Rheumatology & Haematology — MCQs

A 73-year-old woman with rheumatoid arthritis is admitted with suspected septic arthritis of the right knee. She takes methotrexate 20mg weekly, folic acid 5mg weekly, and etanercept 50mg subcutaneously weekly. Blood cultures are taken and empirical antibiotics started. What is the most appropriate management of her immunosuppressive medications?

Q63

A 36-year-old man presents with a 2-week history of progressive dyspnoea and pleuritic chest pain. He is a long-distance lorry driver. He has no significant past medical history. CTPA confirms bilateral pulmonary emboli. His father had a 'clot in the lung' aged 44. Routine blood tests are normal. What is the most important additional investigation to guide long-term management?

Q64

A 61-year-old man presents with severe pain and swelling of his right knee. Joint aspiration reveals weakly positively birefringent rhomboid-shaped crystals. Serum calcium is 2.85 mmol/L (normal 2.20-2.60), phosphate 0.95 mmol/L (normal 0.80-1.40), and PTH 8.2 pmol/L (normal 1.6-6.9). What is the most likely underlying diagnosis?

Q65

A 47-year-old woman with established seropositive rheumatoid arthritis has progressive disease despite methotrexate 25mg weekly and sulfasalazine 2g daily. She has no history of tuberculosis or recurrent infections. Chest X-ray is normal. What is the most appropriate next step in management?

Q66

A 54-year-old man is diagnosed with an unprovoked deep vein thrombosis of the left leg. He has no past medical history and takes no regular medications. He has never smoked and drinks alcohol occasionally. Thrombophilia screening reveals heterozygous Factor V Leiden mutation. He completes 3 months of anticoagulation with apixaban. What is the most appropriate long-term management?

Q67

A 28-year-old woman presents with fatigue and frequent infections. Blood tests show: Hb 82 g/L, MCV 102 fL, WCC 3.1 × 10⁹/L, neutrophils 1.2 × 10⁹/L, platelets 95 × 10⁹/L, reticulocytes 35 × 10⁹/L (normal 50-100). Blood film shows hypersegmented neutrophils. She follows a strict vegan diet and takes no supplements. What is the most appropriate initial investigation?

Q68

A 42-year-old woman with newly diagnosed rheumatoid arthritis is being considered for methotrexate therapy. She has a history of obesity (BMI 34 kg/m²), non-alcoholic fatty liver disease with ALT 78 U/L (normal <40), and type 2 diabetes. She drinks no alcohol. What is the most appropriate action regarding methotrexate initiation?

Q69

A 68-year-old woman with chronic kidney disease stage 3b (eGFR 38 mL/min/1.73m²) presents with fatigue. Blood tests show: Hb 97 g/L, MCV 86 fL, WCC 6.2 × 10⁹/L, platelets 245 × 10⁹/L, ferritin 185 μg/L, transferrin saturation 18%, serum iron 8 μmol/L, CRP 4 mg/L. She has no history of bleeding. What is the most likely diagnosis?

Q70

A 35-year-old man presents with acute onset pain and swelling of his left wrist. He had a similar episode affecting his right ankle 3 months ago which resolved spontaneously. He has hypertension treated with bendroflumethiazide. Examination reveals an effusion of the left wrist with erythema. Joint aspiration shows negatively birefringent needle-shaped crystals. Serum urate is 0.52 mmol/L (normal <0.42). What is the most appropriate long-term management?

Rheumatology & Haematology UK Medical PG Practice Questions and MCQs

Question 61: What is the primary mechanism by which hepcidin regulates iron homeostasis in the body?

