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Heme > Acute Leukemia (Goorha) > Flashcards

Acute Leukemia (Goorha) Flashcards

1
Q

What are the two divisions of acute leukemia?

A

acute myeloid and acute lymphoblastic leukemia

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2
Q

What cellular feature is characteristic of leukemia?

A

accumulation of malignant WBCs in BM and blood

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3
Q

What causes the morbidity and mortality associated with leukemia?

A
  1. BM failure
    (anemia, neutropenia, thrombocytopenia)
  2. Infiltration of organs
    (such as liver, spleen, lymph nodes, meninges, brain, skin, testes)
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4
Q

FAB classification of acute myeloid leukemia:

A

M0-M7

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5
Q

FAB classification of acute lymphoblastic leukemia:

A

L1-L3

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6
Q

Most common form of leukemia in children

A

ALL

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7
Q

Acute leukemia that occurs in all age groups:

A

AML

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8
Q

Highest in kids ages 3-7

A

ALL

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9
Q

Increasingly common with advanced age

A

AML

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10
Q

What is the difference between primary and secondary AML?

A

primary AML = de novo

secondary AML develops from myelodysplastic syndrome or other hematatological malignancies

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11
Q

Which is more difficult to treat: primary or secondary AML?

A

secondary

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12
Q

Acute leukemia that shows a notable rise in patients around 40 years old:

A

ALL

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13
Q

Three treatment phases of ALL:

A
  1. remission induction
  2. consolidation (intensification)
  3. maintenance
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14
Q

Why is allopurinol administered to ALL patients receiving treatment?

A

it counters hyperuricemia resulting from tumor cell breakdown

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15
Q

Do adults or children with ALL have better cure rate? Why?

A

Children; this is possibly due to worse genetic features in adults

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16
Q

Disorders associated with causing acute leukemia (etiology):

A
  1. Myelodysplastic syndromes
  2. Myeloproliferative diseases
  3. Down’s syndrome
  4. Fragile chromosome syndromes (Fanconi’s anemia)
  5. Aplastic anemia + Paroxysmal Nocturnal Hemoglobinuria
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17
Q

Etiologies of acute leukemia related to exposure:

A
  1. Idiopathic (vast majority)
  2. Prior chemotherapy
  3. Prior radiotherapy
  4. Chemical exposure (benzene)
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18
Q

Where does malignant transformation occur in acute leukemia?

A

hematopoetic stem cells or early progenitors

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19
Q

What does genetic damage lead to, in acute leukemia?

A

(1) increased rate of proliferation
(2) reduced apoptosis
(3) block in cellular differentiation

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20
Q

Collectively, what is the result of genetic damage associated with acute leukemia?

A

accumulation of blast cells (early BM hematopoietic cells)

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21
Q

Acute leukemia is defined as:

A
  1. > 20% blasts in blood or BM

2. cytogenetic or molecular genetic abnormalities (even if blasts are <20%)

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22
Q

T/F: Acute leukemias are aggressive diseases.

A

T: no treatment = death

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23
Q

What is immunotyping (in terms of AML/ALL)?

A

analysis of the pattern of antigen expression on surface of blast cells

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24
Q

What is FAB AML classification M0?

A

undifferentiated

25
Q

What are FAB AML classification M1 and M2?

A

M1: no maturation
M2: granulocytic maturation

26
Q

What is FAB AML classification M3?

A

acute promyelocytic

27
Q

What is FAB AML classification M4?

A

granulocytic and monocytic maturation

28
Q

What is FAB AML classification M5?

A

monoblastic or monocytic

29
Q

What are FAB AML classification M6 and M7?

A

M6: erythroleukemia
M7: megakaryocytic

30
Q

What is FAB ALL classification L1?

A

small, uniform blast cells with a high nucleus:cyto ratio

31
Q

What is FAB ALL classification L2?

A

larger, heterogenous blast cells with a lower nucleus:cyto ratio

32
Q

What is FAB ALL classification L3?

A

blasts with vacuoles and basophilic cytoplasm

33
Q

What morphologic structure is diagnostic of AML?

A

auer rods

34
Q

What tests may be useful when trying to differentiate between ALL and AML?

