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Blood and Lymph Unit 2 > Acute Leukemia > Flashcards

Acute Leukemia Flashcards

1
Q

What is acute leukemia?

A

Clonal, neoplastic proliferation of immature myeloid or lymphoid cells.

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2
Q

What are the two major categories of acute leukemia?

A
  1. Acute myeloid leukemia (AML)

2. Acute lymphoblastic leukemia (ALL)

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3
Q

What is the cause for the signs and symptoms of acute leukemia?

A

The loss of normal hematopoietic elements, and subsequently a loss of normal peripheral blood cells

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4
Q

True or False:

Acute leukemia is rapidly fatal without treatment

A

True

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5
Q

What is the most common etiology of acute leukemia?

A

Chromosomal abnormalities

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6
Q

What are two consequences of chromosomal abnormalities in acute leukemias?

A
  1. Maturation/ differentiation is blocked

2. Cells are not dependent on external factors for growth stimulation

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7
Q

Acute myeloid leukemia includes which types of cells?

A

Granulocytic
Monocytic
Erythroid
Megakaryocytic

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8
Q

Acute lymphoid leukemia includes which types of cells?

A

B or T-cell lineages

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9
Q

Name some risk factors for acute leukemia.

A 
Previous chemotherapy 
Tobacco smoke
Ionizing radiation
Benzene exposure
Genetic syndromes
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10
Q

Can acute lymphoblastic leukemia present as a solid mass?

A

Yes. It is called lymphoblastic lymphoma or LBL

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11
Q

What are the two main types of ALL?

A
  1. B-lymphoblastic ALL (B-ALL)

2. T-lymphoblastic ALL (T-ALL)

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12
Q

What patient population does ALL most commonly present in?

A

Children under 6

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13
Q

What would you expect the peripheral white blood cell count to be in a patient with ALL?

A

It could be increased, normal, decreased

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14
Q

What cell surface marker can be found on the surface of lymphoblasts?

A

CD34

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15
Q

What enzymes do lymphoblasts express that can be used to identify them?
Hint: It is not expressed in mature lymphocytes & it adds nucleotides to V(D)J exons during antibody recombination

A

Terminal deoxynucleotidyl transferase (TdT)

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16
Q

Are the majority of ALL cases B-ALL or T-ALL?

A

B-ALL

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17
Q

What three B-lineage antigens are found on B-lymmphoblasts?

A

CD19
CD22
and/or
CD79a

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18
Q

Do B-lymphoblasts express CD20?

A

No

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19
Q

What are three cytogenetic changes seen in B-ALL?

A
  1. B-ALL with t(9;22)(q34;q11.2); BCR-ABL1
  2. B-ALL with translocations of 11q23; MLL
  3. B-ALL with t(12;21)(p13;q23); ETV6-RUNX1
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20
Q

What protein product is produced by t(9;22)?

A

This is called the Philadelphia Chromosome

BCR-ABL fusion protein 190kd

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21
Q

Only 25% of cases of adult B-ALL involve the Philadelphia chromosome. How does the presence of this protein effect the prognosis?

A

B-ALL with Philadelphia chromosome has the worst prognosis of all subtypes of ALL.

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22
Q

B-ALL with abnormalities of MLL is frequently seen in what patient population?

What is the prognosis?

A

Neonates and young infants

poor prognosis

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23
Q

B-ALL with ETV6-RUNX1 is seen in what patient population?

Prognosis?

A

25% cases of childhood B-ALL

Very favorable prognosis

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24
Q

What type of leukemia is more often seen in adolescents and young adults?

A

T-lymphoblastic ALL

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25
Q

T-ALL more frequently presents with a component of lymphoblastic lymphoma (T-LBL). Where does this mass most often present?

A

It presents as a large mediastinal mass.

26
Q

How does T-ALL present?

A

High white blood count

27
Q

Does T-ALL/ T-LBL favor males or females?

A

Males

28
Q

What T-lineage antigens are expressed on T-lymphoblasts?

A

CD2, CD3, &/ or CD7

CD4 and CD8 CONCURRENTLY

CD99 and CD1a

29
Q

What factors influence the prognosis of ALL?

A

AGE: worse in infants (10, and adults

WHITE BLOOD CELL COUNT: worse for markedly elevated WBC count

SLOW RESPONSE TO THERAPY/ SMALL AMOUNTS OF RESIDUAL DISEASE AFTER THERAPY

NUMBER OF CHROMOSOMES: very favorable prognosis for hyperdiploidy; poor prognosis for hypodiploidy

B VS. T LINEAGE: T-ALL seems to have a worse prognosis than B-ALL

30
Q

What is the average age of diagnosis of AML?

A

65 years of age

31
Q

How is AML diagnosed?

A

Increased myeloblasts accounting for 20% or more of nucleated cells in the marrow or peripheral blood

32
Q

What are Auer rods?

A

Fused azurophilic granules forming small stick-like structures in the cytoplasm.

