Rheumatology & Haematology — MCQs
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A 62-year-old man presents with a swollen, painful right first metatarsophalangeal joint. Joint aspiration reveals needle-shaped negatively birefringent crystals under polarised light microscopy. Serum urate is 0.38 mmol/L (normal 0.2-0.45). He has hypertension treated with bendroflumethiazide 2.5mg daily and amlodipine 5mg daily. What is the most appropriate management of his antihypertensive therapy?
A 75-year-old woman is found to have the following blood results during investigation for fatigue: Hb 98 g/L, MCV 105 fL, WCC 4.5 × 10⁹/L, platelets 220 × 10⁹/L. Serum vitamin B12 is 185 ng/L (normal 200-900), serum folate is normal. She has no neurological symptoms. Blood film shows hypersegmented neutrophils. Intrinsic factor antibodies are negative. What is the most appropriate next investigation?
A 48-year-old man with chronic tophaceous gout on allopurinol 300mg daily presents with an acute flare affecting his right knee. He has stage 3 chronic kidney disease (eGFR 45 mL/min/1.73m²) and a history of peptic ulcer disease 5 years ago. He is not currently taking a proton pump inhibitor. What is the most appropriate treatment for this acute flare?
A 55-year-old woman with rheumatoid arthritis treated with methotrexate 20mg weekly presents for routine monitoring. Her blood results show: Hb 115 g/L, WCC 3.2 × 10⁹/L, neutrophils 1.8 × 10⁹/L, platelets 180 × 10⁹/L, ALT 45 U/L (normal <40), AST 42 U/L (normal <40). She feels well with no symptoms. What is the most appropriate next step in management?
A 44-year-old woman with seropositive rheumatoid arthritis on methotrexate 25mg weekly and hydroxychloroquine 200mg twice daily continues to have active disease (DAS28 5.6). Before escalating to biologic therapy, her screening tests reveal: positive tuberculosis IGRA test, normal chest X-ray, HIV negative, hepatitis B surface antigen negative, hepatitis B core antibody positive, hepatitis B surface antibody positive. What is the most appropriate management plan?
A 54-year-old man with unprovoked pulmonary embolism diagnosed 2 years ago completed 6 months of anticoagulation and remained asymptomatic off treatment. He now presents with recurrent pulmonary embolism. Thrombophilia screening shows: protein C 68% (normal 70-140%), protein S 65% (normal 70-140%), antithrombin 92% (normal 80-120%), Factor V Leiden negative, prothrombin gene mutation negative, lupus anticoagulant negative. What is the most appropriate duration of anticoagulation following this recurrence?
A 72-year-old woman is investigated for macrocytic anaemia. Blood tests show: Hb 89 g/L, MCV 112 fL, WCC 3.8 × 10⁹/L, platelets 142 × 10⁹/L, serum B12 102 ng/L (normal 200-900), red cell folate normal, serum folate normal. Blood film shows hypersegmented neutrophils. Intrinsic factor antibodies are positive. What is the most appropriate long-term management?
A 59-year-old man presents with severe pain and swelling of his right first metatarsophalangeal joint. He has a history of hypertension treated with bendroflumethiazide. Synovial fluid aspiration shows needle-shaped negatively birefringent crystals. His serum urate is 0.52 mmol/L (normal 0.2-0.45). What is the most important counselling point regarding long-term urate-lowering therapy?
A 41-year-old woman with antiphospholipid syndrome presents at 32 weeks gestation with left leg swelling and pain. Doppler ultrasound confirms proximal deep vein thrombosis. She has been on prophylactic enoxaparin 40mg daily throughout pregnancy. What is the most appropriate modification to her anticoagulation management?
A 63-year-old man presents with progressive fatigue over 6 months. Blood tests show: Hb 102 g/L, MCV 96 fL, WCC 5.8 × 10⁹/L, platelets 198 × 10⁹/L, reticulocyte count 0.8% (normal 0.5-2.5%), ferritin 180 mcg/L, B12 298 ng/L (normal 200-900), serum folate 6.8 mcg/L (normal 3-20). Blood film shows normochromic normocytic red cells with no abnormal cells. What is the most appropriate next investigation?
