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Haematology > Concepts in Malignant Haematology and Acute Leukaemia > Flashcards

Concepts in Malignant Haematology and Acute Leukaemia Flashcards

1
Q

** on every card with exam knowledge **

A

**

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2
Q

Name the 5 processes which are important in the normal kinetics of haempoiesis.

A
  • Self-renewal.
  • Proliferation.
  • Differentiation or lineage commitment.
  • Maturation.
  • Apoptosis.
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3
Q

** What techniques/methods can be used to identify normal (more mature) cells? **

A

** Morphology ** - blood count and film

Cell surface antigens – (glycophorin A would indicate red cells)
* Enzyme expression – (myeloperoxidase, an enzyme, would indicate it is a neutrophil)

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4
Q

The presence of the cell surface antigen glycophorin A would indicate?

A

Red cells

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5
Q

The presence of what enzyme would suggest that the cell was a neutrophil?

A

Myeloperoxidase

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6
Q

What techniques are used to identify morphology of cells?

A

Blood count and blood film

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7
Q

** How can we identify normal progenitor/stem cells? **

A

Immunophenotying

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8
Q

What does immunophenotyping look at?

A

Cell surface antigens e.g CD34

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9
Q

What is the problem with identifying normal progenitor/stem cells?

A

They are more difficult to recognise as they – microscopically – look the same.

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10
Q

How else (apart from immunophenotyping) can we identify normal progenitor/stem cells?

A
  • Cell culture assays.

* Animal models (not practical in routine diagnostic practice).

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11
Q

** What cell surface antigen do haemopoietic stem cells express? **

A

CD34

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12
Q

What is malignant haemopoiesis characterised by?

A

Malignant haemopoiesis is usually characterised by:

  • Increased numbers of abnormal + dysfunctional cells
  • Loss of normal activity
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13
Q

** Increased numbers of abnormal + dysfunctional cells ** is seen in?

A

Malignant haemopoiesis

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14
Q

Acute leukaemias is a malignancy which affects haemopoiesis

A

T

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15
Q

Lymphomas are a malignancy which affects immune function

A

T

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16
Q

Malignant haemopoiesis arises due to ONE OR MORE of which 4 things?

A
  1. Increased proliferation.
  2. Lack of differentiation.
  3. Lack of maturation.
  4. Lack of apoptosis.
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17
Q

** Proliferation of abnormal progenitors (precursors) with block in differentiation /maturation ** what condition is this?

A

Acute leukaemia e.g acute myeloid leukaemia

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18
Q

Describe acute leukaemia.

A

** Proliferation of abnormal progenitors (precursors) with block in differentiation /maturation **

There is lots of abnormal proliferation with no maturation

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19
Q

Give an example of an acute leukaemia.

A

Acute myeloid leukaemia

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20
Q

What is the bone marrow filled with in acute leukaemia.

A

Bone marrow is filled up with primitive cells which proliferate excessively.

The cells are primitive as there is a block of maturation so they cannot divide

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21
Q

Describe the histological appearance of chronic myeloid leukaemia.

A

Although there is an increase in proliferation, maturation is occurring normally i.e. there are lots of different cell types

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22
Q

Describe the histological appearance of acute myeloid leukaemia.

A

There is an increase in proliferation, but failure to mature.

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23
Q

Describe chronic myeloproliferative disorders e.g chronic myeloid leukaemia.

A

Proliferation of abnormal progenitors but NO differentiation/maturation block

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24
Q

** What causes haematological malignancies? **

A
  • Genetic, epigenetic and environmental factors
  • Somatic mutations in regulatory genes – driver mutations vs passenger mutations
  • Recurrent cytogenetic abnormalities
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25
Q

What are driver mutations?

A

Mutations in genes which regulate/drive growth

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26
Q

What is a clone?

A

Population of cells derived from a single parent cell

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27
Q

What are passenger mutations?

A

Mutations which reflect the noise of mutations which the cell is exposed to

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28
Q

What does the single parent cells (that makes a clone) have?

A

A genetic marker (driver mutation or chromosomal change) that is shared by the daughter cells.

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29
Q

Can clones diversify?

A

Yes, but they contain a similar genetic ‘backbone.’

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30
Q

** Normal haemopoiesis is polyclonal **

A

T

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31
Q

** Malignant haemopoiesis is usually monoclonal **

A

T

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32
Q

What do driver mutations do? When are these selected?

A

Confer growth advantage on the cells, and are selected during the evolution of the cancer.

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33
Q

What do passenger mutations do?

