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Kat's Pathology > Acute Leukaemia > Flashcards

Acute Leukaemia Flashcards

1
Q

What are the main features of acute leukaemia (5)

A 
A neoplastic condition characterised by: 
Rapid onset 
Early death if untreated 
Immature cells (blast cells) 
Bone marrow failure
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2
Q

What are the clinical signs of bone marrow failure (3)

A

Anaemia: fatigue, pallor, breathlessness
Neutropenia: infections
Thrombocytopenia: bleeding

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3
Q

Where cell do all blood cells originate

A

Pluripotent haemopoietic stem cell in the bone marrow

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4
Q

What are the main cell types (8)

A 
Erythroid lineage 
Megakaryocyte lineage
Neutrophil lineage 
Monocyte lineage
Eosinophil lineage 
Basophil lineage 
B cells 
T cells
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5
Q

What cells are affected in chronic lymphoblastic leukaemia

A

B cells

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6
Q

What cells are affected in acute lymphoblastic leukaemia

A

T cell precursors (T-ALL)

B cell precursors (B-ALL)

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7
Q

What cells are affected in chronic myeloid leukaemia

A

Pluripotent haemopoietic stem cells

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8
Q

What cells are affected in acute myeloid leukaemia

A

Multipotent myeloid stem cell/progenitor cell

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9
Q

What is the dominant cell type in acute leukaemias

A

Blast cells

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10
Q

Demographics of AML (3)

A

Increases with age
Prognosis worse with increasing age
40% of adults cured

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11
Q

What are the chromosomal abnormalities that lead to leukaemias (5)

A 
Duplication (usually trisomy) 
Loss 
Translocation 
Inversion 
Deletion
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12
Q

What are the chromosomal translocations in AML (2)

A

T(15;17)

T(5;8)

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13
Q

What is the chromosomal inversion in AML

A

Inv(16)

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14
Q

What leukaemias tend to have new fusion genes (2)

A

AML

ALL

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15
Q

What leukaemia tends to have abnormal regulation of genes

A

ALL

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16
Q

What leukaemia can have chromosomal duplication

A

AML

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17
Q

What are hotspot chromosomes for duplication in AML (2)

A

+8
+21

Dosage effect - extra copies of proto-oncogenes

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18
Q

What leukaemia can have chromosomal loss or deletion

A

AML

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19
Q

What are chromosomal hotspots for loss/deletion in leukaemia (2)

A

5/5q

7/7q

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20
Q

How can chromosomal loss/deletion cause leukaemia (3)

A

Possible loss of tumour suppressor genes

Or…one copy of an allele may be insufficient for normal haemopoiesis

Possible loss of DNA repair systems

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21
Q

What molecular abnormalities can occur in leukaemia (4)

A

Point mutation - NPM1, CEBPA
Loss of tumour suppressor genes
Partial duplication - FLT3
Cryptic deletion

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22
Q

What effect does partial duplication of FLT3 have in leukaemia

A

Proliferation and survival effects

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23
Q

What is the pathogenesis of most AML

A

Block of maturation of granulocyte

Accumulation of blast cells

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24
Q

What is the characteristic cell of leukaemia

A

Blast cells

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25
Q

What are the risk factors for AML (5)

A 
Familial or constitutional predisposition 
Irradiation 
Anticancer drugs 
Cigarette smoking 
Unknown
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26
Q

What is the characteristic of leukaemogenesis in AML

A

Multiple genetic hits:

At least 2 interacting molecular defects synergise to give leukaemic phenotype

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27
Q

What two abnormalities occur in leukaemogenesis in AML (2)

A

Type 1 abnormalities - promote proliferation and survival

Type 2 abnormalities - block differentiation (which would normally be followed by apoptosis)

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28
Q

How is cell differentiation mediated

A

Transcription factors:
Bind to DNA
Alter structure to favour transcription
Regulate gene expression

If transcription factor function is disrupted, cells cannot differentiate

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29
Q

What proteins are involved in cell differentiation

A

Core binding factor:
Dimeric transcription factor
Master controller of haematopoiesis

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30
Q

What core binding factor abnormalities cause AML (2)

A

T(8;21) fuses RUNX1 (encoding CBFalpha) with RUNX1T1 - 15% of adult AML

Inv(16) fuses CBFB with MYH11 - 12% of adult AML

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31
Q

What is the histology in t(8;21) AML (2)

A

Some blast cells

Some mature cells

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32
Q

What is the histology in Inv(16), t(16;16)

A

Some maturation to bizzarre eosinophil precursors with giant purple granules

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33
Q

What is important about t(15;17) acute promyelocytic leukaemia (8)

