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Haematology > Concepts of Malignant Haematology > Flashcards

Concepts of Malignant Haematology Flashcards

1
Q

What are the progeny of myeloid precursors?

A

Erythrocytes, platelets, granulocytes, macrophages

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2
Q

What are the progeny of lymphoid precursors?

A

Dendritic cells, T cells, NK cells, B cells

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3
Q

What methods can be used to identify mature myeloid cells?

A

Morphology, cell surface antigens (e.g glycophorin A for red cells), enzyme expression (e.g myeloperoxidase for neutrophils)

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4
Q

What is malignant haemopoiesis characterised by?

A

Increased numbers of abnormal and dysfunctional cells

Loss of normal function (e.g haemopoiesis)

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5
Q

What are the underlying mechanisms of malignant haemopoiesis?

A

Due to one or more of the following = increased proliferation, lack of differentiation, lack of maturation, lack of apoptosis

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6
Q

What occurs in acute leukaemia?

A

Proliferation of abnormal progenitors with block in differentiation/maturation

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7
Q

What does normal cells being replaced by abnormal ones in acute leukaemia cause?

A

Loss of normal haemopoiesis and subsequent failure of blood and bone marrow

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8
Q

What occurs in chronic myeloid leukaemia?

A

Proliferation of abnormal progenitors but no block in differentiation/maturation

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9
Q

What does high power microscopy of chronic myeloid leukaemia show?

A

Wide variety of cell types and neutrophils

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10
Q

What causes haematological malignancy?

A

Genetic, epigenetic and environmental interaction
Acquired somatic mutation in regulatory genes
Recurrent cytogenetic abnormalities

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11
Q

What are driver mutations?

A

Acquired somatic mutations that are actively involved in cancer pathogenesis

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12
Q

What are passenger mutations?

A

Acquired somatic mutations that don’t confer growth advantage but are present in ancestors of cancer cell when they acquired its driver mutation

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13
Q

How important are recurrent cytogenetic abnormalities in causing haematological malignancy?

A

Usually contribute to cancer pathogenesis but are not causative

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14
Q

What ability allows driver mutations to cause cancer?

A

Have ability to select clones = confer growth advantage on cells and are selected during cancer evolution

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15
Q

What are clones?

A

Population of cells derived from a single parent cell = can diversify but share similar genetic backbone

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16
Q

Why is the parent cell of clones important?

A

Contains genetic marker that is shared by daughter cells

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17
Q

How does normal haemopoiesis differ from malignant haemopoiesis?

A

Normal haemopoiesis is polyclonal whereas malignant haemopoiesis is usually monoclonal

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18
Q

What is the classification of haematological malignancy based on?

A

Lineage = myeloid or lymphoid
Developmental stage within lineage
Anatomical site

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19
Q

What does the term lymphoblastic suggest?

A

A defect in primitive cells

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20
Q

What parts of the body does leukaemia involve?

A

Blood

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21
Q

What parts of the body are involved in lymphoma?

A

Lymph node involvement with lymphoid malignancy

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22
Q

Why is chronic lymphocytic anaemia difficult to classify by site?

A

It can involve both blood and lymph nodes

23
Q

What is myeloma?

A

Plasma cell malignancy of marrow

24
Q

How can haematological malignancies by classified by their histology?

A

Aggressive = acute leukaemia, high grade lymphoma

Less aggressive = chronic leukaemia, low grade lymphoma

25
Q

What are some features of histological aggression?

A

Large cells with high nuclear-cytoplasmic ratio
Prominent nuclei
Rapid proliferation

26
Q

What do acute leukaemias usually present with?

A

Failure of bone marrow

27
Q

What cells are affected by chronic myeloid leukaemia and myeloproliferative neoplasms?

A

More primitive progenitors (e.g stem cells)

28
Q

What cells are mostly affected by acute leukaemias?

A

Acute myeloid = multipotent progenitors

Acute lymphoid = lymphoid progenitors

29
Q

What cells are affected by chronic lymphoid leukaemia?

A

B cells

30
Q

What is acute leukaemia?

A

Rapidly progressive clonal malignancy of marrow/blood with maturation defects = decrease/loss of normal haemopoietic reserve

31
Q

What is acute leukaemia defined as?

A

Excess of blasts (>=20%) in either peripheral blood or bone marrow

32
Q

What are the types of acute leukaemia?

A

Myeloid and lymphoid

33
Q

What is acute lymphoid leukaemia?

A

Disease of primitive lymphoid cells = most common childhood cancer

34
Q

What are the features of acute lymphoid leukaemia?

A

Anaemia, infection, bleeding, bone pain
High count with obstruction of circulation
Often extra-haematological involvement = CNS, testes

35
Q

What is the epidemiology of acute myeloid leukaemia?

A

More common in elderly = age >60

May be de novo or secondary

36
Q

What are the features of acute myeloid leukaemia?

A

Presents similar to acute lymphoid leukaemia but with more prominent symptoms of anaemia

37
Q

What are the subtypes of acute myeloid leukaemia?

A

Coagulation defect = DIC in acute promyelocytic leukaemia

Gum infiltration

38
Q

What investigations are done of acute leukaemia?

A

Blood count and film plus coagulation screen
Bone marrow aspirate for morphology
Cytogenetic analysis for prognosis

39
Q

What test is diagnostic for acute leukaemia?

A

Immunophenotyping = distinguishes between acute myeloid and lymphoid leukaemias

40
Q

What test can be done when bone marrow aspirate is suboptimal?

A

Trepine sample = small piece of bone sample

41
Q

What are the features of blood film for acute leukaemia?

A

Reduction in normal cells

Presence of blasts with high nuclear:cytoplasmic ratio

42
Q

What is a blood film feature of acute myeloid leukaemia?

A

Aver rods = granulations on blood film

43
Q

What is the mainstay of treatment for acute leukaemia?

A

Multi-agent chemotherapy

44
Q

What is the treatment programme for acute lymphoid leukaemia?

A

Lasts 2-3 years = different phases of varying intensity, targeted treatment in certain subsets

45
Q

What is the treatment programme for acute myeloid lymphoid?

A

2-4 cycles of chemo = 5-10 days of chemo followed by 2-4 weeks of recovery
Prolonged hospitalisation with some targeted treatment

46
Q

What is a Hickman line?

A

Allows for long term venous access for drug administration = tip sits at junction of IVC and right atrium

47
Q

What haematological issues are associated with marrow suppression?

A

Anaemia, neutropenia, thrombocytopenia

48
Q

What is a life threatening complication of neutropenia in chemotherapy patients?

A

Gram negative sepsis = start broad spectrum antibiotics in presence of neutropenic fever while waiting for culture results

49
Q

What are the complications of chemotherapy?

A

Nausea/vomiting, hair loss, liver/renal dysfunction, tumour lysis syndrome (1st course of treatment), infection, loss of fertility, cardiomyopathy

50
Q

When should anti-fungals be started in a patient undergoing chemotherapy?

A

Prolonged neutropenia and persisting fever unresponsive to anti-bacterial agents

51
Q

What prophylactic treatment is offered to patients with acute lymphoid leukaemia?

A

Prophylaxis for pneumocystis pneumonia

52
Q

How long does it take for bone marrow function to recover if chemotherapy has been successful?

A

4-6 weeks

53
Q

What is the prognosis of acute leukaemia?

A

Childhood lymphoid = >85-90%
Adult lymphoid = 30-40%
Adult myeloid age 60 = 10% or less

Haematology (24 decks)

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