3 - Krafts Acute Leukemia

Front 1

Acute vs Chronic leukemia:
Acute has a ____onset, chronic has a ____ onset
Chronic occurs only in _____
Acute is rapidly _____ without treatment, chronic has long course
Acute in composed of _____ cells and chronic is ______

Back 1

sudden
slow
adults (acute is mostly children, also adults)
fatal
immature (blasts)
mature

Front 2

Acute leukemia is a _____ proliferation of ______ myeloid or lymphoid cells in the ____ ____. Caused by clonal expansion and ______ failure

Back 2

malignant
immature
bone marrow

maturation

Front 3

Bad things that immature cells do in bone marrow:
_____ out normal cells
inhibit ______ cell function and growth
infiltrate other _____

Back 3

crowd
normal
organs

Front 4

Clinical features of AL:
-Sudden onset (___)
-Symptoms of bone marrow failure (_____ - anemia, _____ - dec normal WBC, Bleeding - thrombocytopenia)
-Bone ____(expanding marrow)
-Organ infiltration (liver, spleen, brain, lymphadenopathy)

Back 4

days
fatigue
infections
pain

Front 5

Laboratory Findings of acute leukemia:
•_______ cells in blood.
•Elevated ____ count (usually!).
•Anemia.
•Thrombocytopenia.

Back 5

immature
white

Front 6

Things to know about AML:
Malignant proliferation of ____ blasts in blood, bone marrow
__% cutoff for diagnosis
many subtypes
____ prognosis

Back 6

myeloid
20%
bad

Front 7

AML subtypes:
M0-M3 involve ______ series
M4-M5 involve ______ series
M6 - involves ______ series
M7 - involves _______ series

Back 7

neutrophilic
monocytic
erythroid
megakaryocytic

Front 8

M0 - acute myeloblastic leukemia, ______ differentiated
M1 - acute myeloblastic leukemia without _______
M2 - acute myeloblastic leukemia with _______

Back 8

minimally
maturation
maturation

Front 9

M3 - acute ________ leukemia
M4 - acute _______ leukemia

Back 9

promyelocytic
myelomonocytic

Front 10

M_ - acute erythroblastic leukemia
M_ - acute megakaryoblastic leukemia
M_ - acute monocytic leukemia

Back 10

6
7
5

Front 11

The ______ must comprise at least __% of all the nucleated cells in the blood and/or bone marrow to make the diagnosis of ___

Back 11

blasts
20
AML

Front 12

Clues to myeloid nature
•__________: Disordered granulocyte production (e.g., hypogranularity or
hyposegmentation).
• ___ rods: Consolidation of _______ granules. If present, prove myeloid lineage!

Back 12

Dysgranulopoiesis
Auer
azurophilic

Front 13

Which AML is this?
Lots of myeloblasts
Bland
MPO negative
Need markers

Back 13

M0

Front 14

What kind of cell is the biggest in the myeloid line with lots of primary (coarse, azurophilic) granules

Back 14

Promyelocyte

Front 15

Myeloblasts have a ____ nucleus with ____ chromatin, nucleoli. Then rim of ________ cytoplasm. Few fine granules

Back 15

large
fine
basophilic

Front 16

-Myeloperoxidase (MPO) - + in ______ and _________.
-Sudan black B (SBB) - same pattern as MPO.
-Non-specific esterase (NSE) - + in _______ lineage

Back 16

neutrophils and eosinophils
monocytic

Front 17

_________ used when morphological and cytochemical features are equivocal. Markers like CD33 (pan-myeloid), CD61 (platelets)
Some AML myeloblasts also have _____ markers

Back 17

Immunophenotyping

lymphoid

Front 18

Which abnormalities give a worse prognosis?
-t(8;21)
•t(15;17)
•inv(16)
•11q23
•AML with FLT3 mutation

Back 18

11q23
AML with FLT3 mutation

Front 19

Which AML do you need to use flow cytometry to diagnose because morphology not definitive and cytochemical stains negative?

Back 19

M0

Front 20

Which AML is this?
-Marrow: lots of myeloblasts
•May see a few Auer rods.
•A few of the myeloblasts stain positive for MPO/SBB.

Back 20

M1

Front 21

Which AML?
more myeloblasts
Maturing neutrophils
t(8;21) in some cases

Back 21

M2

Front 22

Which AML?
•Marrow: more myeloblasts, monoblasts, and promonocytes
•inv(16): M4Eo. in some cases Lots of abnormal eosinophils. Better prognosis!
Extramedullary tumor masses (gums)

Back 22

M4

Front 23

Which AML?
lots of promyelocytes
faggot cells ("bundle of sticks")
at risk for DIC
t(15;17) in all cases

Back 23

AML-M3

Categorized as AML with genetic abnormalities now because it has the t(15;17) always and better prognosis than others

Front 24

Which AML?
lots of monocytic cells
NSE positive
extramedullary tumor masses (skin, gums, testes)

Back 24

M5

Front 25

Which AML?
many erythroblasts
many myeloblasts
Dyserythropoiesis (giant and bizarre erythroblasts)

Back 25

M6

Front 26

What AML is this?
increase in megakaryoblasts
Bland blasts
MPO negative
Need markers and EM

Back 26

M7

Front 27

•This type of AML usually looks like an AML-M2 (it has a lot of myeloblasts, with some maturing neutrophilic cells too) – but it has the addition of a translocation between two chromosomes
•Prognosis is favorable.

