Friday - krafts 2 - Acute Myeloid Leukemias Flashcards
Clinical Sx in acute leukemia
Fatigue infections bleeding bone pain organ infiltration (liver, spleen, brain)
Lab finding in acute leukemia
Blasts/immature cells in blood
Leukocytosis (elevated WBC)
Anemia
Thrombocytopenia
In the context of abnormal marrow
If less that 20% of your cells in the bone marrow are nucleated cells, you have =
if its greater than 20, you have=
less than 20 = acute myeloid leukemia
greater = Myelodysplastic syndrome
How do you know if a leukemia is myeloid?
Dysgranulopoiesis - no granules in nucleated cells, neutrophils show improper segmentation and dys- or agranulation.
Auer Rods - long needle structures that are sometimes seen in malignant myeloid blast cells.
What type of stain can you use when studying the cytochemistry of a myeloid leukemia?
NSE - non-specific esterase stain - stains monocytic cells
Also myeloperoxidase for neutrophils
What does immunophenotyping look for in cancer
translocations of chromosomes
What mutation is particularly bad in AML
FLT-3
AML-M0
hallmarks
Large increase in myeloblasts (99% of WBCs)
No maturation, Bland blast cells, no auer rods
Myeloperoxidase negative
You need markers to diagnose via flow cytometry (but this is how you Dx)
AML-M1
hallmarks
Large increase in myeloblasts (99% of WBCs)
No maturation
Auer rods
Myeloperoxidase positive
AML-M2
hallmarks
Increase in myeloblasts with maturing neutophils
t(8;21) in some cases - indicator of better prognosis
AML-M3
hallmarks
LARGE increase in PROMYELOCYTES
Faggot cells (tons of auer rods)
Associated with Disseminated vascular coagulation (DIC)
t(15;17) in all cases
Abnormal retinoic acid receptor prevents maturation
BEST prognosis of all AML’s due to new drug all trans retinoic acid (ATRA) which prevents DIC
AML-M4
hallmarks
increase in myeloblasts
increase in monocytic cells
*extramedullary tumor casses (consisting of monocytes in places like the gums. give special therapy to prevent this from going to the brain/CNS)
inv(16) in some cases - indicates better prognosis
AML-M5
hallmarks
increase in monocytic cells (usually promonocytes - nucleus looks like tissue paper)
Non specific esterase positive (detects monocytes)
Extramedullary tumor masses
AML-M6
hallmarks
increase in erythroblasts
increase in myeloblasts
dyserythropoiesis (abnormal looking RBCs)
AML-M7
hallmarks
increase in megakaryoblasts
bland
MPO neg
Need markers and need to Dx with flow cytometry
New classification
AML with genetic abnormalities
4 main ones
-good prognosis-
t(8;21) - AML-M2
t(15,17) - AML-M3
inv(16) - AML-M4
-meh-
11q23
AML with FLT-3 mutation
mutation of FLT-3 causes defective tyrosine kinase - prevents maturation
very high WBC
Monocytic cells
poor prognosis
AML with multilineage dysplasia
not very common
>20% blasts + dysplaisa in 2 or more cell lines
Severe pancytopenia - only leukemia that does this
chromosome 5,7 abnormalities
poor prognosis
AML therapy related
Previous chemo - occurs 2-5 years later
**alkylating agents (busulfan) or topo II inhibitors (etoposide)
poor prognosis
MDS (myelodysplastic syndrome)
hallmarks
clinical and lab findings
Tx
abnormal stem cells
dysmyelopoiesis
maybe increase in blast cells
can evolve into leukemia
older patients
asymptomatic or BM failure
macrocytic anemia
Tx: if low grade, support and follow. if high grade, Treat agressively. treat like AML
hallmarks of dysplasia of bone marrow cells:
red cells
neutrophils
magakaryocytes
red cells: megaloblastic nuclei, fragmentation
neutrophils: hypogranulation, hyposegmentation
megakaryocytes: small, non lobulated cells
