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Haematology > Concepts in malignant haematology > Flashcards

Concepts in malignant haematology Flashcards

1
Q

What is involved in normal haemopoiesis?

A
  • Self-renewal
  • Proliferation
  • Differentiation or lineage commitment
  • Maturation
  • Apoptosis
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2
Q

How are normal, mature non-lympohid (myeloid) cells identified?

A
  • Morphology
  • Cell surface antigens (glycophorin A = red cells)
  • Enzyme expression (myeloperoidase = neutrophils)
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3
Q

How are normal progenitors/stem cells identified?

A
  • Cell surface antigens (immunophenotyping) e.g. CD34
  • Cell culture assays
  • Animal models
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4
Q

What happens in malignant haemopoiesis?

A
  • Increased numbers of abnormal and dysfunctional cells
  • Loss of normal activity
  • Due to 1 or more of the following:
    • Increased proliferation
    • Lack of differentiation
    • Lack of maturation
    • Lack of apoptosis
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5
Q

What is the mechanism behind acute leukaemia in terms of haemopoiesis?

A

Proliferation of abnormal progenitors with block in differentiation/maturation e.g. acute myeloid leukaemia

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6
Q

Which bone marrow biopsy is normal and which is abnormal? What is the abnormality?

A
  • Top one is normal, bottom is abnormal
  • Acute leukaemia is the abnormality - stains more blue due to acid uptake as a result of DNA/RNA being present
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7
Q

What is the mechanism behind chronic myeloproliferative disorders?

A

Proliferation of abnormal progenitors but NO differentiation/maturation block e.g. chronic myeloid leukaemia (highlighted in yellow)

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8
Q

What causes haematological malignancies?

A
  • Genetic, epigenetic, environmental interaction
  • Somatic mutations in regulatory genes - driver mutations vs passenger mutations
  • Usually multiple hits rather than a single catastrophic event
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9
Q

What is a clone?

A
  • Population of cells derived from a single parent cell
  • This parent cell has a genetic marker that is shared by the daughter cells
  • Clones can diversify but contain a similar genetic backbone
  • Normal haemopoiesis is polyclonal; malignant haemopoiesis is usually monoclonal
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10
Q

What is the difference between driver mutations and passenger mutations in relation to cancer?

A
  • Driver mutations confer growth advantage on the cells and are selected during the evolution of the cancer
  • Passenger mutations do NOT confer growth advantage but happened to be present in an ancestor of the cancer cell when it acquired one of its drivers
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11
Q

What is a haematological cancer called if it involves blood?

A

Leukaemia

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12
Q

What is a haematological cancer called if it involves lymph nodes?

A
  • Lymphoma
  • CLL can involve blood and lymph nodes
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13
Q

What are some features of histological aggression?

A

Large cells with high nuclear-cytoplasmic ratio, prominent nuclei, rapid proliferation

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14
Q

What are some features of clinical aggression?

A

Rapid progression of symptoms

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15
Q

How do acute leukaemias differ from chronic leukaemias in how they present?

A

Acute leukaemias present with failure of normal bone marrow function

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16
Q

How are haematological malignancies classified?

A
  1. Lineage/stage of development
  2. Site involved
  3. Speed of presentation
17
Q

What is the pathological mechanism behind acute leukaemia?

A
  • Rapidly progressive clonal malignancy of the marrow/blood with maturation defect
  • Defined as an excess of blasts (>20%) in either the peripheral blood or bone marrow
  • Decrease/loss of normal haemopoietic reserve
18
Q

Name the types of acute leukaemia

A
  • Acute myeloid leukaemia (AML)
  • Acute lymphoblastic leukaemia (ALL)
19
Q

What is ALL and who does it typically affect?

A
  • ALL is a malignant disease of primitive lymphoid cells (lymphoblasts)
  • Most common childhood cancer
20
Q

How does ALL typically present?

A
  • Due to marrow failure - anaemia, infections, bleeding
  • Leukaemic effects - high count with obstruction of circulation, involvement of areas outside the marrow and blood (extra-medullary) e.g. CNS, testis
  • Bone pain
21
Q

Who does AML typically affect and how does it present?

A
  • More common in elderly
  • May be de novo or secondary
  • Presentation can be similar to ALL
  • Subgroups of AML may have characteristic presentation: DIC and gum infiltration
22
Q

How is acute leukaemia investigated?

A
  • Blood count and film
  • Coagulation screen
  • Bone marrow aspirate - morphology, immunophenotype, cyto/molecular genetics, trephine (piece of bone)
23
Q

What blood disorder is represented on this blood film?

A
  • Acute leukaemia
  • Reduction in normal cells
  • Presence of abnormal cells with a high nuclear:cytoplasmic ratio
24
Q

Why is immunophenotyping necessary to reach a definitive diagnosis for acute leukaemia?

A

The cells of AML and ALL may look alike but they will express different lineage-associated proteins so immunophenotyping is required

25
Q

What is the curative treatment for acute leukaemia?

A

Multi-agent chemotherapy

26
Q

How does curative treatment differ in ALL vs AML?

A
  • ALL - can last up to 2-3 years, different phases of treatment with varying intensities, targeted therapies in certain subsets
  • AML - normally intensive, between 2-4 cycles of chemo, prolonged hospitalisation, targeted treatments in subsets
27
Q

Where is a Hickman line inserted?

A

IVC - usually midway between nipple and collar bone

28
Q

What are some of the problems associated with marrow suppression therapy?

A
  • Anaemia
  • Neutropenia - infections
  • Thrombocytopenia - bleeding (purpura, petechiae)
29
Q

What can gram-negative bacteria cause in neutropenic patients?

A

Fulminant life-threatening sepsis

30
Q

What are some of the side effects of chemotherapy?

A
  • N + V
  • Hair loss
  • Liver, renal dysfunction
  • Tumour lysis syndrome
  • Infection
  • Late effects - infertility, cardiomyopathy with anthracyclines
31
Q

What is important to do if someone develops infection due to chemo?

A
  • Bacterial - empirical treatment with broad spectrum antibiotics (esp covering gram -ve organisms) as soon as neutropenic fever
  • Suspect fungal origin if prolonged neutropenia and persisting fever unresponsive to anti-bacterial agents
32
Q

What are treatment options other than chemotherapy for acute leukaemias?

A
  • Targeted treatments e.g. molecular targeting with kinase inhibitors
  • Allogenic stem cell transplantation in select patients

Haematology (22 decks)

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