Back 27

AML with t(8;21)

Front 28

•This type of AML usually looks like an AML-M4 but it has inversion in chromosome.
•unusual morphologic findings – the presence of huge eosinophils with deep purple granules. These cases are sometimes called “AML-M4 Eo” because of the abnormal eosinophils.
•Prognosis is favorable.

Back 28

AML with inv(16)

Front 29

AML with t(15;17) is also called what?
What does it encode for?

Back 29

AML-M3
abnormal retinoic acid receptor (which blocks cell differentiation)

Front 30

___ is used for therapy in patients with t(15;17). Acts as a differentiating agent, allowing the screwed up promyelocytes to mature into ______

Back 30

ATRA (all-trans retinoic acid)
neutrophils

Front 31

AML with 11q23 abnormalities usually have a ______ component (either M4 or M5)
Two groups of patients are more likely to get this type: infants and patients who have been treated in the past with ________.
____ prognosis

Back 31

monocytic
chemotherapy
poor

Front 32

AML with FLT3 mutation presents in almost a ____ of cases of AML making it the MOST COMMON genetic abnormality in AML

Back 32

third

Front 33

AML with FLT3 mutation has mostly _______ components (M4 or M5). _____ prognosis

Back 33

monocytic
poor (increased relapse rate, shortened survival)

Front 34

AML w/ Multilineage Dysplasia
≥ 20% blasts + dysplasia in ≥ _ cell lines
Elderly
Severe pancytopenia
Chromosome abnormalities (_ and _)
____ prognosis

Back 34

2
5 and 7
poor

Front 35

AML, Therapy-related:
-Previous ________
-_______ agents (Busulfan)
5-6 years to onset, Starts as MDS, Chr abnormalities (5, 7)
-___________ II inhibitors (Etoposide)
2 years to onset, Monocytic cells, Chr abnormalities (11q23)
-Hard to treat

Back 35

chemotherapy
alkylating
Topoisomerase

Front 36

Treatment of AML:
Chemo, ____ ____ transplant*
Prognosis: 2/3 pts remission after initial therapy. 80% die within _ years. Older patients do _____.

Back 36

bone marrow
3
worse

Front 37

Pts with t(8;21), inv (16), and especially t(15;17) survive _____.
Patients with FLT-3 mutations or 11q23 abnormalities have a _____ prognosis

Back 37

longer
worse

Front 38

What syndrome is this?
Abnormal stem cell!
Dysmyelopoiesis
Maybe increase blasts
May evolve into acute leukemia

Back 38

Myelodysplastic syndrome

Front 39

Dysplasia:
Red cells: _________ nuclei, fragmentation
Neutrophils: hypogranulation, hypo_________
Megakaryocytes: ____, non-lobulated

Back 39

megaloblastic
segmentation
small

Front 40

Clinical and Lab Findings in MDS:
____ patients
Asymptomatic, or BM failure
________ anemia

Back 40

Older
Macrocytic

Front 41

-Most cases of ___ occur in patients under 17 years old (peak = 4y).
•most common type of leukemia in children (80-85% of childhood leukemias).
•also occurs in adults, however.

Back 41

ALL

Front 42

What type of leukemia is this?
Malignant proliferation of lymphoid blasts in blood, bone marrow
Classified by immunophenotype (B vs. T)
More common in children
Prognosis often good!

Back 42

Acute Lymphoblastic Leukemia

Front 43

T-lineage ALL: _____ prognosis.
B-lineage ALL:
“B-cell precursor ALL”: ______ prognosis.
“B-cell ALL”: _____ prognosis.

Back 43

worse
better
worse

Front 44

T-cell ALL:
Teenage male with
________ mass
___ usually very high
___ prognosis
Blasts positive for TdT and T-cell markers

Back 44

mediastinal
WBC
bad

Front 45

B-cell precursor ALL
Several sub- and sub-subtypes
TdT _
Rarely Ph +

Back 45

+

Front 46

What type of ALL is this?
= Burkitt lymphoma
Blue cytoplasm with vacuoles
TdT --, surface __ positive
t(8;14)
older child with fast-growing abdominal mass

Back 46

B-cell ALL
Ig

Front 47

What type of Acute leukemia has the starry sky pattern?

Back 47

B-cell ALL (Burkett's lymphoma)

Front 48

Treatment, prognosis of ALL:
What's the best immunophenotype to have?
Age (best __-__ years)
___ (best <10,000)
Cytogenics (best: hyper_____)

Back 48

common early B-cell precursor
1-10 years old
WBC
hyperdiploidy

Front 49

Treatment of ALL:
Children cured with current therapy:
______ with or without ___ ____ transplant

Back 49

chemotherapy
bone marrow