- sudden onset - Adults or children - Rapidly fatal w/out treatment - composed of IMMATURE cells (blasts

- slow onset - Adults only (>40) - longer course - Composed of MATURE cells

Acute Myeloid Leukemia & Myelodysplastic Syndrome -Krafts Flashcards by Morgan Mensink

Myelodysplastic Syndrome (MDS)

Problem: Abnormal stem cells
Dysmyelopoiesis
Maybe increase in blasts
May evolve into acute leukemia

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What does dysplasia of MDS look like?

RBC:
Neutrophils:
Megakaryocytes:

Red cells: megaloblastic nuclei, fragmentation

Neutrophils: hypogranulation, hyposegmentation

Megakaryocytes: small, non-lobulated cells

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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

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MDS: Tx and prognosis

Low grade: support and follow

High grade: be aggressive. be be aggressive.

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Acute Leukemia

sudden onset
Adults or children
Rapidly fatal w/out treatment
composed of IMMATURE cells (blasts

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Chronic Leukemia

slow onset
Adults only (>40)
longer course
Composed of MATURE cells

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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

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Acute Leukemia=

Malignant proliferation of immature myeloid or lymphoid cells in the BM

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Clinical finding in Acute Leukemia:

Symptoms of BM failure:

fatigue
infections
bleeding

Bone pain (expanding marrow)
Organ infiltration

*sudden onset

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Lab findings in acute leukemia:

marked leukocytosis

blasts/immature cells
anemia
thrombocytopenia

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Acute Myeloid Leukemia:

Things you much know

Malignant proliferation of myeloid blasts in blood, bone marrow
*20% cutoff for diagnosis
Many subtypes
BAD prognosis

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M0, M1, M2, M3

Involve neutrophilic series

myeloblasts, promyelocytes…

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M4 and M5

Involve monocytic series

M4: acute MYLEOmonocytic leukemia

M5: acute monocytic leukemia

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acute ERYTHROBLASTIC leukemia

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acute MEGAKARYOBLASTIC leukemia

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acute myeloblastic leukemia, minimally differentiated

M1: acute myeloblastic leukemia -without maturation

M2: acute myeloblastic leukemia WITH maturation

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