding
d. no enlarged lymph nodes, liver, spleen
aplastic anemia lab findings
a. normochromic, macrocytic
b. very low reticulocyte count
d. low granulocytes, normal looking neutrophils, maybe low lymphocytes
e. no abnormal cells in PBS
f. bone marrow hypoplasia with 75% fat
Major leading causes of AML?
pre-existing hematological disorder such as myelodysplastic syndrome
leukemia in children
ALL (kids 3-7 and then in people over 40)
malignant transformation of what cell type results in acute leukemia?
stem cells or early progenitors which causes accumlation of blast cells (early BM hematopoietic cells)
Difference between AML and ALL
based on whether blasts are myeloblasts or lymphoblasts (determined by immunophenotyping)
Differentiating PBS of AML from ALL
AML- auer rods, MPO, CD33, CD13, HLA-DR
ALL- TdT, CD10, CD19, CD20
coagulopathy with elevated INR and decreased fibrinogen,
white blood count of 2.0, haemoglobin of 8.1 and platelet count of 43, with blasts present on peripheral smear.
Acute promyelocytic leukemia (M3 AML)
Acute promyelocytic leukemia (M3 AML) cytogenetics
Chromosome 15,17 translocation
Acute promyelocytic leukemia
40 year old Hispanic male presented with easy bruising, tiredness and sore throat. On examination he had bleeding gums and pallor. Spleen tip was palpable.
His CBC came back with Hb 7gm/dl, WBC 50 x103/dl, platelet 75 x 103/dl. Peripheral smear showed numerous blasts cells with a single Auer rods in some of them.
Immunophenotyping is positive for CD13, CD33, CD34, CD7, CD 117 and Myeloperoxidase and is negative for CD2, CD3, CD19, CD10, TdT.
Differential from bone marrow showed 60% blasts, nuetrophils 30%, promyelocytes 2%, monocytes 4%, myelocytes 3%, eosinphils 1%
Cytogenetics showed t(8;21) and –Y.
He has acute myeloid leukemia FAB M2 on morphology with t(8;21) and –Y. Molecular analysis showed no evidence of c. kit mutation.
What risk group is this patient’s AML?
Standard or intermediate risk
Poor risk group
Treatment for AML
Remission induction therapy: 1 to 2 courses of intensive therapy to achieve a complete response (absence of detectable leukemia cells)
consolidation therapy: 3 to 4 courses of intensive short- course therapy to further reduce the subclinical body burden of tumor
Followed by (in some patients):
maintenance therapy: months to years of less intensive therapy to further prevent recurrenceor
allogeneic bone marrow transplantation
Which ALL patient has the worst prognosis?
a. An 8 year old with ALL with E2a-PBX (chr 1,19) translocation on cytogenetics
b. A 21 year with T-ALL and normal cytogenetics
c. A 16 year old with TEL-AML1 (chr 12,21) translocation on cytogenetics
d. A 51 year old with BCR-ABL1 (chr 9,22) translocation on cytogenetics
good outcome genetics of childhood ALL
E2A-PBX and TEL-AML
poor outcome genetics of adult and child ALL
MLL-AF4 and BCR-ABL