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Path- Haem Qs laz > Acute leukaemias > Flashcards

Acute leukaemias Flashcards

1
Q
  1. Which cell level does CML tend to occur in?
A

Pluripotent haematopoietic stem cell

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2
Q
  1. Which cell level does AML tend to occur in?
A

Pluripotent haematopoietic stem cell
or
multipotent myeloid stem cell

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3
Q
  1. List some types of chromosomal abnormalities that are associated with AML.
A 
Duplications 
Loss 
Translocation 
Inversion 
Deletion
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4
Q
  1. How can an altered DNA sequence lead to leukaemia?
A

By the creation of a fusion gene

By abnormal regulation of genes

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5
Q
  1. Which chromosomal duplications are most commonly associated with AML?
A

8 and 21 (there is a predisposition seen in Down syndrome)

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6
Q
  1. List some molecular abnormalities that can occur in apparently normal chromosomes.
A 
Point mutations 
Loss of function of tumour suppressor genes 
Partial duplication
Cryptic deletion (formation of a fusion gene by deletion of a small section of DNA)
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7
Q
  1. List some risk factors for AML.
A 
Familial
Constitutional (e.g. Down syndrome)
Anti-cancer drugs 
Irradiation 
Smoking
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8
Q
  1. What are type 1 and type 2 abnormalities with regards to leukaemogenesis?
A

Type 1: promote proliferation and survival (anti-apoptosis)
Type 2: block differentiation
NOTE: leukaemogenesis in AML requires multiple genetic hits

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9
Q
  1. What is the main role of transcription factors?
A

They bind to DNA, alter the structure to favour transcription and, ultimately, regulate gene expression

Disruption of transcription factors can result in failure of differentiation

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10
Q
  1. Give an example of how disruption of a transcription factor can lead to leukaemogenesis.
A

Core binding factor (CBF) is the master controller of haemopoiesis

Translocation 8;21 fuses RUNX1 with RUNX1T1 leading to the formation of a fusion gene that drives leukaemia

The fusion transcription factor binds to co-repressors leading to a differentiation block

Inversion of chromosome 16 also affects CBF in a similar way

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11
Q
  1. Which chromosomal aberration causes APML (Acute promyelocytic leukaemia) ?
A

Translocation 15;17

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12
Q
  1. What is a characteristic feature of APML (Acute promyelocytic leukaemia)? Why does this occur?
A

Haemorrhage – this is because APML is associated with DIC and hyperactive fibrinolysis

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13
Q
  1. Name the fusion gene that is responsible for APML.
A

PML-RARA

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14
Q
  1. In what way are the promyelocytes in APML considered ‘abnormal’?
A

They contain multiple Auer rods

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15
Q
  1. Describe how the variant version of APML is different from the original version.
A

The variant form has granules that are below the resolution of a light microscope
They also tend to have bilobed nuclei

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16
Q
  1. Give a type 1 and type 2 mutation for APML.
A

Type 1: FLT3-ITD

Type 2: PML-RARA

17
Q
  1. Give a type 1 and type 2 mutation for CBF (core binding factor) leukaemias.
A

Type 1: sometimes mutated KIT

Type 2: mutations affecting function of CBF

18
Q
  1. Which microscopic feature is pathognomonic of myeloid leukaemias?
A

Auer rods

19
Q
  1. Which stain can be used to distinguish myeloid leukaemias from other leukaemias?
A

Myeloperoxidase

20
Q
  1. Name other similar stains (to distinguish myeloid leukaemias from other leukaemias) that are not used as frequently.
A

Sudan black

Non-specific esterase

21
Q
  1. List the clinical features of AML.
A

Bone marrow failure (anaemia, neutropaenia, thrombocytopaenia)
Local infiltration (splenomegaly, hepatomegaly, gum infiltration, lymphadenopathy, CNS, skin)
Hyperviscosity if WBC is very high (can cause retinal haemorrhages and exudates)

22
Q
  1. Outline the tests that may be used to diagnose AML.
A

Blood film
Bone marrow aspirate
Cytogenetic studies (done in EVERY patient)
Molecular studies and FISH

23
Q
  1. What is aleukaemic leukaemia?
A

When there are no leukaemic cells in the peripheral blood but the bone marrow has been replaced

24
Q
  1. Outline the supportive care given for AML.
A 
Red cells 
Platelets 
FFC/cryoprecipitate in DIC 
Antibiotics 
Allopurinol (prevent gout) 
Fluid and electrolyte balance 
Chemotherapy
25
Q
  1. What are the principles of treatment of AML?
A 
Damage the DNA of the leukaemic cells 
Leave the normal cells unaffected 
Combination chemotherapy is ALWAYS used 
Usually given as 4-5 courses (2 x remission induction + 2/3 x consolidation)
Treatment usually lasts around 6 months
26
Q
  1. List some determinants of prognosis in AML.
A 
Patient characteristics 
Morphology 
Immunophenotyping 
Cytogenetics 
Response to treatment
27
Q
  1. Outline the clinical features of ALL.
A

Bone marrow failure

Local infiltration

28
Q
  1. What is a key difference in the origin of B-lineage and T-lineage ALL?
A

B-lineage starts in the bone marrow

T-lineage can start in the thymus (which may be enlarged)

29
Q
  1. List some possible leukaemogenic mechanisms in ALL.
A

Proto-oncogene dysregulation due to chromosomal abnormalities (resulting in fusion genes, altered gene promoters)

30
Q
  1. List some investigations used in the diagnosis of ALL.
A

FBC and blood film
Bone marrow aspirate
Immunophenotyping
Cytogenetic/molecular analysis

31
Q
  1. What are the four phases of chemotherapy for ALL?
A

Remission induction
Consolidation and CNS therapy
Intensification
Maintenance

32
Q
  1. How long does chemotherapy for ALL usually take? Why is it longer in boys?
A

2-3 years

Longer in boys because the testes are a site of accumulation of lymphoblasts

33
Q
  1. Who receives CNS-directed chemotherapy? How can this be given?
A

All patients should receive CNS-directed chemotherapy

This can be given intrathecally or a high dose of chemotherapy could be given such that it penetrates the BBB

34
Q
  1. Outline the supportive care for ALL.
A

Blood products
Antibiotics
General medical care (central line, gout management, hyperkalaemia management, sometimes dialysis)

Path- Haem Qs laz (4 decks)

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