Rheumatology & Haematology — MCQs

A 65-year-old man presents to the emergency department with sudden onset severe pain, swelling and erythema of his right first metatarsophalangeal joint. He is unable to bear weight. He has a history of hypertension treated with bendroflumethiazide and stage 3 chronic kidney disease (eGFR 42 mL/min/1.73m²). Joint aspiration reveals needle-shaped negatively birefringent crystals under polarized light microscopy. Serum urate is 485 µmol/L. What is the most appropriate acute management?

Q113

A 42-year-old man with known rheumatoid arthritis presents for review. He has been taking methotrexate 20mg weekly for 3 months with good disease control. His recent blood tests show: Hb 118 g/L, WCC 3.2 × 10⁹/L, platelets 145 × 10⁹/L, ALT 95 U/L (normal <40), AST 88 U/L (normal <40). He is taking folic acid 5mg weekly. What is the most appropriate next step in management?

Q114

A 58-year-old woman presents with a 6-month history of symmetrical joint pain and stiffness affecting her hands and feet, particularly severe in the mornings and lasting over an hour. Examination reveals swelling of the metacarpophalangeal and proximal interphalangeal joints bilaterally. Blood tests show rheumatoid factor positive and anti-CCP antibody positive. What is the most appropriate first-line pharmacological treatment to initiate?

Rheumatology & Haematology UK Medical PG Practice Questions and MCQs

Question 111: A 72-year-old woman with recurrent episodes of gout is started on allopurinol for urate-lowering therapy. She has normal renal function. What is the target serum urate level that should be achieved to effectively prevent further acute attacks and reduce tophi formation?

A. Below 300 µmol/L (Correct Answer)
B. Below 360 µmol/L
C. Below 420 µmol/L
D. Below 480 µmol/L
E. Below 540 µmol/L

Explanation: ***Below 300 µmol/L***- Guidelines from the **British Society for Rheumatology (BSR)** recommend a target of **<300 µmol/L** (approx. 5 mg/dL) for patients with recurrent gout, especially those with **tophi** or chronic gouty arthritis.- Achieving this lower target is crucial to effectively **dissolve existing monosodium urate crystals** and prevent new crystal formation, thus reducing acute attacks and promoting **tophi resorption**.*Below 360 µmol/L*- While **360 µmol/L** (6 mg/dL) is the absolute upper limit of "normal" for some guidelines, it is considered a **sub-optimal target** for patients with established gout, particularly with tophi or frequent attacks.- Maintaining levels just below this threshold carries a higher risk of persistent **crystal deposition** compared to the more aggressive <300 µmol/L target.*Below 420 µmol/L*- This level (7 mg/dL) represents the approximate **saturation point** of urate in physiological conditions; exceeding it increases the risk of **precipitation** into joints.- Targeting this level does not provide the necessary **concentration gradient** required to dissolve existing crystals or prevent further acute episodes in patients with established gout.*Below 480 µmol/L*- This level (8 mg/dL) is considered **hyperuricaemic** and is associated with a significantly increased risk of developing **gout flares** and renal complications.- It is far above any recommended therapeutic target for **urate-lowering therapy (ULT)** in clinical practice for patients with recurrent gout.*Below 540 µmol/L*- This concentration (9 mg/dL) is significantly elevated and indicates **uncontrolled gout**, posing a high risk for the development of extensive **polyarticular tophi**.- At this level, **allopurinol** therapy would be considered ineffective or inadequately titrated to meet clinical objectives for gout management.

Question 112: A 65-year-old man presents to the emergency department with sudden onset severe pain, swelling and erythema of his right first metatarsophalangeal joint. He is unable to bear weight. He has a history of hypertension treated with bendroflumethiazide and stage 3 chronic kidney disease (eGFR 42 mL/min/1.73m²). Joint aspiration reveals needle-shaped negatively birefringent crystals under polarized light microscopy. Serum urate is 485 µmol/L. What is the most appropriate acute management?

A. Allopurinol 100mg daily with colchicine cover
B. Colchicine 500 micrograms four times daily
C. Oral prednisolone 30mg daily for 5 days (Correct Answer)
D. Indomethacin 50mg three times daily
E. Febuxostat 80mg daily

Explanation: ***Oral prednisolone 30mg daily for 5 days*** - In patients with **renal impairment** (CKD Stage 3), **corticosteroids** are the safest and most effective first-line treatment for an acute gout flare. - They provide rapid anti-inflammatory action while avoiding the gastrointestinal and renal risks associated with high-dose colchicine or **NSAIDs**. *Allopurinol 100mg daily with colchicine cover* - **Urate-lowering therapy (ULT)** should not be initiated during an **acute attack**, as fluctuations in serum urate levels can worsen or prolong the joint inflammation. - Allopurinol is used for long-term prophylaxis and is typically started at least 2–4 weeks after the acute episode has completely resolved. *Colchicine 500 micrograms four times daily* - This dose is excessively high and increases the risk of **toxicity**, especially in a patient with an **eGFR of 42 mL/min/1.73m²**. - Current guidelines recommend lower doses (e.g., 500mcg twice daily) in renal impairment to avoid side effects like **diarrhoea** and myelosuppression. *Indomethacin 50mg three times daily* - **NSAIDs** like indomethacin are generally **contraindicated** in patients with significant chronic kidney disease due to the risk of further **nephrotoxicity**. - They can worsen renal function by inhibiting prostaglandins that maintain renal blood flow, leading to acute-on-chronic kidney injury. *Febuxostat 80mg daily* - Similar to allopurinol, **febuxostat** is a urate-lowering agent intended for chronic management, not for treating **acute inflammation**. - Starting this during a flare can precipitate further **monosodium urate crystal** deposition and flare-up instability.

