Rheumatology & Haematology — MCQs
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A 48-year-old woman presents 5 days post-total hip replacement with sudden onset pleuritic chest pain and dyspnoea. CT pulmonary angiogram confirms segmental pulmonary embolism. She weighs 68kg with normal renal function (eGFR 88 mL/min/1.73m²). She has no other significant medical history. What is the most appropriate anticoagulation regimen?
A 26-year-old woman of West African descent presents with fatigue. Blood tests show: Hb 78 g/L, MCV 62 fL, ferritin 85 mcg/L, serum iron 18 mcmol/L (normal 10-30), TIBC 55 mcmol/L (normal 45-70). Haemoglobin electrophoresis shows HbA2 6.8% (normal 2.5-3.5%). What is the most likely diagnosis?
A 56-year-old man with rheumatoid arthritis has failed methotrexate and sulfasalazine combination therapy. He continues to have active disease with DAS28 score of 5.8. His consultant is considering biologic therapy. He has a history of pulmonary tuberculosis treated 15 years ago. Chest X-ray shows apical scarring. What is the most appropriate next step before initiating TNF inhibitor therapy?
A 34-year-old woman presents with fatigue and is found to have microcytic anaemia: Hb 95 g/L, MCV 68 fL, ferritin 8 mcg/L. She has no gastrointestinal symptoms and has regular but heavy menstrual periods (changing pads every 2 hours on heavy days, lasting 7 days). What is the most appropriate initial management approach?
A 70-year-old man with chronic kidney disease stage 4 (eGFR 22 mL/min/1.73m²) presents with an acute flare of gout affecting his left ankle. His current medications include amlodipine, bisoprolol, and atorvastatin. He has a history of peptic ulcer disease. What is the most appropriate treatment for his acute gout attack?
A 38-year-old woman presents with a 4-month history of symmetrical hand pain and early morning stiffness lasting 90 minutes. Examination reveals swelling of the MCP and PIP joints bilaterally. Blood tests show: RF negative, anti-CCP antibody positive at high titre (>200 U/mL), CRP 42 mg/L, ESR 38 mm/hr. X-rays of hands show soft tissue swelling only. What is the most accurate prognostic implication of these findings?
A 67-year-old woman with established rheumatoid arthritis has been taking methotrexate 20mg weekly for 18 months with good disease control. Her recent blood tests show: Hb 88 g/L, MCV 108 fL, WCC 3.2 × 10⁹/L, platelets 145 × 10⁹/L. She takes folic acid 5mg once weekly, 48 hours after her methotrexate dose. What is the most appropriate next step in management?
A 45-year-old man presents with acute onset severe pain and swelling of his right knee. Joint aspiration reveals positively birefringent rhomboid-shaped crystals under polarised light microscopy. Which biochemical abnormality is most directly associated with this condition?
A 52-year-old woman with newly diagnosed rheumatoid arthritis is being considered for disease-modifying antirheumatic drug (DMARD) therapy. She has active disease with a DAS28 score of 5.2 and has no contraindications to treatment. According to current UK guidelines, what is the most appropriate first-line DMARD therapy?
A 72-year-old man with metastatic lung cancer develops acute shortness of breath. CT pulmonary angiogram confirms bilateral pulmonary emboli. His platelet count is 45 × 10⁹/L, haemoglobin 88 g/L, creatinine 145 µmol/L (eGFR 38 mL/min/1.73m²). He is haemodynamically stable. What is the most appropriate anticoagulation approach?
Rheumatology & Haematology UK Medical PG Practice Questions and MCQs
Question 91: A 48-year-old woman presents 5 days post-total hip replacement with sudden onset pleuritic chest pain and dyspnoea. CT pulmonary angiogram confirms segmental pulmonary embolism. She weighs 68kg with normal renal function (eGFR 88 mL/min/1.73m²). She has no other significant medical history. What is the most appropriate anticoagulation regimen?
