43 Acute Leukaemia Flashcards
How does acute leukaemia arise?
De novo or terminal event of pr-existing blood disorder.
Which type of cell is seen in the blood in acute leukaemia?
What is the difference in these cells between AML and ALL?
Blast cells.
Bigger nucleus and more cytoplasm in AML.
How does acute leukaemia present? (3).
Anaemia.
Infections.
Easy bruising and haemorrhage.
Where might leukaemia cells infiltrate into in acute leukaemia? (5).
Kidney, spleen, meninges, testes and skin.
Rarer to occur outside marrow in AML.
Which infections commonly occur in leukaemia? (3,3)
Bacterial: septicaemia, pneumonia, skin sepsis.
Fungal: oral, septicaemia, organ
What is acute leukaemia?
Accumulation of early myeloid or lymphoid precursors in the bone marrow, blood or other tissues.
What are the two classifications of AML?
FAB.
WHO.
How is acute leukaemia diagnosed?
Monoclonal antibody determination of surface antigens using immunofluorescence.
Which AML genetic abnormalities have favourable prognosis? (3).
t(15;17)
t(8;21)
inv(16)
Which AML genetic abnormalities have unfavourable prognosis? (4).
t(6;9)
inv(3)
del(5q)
-7, -5
How does the genetic basis of ALL differ to AML?
ALL is mostly changes in chromosome number.
Which chromosomal abnormality has a favourable prognosis in ALL?
High hyperpoloidy, >50 chromosomes.
Which chromosomal changes have a very poor prognosis in ALL?
t(8;14)
t (9;22) Philadelphia chromosome.
What is the name for the t(9;22) translocation?
Philadelphia chromosome.
What fusion product does the t(8;21) translocation result in?
AML-ETO.
Which translocation and associated gene product explains the response of promyelocytic leukaemia to all trans retinoid acid (ATRA)?
t(15;17)
PML-RARα
Which mutation are present in cytologically normal AML?
Associated prognosis?
NPM1 = good. FLT3 = bad.
What are the poor prognostic features in ALL? (6).
Increasing age. High WCC. Male sex. Certain cytogenetic abnormalities. Poor treatment response. T-ALL or null-ALL
How is AML managed?
Induction Rx to obtain remission, then consolidation with further courses of chemo.
Possible bone marrow transplant in young.
How is ALL managed?
Induction chemo, intensive consolidation chemo.
Prophylaxis of meningeal leukaemia: methotrexate + cranial irradiation.
Maintenance chemo.
Bone marrow transplant in high risk.
What are the complications of therapy in acute leukaemia? (2)
Neutropenic sepsis (all patients). Neutropenic fever: pyrexia with neutrophil count under 1x10^9/l.
How is neutropenic sepsis managed?
Immediate empirical broad spectrum IV antibiotics.
Tazocin, gentamicin.
How is neutropenic sepsis prevented? (4).
Protective isolation.
Prophylactic antibiotics: levofloxacin.
Use of GCSF.
Hand hygiene.
Who gets AML vs ALL?
ALL: 2-10 yr olds
AML: adults (risk increase with age)
