Acute Myeloid Leukemia & Myelodysplastic Syndrome -Krafts Flashcards
Myelodysplastic Syndrome (MDS)
- Problem: Abnormal stem cells
- Dysmyelopoiesis
- Maybe increase in blasts
- May evolve into acute leukemia
What does dysplasia of MDS look like?
RBC:
Neutrophils:
Megakaryocytes:
Red cells: megaloblastic nuclei, fragmentation
Neutrophils: hypogranulation, hyposegmentation
Megakaryocytes: small, non-lobulated cells
Clinical/Lab findings in MDS
- older patients (>50)
- Asymptomatic, or BM failure (fills up with abnormal cells and they fail to get out)
- Macrocytic anemia
MDS: Tx and prognosis
Low grade: support and follow
High grade: be aggressive. be be aggressive.
Acute Leukemia
- sudden onset
- Adults or children
- Rapidly fatal w/out treatment
- composed of IMMATURE cells (blasts
Chronic Leukemia
- slow onset
- Adults only (>40)
- longer course
- Composed of MATURE cells
How does Acute Leukemia occur?
Sporadic.
Cause:
- clonal expansion
- maturation failure
Badness:
- crowd out normal cells (worst thing)
- inhibit normal cell function
- infiltrate other organs
Acute Leukemia=
Malignant proliferation of immature myeloid or lymphoid cells in the BM
Clinical finding in Acute Leukemia:
Symptoms of BM failure:
- fatigue
- infections
- bleeding
Bone pain (expanding marrow) Organ infiltration
*sudden onset
Lab findings in acute leukemia:
marked leukocytosis
- blasts/immature cells
- anemia
- thrombocytopenia
Acute Myeloid Leukemia:
Things you much know
- Malignant proliferation of myeloid blasts in blood, bone marrow
- *20% cutoff for diagnosis
- Many subtypes
- BAD prognosis
M0, M1, M2, M3
Involve neutrophilic series
myeloblasts, promyelocytes…
M4 and M5
Involve monocytic series
M4: acute MYLEOmonocytic leukemia
M5: acute monocytic leukemia
M6
acute ERYTHROBLASTIC leukemia
M7
acute MEGAKARYOBLASTIC leukemia
M0
acute myeloblastic leukemia, minimally differentiated
M1
M2
M1: acute myeloblastic leukemia -without maturation
M2: acute myeloblastic leukemia WITH maturation
M3
acute PROmyleocytic leukemia
Need 20% blasts?
Count everything with nucleus (not mature RBCs)
if 20% are myleoblasts ===then you can diagnose acute myeloid leukemia
How do you know if leukemia is myeloid?
- Dysgranulopoiesis: funny looking neutrophils
- Auer rods: only in malignant myeloblasts
- Cytochemistry:
- Nonspecific esterase (NSE) stain will show monocytic cells
- Myleoperoxidase stain stains neutrophils
- Immunophenotyping
- Cytogenetics
AML New Classification
AML with genetic abnormalities AML with FLT-3 mutation AML with multilineage dysplasia AML, therapy-related AML, not otherwise classified
AML-M0
Things you must know
- increased myeloblasts (lots & tons)
- bland (can’t really tell they’ve decided to go myeloid instead of lymphoid)
- MPO negative
- Need markers
AML -M1
Things you must know
- Lots and lots of myeloblasts
- ***No maturation **
- Can tell they decided to be myeloblasts
- Auer rods
- MPO positive
AML-M2
Things you must know
- Increased myeloblasts
- maturing neutorphils
- T(8;21) in some cases ==better prognosis
AML- M3
Things you must know
- lots and lots of PROmyelocytes (at least 20%)
- Faggot cells- lots of Auer rods
- DIC=disseminated intravascular coagulation (b/c cells have pro-coagulates in them)
- ***t(15;17) in ALL cases
**BEST prognosis of all AMLs
AML-M4
Things you must know
- Increased myeloblasts
- increased MONOCYTIC cells
- Extramedullary tumor masses –like to go into CNS put chemo in CSF
- inv(16) in some cases
AML-M5
Things you must know
Increased monocytic cells
NSE positive (stain for monocytes) M5A and M5B (two types) Extramedullary tumor masses
AML-M6
Things you must know
Increased ERYTHROBLASTS
increased myeloblasts
Dyserythropoiesis (cells not growing properly)
AML-M7
Things you mustttt know
increased MEGAKARYOBLASTS
- bland blasts
- MPO negative (stain for neutrophils)
- Need markers
AML with genetic abnormalities
t(8;21) some cases of AML-M2
inv(16) some cases of AML-M4
t(15;17)*** ALL cases of AML-3
11q23 –>bad prognosis (more common in monocytic AMLs)
Top 3 have good prognosis
AML with FLT-3 mutation
- FLT-3 is a tyrosine kinase
Mutation allows:
1. white cell count to get really high
2. cells to divide really quickly - present in 1/3 of cases of AML
- Monocytic cells usually
- POOR prognosis
AML with multilineage dysplasia
funny looking cells in more than one lineage
≥ 20% blasts + dysplasia in ≥ 2 cell lines
Elderly Severe pancytopenia (all cell counts are low, even malignant cells)
PORR prognosis
AML therapy related
Previous chemotherapy
Alkylating agents (Busulfan) or topoisomerase II inhibitors (Etoposide)
2-5 years to onset
Chromosomal abnormalities sometimes (5, 7, 11q23)
Very hard to treat
AML Tx and prognosis
Tx: chemo or BM transplant
Prognosis:
- dismal
- t(8;21), inv(16), t(15;17) better
- FLT-3, therapy-related is worse
