AML and MDS Flashcards
acute leukemia
-onset, age, course, immature vs mature
Sudden onset
Can occur in either adults or children
Rapidly fatal without treatment
Composed of immature cells (blasts)
chronic leukemia
-onset, age, course, immature vs mature
Slow onset
Occurs only in adults
Longer course
Composed of mature cells
malignant proliferation of immature myeloid or lymphoid cells in the bone marrow
acute leukemia
acute leukemia cause
Clonal expansion
Maturation failure
acute leukemia badness
Crowd out normal cells
Inhibit normal cell function
Infiltrate other organs
Clinical findings in acute leukemia
Sudden onset (days) Symptoms of bone marrow failure Fatigue Infections Bleeding Bone pain (expanding marrow) Organ infiltration (liver, spleen, brain)
Things have to know about AML
Malignant proliferation of myeloid blasts in blood, bone marrow
20% cutoff for diagnosis
Many subtypes
Bad prognosis
how many of the nucleated cells have to be malignant/blast to be diagnosed as AML
20%
old classifications of AML - big grouping
M0-3: involve neutrophilic series (myeloblasts, promyelocytes, etc.)
M4-5: involve monocytic series (monoblasts, etc)
M6: involve erythroid series (erythroblasts)
M7: involve megakaryocytic series (megakaryoblasts)
dysgranulopoiesis
not enough lobes or cytoplasm in neutrophils
a clue that acute leukemia is probably myeloid
how to tell if leukemia is myeloid vs. lymphoid
dysgranulopoiesis auer rods cytochemistry (MPO = neutrophils) immunophenotyping Cytogenetics
Auer rods
azurophilic granules strung together in rods
clue that it is AML
Myeloperoxidase shows that cells are from what lineage
neutrophils
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
“Bland” blasts
MPO negative
Need markers
AML-M1 things you must know
INCREASED myeloblasts
No maturation
Auer rods
MPO positive
AML-M2 things you must know
Increased myeloblasts
Maturing neutrophils
t(8;21) in some cases
AML-M3 things you must know
INCREASED promyelocytes (special)
Faggot cells
DIC
t(15;17) in all cases
Faggot cells
tons of auer rods
M3
why is AML-M3 so dangerous
granules stimulate clotting cascade –> clotting and then bleeding = DIC
Treatment AML-M3
Use ATRA (retinoic acid) to overcome block in maturation
Lab findings in acute leukemia
Blasts/immature cells in blood
Leukocytosis
Anemia
Thrombocytopenia
AML-M4 things you must know
increased myeloblasts
increase monocytic cells
extramedullary tumor masses
inv(16) in some cases= good
AML-M5 things you must know
Increased monocytic cells
NSE positive
M5A and M5B
Extramedullary tumor masses
NSE specific for
monocytic cells
AML-M6 things you must know
Inc erythroblasts, inc myeloblasts
dyserythropoiesis
AML-M7 things you must know
Incr megakaryoblasts
“bland” blasts
MPO negative
need markers
t(8;21)
good prognosis (common in M2)
inv(16)
good prognosis (common in M4)
t(15;17)
good prognosis (always in M3)
11q23
worse prognosis
AML with FLT-3 mutation
Mutation of FLT-3 (a tyrosine kinase)
Present in 1/3 of cases of AML!
Monocytic cells
Poor prognosis
AML with multilineage dysplasia
Elderly
Severe pancytopenia
Chromosome abnormalities (5, 7)
Poor prognosis
AML, therapy-related
Previous chemotherapy
2-5 years to onset
Very hard to treat
tx AML
chemotherapy
bone marrow transplant
prognosis AML
dismal
t(8;21), inv(16), t(15;17) better
FLT-3, therapy-related worse
MDS
Problem: abnormal stem cells
Dysmyelopoiesis
Maybe inc blasts
May evolve into acute leukemia
what does dysplasia look like - red cells
megaloblastic nuclei, fragmentation
what does dysplasia look like - neutrophils
hypogranulation, hyposegmentation
what does dysplasia look like - megakaryocytes
small, non-lobulated cells
clinical and lab findings in MDS
older patients
asymptomatic, or BM failure
macrocytic anemia
tx MDS
Low-grade: support, follow.
High-grade: be aggressive.