Rheumatoid Arthritis — Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mrs Jennifer Park is a 42-year-old office worker who presents with a 4-month history of symmetrical inflammatory polyarthritis affecting her wrists, MCPs, PIPs and MTPs, with morning stiffness lasting 2 to 3 hours. She has lost 4 kg and is struggling to work. She has no significant past medical history and is not on any regular medications. She is a non-smoker. [1]

Her main problems are:

1. Newly diagnosed seropositive rheumatoid arthritis — confirmed by the 2010 ACR/EULAR criteria (score 10 out of 10), with strongly positive anti-CCP (above 3 times ULN) and early marginal erosions on hand X-rays, placing her in the high-risk group for rapid erosive progression.
2. High disease activity (DAS28 5.6) requiring immediate disease-modifying therapy.
3. Functional impairment affecting her work and activities of daily living.
4. Cardiovascular risk — RA is a coronary risk equivalent and requires proactive risk management.
5. Psychological impact of a new chronic disease diagnosis. [1]

My management plan follows the treat-to-target paradigm: methotrexate first-line, bridging with glucocorticoids for rapid control, NSAIDs for symptom relief, physiotherapy and occupational therapy for function, cardiovascular risk management, vaccination update, and psychological support. The target is remission (DAS28 below 2.6), assessed every 1 to 3 months, with escalation to triple therapy or a biologic if the target is not met within 3 to 6 months." [1]

Examiner probing questions and model answers

Q1: "Walk me through your rationale for choosing methotrexate as first-line therapy." [1]

"Methotrexate is the anchor DMARD and the recommended first-line therapy for virtually all patients with rheumatoid arthritis, per EULAR and ACR recommendations [3]. My rationale is fourfold: first, it has the best efficacy-to-toxicity ratio of any DMARD — it works within 4 to 8 weeks and achieves the treat-to-target goal in approximately 30 per cent of patients as monotherapy. Second, it can be combined with every biologic DMARD, so it provides a foundation for future escalation. Third, it is inexpensive and available as a PBS-authority subsidised medication. Fourth, decades of observational data, including the ATTRACT trial foundation, confirm its safety and efficacy profile.

I would start at 15 mg orally once weekly, titrating to 20 to 25 mg weekly over 2 to 4 weeks. I prescribe folic acid 5 mg once weekly on a separate day. I counsel her on three critical safety points: the dose is once weekly, not daily — daily methotrexate causes fatal marrow suppression and mucositis; she must use reliable contraception as methotrexate is teratogenic; and she must report immediately any mouth ulcers, sore throat, fever or new respiratory symptoms. I monitor FBC, LFT and creatinine every 2 to 4 weeks for the first 3 months, then every 8 to 12 weeks." [1]

Q2: "How does the TICORA trial support your treat-to-target strategy?" [1]

"The TICORA trial (Grigor et al., 2004) is the landmark evidence that the treatment strategy matters as much as the drugs [4]. It randomised patients with early RA to either intensive tight control — monthly assessment with DAS and protocolised escalation of DMARD therapy if DAS remained above 2.4 — or routine outpatient care. The intensive group had significantly more remission (42 per cent versus 16 per cent), less radiographic damage progression, and better physical function. This established that measuring disease activity regularly and escalating therapy when the target is not met is superior to treating by clinical impression alone. For this patient, I will assess her every 1 to 3 months with DAS28 (using ESR), and if she has not reached remission or low disease activity within 3 to 6 months, I will escalate."