A

A very special type of acute leukaemia
The molecular mechanism is understood
Molecular treatment can be applied
The great majority of patients can now be cured
An excess of abnormal promyelocytes
Disseminated intravascular coagulation (DIC)
Two morphological variants but the same disease

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34
Q

When is maturation blocked in t(15;17) AML

A

Later than in other AML

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35
Q

What are the leukaemogenesis abnormalities in acute promuelocytic leukaemia (2)

A

Type 1 abnormalities - FLT3-ITD

Type 2 abnormalities - t(15;17) PML-RARA

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36
Q

What are the leukaemogenesis abnormalities in CBF leukaemias (2)

A

Type 1 abnormalities - sometimes mutated KIT

Type 2 abnormalities - mutation affecting function of CBF

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37
Q

How can you distinguish between AML and ALL (3)

A

Cytological features
Cytochemistry
Immunophenotyping

38
Q

What stains are used for AML cytology (3)

A

Myeloperoxidase (positive reaction confirms myeloid cells)
Non-specific esterase
Sudan black B

39
Q

What stains are used in ALL

40
Q

What does immunophenotyping detect

A

Cell surface and cytoplasmic antigens

41
Q

What are some forms of immunopheotyping (3)

A

Flow cytometry
Immunocytochemistry
Immunohistochemistry

42
Q

When is flow cytometry used in leukaemia diagnosis

A

When samples are similar under microscopy

43
Q

What are some ALL immunophenotype markers (3)

A

Precursor-B cell: CD19, CD20, TdT, CD10
B-cell: CD19, CD20, surface Ig
T-cell: CD2, CD3, CD4, CD8, TdT

44
Q

What are some AML immunophenotype markers

A 
MPO
CD13
CD33
CD14
CD15
Glycophorin (E)
Platelet antigens
45
Q

What are some ALL and AML immunophenotype markers (3)

A

CD34
CD45
HLA-DR

46
Q

Clinical features of AML (2)

A

Bone marrow failure

Local infiltration

47
Q

What are features of bone marrow failure (3)

A

Anaemia
Neutropenia
thrombocytopenia

48
Q

What are some clinical features of local infiltration of AML (5)

A 
Splenomegaly 
Hepatomegaly 
Gum infiltration (if monocytic) 
Lymphadenopathy (only occasionally)
Skin, CNS or other sites
49
Q

Skin infiltration, gum infiltration and organomegaly

50
Q

CNS disease

A

Particularly with monocytic differentiation (and ALL)

51
Q

Clinical manifestation of bone marrow failure

A

Infection (chest, skin, soft tissue, may be severe and life threatening - septic shock, renal failure, DIC)

52
Q

Clinical manifestation of thrombocytopenia

A

DIC

Bleeding

53
Q

What leukaemia can cause DIC

A

Acute promyelocytic leukaemia

54
Q

Eye manifestations in AML (2)

A

Hyperviscosity if WBC is very high
Retinal haemorrhages
Retinal exudates

55
Q

How is AML diagnosed

A

Blood film usually diagnostic

56
Q

What are the blood film features in AML (2)

A 
Circulating blasts
Aurer rods (proves myeloid)
57
Q

How can you tell the difference between AML and ALL if no blood film signs

A

Immunophenotyping

58
Q

How do you diagnose leukaemia if there are no leukaemic cells in the blood

A

Bone marrow aspirate

59
Q

Diagnostic methods for AML (2)

A

Blood films

Bone marrow aspirate

60
Q

What is the point of cytogenetic and molecualr studies/FISH in AML

A

Prognostic value and helps select treatment

61
Q

Good prognostic cytogenetics in AML (3)

A

T(15;17)
T(8;21)
Inv(16)

62
Q

What are the two treatment strategies for AML (2)

A

Supportive care

Chemotherapy

63
Q

What is involved in supportive care for AML (6)

A

Red cells
Platelets
Fresh frozen plasma/cryoprecipitate if DIC
Antibiotics
long line
Allopurinol, fluid and electrolyte balance

64
Q

What does chemotherapy do to cells

A

Damages DNA

65
Q

How does chemotherapy work

A

Normal stem cells - often quiescent, checkpoints allow repair of DNA damage
Leukaemia cells - continously dividing, lack of cell cycle checkpoint control

66
Q

What is the point of combination chemotherapy (3)

A

Different mechanisms of action
Synergy
Non-overlapping toxicity IMPORTANT

67
Q

What is the chemotherapy treatment for AML (4)

A

Mainly cell cycle specific drugs
4-5 courses (remission induction x 2, consolidation x 2-3)
About 6 months of therapy
Consider transplantation if poor prognosis

