DMARDs & biologics flashcards
27 high-yield MRCP Part 1 cards from the Intellect Medicos Rheumatology 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 first-line cDMARD for newly diagnosed active rheumatoid arthritis?
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Oral methotrexate monotherapy (NICE also allows leflunomide or sulfasalazine).
Why? NICE NG100 advises cDMARD monotherapy as soon as possible, ideally within 3 months of persistent symptoms, escalating the dose as tolerated.
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What is the mechanism of action of methotrexate?
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It inhibits dihydrofolate reductase, blocking purine and pyrimidine synthesis.
Why? As a folate antagonist it impairs DNA synthesis in rapidly dividing cells — the source of both its effect and its toxicity.
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In rheumatology, methotrexate is taken ______, together with folic acid supplementation.
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once weekly
Why? Accidental daily dosing has caused fatal toxicity (MHRA warning). Folic acid reduces mucositis, GI upset and liver toxicity.
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In rheumatology, methotrexate is taken once weekly, together with ______ supplementation.
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folic acid
Why? Accidental daily dosing has caused fatal toxicity (MHRA warning). Folic acid reduces mucositis, GI upset and liver toxicity.
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Which blood tests are used to monitor methotrexate?
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FBC, renal function and LFTs — at baseline, frequently after starting or any dose change, then usually every 3 months once stable.
Why? Methotrexate can cause myelosuppression and hepatotoxicity, and is renally excreted so toxicity rises in renal impairment.
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Which serious, potentially fatal lung adverse effect of methotrexate must patients be warned about?
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Pneumonitis (which can progress to pulmonary fibrosis).
Why? It presents with new cough, breathlessness and fever. BSR 2025 no longer advises routine lung screening before csDMARDs; lung assessment (lung function tests rather than chest X-ray) is guided by the diagnosis, symptoms and examination.
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What is the antidote for methotrexate toxicity such as myelosuppression?
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Folinic acid (calcium folinate, leucovorin), given IV as soon as possible.
Why? Folinic acid is already reduced, so it bypasses the blocked dihydrofolate reductase.
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Which commonly prescribed antibiotic should be avoided with methotrexate because of severe bone marrow toxicity?
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Trimethoprim (including co-trimoxazole).
Why? Trimethoprim is also a folate antagonist, so the combination causes additive, sometimes fatal, myelosuppression.
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According to current BSR guidance, how long before planned conception should a woman stop methotrexate?
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At least 1 month before conception (switch to a pregnancy-compatible drug).
Why? Methotrexate is teratogenic at any dose and is also not recommended in breastfeeding.
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A woman taking leflunomide wishes to conceive. What must be done in addition to stopping the drug?
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A cholestyramine washout procedure.
Why? Leflunomide's active metabolite has a very long half-life (it can persist for up to 2 years), and the drug is teratogenic.
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Name two important adverse effects of leflunomide that need monitoring.
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Hepatotoxicity and hypertension (also myelosuppression).
Why? LFTs, FBC and blood pressure are checked regularly on leflunomide.
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What effect on male fertility can sulfasalazine cause?
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Reduced sperm count (oligo-/azoospermia), which is reversible on stopping.
Why? BSR 2022: men need not routinely stop sulfasalazine before conception; consider stopping it only if conception is delayed beyond 12 months. It is compatible with pregnancy (with folic acid 5 mg).
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In which inherited enzyme deficiency can sulfasalazine trigger haemolysis?
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G6PD deficiency.
Why? The sulfapyridine component is an oxidant stress, like other sulpha drugs.
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What is the key long-term toxicity of hydroxychloroquine?
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Retinopathy (bull's-eye maculopathy).
Why? The damage is irreversible, so patients are screened to detect it before symptoms develop.
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When should annual retinal screening start for a patient on long-term hydroxychloroquine (RCOphth)?
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After 5 years of treatment — or after 1 year if there are extra risk factors (e.g. dose >5 mg/kg/day, eGFR <60, tamoxifen).
Why? Risk of retinopathy is cumulative and rises steeply after about 5 years.
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Which enzyme activity should be measured before starting azathioprine?
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Thiopurine methyltransferase (TPMT).
Why? Low TPMT activity leads to toxic thioguanine levels and severe myelosuppression.
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Why is co-prescribing allopurinol with azathioprine dangerous?
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Allopurinol blocks xanthine oxidase, which breaks down 6-mercaptopurine, so levels rise and cause severe myelosuppression.
Why? Azathioprine is converted to 6-mercaptopurine; with xanthine oxidase inhibited, more is shunted to toxic thioguanine nucleotides.
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Apart from bone marrow suppression, name two adverse effects of azathioprine.
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Hepatotoxicity and pancreatitis.
Why? Azathioprine is a purine analogue (via 6-MP); FBC and LFTs are monitored throughout.
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Which infection must be screened for before starting a TNF inhibitor?
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Tuberculosis — active and latent (history, chest X-ray, IGRA such as QuantiFERON).
Why? TNF is essential for granuloma maintenance, so blocking it can reactivate latent TB, often as extrapulmonary disease.
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Screening before anti-TNF therapy shows latent TB. What chemoprophylaxis is given?
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3 months of rifampicin plus isoniazid, or 6 months of isoniazid (isoniazid always with pyridoxine).
Why? Treating latent infection before biologics prevents reactivation.
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Name two conditions (other than active infection) in which TNF inhibitors should be avoided.
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Moderate–severe heart failure (NYHA III–IV) and demyelinating disease such as multiple sclerosis.
Why? TNF blockade has worsened heart failure in trials and can trigger or worsen demyelination.
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Which TNF inhibitor has no or minimal placental transfer, so the infant needs no change to its vaccination schedule?
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Certolizumab pegol.
Why? It lacks an Fc region, so it is not actively transported across the placenta.
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Rituximab is a monoclonal antibody against ______ on B cells.
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CD20
Why? It depletes B cells; in RA it is used with methotrexate after TNF-inhibitor failure, and it is an induction option in ANCA vasculitis.
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Tocilizumab blocks the ______.
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IL-6 receptor
Why? It is used in RA after biologic failure and as a steroid-sparing drug in giant cell arteritis.
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What is the mechanism of abatacept?
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A CTLA4-Ig fusion protein that blocks T-cell co-stimulation (CD80/86 binding to CD28).
Why? Without the second (co-stimulatory) signal, T cells are not fully activated.
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Above what DAS28 score is RA classed as severe for NICE biologic eligibility (after failure of intensive cDMARD therapy)?
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DAS28 greater than 5.1.
Why? TNF inhibitors (or a JAK inhibitor) are then offered, usually with methotrexate.
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Name three major risks that limit JAK inhibitor (e.g. tofacitinib) use according to MHRA advice.
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Major cardiovascular events, malignancy, venous thromboembolism (also serious infection).
Why? MHRA (2023) advises using them in people aged 65 or over, current or long-time ex-smokers, or those with CV or cancer risk factors only if there is no suitable alternative.