43 Acute Leukaemia Flashcards Preview

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Flashcards in 43 Acute Leukaemia Deck (24)
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1
Q

How does acute leukaemia arise?

A

De novo or terminal event of pr-existing blood disorder.

2
Q

Which type of cell is seen in the blood in acute leukaemia?

What is the difference in these cells between AML and ALL?

A

Blast cells.

Bigger nucleus and more cytoplasm in AML.

3
Q

How does acute leukaemia present? (3).

A

Anaemia.
Infections.
Easy bruising and haemorrhage.

4
Q

Where might leukaemia cells infiltrate into in acute leukaemia? (5).

A

Kidney, spleen, meninges, testes and skin.

Rarer to occur outside marrow in AML.

5
Q

Which infections commonly occur in leukaemia? (3,3)

A

Bacterial: septicaemia, pneumonia, skin sepsis.
Fungal: oral, septicaemia, organ

6
Q

What is acute leukaemia?

A

Accumulation of early myeloid or lymphoid precursors in the bone marrow, blood or other tissues.

7
Q

What are the two classifications of AML?

A

FAB.

WHO.

8
Q

How is acute leukaemia diagnosed?

A

Monoclonal antibody determination of surface antigens using immunofluorescence.

9
Q

Which AML genetic abnormalities have favourable prognosis? (3).

A

t(15;17)
t(8;21)
inv(16)

10
Q

Which AML genetic abnormalities have unfavourable prognosis? (4).

A

t(6;9)
inv(3)
del(5q)
-7, -5

11
Q

How does the genetic basis of ALL differ to AML?

A

ALL is mostly changes in chromosome number.

12
Q

Which chromosomal abnormality has a favourable prognosis in ALL?

A

High hyperpoloidy, >50 chromosomes.

13
Q

Which chromosomal changes have a very poor prognosis in ALL?

A

t(8;14)

t (9;22) Philadelphia chromosome.

14
Q

What is the name for the t(9;22) translocation?

A

Philadelphia chromosome.

15
Q

What fusion product does the t(8;21) translocation result in?

A

AML-ETO.

16
Q

Which translocation and associated gene product explains the response of promyelocytic leukaemia to all trans retinoid acid (ATRA)?

A

t(15;17)

PML-RARα

17
Q

Which mutation are present in cytologically normal AML?

Associated prognosis?

A
NPM1 = good.
FLT3 = bad.
18
Q

What are the poor prognostic features in ALL? (6).

A
Increasing age.
High WCC.
Male sex. 
Certain cytogenetic abnormalities.
Poor treatment response.
T-ALL or null-ALL
19
Q

How is AML managed?

A

Induction Rx to obtain remission, then consolidation with further courses of chemo.
Possible bone marrow transplant in young.

20
Q

How is ALL managed?

A

Induction chemo, intensive consolidation chemo.
Prophylaxis of meningeal leukaemia: methotrexate + cranial irradiation.
Maintenance chemo.
Bone marrow transplant in high risk.

21
Q

What are the complications of therapy in acute leukaemia? (2)

A
Neutropenic sepsis (all patients).
Neutropenic fever: pyrexia with neutrophil count under 1x10^9/l.
22
Q

How is neutropenic sepsis managed?

A

Immediate empirical broad spectrum IV antibiotics.

Tazocin, gentamicin.

23
Q

How is neutropenic sepsis prevented? (4).

A

Protective isolation.
Prophylactic antibiotics: levofloxacin.
Use of GCSF.
Hand hygiene.

24
Q

Who gets AML vs ALL?

A

ALL: 2-10 yr olds
AML: adults (risk increase with age)

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