Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

genetically damaged hematopoietic stem cell

A 
malignant transformation
- probable mechanisms:
 > increased + unregulated proliferation
 > impaired maturation/differentiation
 > blockage in apoptosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

clinical features of acute leukemia

A 
cytopenias from BM failiure
organ infiltration (leukostasis, bone pain, hepato- & splenomegaly, extramedullary infiltration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute Leukemia treatment

A
  • intensive multi-agent chemotherapy (very toxic side effects)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

primary classification of acute leukemia is based on…

A

lineage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

cytogenetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

90% of adult leukemias; 15% of childhood leukemias

A

acute myeloid leukemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

F, it’s poor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

most effective acute leukemia treatment

A

hematopoietic stem cell/BM transplant

- most effective bt associated with significant morbidity and mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

immunophenotyping for acute leukemia

A
  • specific patterns of molecules associated with different cell lineages
  • used with morphology
  • tool = flow cytometry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

APL t(15;17) morphology

A
  • 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
Q

What are Auer rods?

A
  • 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
Q

T or F. Auer rods are specific to APL

A

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
Q

when is AML with myelodysplasia-related changes diagnosed?

A
  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
Q

AML with MRC prognosis

A

usually very poor; also poor response to treatment

30
Q

therapy-related myeloid neoplasms

A

can be AML or MDS

  • late-onset complication of cytotoxic chemotherapy and/or radiation therapy
  • arise after few to many years of chemo
31
Q

1 to 5 yrs of chemotherapy (Therapy-related myeloid neoplasm)

A

DNA topoisomerase type II inhibitors (mitoxantrone, etoposide, doxo, daunorubicin)

balanced chromosomal translocations

32
Q

5 to 10 yrs of chemotherapy (Therapy-related myeloid neoplasm)

A

alkylating agents and ionizing radiation (cisplatin, chlorambucil, cyclophosphamide)

unbalanced loss of genetic material (often 5 and/or 7)

33
Q

most ALL’s are __ ____

A

de novo

- due to acquired genetic errors in HPSC

34
Q

clinical features of B-ALL

A
  • 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
Q

B-ALL imunophenotype

A
  • CD19, CD20
  • sometimes CD34, TdT as immaturity markers
  • +/- aberrancy = expression of non-B cell antigens; myeloid markers CD13, CD33 common, but never cMPO
36
Q

recurrent genetic subtypes of B-ALL

A

B-LL/L with t(9;22); BCR-ABL1
B-LL/L with hyperdiploidy

ALL and CML usually have different breakpoints

37
Q

B-LL/L with t(9;22); BCR-ABL1

A
  • 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
Q

B-LL/L with hyperdiploidy

A
  • 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
Q

T-ALL epidemiology

A

more common in adolescents than younger children

- 80% males

40
Q

T or F. B-AL often presents as a lymphoma

A

F! T-ALL

  • or leukemia with significant nodal or extranodal involvement
  • marrow involvement is still common
41
Q

clinical features of T-ALL

A
  • often present as lymphoma
  • extranodal sites = 50% mediastinal mass (thymus); hepatosplenomegaly, lymphadenopathy very common; tonsils, skin, CNS, testes
  • hyperleukocytosis (high WBC)
42
Q

lymphoblastic leukemia in a boy with an anterior midline chest mas

A

probs T-ALL

43
Q

T-ALL immunophenotype

A
  • 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
Q

T or F. T-ALL is not classified based on genetics by WHO 2017

A

T! 50-70% have abnormal karyotypes though

45
Q

acute leukemias of ambiguous lineage

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions