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MedEd + PathSoc + Laz's Qs + Romesh Path > Haematology 2: Acute Leukaemias > Flashcards

Haematology 2: Acute Leukaemias Flashcards

1
Q

<p>Which acute leukaemia is an emergency ?</p>

A

<p>APML (acute promyeloid)</p>

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2
Q

<p>What translocation causes Acute promyelocytic leukaemia (APML), which fusion gene?</p>

A

<p>T(15;17)

| <br></br><br></br>Fusion gene = (PML-RARA) (promyelocytic leukemia/retinoic acid receptor alpha)</p>

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3
Q

<p>Which leukaemia is more common in patients with Down’s syndrome ?</p>

A

<p>ALL+ AML </p>

  • Thought to be dose effect (they have more of the protoncogene)
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4
Q

<p>What signs is characteristic in APML ?</p>

A

<p>Sudden onset Haemorrhage (bruising and bleeding)
<br></br>
<br></br>
<br></br>This is because APML is associated w/ DIC + Hyperactive fibrinolysis</p>

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5
Q

<p>Which feature is characteristic of APML on microscopy ?</p>

A

<p>Multiple auer rods in promyelocytes</p>

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6
Q

<p>What does the variant of APML without auer rods look like on microscopy ?</p>

A

<p>Promyelocytes with Bilobed nuclei</p>

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7
Q

<p>Which 2 stains are possitive in AML but not In ALL ?</p>

A

<p>Myeloperoxidase stain<br></br>Sudan black B stain</p>

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8
Q

<p>Which leukaemia causes Gum infiltration ?</p>

A

<p>Monocytic AML</p>

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9
Q

<p>List 5 signs of AML ?</p>

A

<p>Anaemia- SOB, Pallor<br></br>Neutropenia- infections <br></br>Thrombocytopenia- easy Bruising and bleeding, DIC<br></br>Hepatosplenomegally <br></br>Retinal haemorrhage/exudates</p>

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10
Q

<p>What is the most important diagnostic test for Leukaemias ?</p>

A

<p>Immunophenotyping</p>

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11
Q

<p>What is the most common leukaemia in childhood ?</p>

Who else can commonly have this?

Prognosis?

A

<p>ALL</p>

Bimodal distribution - another peak in old age (this has higher incidence of philadelphia +ve cases) - t(9;22)

85% of children are cured, old age = poor prognosis as less likely to cope w/ chemo + philadelphia +ve is more severe

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12
Q

<p>List 5 signs of ALL ?</p>

A

<p>BM failure:
<br></br>- Anaemia- SOB, pallor
<br></br>- Neutropenia- infections
<br></br>- Thrombocytopenia- Easy bruising, bleeding
<br></br>
<br></br>Lymphadenopathy
<br></br>Hepatosplenomegaly</p>

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13
Q

<p>Which drug is used to treat CML or ALL with the Philadelphia chromosome abnormality ?</p>

A

<p>Tyrosine kinase inhibitor- Imatinib</p>

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14
Q

<p>Which cell level does CML tend to occur in? and AML?</p>

A

<p>CML:
Pluripotent haematopoietic stem cell<br></br>
AML:
Pluripotent haematopoietic stem cell or multipotent myeloid stem cell or granulocyte-monocyte precursor</p>

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15
Q

<p>Chromosomal abnormalities associated with AML? (5)</p>

A

<p>Duplications

Loss

Translocation

Inversion

Deletion</p>

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16
Q

<p>How can an altered DNA sequence lead to leukaemia?</p>

A

<p>By the creation of a fusion gene
<br></br>
<br></br>By abnormal regulation of genes</p>

17
Q

<p>Which chromosomal duplications are most commonly associated with AML?</p>

A

<p>8 and 21 (there is a predisposition seen in Down syndrome)</p>

18
Q

<p>List some molecular abnormalities that can occur in apparently normal chromosomes.</p>

A

<p>Point mutations
<br></br>Loss of function of tumour suppressor genes
<br></br>Partial duplication
<br></br>Cryptic deletion (formation of a fusion gene by deletion of a small section of DNA)</p>

19
Q

<p>What are type 1 and type 2 abnormalities with regards to leukaemogenesis?</p>

leukaemogenesis in AML?