Question 113: A 42-year-old man with known rheumatoid arthritis presents for review. He has been taking methotrexate 20mg weekly for 3 months with good disease control. His recent blood tests show: Hb 118 g/L, WCC 3.2 × 10⁹/L, platelets 145 × 10⁹/L, ALT 95 U/L (normal <40), AST 88 U/L (normal <40). He is taking folic acid 5mg weekly. What is the most appropriate next step in management?

A. Stop methotrexate immediately and arrange urgent liver ultrasound
B. Continue methotrexate and increase folic acid to daily dosing
C. Withhold methotrexate temporarily and recheck liver function in 2 weeks (Correct Answer)
D. Switch to sulfasalazine as an alternative DMARD
E. Continue methotrexate at current dose and monitor monthly

Explanation: ***Withhold methotrexate temporarily and recheck liver function in 2 weeks***- The patient exhibits **hepatotoxicity** with **ALT/AST levels** more than twice the upper limit of normal (>2x ULN) and mild **leucopenia**, necessitating a temporary pause in treatment.- According to **BSR guidelines**, withholding the drug and monitoring allows the liver enzymes to normalize before deciding whether to restart at a **lower dose** or switch therapies.*Stop methotrexate immediately and arrange urgent liver ultrasound*- Immediate permanent cessation is premature as the **transaminitis** is moderate (<3x ULN) and may be transient.- An **urgent ultrasound** is not the first-line step for drug-induced liver injury unless there are signs of biliary obstruction or chronic liver disease.*Continue methotrexate and increase folic acid to daily dosing*- **Folic acid** can reduce gastrointestinal side effects, but it cannot reverse or safely manage active **drug-induced hepatotoxicity**.- Continuing the dose despite significant **enzyme elevation** (>2x ULN) and low **WCC** risks progressive bone marrow suppression and liver damage.*Switch to sulfasalazine as an alternative DMARD*- While **sulfasalazine** is an alternative, it is premature to switch before confirming if the toxicity resolves with a temporary break and **dose adjustment**.- The patient previously had **good disease control** on methotrexate, making it preferable to maintain the therapy if safety parameters allow.*Continue methotrexate at current dose and monitor monthly*- Continuing the current dose is unsafe when **ALT** is significantly elevated and **leucopenia** is present, as it leads to increased toxicity risk.- **Monthly monitoring** is insufficient; more frequent (biweekly) rebalancing is required until blood counts and liver enzymes stabilize.

Question 114: A 58-year-old woman presents with a 6-month history of symmetrical joint pain and stiffness affecting her hands and feet, particularly severe in the mornings and lasting over an hour. Examination reveals swelling of the metacarpophalangeal and proximal interphalangeal joints bilaterally. Blood tests show rheumatoid factor positive and anti-CCP antibody positive. What is the most appropriate first-line pharmacological treatment to initiate?

A. Methotrexate with folic acid supplementation (Correct Answer)
B. Prednisolone 60mg daily as monotherapy
C. Hydroxychloroquine monotherapy
D. Etanercept subcutaneous injection
E. Oral NSAIDs with proton pump inhibitor

Explanation: ***Methotrexate with folic acid supplementation***- **Methotrexate** is the gold-standard, first-line **Conventional Synthetic Disease-Modifying Antirheumatic Drug (csDMARD)** recommended for patients with rheumatoid arthritis (RA) to reduce disease activity and prevent joint destruction.- **Folic acid supplementation** is essential to reduce the risk of side effects such as **hepatotoxicity**, gastrointestinal distress, and **stomatitis** and must be taken on a different day than the methotrexate dose.*Prednisolone 60mg daily as monotherapy*- While **glucocorticoids** are used as **bridging therapy** to provide rapid symptomatic relief while DMARDs take effect, they should not be used as monotherapy.- Long-term high-dose steroid use is avoided due to significant risks of **osteoporosis**, infection, and **metabolic disturbances**.*Hydroxychloroquine monotherapy*- This is generally reserved for **mild, seronegative disease** or as part of a combination therapy; it is typically insufficiently potent for **seropositive RA** with severe symptoms.- It has a slower onset of action and lacks the robust evidence for **prevention of erosive joint damage** compared to methotrexate.*Etanercept subcutaneous injection*- **Etanercept**, a TNF-inhibitor (Biologic DMARD), is reserved for patients who have an inadequate response to at least two **conventional DMARDs**, including methotrexate.- Initiating biologics as the very first pharmacological step is not cost-effective and does not follow the standard **step-up management** guidelines.*Oral NSAIDs with proton pump inhibitor*- **NSAIDs** provide only **symptomatic relief** for pain and inflammation and do not alter the course of the disease or prevent joint damage.- They are used as adjuncts for pain management but must never replace **DMARDs** in the treatment of active rheumatoid arthritis.

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