A. Direct inhibition of transferrin synthesis in the liver
B. Degradation of ferroportin, preventing iron export from cells (Correct Answer)
C. Enhanced absorption of dietary iron in the duodenum
D. Increased erythropoietin production by the kidneys
E. Promotion of iron release from ferritin stores

Explanation: ***Degradation of ferroportin, preventing iron export from cells***- **Hepcidin** acts as the master regulator of iron by binding to **ferroportin**, the primary iron exporter on the surface of enterocytes, macrophages, and hepatocytes.- This binding triggers the **internalization and lysosomal degradation** of ferroportin, sequestering iron within cells and lowering plasma iron levels.*Direct inhibition of transferrin synthesis in the liver*- Hepcidin is produced by the **liver**, but it does not directly control the synthesis of **transferrin**, which is the primary carrier protein for iron in the blood.- Transferrin levels are typically regulated by **body iron stores** and liver function rather than hepcidin-mediated degradation.*Enhanced absorption of dietary iron in the duodenum*- High levels of hepcidin actually **inhibit** iron absorption by degrading ferroportin on the basolateral membrane of **duodenal enterocytes**.- Suppression of hepcidin is what allows for enhanced absorption when iron stores are low or **erythropoietic demand** is high.*Increased erythropoietin production by the kidneys*- **Erythropoietin (EPO)** production is stimulated by **hypoxia** and is not a direct downstream effect of hepcidin activity.- In fact, high hepcidin levels can contribute to **anemia of chronic disease** by making iron unavailable for erythropoiesis, despite normal EPO levels.*Promotion of iron release from ferritin stores*- Hepcidin **prevents** the release of iron from **ferritin** stores by blocking the exporter (ferroportin) needed to move iron out of macrophages and hepatocytes.- This results in increased **intracellular ferritin** levels and low serum iron, a hallmark of inflammatory states.

Question 62: A 73-year-old woman with rheumatoid arthritis is admitted with suspected septic arthritis of the right knee. She takes methotrexate 20mg weekly, folic acid 5mg weekly, and etanercept 50mg subcutaneously weekly. Blood cultures are taken and empirical antibiotics started. What is the most appropriate management of her immunosuppressive medications?

A. Stop methotrexate and etanercept immediately; restart once infection resolved (Correct Answer)
B. Continue methotrexate but stop etanercept; restart biologic when infection controlled
C. Continue both medications to prevent arthritis flare during acute illness
D. Stop etanercept but continue methotrexate at reduced dose of 10mg weekly
E. Stop both medications and start prednisolone 20mg daily to control inflammation

Explanation: ***Stop methotrexate and etanercept immediately; restart once infection resolved*** - In the presence of a **serious infection** like **septic arthritis**, all immunosuppressive agents, including **methotrexate** (a conventional DMARD) and **biologic DMARDs (e.g., etanercept)**, must be immediately withheld. - This action allows the patient's immune system to effectively combat the pathogen, preventing the infection from worsening or leading to **sepsis** and permanent joint damage; medications are restarted only after full resolution. *Continue methotrexate but stop etanercept; restart biologic when infection controlled* - While **etanercept** (a biologic anti-TNF agent) carries a high risk for serious infections and should be stopped, **methotrexate** is also a significant immunosuppressant. - Continuing **methotrexate** during active **septic arthritis** can impair cellular immunity and delay the body's ability to clear the infection, potentially leading to prolonged or more severe disease. *Continue both medications to prevent arthritis flare during acute illness* - Prioritizing the prevention of a **rheumatoid arthritis flare** over managing a **life-threatening infection** like septic arthritis is clinically inappropriate. - Continuing potent **immunosuppressive medications** during active infection significantly increases the risk of **sepsis**, organ damage, and mortality. *Stop etanercept but continue methotrexate at reduced dose of 10mg weekly* - There is no clinical guideline supporting a **reduced dose** of methotrexate as a safe alternative to complete cessation during a severe acute infection. - Even at a lower dose, **methotrexate** can still compromise immune function, potentially hindering the body's ability to effectively fight the bacterial infection. *Stop both medications and start prednisolone 20mg daily to control inflammation* - Introducing high-dose **prednisolone** (a corticosteroid) during active **septic arthritis** is contraindicated as it further suppresses the immune system. - **Corticosteroids** can mask signs of infection, impair **leukocyte function**, and worsen the patient's ability to clear the bacterial pathogen, increasing the risk of complications.

Question 63: A 36-year-old man presents with a 2-week history of progressive dyspnoea and pleuritic chest pain. He is a long-distance lorry driver. He has no significant past medical history. CTPA confirms bilateral pulmonary emboli. His father had a 'clot in the lung' aged 44. Routine blood tests are normal. What is the most important additional investigation to guide long-term management?