68
Q

Why have results of treatment of AML improved (3)

A

Better supportive care
Identification of bad prognosis groups for more intensive treatment (more intensive chemotherapy or transplantation)
Specific treatment for acute promyelocytic leukaemia

69
Q

Features of ALL (4)

A

Peak incidence in childhood
Most common childhood malignancy
85% of children cured
Prognosis worse with increasing age

70
Q

What is prognosis dependent on in AML (6)

A 
Patient characteristics 
Morphology 
Immunophenotyping 
Cytogenetics 
Genetics 
Response to treatment
71
Q

Clinical features of ALL (2)

A

Bone marrow failure: anaemia, neutropenia, thrombocytopenia
Local infiltration: lymphadenopathy (+/- thymic enlargement), splenomegaly, hepatomegaly, testes, CNS, kidneys or other sites, bone (causing paiN)

72
Q

Blood film in ALL (4)

A

Anaemia
Neutropenia
Thrombocytopenia
Usually lymphoblasts

73
Q

Bone marrow in ALL

A

Lymphoblast infiltration - may be B or T cell lineage

74
Q

Difference between B lineage or T lineage ALL

A

B lineage - starts in the bone marrow
T lineage - starts in the thymus and thymus may be enlarged

Genetics different

75
Q

Genetic features of ALL (4)

A

As for AML, prognosis is very dependent on cytogenetic/genetic subgroups, particularly for B lineage ALL Hyperdipoidy, t(12;21), t(1;19) – good prognosis
T(4;11), hypodiploidy – poor prognosis
T(9;22) – improved prognosis with tyrosine kinase inhibitors

76
Q

Good prognosis genetics ALL (3)

A

Hyperdiploidy
T(12;21)
T(1;19)

77
Q

Poor prognosis ALL (2)

A

T(4;11)

Hyperdiploidy

78
Q

How does proto-oncogene dysregulation occur in ALL (leukaemogenic mechanisms)

A

Chromosonal translocation (fusion genes, wrogn gene promoter, dysregulation by proximity to T cell receptor (TCR) or immunoglobulin heavy chain loci)

79
Q

What is the philadelphia chromosome

A

T(9;22) - in ALL

bcr-abl gene in chromosome 22

80
Q

Diagnosis of ALL (6)

A 
Clinical suspicion
Blood count and film
Bone marrow aspirate
Immunophenotyping
Cytogenetic/molecular genetic analysis
Blood group, LFTs, creatinine, electrolytes, calcium, phosphate, uric acid, coagulation screen
81
Q

Why is immunophenotype of leukaemia matter (2)

A

AML and ALL are treated differently

T lineage ALL and B lineage ALL are treated differently

82
Q

Why is cytogenetic/molecular genetic category important in ALL treatment (2)

A

Ph-positive needs imatinib

Treatment must be tailored to the prognosis

83
Q

General principles of ALL treatment (2)

A

Specific therapy

Supportive care

84
Q

Specific therapy in ALL (2)

A

Systemic chemotherapy

CNS directed therapy

85
Q

Supportive treatment in ALL (9)

A

Central venous catheter
Red blood cell and platelet transfusions
Broad spectrum antibiotics for fever
Prophylaxis for Pneumocystis jirovecii infection
Hyperuricaemia: hydration, urine alkalinization and allopurinol or rasburicase
Hyperphosphataemia; aluminum hydroxide, calcium
Hyperkalemia: fluids, diuretics
Extreme leukocytosis (WBC > 200 × 109/l): leukapheresis
Sometimes haemodialysis

86
Q

Chemotherapy for ALL features (6)

A 
Induction cycle
Intensification/consolidation cycles
Early intrathecal chemotherapy for all (to treat occult CNS disease)
Prolonged continuation/maintenance phase
Two to three years of therapy
Special measures for poor prognosis
87
Q

How long is ALL chemotherapy treatment in boys and girls (2)

A

2 years in girls

3 years in boys

88
Q

CNS therapy for ALL key features (4)

A

Intrathecal chemotherapy even if initial LP is negative (6‒8 treatments)
More frequent, intensive and prolonged intrathecal chemotherapy for patients with lymphoblasts in CSF
Systemic chemotherapy that penetrates CNS (e.g. high dose cytarabine)
Cranial irradiation now less frequently used

89
Q

Why is cranial irradiation less frequently used for ALL treatment

A

It causes cognitive impairment

Now that more children are cured, thinking about long term morbidity of treatment is increasingly important

90
Q

ALL treatment results in children

A

5 year disease free survival 80%

91
Q

ALL treatment results in adults

A

5 year disease free survival 30-40%

Kat's Pathology (105 decks)

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