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IHO Week 3 > Acute Myeloid Leukemia > Flashcards

Acute Myeloid Leukemia Flashcards

1
Q

Generally, what are the big differences between acute and chronic leukemias?

A
  1. acute have sudden onset (days), chronic have longer onset (months)
  2. acute is in both kids and adults, chornic is only in adults
  3. acute has a more rapid course
  4. acute is composed of blast cells, chronic composed of mature cells
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2
Q

Besides acute and chronic, what are the two types of leukemias/

A

myeloid and lymphoid (lymphoblastic)

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3
Q

Leukemia is a malignant proliferation of immature myeloid or lymphoid cells in the bone marrow or lymph nodes?

A

bone marrow

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4
Q

As for the cause, what are the two general things the cells do in leukemias?

A
  1. clonal expansion

2. maturation failure

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5
Q

Why are leukemias bad?

A
  1. crowd out normal cells from the bone marrow
  2. inhibit normal cell function
  3. infiltrates other organs
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6
Q

What will the general symptoms of an acute leukemia be?

A

sudden onset of bone marrow failure symptoms: fatigue, infections, bleeding, etc. and bone pain
potentially organ infiltration - so confusion if in the CNS

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7
Q

What will the general lab findings be in acute leukemia

A
  1. blasts/immature cells in blood smear
  2. leukocytosis (all bad cells)
  3. anemia
  4. trombocytopenia
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8
Q

What percentage of the blood cells need to be blasts to get the AML diagnosis?

A

at least 20%

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9
Q

AML: good or bad progrnosis in general?

A

bad

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10
Q

What’s the old classification system for AML?

A

M0-M7

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11
Q

What cells are involved in M0?

A

myeloblasts (neutrophilic series) - minimally differentiated.

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12
Q

M1?

A

myeloblasts (neutrophilic series) - without maturation

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13
Q

M2?

A

myeloblasts (neutrophilic series) - with maturation

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14
Q

M3?

A

promyelocytes (neutrophilic series)

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15
Q

M4?

A

myelomonocytes

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16
Q

M5?

A

monocytes

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17
Q

M6?

A

erythroblasts

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18
Q

M7?

A

megakaryoblasts

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19
Q

What are some of the ways you can tell a leukemia is myeloid?

A
  1. dysgranulopoiesis
  2. AEUR RODS!
  3. cytochemistry - use specific stains
  4. immunophenotyping
  5. cytogenetics
20
Q

What are the categories in the “new” classificaiton for AML?

A 
AML with genetic abnormalities
AML with FLT-3 mutstion
AML with multilineage dysplasia
AML, therapy related
AML, NOC
21
Q

For AML M0, what’s the only way you can diagnose it?

A

you need to do immunophenotyping - you need to use markers

22
Q

What’s the main difference between AML M0 and M1?

A

In M1 they have committed themselves to a lineage, but still minimal to no maturation

23
Q

What’s the diagnostic tipoff for M1?

A

auer rods!

24
Q

What enzyme does M1 have that M0 doesn’t?

A

myeloperoxidase (MPO)

25
Q

What genetic abnormaltiy occurs in some cases of M2 and leads to a better prognosis?

A

translocation of chromosone 8 and 21

26
Q

What cells are diagnostic of AML M3?

A

Faggot cells (bundle of sticks - just TONS of Auer rods)

27
Q

Why is treatment of M3 different from all the others?

A

The promyelocytes have pro-thrombotic granules that will cuase DIC if treated like normal leukemias, so you give a drug that removes the block to maturation, so the malignant cells just mature out and disappear!

28
Q

What genetic abnormality is present in ALL cases of M3?

A

a translocation of chromosone 15 and 17

29
Q

Why do you need to worry about extramedullary tumor masses in M4?

A

Because it’s a leukemia of monocytes, which travel through the body

30
Q

What genetic abnormality is present in some cases of M4 and leads to better prognosis?

A

inversion of chromosome 16

31
Q

Why is M4 sometimes considered a dual leukemia?

A

You can get an increase in both myeloblasts and monocytic cells

32
Q

What enzyme will M5 be positive for?

A

nonspecific esterase (from the monoblasts)

33
Q

Will M7 be positive for myeloperoxidase?

A

no - it’s not in the monocyte series

34
Q

Of the AMLs with genetic abnormatlities, which one confers a poor prognosis?

A

11q23

35
Q

What AML technically has a genetic abnormality but is in a group all it’s own?

A

FLT-3 mutation: present in a third of all AML cases!

36
Q

Does the FLT3 mutation lend a good or bad prognosis? Why?

A

bad - they’re so much more likely to relapse and relapse rapidly (this was the case)

37
Q

What are the characteristics of AML with multilineage dysplasia?

A

you have dysplasia in at least 2 different cell lines

typically in elderly patients

you get severe pancytopenia

38
Q

What chromosomes are often abnormal in AML with multilineage dysplasia?

A

5 and 7

39
Q

multilineage dysplasia: good or bad prognosis?

A

bad

40
Q

What drugs are particular cultprits for AML, therapy related?

A

alkylating agents like busulfan and topo 2 ihibitors like etoposide

41
Q

What’s the typical onset for AML, therapy related?

A

2-5 years

42
Q

therapy related - easy or hard to treat?

A

VERY hard

43
Q

What is the treatment for AML?

A

chemo and bone marrow transplant

44
Q

In general, what is myelodysplastic syndrome? Why is this included in this discussion?

A

there’s something abnormal about the stem cells in the marrow so you get dysmyelopoiesis and maybe increased blasts - but not as high as 20%
sometimes can evolved into acute leukemia

45
Q

What sort of anemia is usually present in myelodysplastic syndrome?

A

macrocytic, but often asymptomatic

46
Q

Who gets MDS?

A

elderly

IHO Week 3 (10 decks)

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