Friday - krafts 2 - Acute Myeloid Leukemias Flashcards

1
Q

Clinical Sx in acute leukemia

A
Fatigue
infections
bleeding
bone pain
organ infiltration (liver, spleen, brain)
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2
Q

Lab finding in acute leukemia

A

Blasts/immature cells in blood
Leukocytosis (elevated WBC)
Anemia
Thrombocytopenia

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3
Q

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=

A

less than 20 = acute myeloid leukemia

greater = Myelodysplastic syndrome

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4
Q

How do you know if a leukemia is myeloid?

A

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.

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5
Q

What type of stain can you use when studying the cytochemistry of a myeloid leukemia?

A

NSE - non-specific esterase stain - stains monocytic cells

Also myeloperoxidase for neutrophils

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6
Q

What does immunophenotyping look for in cancer

A

translocations of chromosomes

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7
Q

What mutation is particularly bad in AML

A

FLT-3

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8
Q

AML-M0

hallmarks

A

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)

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9
Q

AML-M1

hallmarks

A

Large increase in myeloblasts (99% of WBCs)
No maturation
Auer rods
Myeloperoxidase positive

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10
Q

AML-M2

hallmarks

A

Increase in myeloblasts with maturing neutophils

t(8;21) in some cases - indicator of better prognosis

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11
Q

AML-M3

hallmarks

A

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

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12
Q

AML-M4

hallmarks

A

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

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13
Q

AML-M5

hallmarks

A

increase in monocytic cells (usually promonocytes - nucleus looks like tissue paper)
Non specific esterase positive (detects monocytes)
Extramedullary tumor masses

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14
Q

AML-M6

hallmarks

A

increase in erythroblasts
increase in myeloblasts
dyserythropoiesis (abnormal looking RBCs)

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15
Q

AML-M7

hallmarks

A

increase in megakaryoblasts
bland
MPO neg
Need markers and need to Dx with flow cytometry

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16
Q

New classification
AML with genetic abnormalities

4 main ones

A

-good prognosis-
t(8;21) - AML-M2
t(15,17) - AML-M3
inv(16) - AML-M4

-meh-
11q23

17
Q

AML with FLT-3 mutation

A

mutation of FLT-3 causes defective tyrosine kinase - prevents maturation
very high WBC
Monocytic cells
poor prognosis

18
Q

AML with multilineage dysplasia

A

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

19
Q

AML therapy related

A

Previous chemo - occurs 2-5 years later
**alkylating agents (busulfan) or topo II inhibitors (etoposide)
poor prognosis

20
Q

MDS (myelodysplastic syndrome)
hallmarks
clinical and lab findings
Tx

A

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

21
Q

hallmarks of dysplasia of bone marrow cells:

red cells
neutrophils
magakaryocytes

A

red cells: megaloblastic nuclei, fragmentation

neutrophils: hypogranulation, hyposegmentation
megakaryocytes: small, non lobulated cells