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24 Cards in this Set

  • Front
  • Back
How is abnormal bone marrow distinguished?
Heavy infiltrate (blue) and absence of fat spaces
In which leukaemia is bone marrow failure not a feature?
None- it is a feature of all leukaemias
Why do those with leukaemia sometimes get tissue ulceration and cavitating lung lesions?
Ulceration is from tissue breakdown in the presence of neutropenia
Cavitating lung lesions form after a fungal infection of a neutropenic person
What sort of leukaemia does benzene exposure lead to?
Acute myeloid leukaemia
What is the collection of identical cells (from a single progenitor) called in leukaemia?
A clone
What tests are done to confirm clonality? (remember, clonality leads to Dx!)
PCR- polymerase chain reaction. Seen in B cells sharing immunoglogulin gene rearrangement (get single line, not smear)
Flow cytometry- stain B cells with monoclonal antibody and see a population skew towards kappa or lambda
Discuss morphological characteristics of AML vs ALL
AML- delicate chromatin, much cytoplasm, fine granules in cytoplasm of myoblast that can coalesce into little rods (Auer rods)
ALL- clumped chromatin, scant cytoplasm, no granules
Discuss classification of AMLs
Most are granulocyte differentiation M0, M1, M2, M3 (M3, APML, is an emergency, recognised by heavy granules is cytoplasm)
Monocytic differentiation M4, M5
Erythroid differentiation M6
Magekaryocytic differentiation M7
Discuss classification of ALLs
Most are L1, but there are also L2 and L3
Why is acute promyeloid leukaemia an emergency?
It is frequently associated with disseminated intravascular coagulation (DIC) that cn be rapidly fatal in the initial week of therapy
Discuss the genetic origins of APML
Typical translocation is the 15,17 translocation (PML/RARalpha fusion gene)
Discuss the treatment target of APML
The PML/RARalpha fusion gene product is a protein which is the target to therapy called All-trans-retanoic-acid (a vitamin A derivative or retinoid)
Inhibition of cell cycling by ATRA leads to differentiation and cell death
In which leukaemias is the Phildelphia chromosome present?
9,22 translocation
Present in:
95% of CML cases
25-30% of adult ALL cases, 2-10% of ALL paediatric cases
Occasionally in AML
What is the genetic abnormality in Philadelphia positive leukaemias? What is the treatment targeting this?
The genetic abnormality is a BCR-abl fusion gene, the product of which is a protein with tyrosine-kinase activity. This activity is autonomous and leads to malignant transformation
Imatinib is an inhibitor of the BCR-abl tyrosine kinase
Discuss characteristics of and treatment of leukaemias resulting from inversion 6 and t(8,21) and CBF (core binding factor) abnormalities
Acute myelomonocytic leukaemia (M4) with very abnormal eosinophils.
Occurs mainly in young adults
Good prognosis! (unlike most AMLs)
High clearance after high dose Cytarabine
Whatr are the 4 steps in the principles of treatment of acute leukaemias?
1. Induction chemotherapy (using a combination of chemo to induce remission)
2. Consolodation chemotherapy, may be intermediate or intense dose
3. Maintenance therapy in ALL (often for a number of years after remission)
4. Bone marrow transplantation allows the use of much higher doses of chemo than would otherwise be possible in induction chemo.
What are the remission and cure rates of childhood ALL and adult AML and ALL?
Childhood ALL: >90% remission, 80% cure
Adult AML and ALL: 60-75% remission, 25-35% cure
What are the features of CML?
-Features all stages of granulocyte development (including mature forms) in peripheral blood and bone marrow
-Either low or high platelet count
-Hyperviscous blood from high white cell count
--Philadelphia chromosome
What are the features of CLL?
-Mostly mature lymphocytes in the peripheral blood and bone marrow
-Hepatosplenomegaly in advanced cases
-Bone marrow failure in advanced cases
-Autoimmune complications
A distinct pattern of surface proteins is diagnostic (clonal expansion of a single cell)
How is CML treated?
Targeted therapies oare very effective
Imatinib, transplantation and failing that, chemotherapy
How is CLL treated?
If not symptomatic, then nil
Otherwise, chemotherapy or anti CD-20 antibody
Where are granulocytes and monocytes produced in an audlt?
Only in the bone marrow
How long to neutrophils take to produce? How long do they remain in the circulation?
6-10 days from stem cell to mature cell.
They have a half-time in the blood of 6-7 hours
Do neutrophils act on bacteria, viruses or fungi?