Rheumatology & Haematology UK Medical PG Practice Questions and MCQs
Question 81: A 62-year-old man presents with a swollen, painful right first metatarsophalangeal joint. Joint aspiration reveals needle-shaped negatively birefringent crystals under polarised light microscopy. Serum urate is 0.38 mmol/L (normal 0.2-0.45). He has hypertension treated with bendroflumethiazide 2.5mg daily and amlodipine 5mg daily. What is the most appropriate management of his antihypertensive therapy?
- A. Continue current antihypertensive therapy unchanged
- B. Stop bendroflumethiazide and increase amlodipine to 10mg daily (Correct Answer)
- C. Stop amlodipine and increase bendroflumethiazide to 5mg daily
- D. Stop both medications and start ramipril
- E. Add losartan to current therapy
Explanation: ***Stop bendroflumethiazide and increase amlodipine to 10mg daily*** - **Thiazide diuretics** like **bendroflumethiazide** increase serum urate levels by reducing renal excretion; they should be discontinued in patients presenting with **gout**. - Increasing the dose of **amlodipine** is a practical strategy to maintain blood pressure control while removing a known precipitant of the patient's **monosodium urate crystals**. *Continue current antihypertensive therapy unchanged* - Continuing **bendroflumethiazide** maintains a high risk for recurrent **gout flares** due to its inhibitory effect on urate excretion. - A **normal serum urate** during an acute attack is common due to urate deposition in the joint and does not justify continuing a causative medication. *Stop amlodipine and increase bendroflumethiazide to 5mg daily* - Increasing the dose of **bendroflumethiazide** would worsen **hyperuricaemia** and likely exacerbate the patient's joint inflammation. - **Amlodipine** is urate-neutral and does not need to be stopped; removing it while increasing a diuretic is contraindicated in this clinical scenario. *Stop both medications and start ramipril* - Stopping both medications unnecessarily risks a **hypertensive crisis** or poor long-term pressure control when only the thiazide is problematic. - While **ACE inhibitors** like **ramipril** are urate-neutral, there is no clinical indication to discontinue the tolerated **amlodipine**. *Add losartan to current therapy* - Although **losartan** has beneficial **uricosuric properties**, adding it without stopping the **bendroflumethiazide** fails to address the underlying drug-induced cause. - Polypharmacy should be avoided; the priority in **gout management** is the removal of offending agents before adding more antihypertensive medications.
Question 82: A 75-year-old woman is found to have the following blood results during investigation for fatigue: Hb 98 g/L, MCV 105 fL, WCC 4.5 × 10⁹/L, platelets 220 × 10⁹/L. Serum vitamin B12 is 185 ng/L (normal 200-900), serum folate is normal. She has no neurological symptoms. Blood film shows hypersegmented neutrophils. Intrinsic factor antibodies are negative. What is the most appropriate next investigation?
- A. Schilling test
- B. Anti-parietal cell antibodies
- C. Upper gastrointestinal endoscopy
- D. Serum methylmalonic acid and homocysteine levels (Correct Answer)
- E. Bone marrow biopsy
Explanation: ***Serum methylmalonic acid and homocysteine levels*** - These metabolic markers are the most appropriate next step when **vitamin B12 levels** are in the **borderline range** (typically 150–400 pg/mL) to confirm a functional cellular deficiency. - An elevation in **methylmalonic acid (MMA)** is highly specific for Vitamin B12 deficiency, whereas **homocysteine** is elevated in both B12 and folate deficiencies. *Schilling test* - This was historically used to determine the cause of **vitamin B12 malabsorption**, but it is now largely obsolete and rarely available in clinical practice. - It involves the use of **radiolabeled B12** and does not help in the initial confirmation of a borderline deficiency state. *Anti-parietal cell antibodies* - While these have high **sensitivity** (approx. 90%) for **pernicious anemia**, they have very low specificity and are frequently positive in other autoimmune conditions or healthy elderly patients. - Confirming the deficiency itself with **metabolic markers** is prioritized over testing for these low-specificity antibodies, especially when **intrinsic factor antibodies** are negative. *Upper gastrointestinal endoscopy* - This may be indicated later to screen for **gastric adenocarcinoma** or **carcinoid tumors** if **pernicious anemia** is confirmed due to associated **atrophic gastritis**. - It is not a diagnostic tool for confirming the underlying **macrocytic anemia** or vitamin deficiency state itself. *Bone marrow biopsy* - While a biopsy would show **megaloblastic erythropoiesis**, it is an invasive procedure that is unnecessary when peripheral findings like **hypersegmented neutrophils** and **macrocytosis** are present. - Diagnostic confirmation should be achieved through less invasive **biochemical testing** of B12 metabolites before considering marrow examination.