- A. Apixaban 10mg twice daily for 7 days, then 5mg twice daily (Correct Answer)
- B. Rivaroxaban 15mg twice daily for 21 days, then 20mg once daily
- C. Dabigatran 150mg twice daily
- D. Low molecular weight heparin for 5 days then warfarin (target INR 2-3)
- E. Unfractionated heparin infusion followed by warfarin
Explanation: ***Apixaban 10mg twice daily for 7 days, then 5mg twice daily*** - This regimen is in line with **NICE guidelines** recommending **Direct Oral Anticoagulants (DOACs)** as first-line treatment for provoked pulmonary embolism in patients with normal renal function. - Apixaban is a **monotherapy** that does not require initial parenteral bridging, with a **loading dose** for 7 days followed by a maintenance dose. *Rivaroxaban 15mg twice daily for 21 days, then 20mg once daily* - While rivaroxaban is an appropriate first-line DOAC, its standard loading dose duration for acute **Venous Thromboembolism (VTE)** is **21 days**, which is a different regimen compared to the 7-day apixaban load. - Both are valid options, but the specific apixaban regimen is a commonly cited and guideline-supported choice for acute PE. *Dabigatran 150mg twice daily* - This option is incorrect because dabigatran requires an **initial lead-in therapy** with parenteral anticoagulation (e.g., **Low Molecular Weight Heparin (LMWH)**) for at least 5 days before the oral dose is started. - Initiating dabigatran immediately without **heparin bridging** in an acute PE deviates from established clinical protocols. *Low molecular weight heparin for 5 days then warfarin (target INR 2-3)* - The traditional **LMWH to warfarin bridging** regimen is now generally considered **second-line** treatment unless DOACs are contraindicated, such as in patients with **antiphospholipid syndrome**. - This regimen necessitates regular **INR monitoring** and carries a higher risk of dietary and drug interactions compared to DOACs. *Unfractionated heparin infusion followed by warfarin* - **Unfractionated heparin (UFH)** is typically reserved for patients with **haemodynamic instability** (massive PE), severe renal impairment (CrCl < 15), or those at high risk of bleeding who may require rapid reversal. - This patient is stable with **normal renal function**, making the continuous infusion and intensive monitoring of UFH unnecessary.
Question 92: A 26-year-old woman of West African descent presents with fatigue. Blood tests show: Hb 78 g/L, MCV 62 fL, ferritin 85 mcg/L, serum iron 18 mcmol/L (normal 10-30), TIBC 55 mcmol/L (normal 45-70). Haemoglobin electrophoresis shows HbA2 6.8% (normal 2.5-3.5%). What is the most likely diagnosis?
- A. Iron deficiency anaemia with concurrent inflammation
- B. Beta-thalassaemia trait (Correct Answer)
- C. Alpha-thalassaemia trait
- D. Sickle cell trait
- E. Anaemia of chronic disease
Explanation: ***Beta-thalassaemia trait*** - The pathognomonic finding is an **elevated HbA2 (>3.5%)**, which in this patient is 6.8%, representing a compensatory increase in delta-chain production due to reduced beta-chain synthesis. - It presents as a **microcytic anaemia** with a strikingly low **MCV** relative to the mildness of the anaemia, while **ferritin** and iron studies remain within normal limits, ruling out iron deficiency. *Iron deficiency anaemia with concurrent inflammation* - While inflammation can elevate ferritin levels, **TIBC** is typically low or normal in inflammation. Here, TIBC is normal, but the key differentiator is the **elevated HbA2**, which is not seen in iron deficiency. - True iron deficiency would demonstrate **low ferritin** and often **elevated TIBC**, neither of which is present in this clinical picture. *Alpha-thalassaemia trait* - **Hb electrophoresis** is typically normal in alpha-thalassaemia trait because all hemoglobin types (HbA, HbA2, HbF) require alpha chains for their formation. - Diagnosis usually requires **DNA analysis** to identify gene deletions, as it does not present with the elevated **HbA2** seen in beta-thalassaemia trait. *Sickle cell trait* - Characterized by the presence of **HbS** on electrophoresis, usually making up about 25-45% of the total hemoglobin, which is not indicated by the elevated HbA2. - Patients with sickle cell trait typically have **normal red cell indices** (MCV and MCH) and do not present with microcytic anaemia. *Anaemia of chronic disease* - Characterized by **low serum iron**, low TIBC, and normal-to-high ferritin levels due to iron trapping in macrophages. - It typically presents as a normocytic or mildly microcytic anaemia, but it never causes an **elevation in HbA2**.
Question 93: A 56-year-old man with rheumatoid arthritis has failed methotrexate and sulfasalazine combination therapy. He continues to have active disease with DAS28 score of 5.8. His consultant is considering biologic therapy. He has a history of pulmonary tuberculosis treated 15 years ago. Chest X-ray shows apical scarring. What is the most appropriate next step before initiating TNF inhibitor therapy?
