Vasculitis, GCA & PMR flashcards
16 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 investigation for suspected giant cell arteritis in a fast-track pathway?
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Temporal (± axillary) artery ultrasound, looking for a "halo" sign.
Why? Ultrasound is quick and non-invasive. ESR and CRP are raised, but treatment must not wait for any test.
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What is the gold-standard diagnostic test for giant cell arteritis, and why can it be falsely negative?
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Temporal artery biopsy (granulomatous inflammation with multinucleated giant cells); it can miss "skip lesions".
Why? Take at least 1 cm of artery (BSR 2020). Biopsy yield also falls the longer steroids have been given, so do it promptly — but never delay steroids.
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A 72-year-old woman has a new temporal headache, scalp tenderness when combing her hair and pain in her jaw when chewing. Vision is normal. ESR is 85 mm/h. What is the immediate management?
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Start oral prednisolone 40–60 mg daily straight away, then arrange urgent ultrasound/biopsy.
Why? Untreated GCA can cause irreversible blindness; treatment does not wait for confirmation.
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How is giant cell arteritis with visual symptoms (e.g. amaurosis fugax, visual loss) treated initially?
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Urgent IV methylprednisolone (500 mg–1 g daily for up to 3 days), then oral prednisolone, with same-day ophthalmology review.
Why? Visual loss from anterior ischaemic optic neuropathy is usually permanent, so the aim is to protect the other eye.
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Which biologic is used as a steroid-sparing drug in giant cell arteritis?
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Tocilizumab (IL-6 receptor blocker).
Why? It reduces relapses and cumulative steroid dose; methotrexate is an alternative steroid-sparing agent.
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What is the first-line treatment of polymyalgia rheumatica?
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Oral prednisolone 15 mg daily, tapered slowly over months to years.
Why? The response is dramatic within days; offer bone protection and keep screening for GCA symptoms.
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In polymyalgia rheumatica, what are the typical ESR/CRP and creatine kinase results?
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ESR and CRP are raised; CK is normal.
Why? A normal CK separates PMR (pain and stiffness, no true weakness) from polymyositis (weakness with raised CK).
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Which HLA allele is associated with Behçet's disease?
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HLA-B51.
Why? Behçet's is commonest along the Silk Road (Mediterranean, Middle East, East Asia) in young adults.
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In Behçet's disease, what is the pathergy test?
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A minor needle prick to the skin produces an exaggerated papule or pustule within 24–48 hours.
Why? It reflects neutrophil hyper-reactivity; it supports the diagnosis but is not diagnostic on its own.
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Which viral infection is classically associated with polyarteritis nodosa?
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Hepatitis B.
Why? PAN is a necrotising vasculitis of medium-sized arteries causing microaneurysms; hepatitis B-related PAN is treated with antivirals plus immunosuppression.
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A 50-year-old man has fever, weight loss, testicular pain, new hypertension, livedo reticularis and a right foot drop. His urine shows no red cell casts. Which investigation finding confirms the likely diagnosis?
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Microaneurysms on renal or mesenteric angiography (or necrotising arteritis on biopsy) — polyarteritis nodosa.
Why? PAN affects medium arteries, causing mononeuritis multiplex, renal artery hypertension and gut ischaemia, but spares glomeruli and lungs.
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Granulomatosis with polyangiitis is associated with ______, while microscopic polyangiitis is associated with p-ANCA (anti-MPO).
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c-ANCA (anti-PR3)
Why? GPA causes ENT destruction (sinusitis, saddle nose) and cavitating lung nodules; MPA has no granulomas or ENT disease. Both cause pauci-immune crescentic GN.
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Granulomatosis with polyangiitis is associated with c-ANCA (anti-PR3), while microscopic polyangiitis is associated with ______.
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p-ANCA (anti-MPO)
Why? GPA causes ENT destruction (sinusitis, saddle nose) and cavitating lung nodules; MPA has no granulomas or ENT disease. Both cause pauci-immune crescentic GN.
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What is the induction treatment for organ-threatening GPA or MPA?
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High-dose glucocorticoids plus rituximab or cyclophosphamide.
Why? Rituximab is often preferred in younger patients to avoid cyclophosphamide's infertility and cancer risks. BSR 2025: consider avacopan to reduce steroids; rituximab is the preferred maintenance drug.
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Which anti-IL-5 biologic is used in eosinophilic granulomatosis with polyangiitis (EGPA)?
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Mepolizumab.
Why? EGPA features late-onset asthma and eosinophilia, with p-ANCA (MPO) in about 40%; IL-5 drives eosinophils.
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In anti-GBM (Goodpasture) disease, what does renal biopsy immunofluorescence show, and what is the key treatment?
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Linear IgG deposition along the basement membrane; treat with plasma exchange plus steroids and cyclophosphamide.
Why? Plasma exchange removes the circulating anti-GBM antibody. ANCA vasculitides instead show pauci-immune staining.