Haematological Malignancies Flashcards

1
Q

What occurs in acute haematological malignancies?

A

Increased rate of apoptosis,
Decreased apoptosis
Differentiation block

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2
Q

What occurs in chronic?

A

Build up of mature differentiated cells
Proliferation increased
NO differential block like in acute

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3
Q

Why is acute leukaemia a heterogenous disease?

A

Because the acute phase can happen at any point of differentiation

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4
Q

What % of blasts in the bone marrow is required to diagnose acute leukaemia?

A

20% (can be less for molecular mechanism in place)

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5
Q

What cells are found in hodgekins lymphoma?

A

Reed-Sternberg cells

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6
Q

What are risks for haematological malignancies

A

Radiation
Benzene
Viruses
Genetic disorders- fanconi anaemia , Down syndrome etc.

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7
Q

What malignancy is associated with the Epstein- Barr virus?

A

Lymphoma

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8
Q

What malignancy is associated with heliocobacter pylori infection?

A

Gastric lymphoma B-cell

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9
Q

Explain how FACS works?

A

Anti surface antigen antibodies are labelled with fluorochromes and used to Bind to CD molecules- analysed on the single cell level by flow cytometry

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10
Q

What mutation is found in 30% of AML?

A

FLIT3

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11
Q

What is the most common change found in b and T cell malignancies?

A

Clonal Ig or TCR rearrangements

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12
Q

What is the incidence of CML?

A

0.9% per 100,000

500/year in uk

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13
Q

What is the most frequent age of CML?

A

40-60 years

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14
Q

What are the 3 phases of CML?

A

Chronic
Accelerated
Blast crisis

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15
Q

What are the symptoms of the chronic stage of CML and how long does it last?

A

Often asymptomatic- can last up to 5 years

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16
Q

What are the symptoms of the accelerated stage of CML and how long does it last?

A

Anaemia and thrombocytopenia and increased blasts in BM

Last several months

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17
Q

What is required to move from chronic to accelerated or blast crisis? (CML)

A

Additional chromosomal abnormalities

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18
Q

What is the blast count during blast crisis (CML) ?

A

> 20%

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19
Q

True or false CML can become AML or ALL?

A

True

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20
Q

What is the BCR able translocation?

A

t(9;22)(q34;q11)

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21
Q

What does BCR-ABL generate?

A

A highly active oncogene tyrosine kinase 210 kda

22
Q

How do you test BCR-ABL negative CML patients?

A

As if they have a myloproliferative disorder

23
Q

What other disorder is the Philadelphia gene found in?

A

ALL

24
Q

What does a blood film of a CML patient look like?

A

Neutrophilic leucocytes is with immature precursors you normally wouldn’t see and lots of basophils

25
Q

What will a PB blood film in CML often resemble?

A

A Bone marrow asparate

26
Q

What does bone marrow look like inCML?

A

Hypercellular see all stages of myeloid maturation and an increase in basophils and eosinophils

27
Q

What are the symptoms of CML?

A

Usually associated with hyper metabolism - splenomegaly or anaemia (normochromic normocytic)

28
Q

How much is leucocytosis?

A

> 50 X 10^9/L

29
Q

If imatinib is not successful what is second generation inhibitor?

A

Disastinib

30
Q

What is the frequency of AML?

A

4.1% per 100,000

31
Q

What is the median age of AML?

A

70

32
Q

What is the most common form of adult leukaemia?

A

AML

33
Q

Is AML one disease?

A

No, many diseases as leukaemia occur at different stages

34
Q

How many types of AML based on FAB?

A

8 types based on morphology moos all abnormality

35
Q

How many classifications of AML based on WHO 2008

A

4

36
Q

What is class 1 of WHO 2008 and what is the prognosis ?

A

AML with recurrent genetic abnormalities - good prognosis

37
Q

Name the four genetic abnormalities associated with group 1 of AML?

A

Inv(16)
T(8;21)
T(16;6)
T(15;17)

38
Q

What is group 2 (who)

A

AML with myelodysplasia related changes including patients with previous myledysplastic syndromes- POOR PROGNOSIS

39
Q

What is group 3 (who)

A

Therapy related AML t-AML and t-MDS

40
Q

What is group 4 (who)

A

All other AML

41
Q

Deletions of what chromosome have a v.poor prognosis in AML ?

A

Chromosome 5 and chromosome 7

42
Q

Is the FLT interval repeat in AML a good prognosis or bad?

A

Bad

43
Q

What are the clinical features of AML?

A

Related to leukaemic cells replacing cells in bone marrow - decrease in rbc, platelets and WBCs
Anaemia (normochromic normocytic)
Thrombocytopenia
Infections

44
Q

What does bone marrow look like in AML?

A

Hypercellular with blasts- large unusual nucleus and open chromatin

45
Q

What can be seen in AML myeloblasts?

A

Auer rods

46
Q

What is involved in the induction treatment of AML?

A

Attempt to reduce blast numbers in BM to less than 5%

Use daunarubican, ara-c and etoposide

47
Q

What is the second stage of AML treatment?

A

Consolidation- attempt to eliminate the disease using daunarubican , ara-c and etopside

48
Q

What disorder is defined by the 15-17 translocation?

A

Acute promyloific leukaemia (APL)

49
Q

How do you treat APL ?

A

Using ATRA

50
Q

What is ATRA?

A

All trans retinoic acid - a non chemotherapy drug that induces differentiation of promyleocytes and once they differentiate they under go apoptosis