A. Thrombophilia screen including protein C, protein S, antithrombin, and Factor V Leiden
B. Lupus anticoagulant, anticardiolipin antibodies, and anti-β2-glycoprotein-I antibodies (Correct Answer)
C. D-dimer levels to assess thrombotic burden
D. CT abdomen and pelvis to exclude underlying malignancy
E. Echocardiogram to assess right ventricular function

Explanation: ***Lupus anticoagulant, anticardiolipin antibodies, and anti-β2-glycoprotein-I antibodies*** - Testing for **Antiphospholipid Syndrome (APS)** is crucial because a diagnosis mandates **lifelong anticoagulation** to prevent recurrent events, regardless of initial provoking factors. - These tests (lupus anticoagulant, anticardiolipin, and anti-β2-glycoprotein-I antibodies) are part of the diagnostic criteria for APS and require repeat testing after 12 weeks for confirmation. *Thrombophilia screen including protein C, protein S, antithrombin, and Factor V Leiden* - While the family history is suggestive of an underlying clotting disorder, results for most **hereditary thrombophilias** rarely change the duration of anticoagulation for a first provoked VTE event. - Testing for **protein C, protein S, and antithrombin** is often inaccurate during the **acute phase** of thrombosis or while on anticoagulation, requiring deferral. *D-dimer levels to assess thrombotic burden* - **D-dimer** is primarily a screening tool with a high negative predictive value to *exclude* VTE, not to quantify the size or extent of a confirmed clot. - It has no role in guiding the **duration of long-term anticoagulation** once the diagnosis of pulmonary emboli is established. *CT abdomen and pelvis to exclude underlying malignancy* - Extensive screening for **occult malignancy** is generally reserved for patients with truly **unprovoked VTE** or those with other suggestive symptoms (e.g., weight loss, unexplained anemia). - This patient has a clear **provocative risk factor** (prolonged sitting as a lorry driver) and a family history suggesting a primary thrombophilia, making malignancy screening less of an immediate priority for long-term management guidance. *Echocardiogram to assess right ventricular function* - An **echocardiogram** is valuable for **acute risk stratification** in pulmonary embolism, assessing for right ventricular strain and guiding immediate management. - While it provides prognostic information, it does not determine the **required length or type of long-term anticoagulant therapy** for secondary prevention.

Question 64: A 61-year-old man presents with severe pain and swelling of his right knee. Joint aspiration reveals weakly positively birefringent rhomboid-shaped crystals. Serum calcium is 2.85 mmol/L (normal 2.20-2.60), phosphate 0.95 mmol/L (normal 0.80-1.40), and PTH 8.2 pmol/L (normal 1.6-6.9). What is the most likely underlying diagnosis?

A. Primary hyperparathyroidism (Correct Answer)
B. Hypervitaminosis D
C. Parathyroid carcinoma
D. Multiple myeloma
E. Tertiary hyperparathyroidism

Explanation: ***Primary hyperparathyroidism***- The patient's presentation of **pseudogout**, identified by **weakly positively birefringent rhomboid-shaped crystals** in the joint fluid, is frequently associated with metabolic disturbances, particularly conditions causing **hypercalcemia**.- The biochemical findings of **elevated serum calcium** (2.85 mmol/L) alongside an **elevated parathyroid hormone (PTH)** level (8.2 pmol/L) are the classic diagnostic markers for **primary hyperparathyroidism**.*Hypervitaminosis D*- While **hypervitaminosis D** causes **hypercalcemia**, it leads to feedback **suppression of PTH**, which contradicts the high PTH level observed in this patient.- This condition typically results from excessive vitamin D intake and would likely show significantly elevated **25-hydroxyvitamin D** levels.*Parathyroid carcinoma*- **Parathyroid carcinoma** is a rare malignancy that usually presents with much more **severe hypercalcemia** (often >3.5 mmol/L) and significantly higher PTH levels than seen here.- Clinical presentation may also include a **palpable neck mass** and more pronounced systemic symptoms of hypercalcemia.*Multiple myeloma*- **Multiple myeloma** causes **hypercalcemia** primarily through osteolytic bone destruction, which results in the **suppression of PTH**.- Diagnosis typically involves detecting a **monoclonal protein** (M-spike) and other features like anemia, renal impairment, or lytic bone lesions, none of which are characteristic of pseudogout crystals.*Tertiary hyperparathyroidism*- **Tertiary hyperparathyroidism** occurs after long-standing **chronic kidney disease (CKD)**, leading to autonomous PTH secretion and often hypercalcemia.- In this patient, the **phosphate level is normal**, and there is no clinical or biochemical evidence to suggest underlying advanced renal failure.

