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MLSCI 230 > Acute Leukemia > Flashcards

Acute Leukemia Flashcards

1
Q

high proliferation rate, high blast count (immture) and happens rapidly

A

acute leukemia

an emergency!

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2
Q

malignancy of immature white cells called blasts

A

acute leukemia

  • uncontrolled proliferation of immature cells in BM which manifests in the PB
  • cytopenias + increased blast %
  • acute is aggressive =emergency!
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3
Q

genetically damaged hematopoietic stem cell

A 
malignant transformation
- probable mechanisms:
 > increased + unregulated proliferation
 > impaired maturation/differentiation
 > blockage in apoptosis
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4
Q

T or F. Children are more at risk for acute myeloblastic leukemia

A

F! lymphoblastic (adults more at risk for myeloblastic)

incidence = first peak in children <5 y/o then another peak in old age

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5
Q

risk factors for acute leukemia (or bad luck cancer)

A
  • increasing age (genetic mutations accumulate)
  • acquired marrow disorders (myelodysplasia, myeloproliferative neoplasms, aplastic anemia)
  • mutagen exposure (toxic chemicals, chemotherapy, radiation)
  • inherited chromosomal disorders that can affect BM (Down’s, Fanconi’s)
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6
Q

clinical features of acute leukemia

A 
cytopenias from BM failiure
organ infiltration (leukostasis, bone pain, hepato- & splenomegaly, extramedullary infiltration)
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7
Q

Acute Leukemia treatment

A
  • intensive multi-agent chemotherapy (very toxic side effects)
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8
Q

primary classification of acute leukemia is based on…

A

lineage

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9
Q

the fundamental basis of diagnosis

A
  • morphology
  • diagnosis requires >20% of WBCs to be blasts (either in PB or BM diffs)
  • several exceptions*
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10
Q

How to know if a blast is myeloid or lymphoid

A

very variable!! morphology is not infallible

  • only Auer rods are definitive (myeloid)
  • it is important to recognize when blasts are present in general
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11
Q

after lineage, the next most important factor for classification of acute leukemia is

A

cytogenetics

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12
Q

90% of adult leukemias; 15% of childhood leukemias

A

acute myeloid leukemia

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13
Q

T or F. overall survival in adults for AML remains great

A

F, it’s poor

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14
Q

most effective acute leukemia treatment

A

hematopoietic stem cell/BM transplant

- most effective bt associated with significant morbidity and mortality

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15
Q

immunophenotyping for acute leukemia

A
  • specific patterns of molecules associated with different cell lineages
  • used with morphology
  • tool = flow cytometry
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16
Q

used to detect specific gene fusion transcripts that arise from certain mutations or translocations

A

PCR (molecular pathology)

  • NPM1, FLT3, t(9;22), etc.
  • next gen sequencing
  • risk stratification and prognosis
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17
Q

90% of adult leukemias

A

AML

  • mostly in elderly but can occur at any age (prolonged exposure to environmental carcinogens)
  • 15% of childhood leukemias
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18
Q

most common risk factors for AML

A
  • radiation, toxins, chemicals, chemo
  • arising from another myeloid neoplasm (MDS, MPN, MDS/MPN)
  • from non-neoplastic marrow disorders = aplastic anemia, inherited bone marrow failure syndrome (Fanconi, Shwachmann-Diamond, etc.)
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19
Q

AML with recurrent genetic abnormalities (3)

A
  • t(15;17)
  • t(8;21)
  • t(16;16) or inv(16)

<20% lasts; oligoblastic; good prognosis leukemias

20
Q

CBFB-MYH11

A

inv(16) or t(16;16)

  • good prognosis AML
  • core-binding factor B
  • affects proper myeloid maturation
  • less common in older
  • frequently accompanies with or a relapse if myeloid sarcomas = tumour-like collection of blasts
21
Q

AML with inv(16) morphology

A
  • myelomonocytic = blasts show granulocytic and monocytic differentiation
  • increase eos in BM
  • abnormal marrow eos
    > “amphophilic”
    > both pink AND purple-violet baso granules
    > granules large and chunky
22
Q

explain FISH

A
  • red and green fluorescent probes target and flank both sides of a known chromosome break point
  • yellow fluorescence = probes are together (chromosome is intact)
  • separate red and green = chromosome has broken
23
Q

APL with t(15;17)