- A. Proceed with TNF inhibitor as TB was adequately treated previously
- B. Perform interferon-gamma release assay (IGRA) and treat if positive
- C. Start prophylactic isoniazid for 3 months before TNF inhibitor (Correct Answer)
- D. Consider alternative biologic therapy such as rituximab
- E. Arrange CT thorax to assess for active TB
Explanation: ***Start prophylactic isoniazid for 3 months before TNF inhibitor*** - **TNF inhibitors** facilitate the breakdown of **granulomas**, significantly increasing the risk of **latent Mycobacterium tuberculosis reactivation** even in patients previously treated. - Current guidelines (BSR/NICE) mandate prophylactic anti-TB therapy (e.g., **isoniazid** for 3–6 months) for patients with **radiological evidence** of past TB (apical scarring) before starting therapy to ensure safety. *Proceed with TNF inhibitor as TB was adequately treated previously* - Adequate prior treatment does not eliminate the risk of **reactivation** of residual dormant bacilli when **TNF-alpha secondary defense mechanisms** are inhibited. - Proceeding without prophylaxis in a patient with **apical scarring** carries an unacceptably high risk of disseminated or extrapulmonary TB. *Perform interferon-gamma release assay (IGRA) and treat if positive* - **IGRA** and TST status are often irrelevant in patients with clear **radiographic evidence** of prior TB infection, as prophylaxis is indicated based on the chest X-ray findings alone. - A negative IGRA would not override the clinical and radiological history of **pulmonary tuberculosis** in the context of high-risk immunosuppression. *Consider alternative biologic therapy such as rituximab* - While **rituximab** (B-cell depletion) has a lower risk of TB reactivation than TNF inhibitors, it is typically reserved for patients who fail an initial TNF inhibitor or have specific contraindications. - The presence of treated TB is not a contraindication to TNF inhibitors, provided appropriate **chemoprophylaxis** is administered. *Arrange CT thorax to assess for active TB* - **CT thorax** is not routinely indicated if the clinical assessment and **chest X-ray** do not suggest current active infection (e.g., no new infiltrates, fever, or weight loss). - The primary concern here is **latent TB reactivation**, which is managed via prophylaxis rather than diagnostic imaging for active disease stage.
Question 94: A 34-year-old woman presents with fatigue and is found to have microcytic anaemia: Hb 95 g/L, MCV 68 fL, ferritin 8 mcg/L. She has no gastrointestinal symptoms and has regular but heavy menstrual periods (changing pads every 2 hours on heavy days, lasting 7 days). What is the most appropriate initial management approach?
- A. Oral iron supplementation and gynaecology referral for menorrhagia management (Correct Answer)
- B. Upper and lower GI endoscopy to exclude malignancy
- C. Blood transfusion followed by oral iron therapy
- D. Intravenous iron infusion
- E. Coeliac serology and proceed to endoscopy regardless of result
Explanation: ***Oral iron supplementation and gynaecology referral for menorrhagia management*** - The patient has **microcytic anaemia** with severely **low ferritin** (8 mcg/L), highly suggestive of **iron deficiency anaemia**, which is clearly attributed to **menorrhagia** (heavy menstrual periods). - The initial management involves replenishing iron stores with **oral iron supplementation** and addressing the underlying cause of chronic blood loss by referral for **menorrhagia management**. *Upper and lower GI endoscopy to exclude malignancy* - **GI endoscopy** is typically indicated for iron deficiency anaemia in men, **postmenopausal women**, or individuals with **gastrointestinal symptoms** or a family history of GI malignancy. - In a **premenopausal woman** with a clear physiological cause of blood loss (menorrhagia) and no GI symptoms, extensive GI investigation is not the most appropriate initial step. *Blood transfusion followed by oral iron therapy* - **Blood transfusion** is reserved for patients with **severe symptomatic anaemia** (e.g., Hb < 70 g/L) or those with cardiovascular instability, which is not the case for this patient (Hb 95 g/L). - For stable patients, **oral iron therapy** is the standard first-line treatment to gradually correct iron deficiency. *Intravenous iron infusion* - **Intravenous iron** is indicated when **oral iron** is poorly tolerated, ineffective, or when rapid correction of iron deficiency is clinically necessary (e.g., severe malabsorption, ongoing significant blood loss, or pre-surgical requirements). - As an initial approach, **oral iron** is preferred given its safety and cost-effectiveness, and there is no contraindication or urgency warranting IV iron in this stable patient. *Coeliac serology and proceed to endoscopy regardless of result* - While **Coeliac serology** can be a screening tool for malabsorption in unexplained iron deficiency, proceeding directly to **endoscopy regardless of the result** is an overinvestigation without gastrointestinal symptoms. - The primary focus should remain on the identified cause of **menorrhagia** and initiating **oral iron** before considering invasive procedures for other potential causes.