Q3: "What are her escalation options if methotrexate monotherapy fails?" [1]

"If her DAS28 remains above the target after 3 to 6 months of optimised methotrexate, I have three escalation pathways. First, triple therapy — adding sulfasalazine 2 to 3 g daily and hydroxychloroquine 200 to 400 mg daily to her methotrexate. The TEAR and RACAT trials showed triple therapy is non-inferior to anti-TNF plus methotrexate in many patients, though onset is slower. This is an evidence-based, lower-cost option. [1]

Second, I can add a biologic DMARD — anti-TNF is the first-line biologic class. I would use adalimumab 40 mg subcutaneously every 2 weeks, etanercept 50 mg weekly, or certolizumab 400 mg then 200 mg every 2 weeks. If she is planning pregnancy, certolizumab is preferred because it does not cross the placenta. Before any biologic, I would screen for latent TB with an IGRA, check HBV and HCV serology, ensure vaccinations are up to date, and counsel on infection risk. [1]

Third, I could use a JAK inhibitor — tofacitinib, baricitinib or upadacitinib — which are oral and rapid-acting. However, the ORAL Surveillance study showed that in patients above 50 with cardiovascular risk factors, tofacitinib had higher MACE and malignancy rates than anti-TNF [5]. At 42 years old she does not yet fall into the high-risk group, so a JAK inhibitor would be a reasonable option, but I would be cautious if she developed cardiovascular risk factors."

Q4: "She is 42 and may want children. How does that affect your treatment plan?" [1]

"Pregnancy planning is a critical conversation to have at diagnosis, not after a treatment has caused harm. The key principles are: first, methotrexate and leflunomide are absolutely contraindicated in pregnancy and must be stopped 3 to 6 months before conception — methotrexate is teratogenic and leflunomide has a 2-year active metabolite half-life requiring cholestyramine washout. Second, sulfasalazine and hydroxychloroquine are safe in pregnancy and should be continued. Third, anti-TNF agents can be continued through pregnancy — certolizumab is preferred because it does not cross the placenta (it lacks the Fc portion), while adalimumab and infliximab cross the placenta in the third trimester but are generally cleared from the neonatal circulation by 6 months. Fourth, rituximab should be avoided in the third trimester (it can cause neonatal B-cell depletion). Fifth, JAK inhibitors are contraindicated in pregnancy. Sixth, NSAIDs should be avoided in the third trimester (premature closure of the ductus arteriosus). [1]

The most important principle: active maternal RA is worse for the pregnancy than well-chosen medications. Uncontrolled inflammation increases the risk of preterm birth, low birth weight and preeclampsia. So I would ensure her disease is well controlled before she conceives, using pregnancy-compatible medications, and manage the transition actively with her obstetrician." [1]

Q5: "What is the role of anti-CCP in her prognosis and how does it influence your treatment intensity?" [1]

"Anti-CCP is the single strongest serological predictor of erosive disease and radiographic progression [2]. The Nishimura meta-analysis confirmed anti-CCP specificity of 90 to 98 per cent for RA and a stronger association with erosive disease than RF. This patient's anti-CCP is strongly positive (above 3 times ULN), which, combined with her early marginal erosions on X-ray at presentation, places her in the high-risk group for aggressive, destructive disease. This directly influences my treatment intensity: I will not delay methotrexate, I will use bridging glucocorticoids to control inflammation immediately while methotrexate takes effect, I will monitor her closely (every 1 to 2 months initially), and I will escalate early if she does not achieve rapid remission. The damage window in early RA is real — most erosions occur in the first 1 to 2 years and are irreversible."

Q6: "How would you manage her cardiovascular risk?" [1]

"RA is a coronary risk equivalent — the Avina-Zubieta meta-analysis showed a 48 per cent increased risk of incident cardiovascular events in RA patients compared with the general population, comparable to diabetes [8]. Chronic systemic inflammation accelerates atherosclerosis through endothelial dysfunction, procoagulant effects and lipid derangement. For this patient, I would calculate her cardiovascular risk using QRISK (which incorporates RA as a risk multiplier) or the Australian Absolute Cardiovascular Risk calculator with clinical upward adjustment. I would optimise her blood pressure (target 130/80 or below), check a fasting lipid panel and start a statin if indicated, encourage regular exercise (adapted for her joints), ensure she remains a non-smoker, and minimise her NSAID and glucocorticoid exposure over time. As her RA inflammation comes under control with effective disease-modifying therapy, her cardiovascular risk should also decrease — this is another reason to treat to target aggressively."

