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IHO Week 3 - WLB > Acute Myeloid Leukemia & Myelodysplastic Syndrome - Krafts > Flashcards

Acute Myeloid Leukemia & Myelodysplastic Syndrome - Krafts Flashcards

1
Q

What is the official definition of leukemia?

A

malignant proliferation of immature myeloid or lymphoid cells in the bone marrow

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2
Q

What are the two types of acute leukemia?

A
  1. Acute myeloid leukemia
  2. Acute lymphoblastic leukemia
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3
Q

What is the etiology behind leukemia?

A
  • most are sporadic (spontaneous)
  • toxins (benzene)
  • genetic conditions increase chance
    • e.g. Down’s syndrome
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4
Q

What is the cause of acute leukemia?

A
  • clonal expansion
  • maturation failure (arrest)
    • get stuck somewhere in myelopoiesis
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5
Q

What is so bad about acute leukemia?

A
  • Crowd out normal cells
    • fill up marrow space
    • no room for RBCs
  • Inhibit normal cell function
  • Infiltrate other organs (worst)
    • especially bad if enter the brain
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6
Q

What are most morphologic cell types in acute leukemia?

A

Immature cells

(most blast cells)

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7
Q

What are the clinical findings in acute leukemia?

A
  • sudden onset (days)
  • Symptoms of bone marrow failure
    • fatigue (not enough red cells)
    • infections (not enough white cells)
    • bleeding (can’t make platelets)
  • Bone pain (due to expanding marrow)
  • Organ infiltration (liver, spleen, brain)
    • leave bone marrow and enter organ
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8
Q

What are the laboratory findings in acute leukemia?

A
  • Marked leukocytosis (really high white count)
    • Blasts/immature cells in blood
  • Anemia
  • Thrombocytopenia
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9
Q

What is the “Old” Classification system of AML based on?

A

only morphology

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10
Q

What percent blast cells do you need to diagnose Acute Myeloid Leukemia?

A

Neet at least 20%

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11
Q

What charactizes a blast cell in Acute Myeloid Leukemia?

A
  • Immature white cells:
  • Large nucleus
  • Small amount of cytoplasm
  • Fine chromatin (see through it)
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12
Q

How do you know when a leukemia is myeloid?

A
  • Dysgranulopoiesis
    • nucleus is not segmenting properly (one big lobe)
    • cytoplasm does not have any specific granulation (or unable to detect it at all)
  • Auer rods
    • long needle-like structures in cytoplasm
    • only occur in malignant myeloid cells (usually only blast cells)
    • not all cases have them
  • Cytochemistry
    • non-specific esterase stain - stains monocytes
    • myeloperoxidase - stains neutrophils
  • Immunophenotyping
  • Cytogenetics
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13
Q

How is the “New” classification of AML different from the “old”?

A
  • more characteristics than just morphology
  • identifies cytogenetic abnormality
  • has therapy-related category (developed after chemo)
  • gives better idea of prognosis
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14
Q

What classifies AML as “M0”?

A
  • least mature (so immature)
    • barely differentiated into myeloid
  • significantly increased myeloblast count
  • bland cells
    • no auer rods
    • no granules
    • can’t tell what they are
  • MPO (myeloperoxidase) negative
  • Need markers (on cell surface)
    • flow cytometry detects these
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15
Q

What classifies AML as “M1”?

A
  • <90% myeloblasts
  • No maturation (all blasts, none beyond this stage)
  • Auer rods present
  • MPO (myeloperoxidase) positive
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16
Q

What classifies AML as “M2”?

A
  • increased myeloblasts
  • maturing neutrophils
  • t(8;21) in some cases
    • special translocation
    • better prognosis
17
Q

What classifies AML as “M3”?

A
  • increased promyelocytes (at least 20%)
    • not a lot of blast cells present
  • Faggot cells (“bundle of sticks”)
    • has a ton of auer rods
  • DIC (disseminated intravascular coagulation)
    • cells bust open and lead to clots
    • granules stimulate coagulation
    • use up all coag factors and then start bleeding
  • t(15;17) in ALL cases
    • particular translocation that gives the patient a better prognosis (best for AML)
    • involves retinoic acid receptor - drug is Tretinoin (ATRA)
      • allows immature cells to mature
18
Q

What classifies AML as “M4”?

A
  • Increased myeloblasts (at least 20% present)
  • Increased monocytic cells
  • Extramedullary tumor masses
    • tumor leaves bone marrow and goes into tissues (esp. CNS, gums)
  • inv(16) in some cases
    • well-known translocation that gives patient a better prognosis
19
Q

What classifies AML as “M5”?

A
  • Increased monocytic cells
    • promonocyte (overlapping, folds in nucleus)
  • NSE (non-specific esterase) positive
  • M5A (monoblasts) and M5B (promonocytes)
  • Extramedullary tumor masses
20
Q

What classifies AML as “M6”?

A
  • increased erythroblasts
  • increased myeloblasts
  • dyserythropoiesis
    • red cells are not growing properly
    • look abnormal
21
Q

What classifies AML as “M7”?

A
  • Increased megakaryoblasts
  • Bland blasts
  • MPO (myeloperoxidase) negative
  • Need markers
    • identified by flow cytometry
22
Q

What are the four specific types of AML with genetic abnormalities?

A
  • t(8;21)
    • AML-M2
  • inv(16)
    • AML-4
    • neutrophilic and monocytic
    • super dark granules
  • *t(15;17)
    • in ALL cases of AML-3
    • treat with ATRA to let cells mature
  • 11q23
    • not associated with any one leukemia
    • monocytic AML
    • bad prognosis
23
Q

What is the significant about AML with FLT-3 mutation?

A
  • Mutation of FLT-3 (a tyrosine kinase)
    • allows white cell count to get REALLY high
    • increased proliferation rate of WBCs
  • Present in 1/3 of cases of AML!
  • Monocytic cells
  • Poor prognosis
24
Q

What is significant about AML with multilineage dysplasia?

A
  • Not very common
  • Type of acute myeloid leukemia that has dysplasia (funny looking cells) in more than one myeloid lineage
    • at least 20% blasts + dysplasia in at least 2 cell lines
  • More common in Elderly
  • Severe pancytopenia
    • all cell counts are DOWN
  • Chromosome abnormalities (5, 7)
  • Poor prognosis
25
Q

What is significant about therapy-related AML?

A
  • Previous chemotherapy treatment
    • alkylating agents (Busulfan) or topoisomerase II inhibitors (Etoposide)
  • 2-5 years to onset
  • Chromosomal abnormalities sometimes (5, 7, 11q23)
  • VERY HARD TO TREAT!!!!
26
Q

How do you treat AML?

A
  • Know type of AML
    • specific treatments for some (ATRA)
  • Chemotherapy
    • get rid of bulk of tumor
  • Bone marrow transplant
    • if patient can tolerate it
    • do not need for AML-M3
    • only hope for permanent cure
27
Q

What is the prognosis of AML?

A
  • Dismal, bad
    • better prognosis in kids
  • t(8;21), inv(16), t(15;17) have better prognosis
  • FLT-3, therapy-related have worse prognosis
28
Q

What classifies Myelodysplastic Syndrome (MDS)?

A
  • Problem: abnormal stem cells
  • Dysmyelopoiesis
  • May have increased blasts
  • May evolve into acute leukemia
  • Varied types & features
29
Q

What does dysplasia look like in red cells?

A

Megaloblastic nuclei

Fragmentation

30
Q

What does dysplasia look like in neutrophils?

A

hypogranulation

hyposegmentation

31
Q

What does dysplasia look like in megakaryocytes?

A

small, non-lobulated cells

(actually get smaller)

32
Q

What are the clinical/lab findings in Myelodysplastic Syndrome?

A
  • Older patients
  • Asymptomatic OR bone marrow failure symptoms
    • fatigue
    • infection
    • bleeding
  • Macrocytic anemia
33
Q

What is the treatment for Myelodysplastic Syndrome?

A
  • Low-grade
    • support
    • follow
  • High-grade
    • be aggressive
    • could turn into leukemia

IHO Week 3 - WLB (10 decks)

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