A

Do not confer growth advantage, but happen to be present in an ancestor of the cancer cell when it acquired one of its drivers.

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34
Q

What, observed in 10% of people older than 65y/o without a blood disorder, can predict the risk of haem malignancy subsequently?

A

Somatic mutations.

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35
Q

Outline how the different types of haematological malignancies are categorised.

A
  1. Based on lineage.
  2. Based on developmental stage (precursor) within lineage.
  3. Based on anatomical site involved.
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36
Q

Based on lineage, what can haematological malignancies be?

A
  • Myeloid – granulocytes, platelets, erythrocytes, monocytes

* Lymphoid – B cell, T cell, NK cell

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37
Q

Based on lineage, what can haematological malignancies be?

A
  • Myeloid – granulocytes, platelets, erythrocytes, monocytes

* Lymphoid – B cell, T cell, NK cell

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38
Q

Based on anatomical site involved, what can haematological malignancies be?

A
  1. Blood involvement: a leukaemia.

2. Lymph node involvement: a lymphoma.

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39
Q

What can chronic lymphocytic leukaemia involve?

A

Blood + Lymph nodes

40
Q

What is a myeloma?

A

A plasma cell malignancy in marrow.

41
Q

A malignancy under the term ‘myeloid’ can involve what?

A
  • Granulocytes
  • Platelets
  • Erythrocytes
  • Monocytes
42
Q

A malignancy under the term ‘lymphoid’ can involve what?

A
  • B cells
  • T cell
  • NK cell
43
Q

Acute leukaemia and high-grade lymphoma (1)
Vs
Chronic leukaemia and low-grade lymphoma (2)

Which is more aggressive?

A

1

44
Q

What are the histological features of an aggressive cancer?

A
  • Large cells with high nuclear-cytoplasmic ratio.
  • Prominent nucleoli.
  • Rapid proliferation.
45
Q

What is the main feature of clinical aggression?

A

Rapid progression of symptoms

  • Open chromatin – smooth and active
46
Q

Acute leukaemias (in contrast to chronic leukaemias) present with failure of normal bone marrow function

A

T

47
Q

Acute leukaemia are usually problems with more primitive precursors

A

T

48
Q

Describe acute leukaemia.

A

A rapidly progressive CLONAL malignancy of the marrow/blood with maturation defects

49
Q

What is acute leukaemia defined as (in terms of scientific parameters)?

A

An excess of ‘blasts’ (≥20%) in either the peripheral blood or bone marrow

50
Q

What is there a decreased/loss of in acute leukaemia?

A

Decrease/loss of normal haemopoietic reserve – because of the block in maturation, normal red cells, neutrophils and platelets do not appear.

51
Q

What are the 2 main types of acute leukaemia?

A
  • Acute myeloid leukaemia

* Acute lympoblastic leukaemia

52
Q

Compare AML to ALL.

A

AML is more aggressive and involves the bone marrow

53
Q

What is ALL a disease of?

A

Primitive lymphoid cells (lymphoblasts)

54
Q

What is the name for primitive lymphoid cells?

A

Lymphoblasts

55
Q

What is the - MOST COMMON CHILDHOOD CANCER (30-40 cases/million)?

A

ALL

56
Q

ALL is the most common ….

A

Childhood cancer

57
Q

What is the clinical presentation of ALL due to?

A

Marrow failure …

  • Anaemia (low red cells)
  • Infections (low neutrophils)
  • Bleeding (low platelets)
58
Q

** What are the important leukaemia effects to be aware of in ALL? **

A
  • High count with obstruction of circulation
  • Involvement of areas outside the marrow and blood (extramedullary) e.g. CNS, testis
  • BONE PAIN !!!!!
59
Q

What symptom is a big indicator that someone has ALL?

A

BONE PAIN !!!!

60
Q

Who gets AML?

A

> 60 yo

61
Q

How can AML arise?

A

Either ‘de novo’ or secondary to another cancer.

62
Q

What can the presentation of AML be similar to? Why?

A

ALL - also associated with marrow failure

63
Q

Some subgroups of AML may have a characteristic presentation. Give examples (2).

A
  • Coagulation defect – called DIC.

* Gum infiltration – the type that affects monoblasts.

64
Q

What are the 3 main Ix’s done for acute leukaemia?

A
  1. Blood count and film
  2. Coagulation screen
  3. Bone marrow aspirate
65
Q

What will a blood count of someone with acute leukaemia show?

A
  • Anaemia
  • Thrombocytopenia
  • Neutropenia

BUT might have a high white cell count because of lots of immature cells.