Short Case Discussion

Examination of the rheumatoid hand

Examiner instruction: "Examine this patient's hands. She is a 60-year-old woman with long-standing arthritis." [1]

Candidate's model answer: [1]

"I would like to examine this patient's hands systematically — inspection, palpation, movement, function, and then a screen for extra-articular manifestations of rheumatoid disease. [1]

Inspection: I am looking at the dorsal and palmar surfaces of both hands, comparing side to side. I can see symmetrical deformities affecting the small joints. At the MCP joints there is ulnar deviation and palmar subluxation. At the PIP joints there is hyperextension — a swan-neck deformity — with associated DIP flexion. There is a Z-deformity of the thumb with MCP flexion and IP hyperextension. The wrist shows a prominent ulnar styloid — caput ulnae — consistent with dorsal subluxation of the distal radioulnar joint. There are firm, non-tender subcutaneous nodules on the extensor surface of the right elbow — rheumatoid nodules. There is mild muscle wasting of the thenar and hypothenar eminences. There is no nail change to suggest psoriasis (no pitting, onycholysis), and the DIP joints are spared — these are important negative findings that distinguish RA from psoriatic arthritis and osteoarthritis. [1]

Palpation: I am palpating each joint individually. The MCP joints feel boggy with palpable synovial thickening. The PIP joints are also thickened. The wrists are tender with a palpable synovial proliferation. I am performing the MTP squeeze test — squeezing across the metatarsal heads of the feet would elicit pain in active disease. I am testing the caput ulnae sign — pressing down on the prominent ulnar head, which depresses and springs back like a piano key, confirming dorsal subluxation of the distal radioulnar joint. The extensor tendons are intact — I am asking the patient to extend her fingers against resistance to exclude extensor tendon rupture, which can occur from friction over a subluxed ulnar head. [1]

Movement: I am assessing active and passive range of motion at the wrists, MCPs, PIPs and DIPs. There is restricted flexion and extension at the MCP joints and reduced wrist extension and supination. [1]

Function: I am assessing hand function — grip strength, pinch grip, the ability to make a fist, to button a shirt, to turn a key, and to write. Functional limitation is the clinical endpoint that matters most to the patient. [1]

Synthesis: My findings are symmetrical inflammatory polyarthritis with classical rheumatoid deformities — ulnar deviation, palmar subluxation, swan-neck deformity, Z-thumb and caput ulnae — with rheumatoid nodules on the extensor surface, DIP sparing, and no psoriatic nail changes. This is consistent with long-standing seropositive rheumatoid arthritis. I would like to complete my examination by screening for extra-articular manifestations: examining the eyes for scleritis or episcleritis, the chest for pleural effusion or interstitial lung disease, the heart for pericardial rub, the abdomen for splenomegaly (Felty syndrome), and the legs for vasculitic lesions or leg ulcers. I would also examine the cervical spine for signs of atlantoaxial subluxation." [1]

Examiner: "What is the mechanism of the swan-neck deformity?" [1]

"A swan-neck deformity consists of PIP hyperextension with DIP flexion. The mechanism is intrinsic muscle tightness — the lumbricals and interossei become shortened and tight in chronic synovitis — combined with attenuation of the extensor mechanism at the DIP. This is distinct from boutonniere deformity, which is PIP flexion with DIP hyperextension caused by rupture of the central slip of the extensor tendon at the PIP joint, allowing the lateral bands to slip palmarward. The two deformities are mirror images and are a classic exam discriminator: swan-neck is PIP hyperextension plus DIP flexion; boutonniere is PIP flexion plus DIP hyperextension." [1]

Examiner: "What would you do if she presented with sudden inability to extend one finger?" [1]

"This is likely an extensor tendon rupture — most commonly the extensor digitorum communis or extensor digiti minimi — caused by chronic friction of the tendon over a dorsally subluxed ulnar head. The management is urgent hand surgery referral for tendon transfer or repair. I would also address the underlying cause by stabilising the distal radioulnar joint (Darrach procedure or similar) to prevent further ruptures of adjacent tendons. This is one of the surgical indications in RA alongside joint replacement for severe pain or instability, and cervical spine stabilisation for atlantoaxial subluxation." [1]