Question 65: A 47-year-old woman with established seropositive rheumatoid arthritis has progressive disease despite methotrexate 25mg weekly and sulfasalazine 2g daily. She has no history of tuberculosis or recurrent infections. Chest X-ray is normal. What is the most appropriate next step in management?

A. Add prednisolone 10mg daily for long-term disease control
B. Switch to hydroxychloroquine and leflunomide combination
C. Add a biologic DMARD such as a TNF inhibitor (Correct Answer)
D. Increase methotrexate to 30mg weekly with folic acid adjustment
E. Add low-dose oral methotrexate and increase to subcutaneous route

Explanation: ***Add a biologic DMARD such as a TNF inhibitor*** - Patients with **seropositive rheumatoid arthritis** who have failed to respond adequately to two **conventional synthetic DMARDs** (like methotrexate and sulfasalazine) with ongoing progressive disease should be escalated to a **biologic DMARD** or a targeted synthetic DMARD. - Given her optimal methotrexate dose (25mg weekly) and no contraindications (no history of **tuberculosis** or recurrent infections, normal **chest X-ray**), a **TNF inhibitor** is the most appropriate next step in management. *Add prednisolone 10mg daily for long-term disease control* - **Corticosteroids** like prednisolone are used for **short-term management** of flares or as **bridging therapy**, not for long-term disease control in progressive rheumatoid arthritis. - Long-term steroid use at this dose is associated with significant **adverse effects** such as osteoporosis, cataracts, and metabolic disturbances, and does not modify the underlying disease process to prevent joint damage. *Switch to hydroxychloroquine and leflunomide combination* - The patient has already failed a robust combination of two conventional DMARDs (**methotrexate and sulfasalazine**) for progressive disease. - Switching to another **conventional DMARD combination** is unlikely to be effective for severe, progressive disease and would delay the use of more potent biologic therapies. *Increase methotrexate to 30mg weekly with folic acid adjustment* - For **oral methotrexate**, doses above **20-25mg weekly** typically do not significantly increase efficacy due to **saturated absorption** in the gastrointestinal tract. - Increasing the oral dose beyond this level primarily increases the risk of **gastrointestinal side effects** and **hepatotoxicity** without providing substantial additional clinical benefit. *Add low-dose oral methotrexate and increase to subcutaneous route* - The patient is already on a high dose of **oral methotrexate** (25mg weekly), making the suggestion to "add low-dose oral methotrexate" illogical. - While switching to **subcutaneous methotrexate** can improve bioavailability, it is usually considered when oral absorption is suboptimal or to reduce gastrointestinal side effects, but it is insufficient as the sole escalation strategy for a patient who has failed combination csDMARDs with progressive disease.

Question 66: A 54-year-old man is diagnosed with an unprovoked deep vein thrombosis of the left leg. He has no past medical history and takes no regular medications. He has never smoked and drinks alcohol occasionally. Thrombophilia screening reveals heterozygous Factor V Leiden mutation. He completes 3 months of anticoagulation with apixaban. What is the most appropriate long-term management?