Question 83: A 48-year-old man with chronic tophaceous gout on allopurinol 300mg daily presents with an acute flare affecting his right knee. He has stage 3 chronic kidney disease (eGFR 45 mL/min/1.73m²) and a history of peptic ulcer disease 5 years ago. He is not currently taking a proton pump inhibitor. What is the most appropriate treatment for this acute flare?
- A. Increase allopurinol to 600mg daily
- B. Colchicine 500 micrograms twice daily
- C. Naproxen 500mg twice daily with omeprazole 20mg daily
- D. Intra-articular corticosteroid injection to the affected knee (Correct Answer)
- E. Stop allopurinol and start febuxostat
Explanation: ***Intra-articular corticosteroid injection to the affected knee*** - **Intra-articular steroids** are the treatment of choice for a **monoarticular gout flare** when systemic options like NSAIDs or colchicine are contraindicated due to **Stage 3 CKD** or GI risks. - This approach provides rapid, localized anti-inflammatory relief without increasing the risk of systemic side effects or worsening **renal function**. *Increase allopurinol to 600mg daily* - **Urate-lowering therapy (ULT)** should never be initiated or increased during an **acute flare**, as rapid changes in serum urate can prolong or worsen the attack. - Allopurinol dose adjustments should only be considered during **intercritical periods** once the acute inflammation has fully resolved. *Colchicine 500 micrograms twice daily* - Colchicine requires significant **dose reduction** or avoidance in patients with **chronic kidney disease (CKD)** due to the risk of accumulation and toxicity. - While still an option at very low doses in some CKD patients, it is less ideal than local steroids in this clinical scenario given the **eGFR of 45 mL/min**. *Naproxen 500mg twice daily with omeprazole 20mg daily* - **NSAIDs** are generally avoided in patients with **Stage 3 CKD** as they can cause further reduction in renal perfusion and acute kidney injury. - Additionally, despite the use of a PPI, a history of **peptic ulcer disease** makes NSAID therapy a higher-risk choice compared to local corticosteroids. *Stop allopurinol and start febuxostat* - **Stopping allopurinol** during a flare is unnecessary and may result in further fluctuations of urate levels, potentially extending the duration of the attack. - Switching to **febuxostat** is a strategy for long-term management of hyperuricaemia, not for the immediate treatment of **acute gouty inflammation**.
Question 84: A 55-year-old woman with rheumatoid arthritis treated with methotrexate 20mg weekly presents for routine monitoring. Her blood results show: Hb 115 g/L, WCC 3.2 × 10⁹/L, neutrophils 1.8 × 10⁹/L, platelets 180 × 10⁹/L, ALT 45 U/L (normal <40), AST 42 U/L (normal <40). She feels well with no symptoms. What is the most appropriate next step in management?
- A. Continue methotrexate at current dose and repeat bloods in 2 weeks (Correct Answer)
- B. Stop methotrexate immediately and repeat bloods in 1 week
- C. Reduce methotrexate dose to 15mg weekly and repeat bloods in 2 weeks
- D. Continue methotrexate and add folic acid 5mg three times weekly
- E. Stop methotrexate and start sulfasalazine
Explanation: ***Continue methotrexate at current dose and repeat bloods in 2 weeks***- According to **British Society for Rheumatology (BSR)** guidelines, methotrexate should only be withheld if **neutrophils** are <1.5 × 10⁹/L or **transaminases** (ALT/AST) are >3x the upper limit of normal.- Since the patient’s neutrophils (1.8 × 10⁹/L) and liver enzymes are only **mildly elevated** (less than 2x normal), it is safe to continue treatment with closer **monitoring**.*Stop methotrexate immediately and repeat bloods in 1 week*- Stopping the medication is premature because the lab abnormalities do not meet the mandatory **toxicity thresholds** for cessation.- Abruptly stopping therapy without clinical indications like **severe leukopenia** or jaundice may lead to a flare of the patient's **rheumatoid arthritis**.*Reduce methotrexate dose to 15mg weekly and repeat bloods in 2 weeks*- Dose reduction is typically considered if there is a **persistent minor derangement** in blood results or if the patient is experiencing side effects.- For a first instance of borderline lab values in an asymptomatic patient, the standard approach is to repeat labs to confirm a trend before adjusting the **therapeutic dose**.*Continue methotrexate and add folic acid 5mg three times weekly*- **Folic acid** is already a standard co-prescription to reduce GI and mucosal side effects, but increasing its frequency does not replace the need for **repeat blood monitoring**.- While folic acid helps mitigate **methotrexate toxicity**, the immediate clinical priority is ensuring the **neutrophil count** remains stable.*Stop methotrexate and start sulfasalazine*- Switching to a different **DMARD** (Disease-Modifying Anti-Rheumatic Drug) like **sulfasalazine** is an escalation of management not warranted by these mild lab results.- Methotrexate is the **gold-standard** treatment, and switching is only indicated if the patient is intolerant or fails to respond after optimization.