A

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

20
Q

<p>Give a type 1 and type 2 mutation for APML.</p>

A

<p>Type 1: FLT3-ITD (internal tandem duplication)

| <br></br><br></br>Type 2: PML-RARA</p>

21
Q

<p>Give a type 1 and type 2 mutation for CBF (core binding factor) leukaemias.</p>

A

<p>Type 1: sometimes mutated KIT
<br></br>
<br></br>Type 2: mutations affecting function of CBF</p>

22
Q

<p>Which microscopic feature is pathognomonic of myeloid leukaemias?</p>

A

<p>Auer rods</p>

23
Q

<p>What is aleukaemic leukaemia?</p>

A

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

24
Q

<p>What is a key difference in the origin of B-lineage and T-lineage ALL?</p>

A

<p>B-lineage starts in the bone marrow (85%)

| <br></br><br></br>T-lineage can start in the thymus (which may be enlarged) (15%)</p>

25
Q

<p>How long does chemotherapy for ALL usually take? Why is it longer in boys?</p>

A

<p>2-3 years
<br></br>
<br></br>Longer in boys because the testes are a site of accumulation of lymphoblasts
<br></br>
<br></br>NB. can also accumulate in CNS</p>

26
Q

<p>What are the four phases of chemotherapy for ALL?</p>

A

<p>Remission induction

Consolidation and CNS therapy

Intensification

Maintenance</p>

27
Q

<p>Who receives CNS-directed chemotherapy? How can this be given?</p>

A

<p>All patients should receive CNS-directed chemotherapy
<br></br>
<br></br>This can be given intrathecally or a high dose of chemotherapy could be given such that it penetrates the BBB</p>

28
Q

<p>Recall some clinical signs that can be used to identify AML</p>

A

Hepatosplenomegaly

Monocytic gum infiltration

CNS disease

Occasional lymphadenopathy

29
Q

<p>What is the most effective investigation for differentiating AML and ALL, and what results would it show for each?</p>

A

<p>Immunophenotyping:<br></br>
AML: CD13/14/15<br></br><br></br>
ALL: CD3/4/18/19/20</p>

30
Q

<p>Recall some useful supportive therapies for AML</p>

A

Blood products: red cells, platelets and FFP

Antibiotics

Long line

Allopurinol (as uric acid may be released from dying cells when treatment is started)

31
Q

<p>Recall some sites of leukaemic involvement in ALL that you wouldnt see in AML</p>

A

<p>Thymus, testes, CNS</p>

32
Q

<p>Which type of leukaemia is most likely to present with long bone pain?</p>

A

<p>ALL</p>

33
Q

What are 3 ways of differentiating between AML and ALL?

A

Cytological features

Cytochemistry

Immunophenotyping

34
Q

Cytological differences between AML and ALL?

A

AML:

  • Abundant amount of cytoplasm w/ granules present
  • Coarse chromatin appearance due to granules
  • 3-4 nuclei
  • Auer rods present

ALL:

  • A rim of cytoplasm w/out chromatin
  • Fine chromatin appearance
  • 1-2 nuclei
  • No auer rods
35
Q

Cytochemistry in ALL v AML?

A

Not used as much anymore however stains used are:

Myeloperoxidase - MAIN
Sudan black
Non-specific esterase

These are all positive in AML but not ALL

36
Q

Prognosis for APML w/ treatment + what treatment?

A

Good prognosis when treated w/ All-trans retinoic acid (high dose vit A)

ATRA

37
Q

Acute leukaemia + t(9;22) + CD19 and TdT =?

A

ALL - t(9;22) present in 30%

MedEd + PathSoc + Laz's Qs + Romesh Path (99 decks)

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