Question 95: A 70-year-old man with chronic kidney disease stage 4 (eGFR 22 mL/min/1.73m²) presents with an acute flare of gout affecting his left ankle. His current medications include amlodipine, bisoprolol, and atorvastatin. He has a history of peptic ulcer disease. What is the most appropriate treatment for his acute gout attack?
- A. Colchicine 500 micrograms four times daily
- B. Naproxen 500mg twice daily with omeprazole
- C. Oral prednisolone 30mg daily (Correct Answer)
- D. Intra-articular corticosteroid injection
- E. Allopurinol 100mg daily
Explanation: ***Oral prednisolone 30mg daily*** - **Oral corticosteroids** are the preferred first-line treatment for acute gout when **NSAIDs** and **colchicine** are contraindicated due to **chronic kidney disease (CKD)**. - This patient's **eGFR of 22 mL/min** and history of **peptic ulcer disease** make systemic steroids the safest and most effective systemic option without risking renal toxicity or GI bleeding. *Colchicine 500 micrograms four times daily* - In **CKD stage 4**, the clearance of colchicine is significantly reduced, leading to high risks of **neuromuscular toxicity** and bone marrow suppression. - The proposed dose of **four times daily** is dangerously high for someone with an **eGFR < 30 mL/min**; a much lower, infrequent dose would be required. *Naproxen 500mg twice daily with omeprazole* - **NSAIDs** are strictly contraindicated in **Stage 4 CKD** because they may further decrease renal blood flow and precipitate **acute-on-chronic kidney injury**. - Despite PPI coverage with **omeprazole**, his history of **peptic ulcer disease** increases the risk of a life-threatening gastrointestinal hemorrhage. *Intra-articular corticosteroid injection* - While effective for **monoarthritis**, oral prednisolone is often prioritized in clinical scenarios where immediate access to specialized **joint aspiration** or injection expertise is unavailable. - Although a valid consideration, **systemic corticosteroids** (oral) are generally the first practical systemic approach for acute flares in patients with multiple comorbidities. *Allopurinol 100mg daily* - **Allopurinol** is a urate-lowering therapy and should not be initiated during an **acute flare**, as rapid changes in serum urate can prolong or worsen the inflammation. - Starting this medication now does not address the **acute pain and swelling** currently experienced by the patient.
Question 96: A 38-year-old woman presents with a 4-month history of symmetrical hand pain and early morning stiffness lasting 90 minutes. Examination reveals swelling of the MCP and PIP joints bilaterally. Blood tests show: RF negative, anti-CCP antibody positive at high titre (>200 U/mL), CRP 42 mg/L, ESR 38 mm/hr. X-rays of hands show soft tissue swelling only. What is the most accurate prognostic implication of these findings?
- A. The negative RF indicates a better prognosis than seropositive disease
- B. High titre anti-CCP antibodies predict more aggressive erosive disease (Correct Answer)
- C. Absence of erosions on initial X-ray indicates low risk of joint damage
- D. Normal inflammatory markers exclude significant disease activity
- E. The diagnosis cannot be confirmed without positive RF
Explanation: ***High titre anti-CCP antibodies predict more aggressive erosive disease***- **Anti-CCP antibodies** are highly specific for rheumatoid arthritis and are strong predictors of **future joint destruction** and radiological progression.- A **high titre** (>200 U/mL) of anti-CCP antibodies indicates a significantly increased risk for a more **aggressive clinical course**, often requiring early and intensive **DMARD therapy**.*The negative RF indicates a better prognosis than seropositive disease*- While **rheumatoid factor (RF)** is a prognostic marker, a negative RF does not negate the poor prognosis associated with **positive anti-CCP antibodies**.- Patients with **anti-CCP positive** but RF negative RA often experience a disease course similar to those who are double-positive for both markers.*Absence of erosions on initial X-ray indicates low risk of joint damage*- In early rheumatoid arthritis, initial X-rays typically show only **soft tissue swelling**, with **bony erosions** developing later in the disease course.- The presence of **high titre anti-CCP antibodies** and elevated **inflammatory markers** (CRP, ESR) predicts a high risk of future joint damage, regardless of initial X-ray findings.*Normal inflammatory markers exclude significant disease activity*- In this patient, both **CRP (42 mg/L)** and **ESR (38 mm/hr)** are significantly elevated, indicating active systemic **inflammation**.- Elevated inflammatory markers are associated with higher disease activity and a greater likelihood of **radiographic progression** and worse prognosis in RA.*The diagnosis cannot be confirmed without positive RF*- Rheumatoid arthritis can be diagnosed based on **ACR/EULAR criteria**, where **anti-CCP antibody positivity** (especially high titre) contributes significantly to the diagnostic score.- Approximately 20% of RA cases are **seronegative for RF** (seronegative RA), and **anti-CCP antibodies** are often present and diagnostic in these cases.
