On this page
Study tools
Exam tags
Write your answer
Saved on this device. No marking — you are the marker.
Viva format
A 10-minute cross-table viva built around escalating questions. Each question carries the examiner's intended trap and the model answer that would score full marks. Defend the why — examiners test reasoning, not lists.
Q1: Define rheumatoid arthritis and how you classify it (2 min)
Examiner: "A 38-year-old woman presents with symmetric small-joint polyarthritis, morning stiffness of 2 hours, anti-CCP positive, erosions on X-ray. What is the diagnosis and how do you formally classify it?"
Model answer: "This is seropositive rheumatoid arthritis, classified by the 2010 ACR/EULAR criteria. The criteria require at least one swollen joint, no better alternative diagnosis, and a score of 6 or more out of 10 across four domains: joint involvement (0–5; 1 large = 1 point, up to more than 10 joints with at least one small = 5), serology (negative RF/ACPA = 0, low-positive = 2, high-positive = 3), acute phase (normal CRP and ESR = 0, abnormal = 1) and duration (under 6 weeks = 0, 6 weeks or more = 1). The DIP, the first CMC and the first MTP are excluded — they are OA sites. This patient scores 10 out of 10: more than 10 small joints (5), high-positive serology (3), abnormal acute phase (1), more than 6 weeks (1)." [1]
Trap: confusing the 2010 (early disease) criteria with the older 1987 ACR criteria (designed for established, erosive disease). Defend why we use the 2010 version — to identify early disease and start DMARD therapy within the window of opportunity.
Q2: Serology — which antibody and why? (2 min)
Examiner: "If you had to choose ONE antibody to confirm the diagnosis, which would it be and why?"
Model answer: "Anti-cyclic citrullinated peptide antibody (anti-CCP / ACPA). It has a specificity of around 95–98% for RA — the highest of any serology in rheumatology — and is positive early, often years before symptoms. It also predicts erosive disease. Rheumatoid factor has similar sensitivity (~70%) but lower specificity (~70–80%) because it is also positive in Sjögren, SLE, chronic hepatitis, infective endocarditis, TB and around 5% of healthy elderly. So if a patient is RF-positive alone, I would still look hard for mimics; if they are anti-CCP positive with symmetric small-joint polyarthritis, I have RA." [3]
Trap: examiner may ask for the antigenic target — anti-CCP recognises citrullinated (deiminated) self-proteins (vimentin, fibrin, fibronectin, alpha-enolase), generated by PAD enzymes converting arginine to citrulline.
Q3: Initial management — drug, dose, monitoring (2 min)
Examiner: "Walk me through your initial drug management."
Model answer: "I would use a treat-to-target strategy aiming for remission (DAS28 below 2.6) or low disease activity, escalating every 3–6 months. The first DMARD is methotrexate 7.5–25 mg once weekly (oral or subcutaneous), titrated up, with folic acid 5 mg weekly to reduce mucosal, hepatic and GI toxicity. I would bridge with a short course of prednisolone 5–10 mg daily, tapering as the methotrexate takes effect (typically 2–3 months), and add a short NSAID such as naproxen 500 mg twice daily with a PPI for symptom control. I would check CBC, LFT, U&E at baseline and every 2–4 weeks for 3 months, then monthly, then 2–3-monthly. I counsel that methotrexate is teratogenic — stop 3 months before conception in both partners, limit alcohol, and report new cough or dyspnoea (pneumonitis). If disease activity remains above target at 3–6 months I add sulfasalazine 1–3 g/day and hydroxychloroquine 200–400 mg/day — triple csDMARD therapy." [2]
Trap: examiner will catch a candidate who says "methotrexate daily" — that is a fatal dosing error. Also be ready for the next step: if csDMARDs fail, choose a biologic (anti-TNF first; tocilizumab, rituximab, abatacept) or a JAK inhibitor (tofacitinib, baricitinib, upadacitinib).
Q4: Pre-biologic screening (1 min)
Examiner: "Before you start an anti-TNF, what must you exclude?"
Model answer: "Latent tuberculosis — interferon-gamma release assay (QuantiFERON-TB) plus chest X-ray; treat latent TB with rifampicin for 4 months or isoniazid for 6–9 months before starting. Hepatitis B and C serology — give entecavir or tenofovir prophylaxis if HBsAg or anti-HBc positive. Active infection — dental, skin, urine, chest. Update vaccination (pneumococcal, influenza, COVID-19, hepatitis B, recombinant zoster) before immunosuppression; avoid live vaccines once on therapy. In heart failure NYHA III/IV, avoid anti-TNF; in demyelinating disease, avoid anti-TNF." [2]
Q5: Atlantoaxial subluxation — the anaesthetic trap (1 min)
Examiner: "This patient needs emergency laparoscopic cholecystectomy. What pre-operative check matters most in RA?"
Model answer: "Lateral cervical spine X-rays in flexion and extension to look for atlantoaxial subluxation — anterior C1 on C2 translation from inflammatory attenuation of the transverse ligament. An atlantodens interval over 3 mm in adults (over 5 mm in children) is abnormal and warrants MRI and neurosurgical opinion. Unrecognised subluxation can cause cord compression during intubation. If symptomatic or significantly subluxed, I would arrange awake fibreoptic intubation and consider atlantoaxial fusion." [10]
Q6: Long-term complication and mortality (1 min)
Examiner: "What is the leading cause of premature death in RA, and what do you do about it?"
Model answer: "Cardiovascular disease — RA carries about a 1.5–2 times population baseline cardiovascular risk, driven by chronic inflammation plus traditional risk factors. The leading excess-risk causes are ischaemic heart disease, sudden cardiac death and stroke. I would perform an annual CV risk assessment with a 1.5× multiplier applied to the calculated score, treat hypertension, lipids and diabetes aggressively, encourage smoking cessation and exercise, and minimise glucocorticoids. Other major causes of death include interstitial lung disease (especially UIP pattern) and infection (disease- and treatment-related)."
Closing trap: examiner may ask "Does DMARD therapy change this?" — yes: tight control with methotrexate and biologics reduces CV events, partly by suppressing systemic inflammation, so treat-to-target also reduces cardiovascular mortality.
References4ShowHide
- [1]Neogi T, Aletaha D, Silman AJ, et al. The 2010 ACR/EULAR classification criteria for rheumatoid arthritis. Arthritis and Rheumatism, 2010.PMID 20872596
- [2]Smolen JS, Landewé RBM, Bijlsma JWJ, et al. EULAR recommendations for the management of rheumatoid arthritis: 2019 update. Annals of the Rheumatic Diseases, 2020.PMID 31969328
- [3]Schellekens GA, Visser H, de Jong BA, et al. The diagnostic properties of rheumatoid arthritis antibodies recognizing a cyclic citrullinated peptide. Arthritis and Rheumatism, 2000.PMID 10643712
- [10]Neva MH, Isomäki P, Hannonen P, et al. Early and extensive erosiveness in peripheral joints predicts atlantoaxial subluxations in RA. Arthritis and Rheumatism, 2003.PMID 12847673