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Pathology by week > W24 - Acute leukaemia > Flashcards

W24 - Acute leukaemia Flashcards

1
Q

A 3-year-old girl develops pain in her legs and is found to have generalised lymphadenopathy and a palpable spleen. Her blood count shows WBC 35.4 × 109/l, Hb 77 g/l and platelet count 85 × 109/l. The most likely diagnosis is

  1. Acute lymphoblastic leukaemia
  2. Chronic lymphocytic leukaemia
  3. Acute myeloid leukaemia
  4. Chronic myeloid leukaemia
A

1.Acute lymphoblastic leukaemia

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2
Q

In acute leukaemia, the dominant cell is a ______ cell

A

blast

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4
Q

AML - the incidence increases/decreases with age

  • median age of diagnosis?
A

AML - the incidence increases with age

  • median age of diagnosis = 65-70
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5
Q

Name 2 chromosomal translocations and 1 inversion that may result in AML

A

t(15;17)

t(5;8)

inv(16)

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6
Q

Name 2 chromosomal duplications that may result in AML - any associated diseases for either one?

A

Trisomy 8 (predisposes to AML)

Trisome 21 (predisposes to Down’s and AML)

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7
Q

Name 2 chromosomal loss or deletion that may result in AML

A

deletions and loss of 5/5q & 7/7q

q = long arm

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8
Q

RFs (4) for development of AML

A
  1. Familial predisposition
  2. Irradiation
  3. Anticancer drugs
  4. Smoking

also idiopathic

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9
Q

This is a inv(16) aka t(16;16)

  • what disease is this?
  • what does the blood film show?
A

AML

  • in this AML subtype, there is some maturation to bizarre eosinophil precursors (with giant granules) and also some blast cells
  • in inv(16) AML the block of differentiation is incomplete
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10
Q

Which is AML? why?

A

Top is likely AML due to fine granules

Bottom is likely lymphoid

*we can’t be 100% certain without immunophenotyping

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11
Q

Cytological features – which are myeloid?

A

auer rods = crystalline inclusion bodies in myeloid blast cells

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12
Q

How does leukamogenesis in AML occur?

A

at least 2 interacting molecular defects, synergise to give leukaemic phenotype via either:

  • promoting proliferation + anti-apoptosis
  • blocking differentiation
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14
Q

Person showing gum infiltration, skin changes (petechaei-like lesions), hepatosplenomegaly and recently feeling very lethargic with some weight loss. Diagnosis?

A

Acute monocytic leukaemia

*Gum infiltration is always monocyte disease

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17
Q

What do you do if you can’t tell if it is AML or ALL?

A

Immunophenotyping (Flow cytometry)

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18
Q

Clinical features (8) of AML

A

BM failure:

  1. Anaemia
  2. Neutropenia
  3. Thrombocytopaenia

Local infiltration:

  1. Splenomegaly
  2. Hepatomegaly
  3. Skin, CNS, or other sites
  4. Lymphadenopathy
  5. Gum infiltration (if monocytic)
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20
Q

If you suspect AML or ALL - what do you do? 4 steps

A
  1. Blood count and blood film
  2. If auer rods + granules => proves myeloid
  3. If not => immunophenotyping
  4. If aleukaemia leukaemia (no leukaemic cells in blood) => BM aspirate
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21
Q

General principals of treatments (4) for AML

A
  1. Supportive care - Red cells, platelets, FFP/cryoprecipitate if DIC, abx, electrolyte balance
  2. Chemotherapy (4-5 courses, 6 months)
  3. Targeted molecular therapy
  4. Transplantation - if poor prognosis
22
Q

What % of children with ALL are cured?

A

85%

23
Q

Clinical features (8) of ALL

A

BM failure:

  1. Anaemia (pallor)
  2. Neutropenia (infections)
  3. Thrombocytopaenia (bruising)

Local infiltration:

  1. Splenomegaly
  2. Hepatomegaly
  3. Lymphadenopathy +/- thymic enlargement
  4. Testes, CNS, kidneys, or other sites
  5. Bone (causing pain, limping)
24
Q

B-ALL or T-ALL - where does each originate?

A

B-ALL = BM

T-ALL = thymus, hence may be enlarged

25
Q

How does leukamogenesis in ALL occur?

A
  1. proto-oncogene dysregulation (via chromosomal translocation like fusion genes, wrong promoter, etc)
  2. unknown - hyperdiploidy
26
Q

Good prognostic factor for ALL

A

Hyperdiploidy

27
Q

poor prognostic factors (2) for ALL

A
  1. Hypodiploidy
  2. Ph + (previously poor, now better prognosis)
28
Q

What % of ALL is B-ALL and T-ALL?

A

B-ALL 85%

T-ALL 15%

29
Q

General principals of treatments (4) for ALL

A
  1. Supportive care => blood products, abx, general medical care
  2. Chemotherapy (systemic + CNS-targeted)
  3. Molecularly targeted treatment
  4. Transplantation

Pathology by week (70 decks)

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