33
Q

What cells do Auer rods differentiate.

A

Myeloblasts are generic looking. Aeur rods differentiate myeloblasts from lymphoblasts

34
Q

What cells are Auer rods found?

A

Only abnormal myeloblasts

35
Q

Myeloblasts often express what cellular markers?

A 
CD34-A generic marker of immaturity
CD117 (C-Kit)
Myeloperoxidase 
CD33
CD13
36
Q

If monocytic differentiation occurs in AML what cellular markers can be seen?

A

CD64

CD14

37
Q

If megakaryoblastic defferentiation occurs in AML what cellular markers can be seen?

A

CD41

CD61

38
Q

What type of genetic abnormality is characteristic for AML?

A

Balanced translocations

39
Q

How are balanced translocations detected?

A 
Cytogenetic analysis (karyotyping or FISH)
Molecular analysis (RT-PCT)
40
Q

What protein is produced in AML with t(8;21)(q22;q22); RUNX1-RUNX1T1?

A

RUNX1 encodes alpha unit of core binding factor (CBF), a transcription factor needed for hematopoiesis. The fusion protein blocks transcription of CBF-dependent genes, thus blocking differentiation.

41
Q

What is the general prognosis of AML with t(8;21)(q22;q22); RUNX1-RUNX1T1?

A

Relatively good prognosis

42
Q

What subtype of AML is characteristic of baso eos in the bone marrow?

A

AML with inv(16)(p13.1;q22) or t(16;16)(p13.1;q22); CBFB-MYH11

43
Q

What are “baso eos”?

A

Immature eosinophils with abnormal baasophilic granules in addition to their eosinophilic granules

44
Q

What cells are often seen in AML with inv(16)(p13.1;q22) or t(16;16)(p13.1;q22); CBFB-MYH11?

A

Increased myeloblasts and increasedmonocytes thus a “myelomonocytic leukemia”

45
Q

Describe the protein produced in AML with inv(16)(p13.1;q22) or t(16;16)(p13.1;q22); CBFB-MYH11?

A

CBFB encodes the beta subunit of core binding factor (CBF), a transcription factor needed for hematopoiesis. The fusion protein blocks transcription of CBF-dependent genes, thus blocking differentiation.

46
Q

What is the general prognosis for AML with inv(16)(p13.1;q22) or t(16;16)(p13.1;q22); CBFB-MYH11?

A

Relatively good prognosis

47
Q

Describe the cells in acute promyelocytic leukemia with t(15;17)(q22;q12); PML-RARA.

A

Abnormal promyelocytes predominate instead of blasts.

Hypergranular promyelocytes with many Auer rods (faggot cells)

48
Q

How can acute promyelocytic leukemia be treated?

A

Supra-physiologic doses of all-transretinoic acid (ATRA) in combinatoinn with arsenic salts

49
Q

APL can give rise to what life-threatening event?

A

Disseminated intravascular coagulation (DIC)

50
Q

Describe the cells in AML with t(1/22)(p13;q13); RBM 15-MKL1.

A

Usually shows megakaryoblastic differentiation

51
Q

What specific patient population is at risk of developing AML with t(1/22)(p13;q13); RBM 15-MKL1.?

A

Infants with Down syndrome

52
Q

What is the general prognosis of an individual with AML with t(1/22)(p13;q13); RBM 15-MKL1.?

A

Relatively good prognosis with intensive chemotherapy

53
Q

Describe the cells of AML with abnormalities of 11q23; MLL.

A

Frequently shows some degreee of monocytic differentiation

54
Q

What is the general prognosis of AML with abnormalities of 11q23; MLL?

A

Poor prognosis

55
Q

AML (t-AML) can be caused by what therapies?

A

Alkylating agents

Topoisomerase-II inhibitors

Ionizing radiation

56
Q

t-AML secondary to alkylating agents or radiations occurs due to what cytological abnormality?

What is the latency period?

A

Whole or partial loss of chromosomes 5 and/or 7

2-8 years

57
Q

t-AML secondary to topoisomerase-II inhibitors occurs due to what cytological abnormality?

A

Rearrangement of the MLL gene (11q23)

58
Q

Generally all types of t-AML have what prognosis?

A

Very poor

59
Q

Monocytic differentiation is important to note as leukemic monocytes because…

A

They often infiltrate the skin and gums, resulting in many small lesions

60
Q

Megakaryoblasts in AML, NOS (not otherwise specified) usually are accompanied by what life threatening disorder?

A

Marrow fibrosis

61
Q

What is the most important prognostic finding for AML, NOS?

A

The presence of certain molecular findings

  1. FLT3 ITD- NEGATIVE prognostic factor
  2. NPM1- POSITIVE prognostic factor
  3. CEBPA- POSITIVE prognostic factor
62
Q

What is the general prognosis for AML?

A

variable. 60% of AML cases will reach complete remission after chemotherapy

Blood and Lymph Unit 2 (9 decks)

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