Acute leukaemia Flashcards Preview

Clinical Pathology > Acute leukaemia > Flashcards

Flashcards in Acute leukaemia Deck (22):
1

What is acute leukaemia?

Result of accumulation of early myeloid or lymphoid precursors in the bone marrow, blood and other tissues

2

How does acute leukaemia arise?

- Probably occurs by somatic mutation in a single cell within a population of early progenitor cells
- May arise de novo or be the terminal event of a pre-existing blood disorder

3

What are the two main subgroups of acute leukaemia?

- Acute myeloid leukaemia (AML)
- Acute lymphoblastic leukaemia (ALL)

4

What criteria is used to further divide acute leukaemia in various subcategories?

Morphological

5

What are the clinical features of acute leukaemia?

- Presents with features of bone marrow failure: anaemia, infections, easy bruising and haemorrhage
- Organ infiltration by leukaemia cells may occur e.g. spleen, liver, meninges, testes and skin

6

What are the two different ways of classifying AML?

- FAB classification – ‘morphological’
- WHO classification – ‘risk adapted’

7

What molecular technique lies at the cornerstone of leukaemia diagnosis?

- Monoclonal antibody determination of surface antigen expression
- Immunoflouresence and particularly flouresence activated cell sorting (FACS) allows rapid leukaemia diagnosis

8

How might cytogenetic analysis be useful?

May help confirm the diagnosis and indicate subtype

9

What is the Philadelphia chromosome?

Tranclocation between the long arms of ch9 and 22 resulting in a bcr-abl fusion protein with tyrosine kinase activity. Causes cell to divide uncontrollably. Found in CML and ALL.

10

What mutations cause abnormal cell proliferation in AML?

- FLT3 mutations
- Ras mutations
- Others: c-KIT mutations

11

What mutations cause blocks in cell differentiation in AML?

- CBF AML (t(8;21) and inv(16))
- PML-RARα (t(15;17))
- MLL translocations (11q23)

12

Which mutation suppresses tumour suppression?

NPM1

13

What can cytogenetics tell you about the prognosis of AML?

- Mutations in NPM1 = good

- Mutations in FLT3 = bad

- NPM1+ve/FLT3 ITD-ve gives improved relapse free (61% v 47%) and overall (57% v 23%) survival at 4 years compared with other way round

14

What is minimal residual disease monitoring and how may it be useful?

- May allow detection of early relapse and allow earlier treatment in some sub-types eg APML

15

What are the poor prognostic factors in ALL?

Increasing age
High WCC
Male sex
Certain cytogenetic abnormalities
Poor response to treatment
T-ALL and null-ALL

16

How is AML managed?

- Induction treatment to obtain remission, then consolidation with further courses of combination chemotherapy
- In younger patients consider bone marrow transplantation (sibling or MUD)

17

How is ALL managed?

- All patients receive induction chemotherapy, intensive consolidation chemotherapy and prophylaxis of meningeal leukaemia with intrathecal methotrexate and cranial irradiation
- Following this maintenance chemotherapy is given, or bone marrow transplantation in ‘bad-risk’ patients

18

What is the most serious complication of therapy?

All patients with acute leukaemia receiving intensive chemotherapy will become neutropenic for 10 – 21 days

19

What is neutropenic fever?

Defined as pyrexia in the presence of a neutrophil count of less than 1.0 x 10^9/l

20

What is neutropenic sepsis?

- Neutropenic patients are in grave danger of developing overwhelming gram negative or gram positive infection

21

How should neutropenic fever be managed?

- Cornerstone of management is immediate administration of broad spectrum IV antibiotics (often Tazocin and Gentamicin) given empirically before the results of cultures are available

22

How can neutropenic sepsis be avoided?

- protective isolation
- prophylactic antibiotics eg levofloxacin
- use of granulocyte colony stimulating factors
- strict hand hygiene

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