A 
chromosomal/genetic analysis
Immunological markers (flow cytometry)
35
Q

4 myeloid antigens:

A

MPO
CD33
CD13
HLA-DR

36
Q

4 lymphoid antigens:

A

TdT
CD10
CD19
CD20

37
Q

What is an example of a genetic translocation linked to acute promyelocytic leukemia?

A

t(15;17)

38
Q

How do ATRA and arsenic counter an oncoprotein (or fusion oncoprotein)?

A
  • -Oncoprotein (gene product) binds to DNA and activates self-renewal of leukemic stem cells
  • -ATRA/arsenic releases the co-repressors bound to the DNA (“deprogramming” leukemia self-renewal)
  • -Normal transcription can now occur, allowing cell to differentiate into a normal cell
39
Q

What’s the diagnosis?

elevated WBC and smear showing auer rods

A

AML

40
Q

How does determining the specific genetic defect associated with an acute leukemia improve patient’s outcome?

A

useful in determining pronosis/treatment

41
Q

What is remission induction therapy (AML)?

A

1 to 2 courses of intensive therapy to achieve a complete response (no detectable leukemia cells)

42
Q

What is post-remission therapy (AML)?

A

“consolidation therapy”, in which 3 to 4 courses of intensive short-course therapy are used to further reduce the subclinical effects of a tumor

43
Q

What often follows post-remission therapy (AML)?

A

Either:

  1. maintenance therapy: months to years of less intensive therapy (further prevents recurrence)
  2. allogeneic bone marrow transplantation
44
Q

T/F: AML treatment is more favorable for older patients.

A

F: younger patients (perhaps because they tolerate chemo better)

45
Q

What are 4 treatment strategies for older adults with AML?

A
  1. Supportive care
  2. Standard intensive chemotherapy, not clear that any consolidation is beneficial
  3. New agents (noncytotoxic agents)
  4. Reduced-intensity conditioning HSCT (has shown a more favorable response than traditional high-intensity treatment)
46
Q

What genetic abnormalities are associated with poor outcomes in adults and children will ALL?

A

MLL-AF4 and BCR-ABL translocations

47
Q

What genetic abnormalities in childhood ALL (rare in adults) are associated with a good outcome?

A

E2A-PBX and TEL-AML

“abnormalities of hyperdiploidy”

48
Q

What is the prophylactic CNS treatment in ALL?

A

intrathecal methotrexate or ARA-C

49
Q

What are maintenance therapy drugs used in ALL?

A

6-MP, methotrexate, prednisone

50
Q

What are induction therapy drug options for ALL?

A
  1. VCR
  2. L-ASP
  3. DEX
  4. PRED +/- Daunorubicin
51
Q

What are consolidation therapy drug options for ALL?

A
  1. Daunorubicin
  2. HD Ara-C
  3. VCR
  4. Etoposide
  5. thioguanine or 6-mercaptopurine
  6. cyclophosphamide
  7. L-ASP

**do we need to know this??

52
Q

In acute leukemia, therapy is tailored to:

A

specific genetic abnormalities

53
Q

What are 4 ways to improve outcomes, in terms of treatment?

A

Treatment at specialized centres
Clinical Trials
Immunotherapy
Stem Cell Transplantation

54
Q

Molecular abnormality associated with poor prognosis in AML:

A

FLT3-ITD

55
Q

Molecular abnormality associated with intermediate prognosis in AML (in addition to cytogenetic abnormalities):

A

c-KIT

56
Q

3 cytogenetic abnormalities associated with good risk in AML:

A
  1. inv(16)
  2. t(8;21)
  3. t(15;17) **ATRA
57
Q

What would you use to treat APML (M3), according to the lecture?

A

ATRA/ARA-C

Anthracycline

58
Q

What would you use to treat inv(16) or t(8;21), according to the lecture (in addition to standard induction)?

A

high dose ARA-C

ultimately, allograft

59
Q

How would you treat a patient positive for FLT3-ITD versus one that was negative?

A

positive: allograft ASAP
negative: high dose ARA-C, allograft if needed

Heme (38 decks)

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