A. Continue anticoagulation indefinitely as he has unprovoked VTE with thrombophilia
B. Stop anticoagulation and restart only if further thrombotic events occur (Correct Answer)
C. Continue anticoagulation for a further 3 months then reassess bleeding risk
D. Reduce apixaban to prophylactic dose (2.5mg twice daily) for extended therapy
E. Switch to aspirin 75mg daily for long-term secondary prevention

Explanation: ***Stop anticoagulation and restart only if further thrombotic events occur***- **Heterozygous Factor V Leiden** is a common, low-risk thrombophilia that alone does not mandate lifelong anticoagulation after a single **unprovoked VTE**.- Standard guidelines recommend **3-6 months** of anticoagulation for a first unprovoked VTE; the presence of this specific mutation does not significantly change the risk-benefit ratio for indefinite therapy.*Continue anticoagulation indefinitely as he has unprovoked VTE with thrombophilia*- Indefinite therapy is usually reserved for **high-risk thrombophilias**, such as **Antiphospholipid Syndrome**, Antithrombin III deficiency, or **homozygous** Factor V Leiden.- For a heterozygous mutation, the **bleeding risk** of long-term anticoagulation often outweighs the benefit of preventing a recurrent event.*Continue anticoagulation for a further 3 months then reassess bleeding risk*- A **3-month course** is already the established standard for a first event; extending it to 6 months without a high-risk profile provides no proven additional long-term benefit.- Reassessing at 6 months is unnecessary since the patient has already completed the primary treatment phase for an **unprovoked event** with a low-risk mutation.*Reduce apixaban to prophylactic dose (2.5mg twice daily) for extended therapy*- While **dose reduction** is a strategy for extended VTE prophylaxis, it is typically indicated for patients deemed to require **lifelong anticoagulation** who have a high risk of bleeding.- This patient does not meet the criteria for **extended secondary prevention** based on a single VTE and a heterozygous Factor V Leiden status.*Switch to aspirin 75mg daily for long-term secondary prevention*- **Aspirin** is significantly less effective than anticoagulants for preventing recurrent VTE and is not first-line therapy for **secondary prevention**.- There is no clinical indication to transition to antiplatelet therapy after completing the treatment for **venous thromboembolism** in this scenario.

Question 67: A 28-year-old woman presents with fatigue and frequent infections. Blood tests show: Hb 82 g/L, MCV 102 fL, WCC 3.1 × 10⁹/L, neutrophils 1.2 × 10⁹/L, platelets 95 × 10⁹/L, reticulocytes 35 × 10⁹/L (normal 50-100). Blood film shows hypersegmented neutrophils. She follows a strict vegan diet and takes no supplements. What is the most appropriate initial investigation?

A. Serum vitamin B12 and red cell folate levels (Correct Answer)
B. Bone marrow aspiration and trephine
C. Anti-intrinsic factor antibodies and anti-parietal cell antibodies
D. Serum methylmalonic acid and homocysteine levels
E. HIV serology and viral screen

Explanation: ***Serum vitamin B12 and red cell folate levels*** - The patient presents with **macrocytic anemia** (MCV 102 fL), **pancytopenia** (low WCC, neutrophils, platelets), and **hypersegmented neutrophils**, which are classic features of **megaloblastic anemia** typically caused by B12 or folate deficiency. - Given her **strict vegan diet** without supplementation, measuring serum levels is the most appropriate first-line step to confirm a nutritional deficiency before more invasive tests or investigating other causes.*Bone marrow aspiration and trephine* - While marrow examination would show diagnostic **megaloblastic maturation**, this is an **invasive procedure** that is not indicated as an initial investigation for suspected nutritional deficiency. - It is generally reserved for cases where initial serology is inconclusive or if a primary **bone marrow disorder** (like MDS) is suspected after ruling out nutritional causes.*Anti-intrinsic factor antibodies and anti-parietal cell antibodies* - These tests are used to diagnose **pernicious anemia**, an autoimmune cause of vitamin B12 malabsorption. - Since the patient has a clear **dietary risk factor** (veganism), confirming the deficiency level precedes testing for specific autoimmune etiologies, making it a second-line investigation.*Serum methylmalonic acid and homocysteine levels* - These are highly sensitive **metabolic markers** used to confirm tissue-level deficiency when direct serum B12 and folate levels are **borderline** or inconclusive. - They are considered **second-line tests** used for diagnostic clarification if initial serum B12 and folate results are ambiguous, not the absolute initial investigation.*HIV serology and viral screen* - Although HIV can cause **pancytopenia**, the pathognomonic finding of **hypersegmented neutrophils** along with macrocytic anemia strongly points toward a megaloblastic process rather than a viral infection. - Nutritional deficiency is far more consistent with the specific hematological findings and the patient's diet than an acute or chronic viral syndrome.

Question 68: A 42-year-old woman with newly diagnosed rheumatoid arthritis is being considered for methotrexate therapy. She has a history of obesity (BMI 34 kg/m²), non-alcoholic fatty liver disease with ALT 78 U/L (normal <40), and type 2 diabetes. She drinks no alcohol. What is the most appropriate action regarding methotrexate initiation?

A. Start methotrexate with more frequent liver function monitoring due to pre-existing liver disease (Correct Answer)
B. Defer methotrexate and use hydroxychloroquine until liver function normalizes
C. Arrange liver biopsy or transient elastography before deciding on methotrexate
D. Contraindicate methotrexate permanently due to liver disease and use alternative DMARD
E. Start methotrexate at reduced dose of 5mg weekly and monitor closely

Explanation: ***Start methotrexate with more frequent liver function monitoring due to pre-existing liver disease***- **Methotrexate** is the first-line DMARD for **Rheumatoid Arthritis**; while it carries a risk of **hepatotoxicity**, it is not contraindicated unless ALT is >3x the upper limit of normal or **cirrhosis** is present.- This patient has risk factors for liver injury (**obesity**, **diabetes**, **NAFLD**), so the most appropriate strategy is initiation with **frequent liver enzyme monitoring** every 2–4 weeks initially.*Defer methotrexate and use hydroxychloroquine until liver function normalizes*- **Hydroxychloroquine** is generally reserved for mild disease or as an adjunct; delaying the gold-standard treatment, **methotrexate**, can lead to irreversible **joint destruction**.- In **NAFLD**, liver enzymes may not normalize without significant weight loss, making this an impractical clinical strategy for controlling active **RA**.*Arrange liver biopsy or transient elastography before deciding on methotrexate*- Routine **liver biopsy** or **FibroScan** is not required before starting methotrexate even in patients with **NAFLD**, provided enzymes are only mildly elevated (ALT 78 U/L is <2x normal).- Advanced imaging or histology is reserved for cases where there is clinical suspicion of **advanced fibrosis** or **cirrhosis**, which is not indicated by an ALT of 78 U/L.*Contraindicate methotrexate permanently due to liver disease and use alternative DMARD*- **NAFLD** is a relative, not an absolute, contraindication; current guidelines permit methotrexate use in these patients if they abstain from **alcohol** and undergo close surveillance.- Permanent avoidance unnecessarily limits therapeutic options for a patient with multiple **metabolic risk factors** who may benefit from aggressive RA control.*Start methotrexate at reduced dose of 5mg weekly and monitor closely*- A starting dose of 5mg is considered **sub-therapeutic** for managing **Rheumatoid Arthritis** effectively; the standard starting dose is typically 10–15mg weekly.- While caution is needed, **dose reduction** is less critical than **frequent monitoring** and supplemental **folic acid** to mitigate toxicity.

Question 69: A 68-year-old woman with chronic kidney disease stage 3b (eGFR 38 mL/min/1.73m²) presents with fatigue. Blood tests show: Hb 97 g/L, MCV 86 fL, WCC 6.2 × 10⁹/L, platelets 245 × 10⁹/L, ferritin 185 μg/L, transferrin saturation 18%, serum iron 8 μmol/L, CRP 4 mg/L. She has no history of bleeding. What is the most likely diagnosis?

A. Functional iron deficiency from chronic kidney disease (Correct Answer)
B. Anaemia of chronic disease
C. Early myelodysplastic syndrome
D. Absolute iron deficiency requiring investigation
E. Combined B12 and folate deficiency

Explanation: ***Functional iron deficiency from chronic kidney disease***- This patient demonstrates **functional iron deficiency (FID)**, where iron stores are present (ferritin >100 μg/L) but cannot be mobilized for erythropoiesis, evidenced by a **transferrin saturation (TSAT) <20%**.- In **CKD**, increased **hepcidin** levels sequester iron in macrophages, limiting its availability for the bone marrow despite adequate total body iron.*Anaemia of chronic disease*- While related, this specifically refers to a **normocytic anaemia** where high inflammatory states fully block iron usage; however, the term **Functional Iron Deficiency** more accurately describes the iron status in CKD management guidelines.- This patient's **low CRP** suggests that a generalized acute inflammatory response is not the primary driver compared to the underlying renal pathology.*Early myelodysplastic syndrome*- **Myelodysplastic syndrome (MDS)** typically presents with **macrocytosis** (high MCV) or other cytopenias like thrombocytopenia or leukopenia.- This patient has a **normocytic MCV (86 fL)** and normal white cell and platelet counts, making a primary bone marrow disorder less likely.*Absolute iron deficiency requiring investigation*- **Absolute iron deficiency** is characterized by a **low ferritin** level (typically <30 μg/L), whereas this patient has a ferritin of 185 μg/L.- The absence of a **bleeding history** and the high ferritin level indicate the issue is iron distribution rather than a total body deficit.*Combined B12 and folate deficiency*- Deficiency in **B12 or folate** typically leads to a **macrocytic anaemia** with an elevated MCV.- A combined deficiency might result in a normocytic picture, but there are no clinical or biochemical markers provided to suggest **megaloblastic** changes.

Question 70: A 35-year-old man presents with acute onset pain and swelling of his left wrist. He had a similar episode affecting his right ankle 3 months ago which resolved spontaneously. He has hypertension treated with bendroflumethiazide. Examination reveals an effusion of the left wrist with erythema. Joint aspiration shows negatively birefringent needle-shaped crystals. Serum urate is 0.52 mmol/L (normal <0.42). What is the most appropriate long-term management?

A. Start allopurinol 100mg daily and increase gradually to achieve target urate <0.30 mmol/L (Correct Answer)
B. Continue current management and only start urate-lowering therapy if he has further attacks
C. Switch bendroflumethiazide to an alternative antihypertensive and monitor serum urate
D. Start febuxostat 80mg daily as first-line urate-lowering therapy
E. Advise lifestyle modifications alone as serum urate is only marginally elevated

Explanation: ***Start allopurinol 100mg daily and increase gradually to achieve target urate <0.30 mmol/L*** - Long-term management with **urate-lowering therapy (ULT)** is indicated due to **recurrent gout attacks** (two episodes) and confirmed diagnosis by **negatively birefringent needle-shaped crystals**. - **Allopurinol** is the first-line ULT; it should be started at a low dose (e.g., **100mg daily**) and titrated upwards to achieve a target serum urate of **<0.30 mmol/L** to dissolve existing crystals and prevent new ones. *Continue current management and only start urate-lowering therapy if he has further attacks* - This approach is inappropriate because the patient has already experienced **recurrent gout attacks** and has confirmed hyperuricemia, which are clear indications for initiating **urate-lowering therapy**. - Delaying ULT increases the risk of further painful flares, **tophi formation**, and progressive **joint damage**. *Switch bendroflumethiazide to an alternative antihypertensive and monitor serum urate* - While **thiazide diuretics** like bendroflumethiazide can exacerbate hyperuricemia, simply switching the antihypertensive is insufficient as the sole long-term management for established and **recurrent gout**. - Although changing to agents like **losartan** or **calcium channel blockers** is beneficial, the patient's significantly elevated urate and history of attacks necessitate active **pharmacological urate lowering** beyond just drug modification. *Start febuxostat 80mg daily as first-line urate-lowering therapy* - **Febuxostat** is typically reserved as a **second-line** urate-lowering therapy for patients who cannot tolerate allopurinol or do not achieve target urate levels with allopurinol. - It is not the initial preferred therapy for most patients due to its higher cost and potential **cardiovascular risk concerns** in certain populations compared to allopurinol. *Advise lifestyle modifications alone as serum urate is only marginally elevated* - A serum urate level of **0.52 mmol/L** is not marginally elevated; it is significantly above the saturation point of urate (0.42 mmol/L) and is associated with crystal formation and gout attacks. - While **lifestyle modifications** are important adjuncts, they typically only reduce serum urate by a modest amount (**10-15%**) and are insufficient as monotherapy for patients with established, recurrent gout and such high urate levels.

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