A
  • very unique
  • acute promyelocytic leukemia
  • PML-RARA
  • middle-age adults
  • pancytopenia and bleeding
    > DIC
    > dysregulated hemostasis and coagulation
24
Q

this is treated differently than other AMLs

A

APL t(15;17)
- specific chemotherapy plus ATRA (all-trans retinoic acid)
> high dose vit A!
> cell maturation = leukemic blasts grow up into neuts and die
- very good prognosis; best of all AMLs

25
APL t(15;17) morphology
- pancytopenia (circulating blasts are often missed) - blasts are abnormal promyelocytes > can be mistaken for myeloid precursors > hypergranular blasts > bilobed or butterfly saddle nuclei > Auer rods and F cells
26
What are Auer rods?
- linear polymer of primary granules - defines myeloid blasts - Auer rods means = myeloid, malignant, aggressive disease (high-grade MDS or AML) - Auer rods are always abnormal!
27
T or F. Auer rods are specific to APL
F! specific to AML (not unique to APL) - can occur in any AML type - f cells highly characteristic for APL - if f cells + Auer rods are easy to find = APL until proven otherwise
28
when is AML with myelodysplasia-related changes diagnosed?
1. prior history of MDS, MDS/MPN 2. significant morphologic dysplasia > dysplasia in >50% of cells in >/= 2 lines 3. MDS-related cytogenetic abnormality
29
AML with MRC prognosis
usually very poor; also poor response to treatment
30
therapy-related myeloid neoplasms
can be AML or MDS - late-onset complication of cytotoxic chemotherapy and/or radiation therapy - arise after few to many years of chemo
31
1 to 5 yrs of chemotherapy (Therapy-related myeloid neoplasm)
DNA topoisomerase type II inhibitors (mitoxantrone, etoposide, doxo, daunorubicin) balanced chromosomal translocations
32
5 to 10 yrs of chemotherapy (Therapy-related myeloid neoplasm)
alkylating agents and ionizing radiation (cisplatin, chlorambucil, cyclophosphamide) unbalanced loss of genetic material (often 5 and/or 7)
33
most ALL's are __ ____
de novo | - due to acquired genetic errors in HPSC
34
clinical features of B-ALL
- blast expansion in BM and organs > bone and joint pain > hepatosplenomegaly, lymphadenopathy > extra-nodal masses - decrease in normal hematopoiesis = anemia, thrombocytopenia, neutropenia - WBC may be decreased, normal or increased (DIFF count is critical)
35
B-ALL imunophenotype
- CD19, CD20 - sometimes CD34, TdT as immaturity markers - +/- aberrancy = expression of non-B cell antigens; myeloid markers CD13, CD33 common, but never cMPO
36
recurrent genetic subtypes of B-ALL
B-LL/L with t(9;22); BCR-ABL1 B-LL/L with hyperdiploidy **ALL and CML usually have different breakpoints**
37
B-LL/L with t(9;22); BCR-ABL1
- high risk, very poo prognosis - chemo resistance - decrease remission, increase relapse - usually need BMT - treatment must include tyrosine kinase inhibitors (imatinib) which targets the BCR-ABL1 fusion protein
38
B-LL/L with hyperdiploidy
- rare in adults - blasts have >50 chromosomes (normal is 46;2N) - additional copies; NO structural abnormalities or translocations - no unique or specific characteristics - favourable prognosis
39
T-ALL epidemiology
more common in adolescents than younger children | - 80% males
40
T or F. B-AL often presents as a lymphoma
F! T-ALL - or leukemia with significant nodal or extranodal involvement - marrow involvement is still common
41
clinical features of T-ALL
- often present as lymphoma - extranodal sites = 50% mediastinal mass (thymus); hepatosplenomegaly, lymphadenopathy very common; tonsils, skin, CNS, testes - hyperleukocytosis (high WBC)
42
lymphoblastic leukemia in a boy with an anterior midline chest mas
probs T-ALL
43
T-ALL immunophenotype
- cCD3 and CD7 most common - immaturity markers may be CD34, nTdT, cytoplasmic CD3 expression without surface CD3 - aberrancy = loss of other T-cell antigens like CD5; expression of CD13, CD33 (non-Tcell antigens)
44
T or F. T-ALL is not classified based on genetics by WHO 2017
T! 50-70% have abnormal karyotypes though
45
acute leukemias of ambiguous lineage
- acute undifferentiated leukemia = no lineage-specific markers; cannot classify as either myeloid or lymphoid - mixed phenotype acute leukemia = lineage-specific markers for >/= 2 lineages **poor prognosis**

MLSCI 230 (36 decks)

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