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Immunology and Haematology Jenna to Sort > Myeloid Malignancy > Flashcards

Myeloid Malignancy Flashcards

1
Q

What is the difference between AML and myeloproliferative disorders?

A

AML is proliferation without differentiation, but also get myeloproliferative disorders where differentiation has occurred:

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2
Q

What are the main groups of myeloid malignancy?

A
  • Acute myeloid leukaemia (AML)
  • Chronic myeloid leukaemia (CML)
  • Myelodysplastic syndromes (MDS)
    • Pre-leukaemia conditions
  • Myeloproliferative neoplasm (MPN)
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3
Q

What does AML stand for?

A
  • Acute myeloid leukaemia (AML)
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4
Q

What does CML stand for?

A
  • Chronic myeloid leukaemia (CML)
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5
Q

What does MDS stand for?

A
  • Myelodysplastic syndromes (MDS)
    • Pre-leukaemia conditions
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6
Q

What does MPN stand for?

A
  • Myeloproliferative neoplasm (MPN)
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7
Q

What is the difference between acute and chronic myeloid leukaemia?

A

Old terms, basically describes how long patients survive with illness:

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8
Q

Compare and contrast acute and chronic myeloid leukaemia for:

  • ability to differentiate
  • bone marrow failure
  • prognosis
  • curability
A
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9
Q

Describe the pathophysiology of AML?

A
  • Acute myeloid leukaemia replaces bone marrow leading to bone marrow failure
  • Proliferation without differentiation
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10
Q

Describe the clinical features of AML?

A
  • Bone marrow failure (triad)
    • Anaemia
    • Thrombocytopenic bleeding (purpura and mucosal membrane bleeding)
    • Infection because of neutropenia (predominantly bacterial and fungal)
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11
Q

What forms the triad of bone marrow failure symptoms?

A
  • Anaemia
  • Thrombocytopenic bleeding (purpura and mucosal membrane bleeding)
  • Infection because of neutropenia (predominantly bacterial and fungal)
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12
Q

What pattern of bleeding occurs in bone marrow failure?

A

Thrombocytopenic bleeding (purpura and mucosal membrane bleeding)

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13
Q

What investigations should be done for AML?

A
  • Blood count and blood film
  • Bone marrow aspirate
    • Blasts > 20% of marrow cells in acute leukaemia
  • Cytogenetics (Karyotype) from leukaemic blasts
    • Prognostic info
  • Immunophenotyping of leukaemic blasts
    • Prognostic info – to identify as myeloid or lymphoid
  • CSF examination if symptoms
    • Prognostic info
  • Targeted molecular genetics for associated acquired gene mutations
    • Looks at individual genes for mutations, such as FLT3 and NPM1
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14
Q

What genetic mutations are potentially important for AML?

A
  • Targeted molecular genetics for associated acquired gene mutations
    • Looks at individual genes for mutations, such as FLT3 and NPM1
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15
Q

What % of cells in bone marrow do blasts form in AML?

A
  • Bone marrow aspirate
    • Blasts > 20% of marrow cells in acute leukaemia
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16
Q

Describe the treatment for AML?

A
  • Supportive care
  • Anti-leukaemic chemotherapy
    • Remission induction (1-2 cycles)
      • Classified as normal blood counts and <5% blasts
    • Consolidation (1-3 cycles)
    • Maintenance
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17
Q

At what % of blasts in bone marrow is considered to be remission in AML?

A
  • Classified as normal blood counts and <5% blasts
18
Q

Describe the pathophysiology of CML?

A
  • Proliferation with differentiation
19
Q

Describe the clinical features of CML?

A
  • Anaemia
  • Splenomegaly
    • Often massive
  • Weight loss
  • Hyperleukostasis
    • Fundal haemorrhage and venous congestion, altered consciousness, respiratory failure
  • Gout
20
Q

What are symptoms of hyperleukostasis?

A
  • Fundal haemorrhage and venous congestion, altered consciousness, respiratory failure
21
Q

What investigations should be done for CML?

