Targeted drugs, biologics & cytotoxics flashcards
22 high-yield MRCP Part 1 cards from the Intellect Medicos Basic sciences & statistics 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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What is the mechanism of action of vinca alkaloids (vincristine, vinblastine)?
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They bind tubulin and inhibit microtubule polymerisation, stopping spindle formation and arresting cells in mitosis (M phase).
Why? Without a mitotic spindle, chromosomes cannot align and separate.
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How do taxanes (e.g. paclitaxel) act on microtubules?
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They stabilise microtubules and prevent depolymerisation, so the spindle cannot break down and mitosis stalls.
Why? Taxanes and vinca alkaloids both block mitosis, but in opposite ways.
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What is the mechanism of action of colchicine?
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It binds tubulin and inhibits microtubule polymerisation, reducing neutrophil migration and activity.
Why? This explains its use in acute gout and pericarditis, where neutrophil-driven inflammation dominates.
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What is the molecular target of rituximab?
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CD20 on B cells.
Why? Rituximab depletes B cells; it is used in B-cell lymphomas, CLL and some autoimmune diseases.
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What is the molecular target of trastuzumab?
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HER2 (ERBB2) receptor.
Why? Used in HER2-positive breast and gastric cancer.
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Cetuximab and panitumumab target which receptor?
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EGFR (epidermal growth factor receptor).
Why? Both are used in metastatic colorectal cancer.
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The checkpoint inhibitor ipilimumab blocks ______, whereas nivolumab blocks PD-1.
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CTLA-4
Why? Blocking these inhibitory receptors releases the brakes on T cells so they attack the tumour (e.g. melanoma).
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The checkpoint inhibitor ipilimumab blocks CTLA-4, whereas nivolumab blocks ______.
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PD-1
Why? Blocking these inhibitory receptors releases the brakes on T cells so they attack the tumour (e.g. melanoma).
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Anakinra blocks the ______ receptor; tocilizumab blocks the IL-6 receptor.
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IL-1
Why? IL-1 and IL-6 are pro-inflammatory cytokines from macrophages; IL-6 drives the acute-phase response (CRP).
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Anakinra blocks the IL-1 receptor; tocilizumab blocks the ______ receptor.
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IL-6
Why? IL-1 and IL-6 are pro-inflammatory cytokines from macrophages; IL-6 drives the acute-phase response (CRP).
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How do ciclosporin and tacrolimus suppress T-cell activation?
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They inhibit calcineurin, reducing IL-2 production and therefore T-cell proliferation.
Why? IL-2 from activated T cells is the main growth signal for T cells.
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A 62-year-old has a gastric mass. Biopsy shows spindle cells that stain for CD117 (c-KIT). CT shows liver metastases. What is the first-line systemic treatment?
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Imatinib (a tyrosine kinase inhibitor).
Why? GISTs arise from interstitial cells of Cajal and are driven by activating c-KIT or PDGFRA mutations, which imatinib blocks.
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What is the first-line treatment for a localised, resectable GIST?
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Surgical resection.
Why? Complete surgical excision is the only curative treatment. Imatinib is first-line for unresectable or metastatic disease.
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Which enzyme does methotrexate inhibit?
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Dihydrofolate reductase.
Why? This depletes tetrahydrofolate, which is needed to make purines and thymidine, so DNA synthesis stops (methotrexate is an antimetabolite acting in S phase).
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Which enzyme deficiency should be tested for before starting 5-fluorouracil or capecitabine?
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Dihydropyrimidine dehydrogenase (DPD) deficiency.
Why? DPD breaks down fluoropyrimidines. Deficient patients get severe, sometimes fatal, toxicity (mucositis, diarrhoea, neutropenia), so the MHRA (2020) advises DPD testing before treatment.
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What is the mechanism of action of bortezomib in multiple myeloma?
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Proteasome inhibition.
Why? The proteasome degrades ubiquitin-tagged proteins. Myeloma cells make huge amounts of immunoglobulin, so blocking protein disposal triggers their apoptosis.
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In chronic myeloid leukaemia, which abnormal kinase does imatinib inhibit?
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The BCR-ABL tyrosine kinase, produced by the t(9;22) Philadelphia chromosome.
Why? BCR-ABL is a constitutively active fusion kinase that drives myeloid proliferation. Imatinib also blocks c-KIT, which is why it treats GIST.
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What is the target of denosumab, and which blood test must be checked before and during treatment?
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RANKL; serum calcium (risk of hypocalcaemia).
Why? Blocking RANKL stops osteoclast formation and activation. Calcium and vitamin D deficiency should be corrected before starting.
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Eculizumab blocks which complement component, and which vaccination is required before starting it?
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C5; meningococcal vaccination.
Why? Blocking C5 prevents formation of the membrane attack complex, which mimics terminal complement deficiency and so carries a high risk of Neisseria meningitidis infection.
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In severe asthma, omalizumab targets ______, whereas mepolizumab targets IL-5.
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IgE
Why? IgE cross-linking on mast cells drives type I hypersensitivity; IL-5 from Th2 cells drives eosinophil growth and activation.
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In severe asthma, omalizumab targets IgE, whereas mepolizumab targets ______.
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IL-5
Why? IgE cross-linking on mast cells drives type I hypersensitivity; IL-5 from Th2 cells drives eosinophil growth and activation.
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How does nusinersen treat spinal muscular atrophy?
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It is an antisense oligonucleotide (given intrathecally) that changes SMN2 pre-mRNA splicing so exon 7 is included, increasing functional SMN protein.
Why? SMA is caused by loss of SMN1. The back-up gene SMN2 usually skips exon 7 and makes mostly truncated protein, so correcting its splicing compensates.