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Q1: Presentation (2 min)
Examiner: A 74-year-old woman presents with new temporal headache and jaw pain on chewing. What is your diagnosis and what must you ask about next?
Candidate: Giant cell arteritis is the leading diagnosis at this age with new cranial pain. I would immediately ask about visual symptoms (amaurosis fugax, diplopia, blurring, sudden loss), because any visual symptom makes this an emergency. I would also ask about scalp tenderness, polymyalgia symptoms (shoulder and pelvic-girdle stiffness with morning stiffness over 45 minutes), constitutional symptoms, limb claudication, and risk factors such as PMR or family history.
Examiner: Why is jaw claudication so specific?
Candidate: Because it reflects ischaemia of the masseteric branch of the external carotid — pain that builds with sustained chewing and eases with rest — which only occurs with arterial inflow limitation, unlike temporomandibular joint pain which is present from the start of chewing.
Examiner: What proportion have a normal ESR?
Candidate: About 5 to 10 percent of biopsy-proven cases have a normal or near-normal ESR, which is why I would also check CRP, and why a normal ESR never excludes GCA.
Q2: Management (3 min)
Examiner: This patient has amaurosis fugax. Walk me through your first hour.
Candidate: This is threatened vision, so I would give IV methylprednisolone 500 mg to 1 g once daily for 3 days immediately, without waiting for bloods, biopsy or imaging. I would convert to oral prednisolone 1 mg/kg (60 mg) daily thereafter, draw baseline ESR, CRP, FBC, UEC, LFT and glucose alongside the first dose, request a temporal artery biopsy within 2 weeks, and arrange same-day ophthalmology review to baseline the eye.
Examiner: Why not wait for the biopsy?
Candidate: Because the diagnostic inflammatory changes persist in the arterial wall for 2 to 4 weeks after steroids are started, while irreversible blindness can develop within hours. The tiny reduction in biopsy yield from a few days of steroids is dwarfed by the catastrophic cost of a delay.
Examiner: How would you taper, and when would you add tocilizumab?
Candidate: Once symptoms and CRP are controlled — usually 2 to 4 weeks — I taper over 12 to 24 months: 10 mg every 2 weeks to 20 mg, then 2.5 mg every 2 to 4 weeks to 10 mg, then 1 mg every 4 weeks, monitoring ESR/CRP and symptoms. I add tocilizumab 162 mg subcutaneously weekly at induction in patients at high risk of steroid toxicity (age over 70, diabetes, osteoporosis), on relapse, or for refractory disease — the GiACTA trial showed sustained remission at 12 months in over half of patients with roughly half the cumulative steroid dose.
Q3: Complications (2 min)
Examiner: What are the complications of this disease and its treatment?
Candidate: The most feared disease complication is permanent visual loss from anterior ischaemic optic neuropathy — 15 to 30 percent of untreated patients lose vision, reduced to under 5 percent with prompt steroids. Other complications include posterior-circulation stroke from vertebral artery involvement, and thoracic aortic aneurysm and dissection which is the chief cause of excess late mortality. Limb claudication, scalp and tongue necrosis are less common.
Treatment complications are dominated by long-term steroids — osteoporotic fracture, diabetes, hypertension, infection, adrenal suppression, cataract, skin thinning — which is exactly why we add tocilizumab early to minimise cumulative steroid. Tocilizumab itself carries infection, neutropenia, transaminitis, hyperlipidaemia and masks CRP/ESR.
Examiner: How do you monitor for the late complications?
Candidate: Annual CT or MR angiography of the aorta for life in large-vessel GCA, because thoracic aneurysm can develop years after remission. Clinical and ESR/CRP review every 4 to 8 weeks during taper, with steroid-toxicity surveillance — DEXA, glucose, lipids and intra-ocular pressure.
Q4: Prognosis and pitfalls (2 min)
Examiner: What is the prognosis, and what are the classic pitfalls?
Candidate: Prognosis is excellent with prompt treatment — overall mortality is similar to the age-matched population, with a modest excess from aortic and cardiovascular disease. Relapse occurs in 30 to 50 percent on tapering, mostly in the first 18 months. Once visual loss occurs it is usually permanent.
The classic pitfalls are: waiting for biopsy before treating; excluding GCA on a normal ESR or a negative biopsy (5 to 10 percent and 10 to 15 percent respectively); missing large-vessel GCA in a patient with fever of unknown origin and a normal cranial examination; chasing the marker rather than the patient during taper; and failing to image the aorta during follow-up. I would also always exclude mimics — non-arteritic AION, infective endocarditis, malignancy, ANCA-associated vasculitis — before committing to prolonged high-dose steroids.