Leukaemias flashcards
18 high-yield MRCP Part 1 cards from the Intellect Medicos Haematology & Oncology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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Which translocation and fusion gene define acute promyelocytic leukaemia (APML)?
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t(15;17) — PML–RARA.
Why? The fusion protein blocks myeloid differentiation at the promyelocyte stage.
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What is the key first-line drug treatment of acute promyelocytic leukaemia?
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All-trans retinoic acid (ATRA), now usually combined with arsenic trioxide.
Why? ATRA overcomes the PML–RARA block so promyelocytes mature, which also quickly improves the coagulopathy.
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During APML treatment, which serious complication causes fever, breathlessness, pulmonary infiltrates and weight gain?
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Differentiation syndrome — treat with dexamethasone.
Why? Rapidly maturing leukaemic cells release cytokines and infiltrate the lungs, causing capillary leak.
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What is standard induction chemotherapy for AML?
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Cytarabine plus an anthracycline (e.g. daunorubicin).
Why? This combination produces remission in most fit patients; consolidation or stem cell transplant follows.
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Name the cytogenetic abnormalities associated with a GOOD prognosis in AML.
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t(15;17), t(8;21) and inv(16).
Why? These lesions respond well to treatment; they define AML even when blasts are below 20%.
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What is the first-line treatment of chronic-phase CML, and how does it work?
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A tyrosine kinase inhibitor that blocks the BCR-ABL1 kinase — classically imatinib (dasatinib and nilotinib are also NICE-approved first-line options).
Why? CML is driven by the Philadelphia chromosome t(9;22), whose BCR-ABL1 fusion gene makes a permanently active tyrosine kinase.
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Which test confirms CLL, and what is the classic marker profile?
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Flow cytometry (immunophenotyping): CD5, CD19, CD20 and CD23 positive.
Why? CLL is a clonal mature B-cell disorder; this profile separates it from other lymphoproliferative disorders.
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A patient with CLL needs treatment and has del(17p)/TP53 mutation. What is first-line therapy?
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A BTK inhibitor, e.g. ibrutinib, acalabrutinib or zanubrutinib.
Why? TP53 loss predicts a poor response to chemoimmunotherapy (FCR), but BTK inhibitors work independently of p53.
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What is the target of venetoclax, and which complication requires a gradual dose ramp-up?
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BCL-2 (an anti-apoptotic protein); tumour lysis syndrome.
Why? Blocking BCL-2 triggers rapid apoptosis of CLL cells, which can release potassium, phosphate and urate.
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What is first-line treatment for hairy cell leukaemia?
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A purine analogue — cladribine (or pentostatin).
Why? Purine analogues give long-lasting remissions in this indolent B-cell disorder.
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In childhood ALL, ______ (ETV6–RUNX1) predicts a good prognosis, whereas t(9;22) (Philadelphia chromosome) predicts a poor prognosis.
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t(12;21)
Why? Cytogenetics guides risk stratification; Philadelphia-positive ALL now has a tyrosine kinase inhibitor added to chemotherapy.
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In childhood ALL, t(12;21) (ETV6–RUNX1) predicts a good prognosis, whereas ______ (Philadelphia chromosome) predicts a poor prognosis.
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t(9;22)
Why? Cytogenetics guides risk stratification; Philadelphia-positive ALL now has a tyrosine kinase inhibitor added to chemotherapy.
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When should ATRA be started in suspected acute promyelocytic leukaemia?
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Immediately on clinical and blood film suspicion — without waiting for genetic confirmation of PML–RARA.
Why? Early deaths in APML are mainly from haemorrhage due to DIC; ATRA quickly corrects the coagulopathy.
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A 55-year-old has weight loss and massive splenomegaly. WBC is 210 × 10⁹/L with basophilia, eosinophilia and a full spectrum of myelocytes and metamyelocytes. Which investigation confirms the diagnosis?
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Cytogenetics/FISH or RT-PCR showing t(9;22) — the Philadelphia chromosome (BCR-ABL1).
Why? CML is defined by the BCR-ABL1 fusion gene; quantitative PCR also gives a baseline for monitoring treatment.
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How is response to tyrosine kinase inhibitor therapy monitored in CML?
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Quantitative RT-PCR for BCR-ABL1 transcripts in peripheral blood (International Scale), usually every 3 months.
Why? Falling transcript levels define molecular response; a rise suggests resistance, e.g. an ABL kinase domain mutation.
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Which second-generation tyrosine kinase inhibitor used in CML commonly causes pleural effusions?
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Dasatinib.
Why? Fluid retention with pleural effusion is a characteristic dasatinib effect, so check a CXR if the patient becomes breathless.
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In CLL, del(13q) is the commonest cytogenetic lesion and is favourable, whereas ______ (TP53 loss) carries the worst prognosis.
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del(17p)
Why? TP53 loss predicts resistance to chemoimmunotherapy, so these patients get a BTK inhibitor (or venetoclax-based therapy) first-line.
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Which arrhythmia is a recognised adverse effect of ibrutinib?
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Atrial fibrillation.
Why? Ibrutinib (a BTK inhibitor) increases the risk of AF, bleeding and hypertension; acalabrutinib and zanubrutinib cause less AF.