66
Q

What will a blood film of someone with acute leukaemia show?

A
  • Reduction in normal cells.
  • Presence of abnormal cells.
  • The abnormal cells (‘blasts’) have a high nuclear:cytoplasmic ratio.
67
Q

Apart from the 3 main Ix’s for acute leukaemia, what other investigations are also very important?

A
  • Morphology – what do the cells look like?

* Immunophenotyping – are there lineage specific proteins on the cell surface

68
Q

In what condition are ‘AUER RODS’ seen?

A

In AML - acute myeloid leukaemia

69
Q

What is the importance of doing a coagulation screen in someone with suspected acute leukaemia?

A

Some acute leukaemias are associated with DIC which can cause life-threatening bleeding

70
Q

NOTE: when taking a bone marrow aspirate from an adult remember to locate which bones in the adult have marrow e.g axial skeleton and long bones

A

T

71
Q

Where can bone marrow in an adult be found?

A

Axial skeleton + long bones

72
Q

** What is required for a DEFINITE diagnosis of acute leukaemia (i.e ALL vs AML)? **

A

** IMMUNOPHENOTYPING **

73
Q

Why is the diagnosis between AML and ALL so important?

A

Because the treatments are very different

74
Q

What is the treatment of acute leukaemia?

A

Multi-agent chemotherapy

Hickman line – used to give chemotherapy

75
Q

Describe the treatment of ALL.

A

Different phases of treatment of varying intensity (induction, consolidation, intensification, maintenance).

Also, targeted treatments in certain subsets

76
Q

How long can treatment of ALL last?

A

2-3 years

77
Q

Describe the treatment of AML.

A

Normally intensive.

Between 2-4 cycles of chemotherapy (5-10days of chemo, followed by 2-4weeks of recovery).

Prolonged hospitalisation.

78
Q

What are the 3 main problems associated with the suppression of bone marrow?

A
  • Anaemia
  • Neutropenia – infection from a gram -ve organism usually
  • Thrombocytopenia – bleeding, purpura, petechiae (plt <20 x 109)
79
Q

What kind of infection do people with bone marrow suppression usually get?

A

Gram -ve

80
Q

Is the gram -ve infection in people with bone marrow suppression usually from them or the environment?

A

Them - usually bowel bacteria

81
Q

What can a gram -ve infection cause in people with bone marrow suppression?

A

Fulminant life-threatening sepsis in neutropenic patients

82
Q

What should you do if you suspect that someone with bone marrow suppression has a gram -ve infection?

A

TREAT WITH ABX ASAP - do not wait for culture results

83
Q

To get bleeding, petechiae, and purpura what must your platelet count be?

A

plt <20 x 109)

84
Q

What causes bleeding, petechiae, and purpura?

A

Thrombocytopenia

85
Q

Outline the 4 main complications of treatment of acute leukaemia (i.e chemo).

A
  • Nausea and vomiting
  • Hair loss
  • Liver, renal dysfunction
  • Tumour lysis syndrome

This usually occurs during the first course of treatment

86
Q

** When should you suspect a bacterial infection in someone with bone marrow suppression? **

A
  • Suspect this as soon as a neutropenic fever onsets
87
Q

** What should you do if you suspect someone with bone marrow suppression has a bacterial infection? **

A

Give empirical treatment with broad spectrum antibiotics (particularly covering gram -ve organisms) as soon as neutropenic fever

88
Q

** When should you suspect a fungal infection in someone with bone marrow suppression? **

A

If there is prolonged neutropenia and persisting fever even after giving antibiotics you should start to suspect this

89
Q

Although bacterial infections are more common, patients are also susceptible to fungal infections

A

T

90
Q

What patients mostly get protozoa infection?

A

ALL therapy patients

91
Q

Give 2 examples of late effects of bone marrow suppression.

A
  • Loss of fertility.

* Cardiomyopathy with anthracyclines.

92
Q

What is remission defined as?

A

<5% marrow blasts with recovery of normal haemopoiesis

93
Q

Many patients go into remission

A

T

94
Q

Unfortunately remissions may not durable depending on the type of acute leukaemia and
many patients will relapse

A

T

95
Q

Patients NEVER die of treatment related toxicity

A

F - some of them do :(

96
Q

What do molecular ‘targeting’ with kinase inhibitors treat?

A

ALL with the PHILADEPHIA chromosome.

97
Q

What is the final Tx of someone with ALL?

A

Allogenic stem cell transplantation in select patients

Haematology (26 decks)

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