A
  • Blood count
    • Massively raised WBC
      • Various different cells raised
    • Raised platelets
    • Immature cells raised
  • Blood film
    • All stages of white cell differentiation with increase basophils
  • Bone marrow aspirate
    • Hypercellular
  • Cytogenetics (Karytype)
    • Philadelphia chromosome in blood cells and bone marrow (chromosome 9 and 22 translocation), putting the BCR-ABL genes together and causing the disease
22
Q

What is seen in the FBC for CML?

A
  • Massively raised WBC
    • Various different cells raised
  • Raised platelets
  • Immature cells raised
23
Q

What is seen in the blood film for CML?

A
  • All stages of white cell differentiation with increase basophils
24
Q

What is seen in the bone marrow aspirate for CML?

A
  • Hypercellular
25
Q

What is often seen in cytogenetics for CML?

A
  • Philadelphia chromosome in blood cells and bone marrow (chromosome 9 and 22 translocation), putting the BCR-ABL genes together and causing the disease
26
Q

Describe the treatment of CML?

A
  • Tyrosine kinase inhibitors (TKIs) of BCR-ABL – first line
    • Drugs
      • Imatinib
      • Dasatinib
      • Nilotinib
      • Bostinib
      • Ponatinib
  • Allogeneic transplantation
    • Only in TKI failure
27
Q

What are some examples of myeloproliferative neoplasms?

A
  • Polycythaemia vera (PV)
  • Essential thrombocythaemia (ET)
  • Idiopathic myelofibrosis
    • Often advanced stages of PV and ET
28
Q

What does PV stand for?

A

Polycythaemia vera

29
Q

What does ET stand for?

A

Essential thrombocythaemia

30
Q

Describe the pathophysiology of MPN?

A
  • Mutation of gene
    • JAK2 gene (95% of PV)
      • Normally indicates red cells to proliferate when signalling protein erythropoietin has binded, but with mutation does not need signalling protein
    • CALR mutation (25% of ET)
31
Q

What genes are often involved in MPN?

A
  • JAK2 gene (95% of PV)
    • Normally indicates red cells to proliferate when signalling protein erythropoietin has binded, but with mutation does not need signalling protein
  • CALR mutation (25% of ET)
32
Q

Describe the clinical features of PV?

A
  • Headaches
  • Itch
  • Vascular occlusion
  • Thrombosis
  • TIA, stroke
  • Splenomegaly
33
Q

What investigations should be done for PV?

A
  • Blood count
    • Raised haemoglobin concentration and haematocrit
    • Raised white cell and platelet count
      • Not as high as in leukaemia
    • Raised uric acid
    • True increase in red cell mass when blood volume is measured
34
Q

What is seen in the FBC for PV?

A
  • Raised haemoglobin concentration and haematocrit
  • Raised white cell and platelet count
    • Not as high as in leukaemia
  • Raised uric acid
  • True increase in red cell mass when blood volume is measured
35
Q

Describe the treatment for PV?

A
  • Venesection
    • To keep haematocrit below 0.45 (45%)
  • Aspirin
  • Cytoreduction
    • Hydroxcarbamide or alpha interferon
    • To bring platelet count and WCC down
  • Ruxolitinib (JAK2 inhibitor)
    • In HC failures with systemic symptoms
36
Q

What are possible complications of PV?

A

Complications:

  • Stroke and other arterial or venous thrombosis
  • Bone marrow failure from development of secondary myelofibrosis
  • Transformation to AML
37
Q

Describe the aetiology of ET?

A
  • JAK2 mutation 50%
  • CALR mutation 25%
38
Q

Describe the presentation of ET?

A
  • Symptoms of arterial and venous thrombosis
  • Digital ischaemia
  • Gout
  • Headache
  • Splenomegaly
    • Mild
39
Q

What investigations should be done for ET?

A
  • Blood count
    • Raised platelet
  • Blood film
    • Thrombocytosis with giant platelets
40
Q

What is seen on the blood count and blood film for ET?

A
  • Blood count
    • Raised platelet
  • Blood film
    • Thrombocytosis with giant platelets
41
Q

Describe the treatment for ET?

A
  • Aspirin
  • Hydroxycarbamide or anagrelide
42
Q

What is a possible complication of ET?

A
  • Can progress to myelofibrosis or AML

Immunology and Haematology Jenna to Sort (23 decks)

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