Lecture 9: Haematological Malignancies (Parts 1-4) Flashcards
Compare AML and ALL:
AML:
Myeloid lineage (CD13+, CD33+)
Auer rods on blood film
Peak in adults
t(15;17) PML-RARA (APL)
ALL:
Lymphoid lineage (CD10+, CD19+)
Agranular blasts with high N:C ratio
Peak in children (3-7 years)
t(12;21) TEL-AML1 (good prognosis)
Key FBC findings in AML?
↓Hb, ↓platelets, ↑WBC (blasts), neutropenia.
What is the first-line treatment for ALL?
Induction chemotherapy (vincristine, dexamethasone, asparaginase) + CNS prophylaxis.
What defines CML?
Philadelphia chromosome t(9;22) → BCR-ABL1 fusion → constitutive tyrosine kinase activity.
Blood film: Myeloid precursors (metamyelocytes, basophilia).
Treatment: Tyrosine kinase inhibitors (imatinib).
How is CLL diagnosed?
Lymphocytosis (>5×10⁹/L), smudge cells on film, CD5+/CD19+/CD23+ on flow cytometry.
Binet staging: Determines prognosis (Stage A: >13 years survival).
Which translocation is diagnostic for CML?
t(9;22)(q34;q11) → BCR-ABL1.
What immunophenotypic markers distinguish B-ALL from T-ALL?
B-ALL: CD10, CD19, TdT.
T-ALL: CD3, CD7, TdT.
What is the significance of Auer rods?
Pathognomonic for AML (seen in myeloblasts).
Classic symptoms of CLL?
Fatigue, lymphadenopathy, recurrent infections, hepatosplenomegaly.
How is APL (AML-M3) treated?
ATRA (All-Trans Retinoic Acid) + arsenic trioxide (targets PML-RARA fusion).
Why is imatinib used in CML?
Inhibits BCR-ABL1 tyrosine kinase → halts proliferation.