Question 85: A 44-year-old woman with seropositive rheumatoid arthritis on methotrexate 25mg weekly and hydroxychloroquine 200mg twice daily continues to have active disease (DAS28 5.6). Before escalating to biologic therapy, her screening tests reveal: positive tuberculosis IGRA test, normal chest X-ray, HIV negative, hepatitis B surface antigen negative, hepatitis B core antibody positive, hepatitis B surface antibody positive. What is the most appropriate management plan?
- A. Proceed with TNF inhibitor therapy as hepatitis B surface antibody is positive indicating immunity
- B. Start antiviral prophylaxis with tenofovir before commencing biologic therapy
- C. Check hepatitis B viral load and commence biologic only if undetectable (Correct Answer)
- D. Commence TB prophylaxis, then start biologic therapy without hepatitis B intervention as core antibody indicates past cleared infection
- E. Defer biologic therapy due to dual infection risk
Explanation: ***Check hepatitis B viral load and commence biologic only if undetectable*** - The patient has **resolved Hepatitis B** (HBsAg negative, anti-HBc positive, anti-HBs positive), but **HBV DNA** must be checked to rule out **occult infection** before starting biologics. - Monitoring **viral load** and transaminases is essential because immunosuppressive therapy, particularly **TNF inhibitors**, can trigger **HBV reactivation** in a core-antibody positive patient. *Proceed with TNF inhibitor therapy as hepatitis B surface antibody is positive indicating immunity* - While **anti-HBs** indicates immunity, the presence of **anti-HBc** means the virus persists in the liver as **covalently closed circular DNA (cccDNA)**. - Immunosuppression can lead to loss of immune control and **viral replication**, making simple observation without baseline viral load assessment risky. *Start antiviral prophylaxis with tenofovir before commencing biologic therapy* - **Routine prophylaxis** with **tenofovir** is generally mandatory for high-risk B-cell depleting agents like **Rituximab** in core-antibody positive patients. - For TNF inhibitors in patients with **resolved HBV**, a "monitor and preemptive treatment" strategy is often preferred over immediate **antiviral prophylaxis** unless HBV DNA is detectable. *Commence TB prophylaxis, then start biologic therapy without hepatitis B intervention as core antibody indicates past cleared infection* - While **TB prophylaxis** is necessary for the **latent TB** (positive IGRA), ignoring the HBV status is dangerous as "cleared" infection can still reactivate. - Guidelines mandate assessing the **HBV viral load** and performing periodic **liver function tests** to ensure safety during biologic therapy. *Defer biologic therapy due to dual infection risk* - **Active RA** (DAS28 5.6) warrants escalation of therapy, and both **latent TB** and **resolved HBV** can be managed concurrently with treatment. - Biologics are not contraindicated; they simply require **prophylactic TB treatment** and **HBV monitoring** or prophylaxis to prevent complications.
Question 86: A 54-year-old man with unprovoked pulmonary embolism diagnosed 2 years ago completed 6 months of anticoagulation and remained asymptomatic off treatment. He now presents with recurrent pulmonary embolism. Thrombophilia screening shows: protein C 68% (normal 70-140%), protein S 65% (normal 70-140%), antithrombin 92% (normal 80-120%), Factor V Leiden negative, prothrombin gene mutation negative, lupus anticoagulant negative. What is the most appropriate duration of anticoagulation following this recurrence?
