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Haematology (E) > Acute Leukaemia > Flashcards

Acute Leukaemia Flashcards

1
Q

What is acute leukaemia?

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 symptoms can occur due to bone marrow failure in acute leukaemia?

A

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

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3
Q

How would you differentiate acute myeloid leukaemia on blood film under microscope?

A

Fine granules

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4
Q

What is the epidemiology of AML?

A

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

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5
Q

What are the risk factors for AML?

A

Irradiation
Certain drugs
Benzene exposure
Mostly unknown

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6
Q

What chromosome features may be found in AML?

A

Many AMLs have aberrations in chromosome count or structure

Such abberations are recurrent and may be directly involved in the development of the leukaemia

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7
Q

List the types of chromosomal abnormalities

A 
Duplication
Loss
Translocation (new chromosome is called a derivative)
Inversion
Deletion
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8
Q

What do chromosomal translocations and inversions in leukaemia lead to?

A

Altered DNA sequence
creation of new fusion genes (AML and ALL)
Abnormal regulation of genes (mainly ALL)

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9
Q

What is the relationship between chromosomal duplication and leukaemia?

A

Common in AML

Disease hotspts: +8, +21 gives predisposition

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10
Q

What is the relationship between chromosomal loss or deletion and leukaemia?

A

Common in AML

Disease hotspots - deletion and loss of 5/5q & 7/7q

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11
Q

What happens in most acute myeloid leukaemia?

A

Block in maturation, blast cells accumulate

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12
Q

Why do people get AML?

A 
Familial or constitutional predisposition
Irradiation
Anticancer drugs
Cigarette smoking
Unknown
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13
Q

How does leukaemogeneis occur in AML?

A

Multiple genetic hits - at least 2 interacting molecular defects, synergise to give leukaemic phenotype

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14
Q

What are the types of abnormalities leading to leukaemogenesis in AML?

A

Type 1 abnormalities: promote proliferation and survival

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

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15
Q

What is required for differentiation?

A

Transcription factors: bind to DNA, alter structure to favour transcription, regulate gene expression

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16
Q

What is the gene abnormality in acute promyelocytic leukaemia?

A

t(15;17)

17
Q

What are features of acute promyelocytic leukaemia?

A

Molecular mechanisms understood so molecular treatment can be applied
An excess of abnormal promyelocytes
Disseminated intravascular coagulation
Auer rods

18
Q

How do we distinguish between AML and ALL?

A

Cytological features: myeloid - granules and auer rods
(Cytochemistry)
Immunophenotyping: cell surface and cytoplasmic antigens

19
Q

What are the features of AML on blood film?

A

Granules

Auer rods

20
Q

What clinical features occur due to bone marrow failure in AML?

A

Anaemia: pallor, fatigue
Neutropenia: infection, may be severe and life threatening (septic shock, renal failure, DIC)
Thrombocytopenia: bleeding

21
Q

What clinical features occur due to local infiltration failure in AML?

A 
Splenomegaly
Hepatomegaly
Gum infiltration (if monocytic)
Lymphadenopathy occasionally
Skin, CNS, other sites
22
Q

What are the steps in diagnosis of AML?

A 
Clinical history
Physical examination
Blood count and film
Bone marrow aspirate (morphology)
Cytogenetic studies
Immunophenotypic
Molecular studies and FISH in selected patient
23
Q

What are the important features of clinical history in AML?

A

Past drug/irradiation exposure

24
Q

What can occur as result of a high white cell count in AML?

A

Hyperviscosity: retinal haemorrhage, retinal exudates

25
Q

Why is blood count and film important in diagnosis of AML?

A

Usually diagnostic: circulating blasts

Auer rods - proves myeloid

26
Q

What are the treatments available for AML?

A 
Supportive care
Chemotherapy
Combination chemotherapy
Targeted molecular therapy
Possibly immunotherapy
Transplantation (haematopoietic stem cell transplantation)
27
Q

What supportive care is given in AML?

A

Correct the effects of inadequate bone marrow function:
Red cells
Platelets
FFP/Cryoprecipitate if DIC
Antibiotics
Long line
Allopurinol, fluid and electrolyte balance

28
Q

How does the chemotherapy affect the bone marrow?

A

Damages DNA
Normal stem cells: often quiescent, checkpoints allow repair of DNA damage
Leukaemia cells: continuously dividing, lack of cell cycle checkpoint control

29
Q

What is combination chemotherapy?

A

Use two or more chemotherapy drugs
Different mechanisms of action
Synergy
Non-overlapping toxicity

30
Q

What determines the prognosis for AML?

A 
Patient characteristics: age, fitness
Morphology
Immunophenotyping
Cytogenetics
Genetics
Response to treatment
31
Q

What is the epidemiology of ALL?

A

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

32
Q

What are the clinical features of ALL?

A

Lymphadenopathy: more common in T-lineage, infiltration of thymus, CNS and testes much more common than AML
Bone marrow failure: anaemia, neutropenia, thrombocytopenia
Local infiltration: lymphadenopathy, splenomegaly, hepatomegaly, kidney, bone

33
Q

What are the peripheral blood pathological features of ALL?

A

Anaemia
Neutrophenia
Thrombocytopenia
Usually lymphoblasts

34
Q

What are the bone marrow and other tissue pathological features of AML?

A

Lymphoblast infiltration
Lymphoblasts may be B or T lineage
B-lineage - starts in bone marrow
T-lineage - starts in thymus

35
Q

What are the leukaemogenic mechanisms of ALL?

A

Proto-oncogene dysregulation: chromosomal translocation - fusion genes, wrong gene promoter, dysregulation by proximity to T cell receptor

36
Q

What is required for the diagnosis of ALL?

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
37
Q

What are the principles of specific therapy in ALL?

A

Systemic chemotherapy
CNS-directed therapy
Molecularly targeted treatment
Transplantation

38
Q

What symptoms in children should make you consider leukaemia as a diagnosis?

A 
Bone pain
Limping
Pallor
Bruising
Organomegaly
39
Q

What symptoms in adults would make you consider leukaemia?

A 
Pallor
Bruising
Bleeding
Infection
Organomegaly

Haematology (E) (14 decks)

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