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ALL Flashcards

1
Q

What is the main characteristic feature of ALL?

A

development of a large number of immature lymphocytes/lymphoblasts

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2
Q

What are the S+S of ALL?

A
  1. Bruising or bleeding
  2. Pallor + fatigue
  3. Infection (recurrent)
  4. Bone/joint pain
  5. Enlarged lymph nodes, liver and/or spleen

(there are way more, but this is probably enough)

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3
Q

Explain why the following symptoms arise:

  1. Bruising or bleeding
  2. Pallor + fatigue
  3. Infection (recurrent)
  4. Bone/joint pain
A
  1. Bruising or bleeding due to thrombocytopenia
  2. Pallor + fatigue due to anaemia
  3. Infection (recurrent) due to neutropenia
  4. Bone/joint pain (increased cell production = bone marrow expansion)
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4
Q

Which chromosome abnormality is commonly implicated in Pro-B ALL?

A

MLL translocation (also known as KMT2A according to Wiki)

but the lecture said MLL, so stick to that x

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5
Q

Which chromosome abnormality is commonly implicated in Pre-B ALL?

A

High hyperdiploidy or ETV6-RUNX1 translocation

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6
Q

Give examples of common and rare mutations associated with ALL?

A

Common:

  • ARID5B
  • CDKN2A/2B
  • CEBPE
  • IKZF1
  • GATA3
  • PIP4K2A

Rare:
- TP53

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7
Q

Why is Down’s syndrome a risk factor for ALL?

A
  • a common translocation in ALL is on chromosome 12 and 21
  • in Down’s syndrome there is trisomy 21
  • more chromosome 21 increases likelihood of translocation occurring
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8
Q

Apart from genetic abnormalities, what are the other risk factors of ALL?

A
  • environmental:
    1. high levels of radiation exposure
    2. high birth weight
    3. secondary leukaemia (after treatment with certain chemotherapies)

also delayed infection hypothesis

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9
Q

What test gives conclusive proof for a diagnosis of ALL? How does it do this?

A

Bone marrow biopsy

>20% fo all cells being leukaemic lymphoblasts = A::

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10
Q

What tests can be done to diagnose ALL?

A
  • medical history
  • physical examination
  • complete blood count
  • blood smears
  • bone marrow biopsy
  • lumbar puncture (see if spina cord + brain have been invaded)
  • kidney function, electrolytes and liver enzyme tests
  • immunophenotyping
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11
Q

What is immunophenotyping? What is the preferred method? Why is it beneficial in the diagnosis of ALL?

A
  • lab technique used to identify proteins that are expressed on their cell surface
  • preferred method = flow cytometry
  • in malignant lymphoblasts there is expression of terminal deoxynucleotidyl transferase (TdT)
  • can help differentiate is rom B or T cell lineage and the level of maturity of the WBCs
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12
Q

What are the different stages in treating ALL? What is the aim of each stage?

A
  1. remission induction
    - kill most tumour cells
    - reduce leukaemic blasts in bone marrow
  2. consolidation/intensification
    - further reduce tumour burden
  3. maintenance
    - kill any residual cells
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13
Q

What types of drugs are used in the remission induction stage?

A
  1. steroids (prednisolone or dexamethasone
  2. vincristine
  3. asparaginase
    * daunorubicin used in adult ALL
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14
Q

What types of drugs are used in the consolidation/intensification stage?

A
  1. vincristine
  2. cyclophosphamide
  3. cytarabine
  4. daunorubicin
  5. etoposide
  6. thioguanine
  7. mercaptopurine

CNS treatment: hydrocortisone, MTX and cytarabine

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15
Q

What types of drugs are used in the maintenance stage?

A
  1. daily oral mercaptopurine
  2. weekly oral methotrexate
  3. monthly 5-day course of UV vincristine and oral corticosteroid
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16
Q

What biological therapy can be used in ALL, and why is it used?

A
  1. tyrosine kinase inhibitors
    - usually used in patients with Bcr-Abl1+ ALL
  2. Blinatumomab (CD19-CD3 bispecific mAb) - engages CD3 T cells with CD19 B cells, causing the T cells to kill the CD19 B cells
17
Q

What factors are favourable in terms of prognosis?

A
  1. 3-5 y/o
  2. Female
  3. Caucasian
  4. Absent organomegaly
  5. Absent mediastinal mass
  6. Absent CVS involvement
  7. Low leukocyte count
  8. Lymphoid cell type
  9. early Pre-B cell lineage
  10. Rapid response to treatment
  11. time to remission <4 weeks

HD (26 decks)

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