- A. 3 months, as this represents a provoked VTE (previous PE is the provoking factor)
- B. 6 months, consistent with standard VTE treatment duration
- C. 12 months, with reassessment of risk-benefit ratio before discontinuation
- D. Lifelong anticoagulation (Correct Answer)
- E. 3 months, followed by aspirin indefinitely
Explanation: ***Lifelong anticoagulation***- Patients with **recurrent unprovoked VTE** (venous thromboembolism) have a very high risk of further recurrence, estimated at approximately **15% per year** without treatment.- Current guidelines from **NICE** and **ESC** recommend **extended (indefinite) anticoagulation** for a second unprovoked event, provided the bleeding risk is not prohibitively high.*3 months, as this represents a provoked VTE (previous PE is the provoking factor)*- A previous VTE is not considered a "provoking factor" (like surgery or trauma); instead, it marks the patient as having a **high baseline risk** for future events.- Short-term treatment (3 months) is only appropriate for VTE provoked by a **major transient risk factor**, which is absent in this history.*6 months, consistent with standard VTE treatment duration*- While 6 months was once a common standard, it is now considered insufficient for **recurrent unprovoked** cases due to the high likelihood of relapse upon discontinuation.- The priority in this patient is **secondary prevention**, which necessitates a longer duration than the initial treatment of a first-time event.*12 months, with reassessment of risk-benefit ratio before discontinuation*- Fixed-term durations like 12 months are not recommended for **recurrent idiopathic** events because the underlying thrombotic tendency remains constant.- Although **annual reassessment** of bleeding risk is required, the default plan should be **permanent therapy** rather than planned discontinuation at one year.*3 months, followed by aspirin indefinitely*- **Aspirin** is significantly less effective than anticoagulants for preventing VTE recurrence and is not the standard of care for high-risk patients.- Anticoagulation (ideally with a **DOAC**) is preferred over aspirin as it offers superior protection against life-threatening **recurrent pulmonary embolism**.
Question 87: A 72-year-old woman is investigated for macrocytic anaemia. Blood tests show: Hb 89 g/L, MCV 112 fL, WCC 3.8 × 10⁹/L, platelets 142 × 10⁹/L, serum B12 102 ng/L (normal 200-900), red cell folate normal, serum folate normal. Blood film shows hypersegmented neutrophils. Intrinsic factor antibodies are positive. What is the most appropriate long-term management?
- A. Oral cyanocobalamin 50 micrograms daily
- B. Intramuscular hydroxocobalamin 1mg three times weekly for 2 weeks, then 1mg every 3 months
- C. Intramuscular hydroxocobalamin 1mg on alternate days until no further improvement, then 1mg every 2 months (Correct Answer)
- D. Oral B12 1000 micrograms daily indefinitely
- E. Blood transfusion followed by oral B12 supplementation
Explanation: ***Intramuscular hydroxocobalamin 1mg on alternate days until no further improvement, then 1mg every 2 months*** - This patient has **pernicious anaemia** confirmed by macrocytic anaemia, low B12, and positive **intrinsic factor antibodies**, requiring parenteral therapy due to malabsorption. - The initial regimen rapidly replets B12 stores, and **1mg every 2 months** is a standard maintenance dose for pernicious anaemia, especially if severe or with neurological considerations. *Oral cyanocobalamin 50 micrograms daily* - This dose is too low to overcome the severe malabsorption due to the absence of **intrinsic factor** in pernicious anaemia. - **Oral supplementation** at this low dose is ineffective for initial or long-term management of B12 deficiency caused by malabsorption. *Intramuscular hydroxocobalamin 1mg three times weekly for 2 weeks, then 1mg every 3 months* - While the initial regimen is standard for B12 deficiency, the **1mg every 3 months** maintenance is typically for deficiency **without neurological features**. - For **pernicious anaemia**, especially with potential for severe symptoms, a more frequent maintenance (like every 2 months) is often preferred to ensure optimal B12 levels. *Oral B12 1000 micrograms daily indefinitely* - High-dose oral B12 can be absorbed via **passive diffusion**, but it is generally not the first-line or gold standard for confirmed autoimmune **pernicious anaemia**. - **Intramuscular injections** are preferred for pernicious anaemia to guarantee consistent therapeutic B12 levels and prevent long-term complications. *Blood transfusion followed by oral B12 supplementation* - **Blood transfusion** is usually reserved for **haemodynamic instability** or very severe anaemia (Hb < 70-80 g/L) and is not typically indicated for stable chronic anaemia at Hb 89 g/L. - **Oral B12 supplementation** is ineffective for long-term management of pernicious anaemia due to the persistent malabsorption caused by the lack of **intrinsic factor**.
Question 88: A 59-year-old man presents with severe pain and swelling of his right first metatarsophalangeal joint. He has a history of hypertension treated with bendroflumethiazide. Synovial fluid aspiration shows needle-shaped negatively birefringent crystals. His serum urate is 0.52 mmol/L (normal 0.2-0.45). What is the most important counselling point regarding long-term urate-lowering therapy?
- A. Allopurinol should be started immediately at 300mg daily to prevent further attacks
- B. Urate-lowering therapy is indicated because serum urate exceeds 0.45 mmol/L
- C. Bendroflumethiazide should be stopped before considering urate-lowering therapy
- D. Urate-lowering therapy should be started after acute attack resolves, with colchicine or NSAID prophylaxis for at least 1 month (Correct Answer)
- E. Dietary modification alone is sufficient as serum urate is only marginally elevated
Explanation: ***Urate-lowering therapy should be started after acute attack resolves, with colchicine or NSAID prophylaxis for at least 1 month*** - Urate-lowering therapy (ULT) should typically be delayed until **2–4 weeks** after an acute gout attack has resolved to avoid exacerbating or prolonging the flare. - Co-prescribing **prophylactic colchicine** or a **low-dose NSAID** is essential for at least 3-6 months when starting ULT to prevent precipitation of further acute attacks due to rapid changes in serum urate levels. *Allopurinol should be started immediately at 300mg daily to prevent further attacks* - Starting allopurinol during an **acute gout attack** can worsen the inflammation and is generally contraindicated. - Allopurinol should be initiated at a **low dose** (e.g., 50-100mg daily), particularly in patients with renal impairment, and slowly titrated upwards to prevent hypersensitivity reactions and acute flares. *Urate-lowering therapy is indicated because serum urate exceeds 0.45 mmol/L* - While the patient's serum urate is elevated, the primary indication for ULT in this case is the **clinical diagnosis of gout** confirmed by synovial fluid crystals, not just a single high urate level. - Serum urate levels can paradoxically be **normal or even low** during an acute gout attack, making crystal analysis the definitive diagnostic test and guide for therapy. *Bendroflumethiazide should be stopped before considering urate-lowering therapy* - Thiazide diuretics, such as bendroflumethiazide, are known to **increase serum urate levels** and should ideally be switched to an alternative, like losartan or a calcium channel blocker. - However, stopping an essential antihypertensive is not a prerequisite for initiating ULT; ULT can be started while a thiazide is still being used, especially if the drug cannot be safely or easily switched. *Dietary modification alone is sufficient as serum urate is only marginally elevated* - Although beneficial, **dietary modifications** (e.g., reducing alcohol, purine-rich foods, sugary drinks) are rarely sufficient to achieve target urate levels (typically **<0.36 mmol/L**) to prevent recurrent attacks in patients with established gout. - This patient has a confirmed diagnosis of gout with crystalline evidence and a significantly elevated urate level, indicating the need for **pharmacological urate-lowering therapy**.
Question 89: A 41-year-old woman with antiphospholipid syndrome presents at 32 weeks gestation with left leg swelling and pain. Doppler ultrasound confirms proximal deep vein thrombosis. She has been on prophylactic enoxaparin 40mg daily throughout pregnancy. What is the most appropriate modification to her anticoagulation management?
- A. Increase enoxaparin to treatment dose (1mg/kg twice daily) and continue until 6 weeks postpartum (Correct Answer)
- B. Switch to warfarin with target INR 2-3
- C. Continue prophylactic dose enoxaparin and add low-dose aspirin
- D. Switch to fondaparinux
- E. Increase enoxaparin to treatment dose and plan for epidural anaesthesia
Explanation: ***Increase enoxaparin to treatment dose (1mg/kg twice daily) and continue until 6 weeks postpartum*** - The confirmation of an **acute proximal deep vein thrombosis (DVT)** in a pregnant woman, especially with antiphospholipid syndrome and breakthrough despite prophylactic enoxaparin, mandates an immediate escalation to **therapeutic anticoagulation** with Low Molecular Weight Heparin (LMWH), typically **enoxaparin 1mg/kg twice daily**. - Anticoagulation for acute VTE in pregnancy must be maintained throughout the remainder of the pregnancy and continued for at least **6 weeks postpartum**, or for a minimum total duration of **3 months**, whichever is longer. *Switch to warfarin with target INR 2-3* - **Warfarin** is generally **contraindicated in pregnancy** as it readily **crosses the placenta**, leading to a risk of **fetal warfarin syndrome** (teratogenicity) during the first trimester and increased risk of **fetal hemorrhage** in later pregnancy. - **LMWH** is the preferred anticoagulant in pregnancy due to its non-placental transfer and superior safety profile for the fetus. *Continue prophylactic dose enoxaparin and add low-dose aspirin* - Continuing a **prophylactic dose** of enoxaparin is inadequate for managing an **established acute DVT**, especially when the clot occurred despite prophylaxis, indicating treatment failure. - While **low-dose aspirin** is often used in antiphospholipid syndrome for obstetric indications, it does not provide sufficient anticoagulation to treat an **acute proximal DVT**. *Switch to fondaparinux* - **Fondaparinux** is an indirect factor Xa inhibitor that may be used in VTE treatment, but it is typically reserved for patients with a documented **heparin allergy** or **heparin-induced thrombocytopenia (HIT)** due to more limited data regarding its safety and efficacy in pregnancy compared to LMWH. - **LMWH** remains the **gold standard** for treating VTE during pregnancy due to its extensive evidence base and favorable safety profile. *Increase enoxaparin to treatment dose and plan for epidural anaesthesia* - Increasing enoxaparin to a **treatment dose** is the correct immediate management for the DVT. However, planning for **epidural anaesthesia** concurrently with therapeutic anticoagulation is problematic. - Patients receiving **therapeutic doses of LMWH** require a mandatory waiting period (typically at least **24 hours**) after the last dose before neuraxial anesthesia can be safely performed to minimize the risk of **spinal hematoma**.
Question 90: A 63-year-old man presents with progressive fatigue over 6 months. Blood tests show: Hb 102 g/L, MCV 96 fL, WCC 5.8 × 10⁹/L, platelets 198 × 10⁹/L, reticulocyte count 0.8% (normal 0.5-2.5%), ferritin 180 mcg/L, B12 298 ng/L (normal 200-900), serum folate 6.8 mcg/L (normal 3-20). Blood film shows normochromic normocytic red cells with no abnormal cells. What is the most appropriate next investigation?
- A. Bone marrow aspirate and trephine biopsy
- B. Haemolysis screen including LDH, haptoglobin, and direct antiglobulin test
- C. Comprehensive metabolic panel including renal function, liver function, and thyroid function (Correct Answer)
- D. Serum erythropoietin level
- E. Repeat full blood count in 2 weeks
Explanation: ***Comprehensive metabolic panel including renal function, liver function, and thyroid function***- This patient presents with a **normocytic normochromic anaemia** with a relatively low **reticulocyte count** (0.8% for Hb 102 g/L), which points towards a hypoproliferative cause rather than hemolysis or acute blood loss.- A comprehensive metabolic screen is the most appropriate next step to rule out common systemic causes such as **chronic kidney disease (CKD)**, **hypothyroidism**, or **liver disease**, which frequently present with this hematological profile.*Bone marrow aspirate and trephine biopsy*- This is an **invasive procedure** that should be reserved for cases where common systemic causes have been excluded or if there is stronger evidence of primary marrow failure or malignancy.- The absence of other **cytopenias** (normal WCC and platelets) and no abnormal cells on the blood film make marrow pathology less likely as the primary initial concern.*Haemolysis screen including LDH, haptoglobin, and direct antiglobulin test*- The **reticulocyte count of 0.8%** is within the normal range and not appropriately elevated for the degree of anaemia, which effectively rules out a vigorous compensatory response seen in **haemolytic anaemia**.- If hemolysis were occurring, one would expect a significantly elevated **reticulocyte count** and potentially abnormal red cell morphology on the blood film.*Serum erythropoietin level*- While **erythropoietin deficiency** (common in CKD) can cause normocytic anaemia, measuring the level is not a standard initial test.- Assessing **renal function (U&Es)** via a metabolic panel is a more practical first step to identify the underlying cause of potentially low erythropoietin production.*Repeat full blood count in 2 weeks*- Waiting for a repeat test is inappropriate in a patient with **progressive fatigue** over 6 months and established **anaemia** (Hb 102 g/L).- Clinical guidelines mandate that an explanation for anaemia in an older patient be sought through **systematic investigation** rather than observation.
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