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IHO WK 3 > Acute Myeloid Leukemia and Myelodysplastic Syndromes Dr. Krafts 5/9/14 > Flashcards

Acute Myeloid Leukemia and Myelodysplastic Syndromes Dr. Krafts 5/9/14 Flashcards

1
Q

Acute v. Chronic Leukemia

A

Acute Leukemia

  • Sudden onset (over period of day (s))
  • Can occur in either adults or children
  • Rapidly fatal without treatment (prognosis poor even w/ Tx)
  • Composed of immature cells (blasts) (located on top part of chart)

Chronic

  • Slow onset (months)
  • Occurs only in adults***
  • Longer course
  • Composed of mature cells (bottom of chart)
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2
Q

Leukemia from neutrophil series

A

CML

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3
Q

Leukemia w/ a large number of normal looking mature lymphocytes

A

CLL

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4
Q

Definition, cause, and badness of acute leukemia

A

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

Cause (many times we don’t know the cause)

  • Clonal expansion
  • Maturation failure (cells expanding and dividing more than normal also)(Tx removes block in maturation)

Badness

  • Crowd out normal cells (fill up marrow)(dies of bleeding because don’t have platelets, anemia, infection, etc)
  • Inhibit normal cell function (e.g. prevents B cells for making antibodies, etc)
  • Infiltrate other organs

Down Syndrome has increased risk of getting leukemia

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5
Q

Clinical findings in acute leukemia

A

Sudden onset*** (days)

Symptoms of bone marrow failure

  • Fatigue (anemic)
  • Infections (not enough WBC)
  • Bleeding (bad nose bleeds, etc)

Bone pain*** (expanding marrow)

Organ infiltration (liver, spleen, brain)

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6
Q

Laboratory findings in Acute Leukemia

A
  • Blasts/immature cells in blood
  • Leukocytosis (will see in almost ever case. These are the malignant blasts)
  • Anemia
  • Thrombocytopenia
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7
Q

Acute Myeloid Leukemia things you must know

A
  • Malignant proliferation of myeloid “blasts” in blood, bone marrow (could be any precursor cell but usually blast)
  • 20% cutoff*** for diagnosis (nucleated cells in blood or marrow everything but red cells)(another disease w/ higher blast count but in that disease may not turn into leukemia and won’t need the heavy Tx and so to separate these cases the 20% stipulation was made)(1-2% blasts is normal)
  • Many subtypes
  • Bad prognosis
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8
Q

AML “old classification”

A

M0 - acute myeloblastic leukemia, minimally differentiated

M1 - acute myeloblastic leukemia without maturation

M2 - acute myeloblastic leukemia with maturation

M3 - acute promyelocytic leukemia (likely to go into DIC)

M4 - acute myelomonocytic leukemia

M5 - acute monocytic leukemia (tend to have cells that crawl out so give Tc in CSF)

M6 - acute erythroblastic leukemia

M7 - acute megakaryoblastic leukemia

Based on what type of cell predominating. (all young and myeloid cells)

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9
Q

Revised AML “old” classification

A

M0, 1, 2, 3-involve neutrophilic series
(myeloblasts, promyelocytes, etc.)

M4, 5-involve monocytic series (monoblasts, etc.)

M6-involves erythroid series (erythroblasts)

M7-involves megakaryocytic series (megakaryoblasts)

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10
Q

How do you know when a leukemia is myeloid?

A
  • Many times blast and can’t tell what they are
  • Dysgranulopoeisis-growing funny/weird looking changes
  • In AML–>auer rods***(composed of primary granules)(little sticks in cytoplasm)(many cases of AML can occur w/o auer rods)
  • Cytochemistry
  • Immunophenotyping
  • Cytogenetics
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11
Q

AML “new” classification

A
  • AML with genetic abnormalities
  • AML with FLT-3 mutation
  • AML with multilineage dysplasia
  • AML, therapy-related (had cancer previously and got chemo and now AML. These are hard to treat)
  • AML, not otherwise classified
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12
Q

AML-M0 things you must know

A
  • Increased myeloblasts
  • Bland
  • MPO negative (stain done on cells to see if part of neutrophil series)
  • Need markers (nothing else you can rely on)(need to do flow on it)
  • Least differentiated of the AML series (usually 90% blasts)
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13
Q

