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SLE & antiphospholipid syndrome flashcards

17 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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  1. SLE is associated with HLA-DR2/DR3 and with inherited deficiency of early complement components such as ______.

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    C1q, C2 and C4

    Why? Early complement helps clear apoptotic debris and immune complexes; without it, nuclear antigens drive autoimmunity.

  2. Which antibody is the best screening test for SLE?

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    Antinuclear antibody (ANA).

    Why? ANA is positive in almost all patients with SLE (highly sensitive) but is also found in many other conditions and healthy people (not specific).

  3. Which antibody is the most specific for SLE but has low sensitivity?

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    Anti-Smith (anti-Sm).

    Why? A positive anti-Sm strongly supports SLE, but most patients with SLE are negative for it.

  4. In SLE, disease activity is tracked with ______ titres, which rise in flares, and C3 and C4 levels, which fall in flares.

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    anti-dsDNA

    Why? Complement is consumed by immune complexes in active disease, especially lupus nephritis.

  5. In SLE, disease activity is tracked with anti-dsDNA titres, which rise in flares, and ______ levels, which fall in flares.

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    C3 and C4

    Why? Complement is consumed by immune complexes in active disease, especially lupus nephritis.

  6. What is the most common cardiac manifestation of SLE?

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    Pericarditis.

    Why? SLE can also cause myocarditis and Libman–Sacks (sterile verrucous) endocarditis.

  7. Which drug should all patients with SLE receive unless contraindicated?

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    Hydroxychloroquine.

    Why? It reduces flares and organ damage and improves survival; patients also need sun protection and retinal screening.

  8. Which drug is the backbone of first-line induction for active proliferative (class III/IV) lupus nephritis, and what is used for maintenance (BSR 2026)?

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    Mycophenolate, combined with belimumab, a calcineurin inhibitor (voclosporin or tacrolimus) or obinutuzumab, plus steroids and hydroxychloroquine. Maintenance: continue the mycophenolate-based regimen for at least 3 years.

    Why? Renal biopsy classifies the nephritis and guides treatment. Azathioprine is the maintenance option if mycophenolate cannot be taken or pregnancy is planned.

  9. Which maternal antibody causes congenital heart block (neonatal lupus)?

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    Anti-Ro (SSA) antibody.

    Why? Anti-Ro crosses the placenta and damages the fetal conducting system; pregnancies are monitored with fetal echo.

  10. A woman with SLE on mycophenolate plans pregnancy. Which immunosuppressant is compatible with pregnancy as a replacement?

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    Azathioprine (hydroxychloroquine and prednisolone are also continued as needed).

    Why? Mycophenolate, methotrexate and cyclophosphamide are teratogenic. BSR advises stopping mycophenolate at least 6 weeks before trying to conceive.

  11. Which antibody is characteristic of drug-induced lupus?

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    Anti-histone antibodies.

    Why? Drug-induced lupus is milder than SLE, rarely affects kidneys or brain, and resolves when the drug is stopped.

  12. Name three drugs that cause drug-induced lupus.

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    Any three: procainamide, hydralazine, isoniazid, minocycline, methyldopa, chlorpromazine, phenytoin, sulphonamides.

    Why? Procainamide and hydralazine are the highest-risk drugs; slow acetylators are more susceptible.

  13. What is the first-line management of discoid lupus erythematosus?

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    Strict sun protection plus potent topical corticosteroids.

    Why? Topical calcineurin inhibitors are an alternative; hydroxychloroquine is the main systemic option for extensive disease.

  14. Which antiphospholipid antibody prolongs the APTT and is most strongly associated with thrombosis?

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    Lupus anticoagulant.

    Why? It interferes with phospholipid-dependent clotting tests in the laboratory, yet in the body it is prothrombotic.

  15. What is the long-term treatment after a first venous thrombosis in antiphospholipid syndrome?

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    Lifelong warfarin, target INR 2–3.

    Why? With recurrent thrombosis on warfarin, the slides advise adding aspirin or aiming for a higher INR (3–4).

  16. Why are DOACs generally avoided in antiphospholipid syndrome?

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    They carry a higher risk of recurrent (especially arterial) thrombosis than warfarin, particularly in triple-positive patients.

    Why? The MHRA advises against DOACs in APS, especially triple-positive disease (lupus anticoagulant, anticardiolipin and anti-β2-glycoprotein I).

  17. How is antiphospholipid syndrome managed during pregnancy?

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    Low-dose aspirin plus LMWH (prophylactic dose for obstetric APS; therapeutic dose if there has been previous thrombosis).

    Why? Warfarin is teratogenic, so it is switched to LMWH; the combination reduces miscarriage and pre-eclampsia risk.

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