Acute Myeloid Leukemia Flashcards
Generally, what are the big differences between acute and chronic leukemias?
- acute have sudden onset (days), chronic have longer onset (months)
- acute is in both kids and adults, chornic is only in adults
- acute has a more rapid course
- acute is composed of blast cells, chronic composed of mature cells
Besides acute and chronic, what are the two types of leukemias/
myeloid and lymphoid (lymphoblastic)
Leukemia is a malignant proliferation of immature myeloid or lymphoid cells in the bone marrow or lymph nodes?
bone marrow
As for the cause, what are the two general things the cells do in leukemias?
- clonal expansion
2. maturation failure
Why are leukemias bad?
- crowd out normal cells from the bone marrow
- inhibit normal cell function
- infiltrates other organs
What will the general symptoms of an acute leukemia be?
sudden onset of bone marrow failure symptoms: fatigue, infections, bleeding, etc. and bone pain
potentially organ infiltration - so confusion if in the CNS
What will the general lab findings be in acute leukemia
- blasts/immature cells in blood smear
- leukocytosis (all bad cells)
- anemia
- trombocytopenia
What percentage of the blood cells need to be blasts to get the AML diagnosis?
at least 20%
AML: good or bad progrnosis in general?
bad
What’s the old classification system for AML?
M0-M7
What cells are involved in M0?
myeloblasts (neutrophilic series) - minimally differentiated.
M1?
myeloblasts (neutrophilic series) - without maturation
M2?
myeloblasts (neutrophilic series) - with maturation
M3?
promyelocytes (neutrophilic series)
M4?
myelomonocytes
M5?
monocytes
M6?
erythroblasts
M7?
megakaryoblasts
What are some of the ways you can tell a leukemia is myeloid?
- dysgranulopoiesis
- AEUR RODS!
- cytochemistry - use specific stains
- immunophenotyping
- cytogenetics
What are the categories in the “new” classificaiton for AML?
AML with genetic abnormalities AML with FLT-3 mutstion AML with multilineage dysplasia AML, therapy related AML, NOC
For AML M0, what’s the only way you can diagnose it?
you need to do immunophenotyping - you need to use markers
What’s the main difference between AML M0 and M1?
In M1 they have committed themselves to a lineage, but still minimal to no maturation
What’s the diagnostic tipoff for M1?
auer rods!
What enzyme does M1 have that M0 doesn’t?
myeloperoxidase (MPO)
What genetic abnormaltiy occurs in some cases of M2 and leads to a better prognosis?
translocation of chromosone 8 and 21
What cells are diagnostic of AML M3?
Faggot cells (bundle of sticks - just TONS of Auer rods)
Why is treatment of M3 different from all the others?
The promyelocytes have pro-thrombotic granules that will cuase DIC if treated like normal leukemias, so you give a drug that removes the block to maturation, so the malignant cells just mature out and disappear!
What genetic abnormality is present in ALL cases of M3?
a translocation of chromosone 15 and 17
Why do you need to worry about extramedullary tumor masses in M4?
Because it’s a leukemia of monocytes, which travel through the body
What genetic abnormality is present in some cases of M4 and leads to better prognosis?
inversion of chromosome 16
Why is M4 sometimes considered a dual leukemia?
You can get an increase in both myeloblasts and monocytic cells
What enzyme will M5 be positive for?
nonspecific esterase (from the monoblasts)
Will M7 be positive for myeloperoxidase?
no - it’s not in the monocyte series
Of the AMLs with genetic abnormatlities, which one confers a poor prognosis?
11q23
What AML technically has a genetic abnormality but is in a group all it’s own?
FLT-3 mutation: present in a third of all AML cases!
Does the FLT3 mutation lend a good or bad prognosis? Why?
bad - they’re so much more likely to relapse and relapse rapidly (this was the case)
What are the characteristics of AML with multilineage dysplasia?
you have dysplasia in at least 2 different cell lines
typically in elderly patients
you get severe pancytopenia
What chromosomes are often abnormal in AML with multilineage dysplasia?
5 and 7
multilineage dysplasia: good or bad prognosis?
bad
What drugs are particular cultprits for AML, therapy related?
alkylating agents like busulfan and topo 2 ihibitors like etoposide
What’s the typical onset for AML, therapy related?
2-5 years
therapy related - easy or hard to treat?
VERY hard
What is the treatment for AML?
chemo and bone marrow transplant
In general, what is myelodysplastic syndrome? Why is this included in this discussion?
there’s something abnormal about the stem cells in the marrow so you get dysmyelopoiesis and maybe increased blasts - but not as high as 20%
sometimes can evolved into acute leukemia
What sort of anemia is usually present in myelodysplastic syndrome?
macrocytic, but often asymptomatic
Who gets MDS?
elderly