AML-M1 things you must know

A
  • Increased myeloblasts
  • No/minimal maturation
  • Auer rods
  • MPO positive
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14
Q

AML-M2 things you must know

A
  • Increased myeloblasts (not as much as 0,1)
  • Maturing neutrophils
  • t(8;21) in some cases (better prognosis)***
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15
Q

AML-M3 things you must know

A
  • Increased promyelocytes
  • Faggot cells (ton of aurer rods)
  • DIC (granules that are procoagulant)
  • t(15;17) in all cases***
  • All trans-retinoic acid overcomes genetic defect. Removes block on promyelocytes and start maturing
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16
Q

AML-M4 things you must know

A
  • Increased myeloblasts
  • Increased monocytic cells
  • Extramedullary tumor masses (anytime have leukemia w/ moncytic. Need to worry about monocytes getting out and need to protect CNS (intrathecal therapy) gums/skin/testes are big 4 involved.)
  • inv(16) in some cases (better prognosis)
  • “Like a dual leukemia”
17
Q

AML-M5 things you must know

A
  • Increased monocytic cells
  • NSE positive
  • M5A and M5B (one form monoblast (5A) other form chromatocytes (5B) “her favorite”)
  • Extramedullary tumor masses
18
Q

MPO and NSE stain what?

A

MPO neutrophil and precursors

NSE monocytic

19
Q

AML-M6 things you must know

A
  • Increased erythroblasts
  • Increased myeloblasts
  • Dyserythropoiesis
20
Q

AML-M7 things you must know

A
  • Increased megakaryoblasts (only one that involves platelet precursors)
  • Bland blasts
  • MPO negative
  • Need markers
21
Q

AML w/ genetic abnormalities (certain cytogenetic changes in AML that can give better or worse prognosis)

A
  • t(8;21) (AML-M2) Looks different than other cases of M2. The cells get gigantic.
  • inv(16) (AML-M4) Gigantic eosinophils w/ dark blue granules instead of little orangish.
  • t(15;17) (AML-M3) All cases have this. (can’t give regular chemotherapy as will burst cell and release granules)
  • 11q23 (something wrong w/ long arm of 11 band 2 subpart 3 (??) could be translocation, deletion, etc) Usually seen in AML w/ monocytic component.

***First three good prognosis w/ the last being bad

22
Q

AML w/ FLT-3 mutation

A
  • Mutation of FLT-3 (a tyrosine kinase)
  • Present in 1/3 of cases of AML!
  • Monocytic cells
  • Poor prognosis (more likely to relapse, cells grow faster) (e.g. WBC 16->102 in one day hard to keep blood flowing at that high of lever)
23
Q

AML w/ multilineage dysplasia (cells growing funny)

A
  • ≥ 20% blasts + dysplasia in ≥ 2 cell lines
  • Elderly
  • Severe pancytopenia*** (every other leukocytosis)
  • Chromosome abnormalities (5, 7)
  • Poor prognosis
24
Q

AML therapy-related

A
  • 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
25
Q

Tx and prognosis of AML

A

Treatment (over ally 60% patients get into 1 complete remission but many will relapse and overall survival is low)

  • Chemo
  • Bone marrow transplant

Prognosis

  • Dismal
  • t(8;21), inv(16), t(15;17) better
  • FLT-3, therapy-related worse
26
Q

Myelodysplastic Syndrome (MDS)

A
  • Problem: abnormal stem cells
  • Dysmyelopoiesis
  • Maybe increased blasts (never up to 20% maybe 3-10%)
  • May evolve into acute leukemia
27
Q

What does dysplasia look like?

A
  • Red cells: megaloblastic nuclei, fragmentation
  • Neutrophils: hypogranulation, hyposegmentation
  • Megakaryocytes: small, non-lobulated cells
28
Q

Clinical/lab findings, Tx, and support in MDS

A
  • Older patients
  • Asymptomatic, or BM failure
  • Macrocytic anemia***
  • Low-grade: support, follow.
  • High-grade: be aggressive.

IHO WK 3 (7 decks)

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