Question 97: A 67-year-old woman with established rheumatoid arthritis has been taking methotrexate 20mg weekly for 18 months with good disease control. Her recent blood tests show: Hb 88 g/L, MCV 108 fL, WCC 3.2 × 10⁹/L, platelets 145 × 10⁹/L. She takes folic acid 5mg once weekly, 48 hours after her methotrexate dose. What is the most appropriate next step in management?
- A. Stop methotrexate and commence sulfasalazine
- B. Continue current dose and recheck bloods in 2 weeks
- C. Reduce methotrexate dose to 15mg weekly
- D. Stop methotrexate temporarily and increase folic acid to daily dosing (Correct Answer)
- E. Arrange urgent bone marrow biopsy
Explanation: ***Stop methotrexate temporarily and increase folic acid to daily dosing***- The patient's blood tests show **macrocytic anemia** (Hb 88 g/L, MCV 108 fL) and **leukopenia** (WCC 3.2 × 10⁹/L), indicative of **bone marrow suppression** likely due to **methotrexate toxicity**.- The most appropriate immediate action is to temporarily cease **methotrexate** and increase the dose of **folic acid** to daily to counteract the folate antagonism and promote hematopoietic recovery.*Stop methotrexate and commence sulfasalazine*- While **sulfasalazine** is an alternative DMARD for rheumatoid arthritis, the immediate and critical concern is the acute **methotrexate toxicity** and **bone marrow suppression**.- Commencing a new medication without first resolving the underlying toxicity is inappropriate and could potentially complicate the clinical picture or delay recovery.*Continue current dose and recheck bloods in 2 weeks*- Continuing **methotrexate** in the presence of significant **leukopenia** and **anemia** is dangerous and substantially increases the risk of severe infections and other life-threatening complications.- Waiting two weeks to recheck bloods is an unacceptable delay for managing drug-induced **myelosuppression** that requires urgent intervention.*Reduce methotrexate dose to 15mg weekly*- Simply reducing the dose is insufficient when there is clear evidence of active and significant **bone marrow suppression** and **toxicity**.- The drug must be completely withheld to allow for hematological recovery before any consideration of reintroduction or dose adjustment.*Arrange urgent bone marrow biopsy*- A **bone marrow biopsy** is generally not the initial step for suspected drug-induced myelosuppression when the offending agent is known and can be immediately discontinued.- The priority is to remove the causative drug and provide supportive care, reserving invasive diagnostics for cases where the etiology is unclear or there is no response to withdrawal.
Question 98: A 45-year-old man presents with acute onset severe pain and swelling of his right knee. Joint aspiration reveals positively birefringent rhomboid-shaped crystals under polarised light microscopy. Which biochemical abnormality is most directly associated with this condition?
- A. Hyperuricaemia
- B. Hypercalcaemia (Correct Answer)
- C. Hyperparathyroidism
- D. Hypomagnesaemia
- E. Hypophosphataemia
Explanation: ***Hypercalcaemia***- Joint aspiration showing **positively birefringent rhomboid-shaped crystals** is diagnostic of **Calcium Pyrophosphate Deposition (CPPD)**, also known as pseudogout.- Elevating serum **calcium levels** directly promotes the formation of these crystals, and its presence warrants screening for underlying metabolic disorders.*Hyperuricaemia*- This biochemical abnormality is the hallmark of **Gout**, not CPPD or pseudogout.- Gout presents with **negatively birefringent needle-shaped crystals** of monosodium urate, distinct from the rhomboid crystals described.*Hyperparathyroidism*- While **primary hyperparathyroidism** is a known risk factor for pseudogout, it is a clinical condition rather than the "direct biochemical abnormality."- It predisposes to CPPD primarily by causing **hypercalcaemia**, which is the more direct metabolic driver for crystal deposition.*Hypomagnesaemia*- Low levels of **magnesium** act as a risk factor because magnesium is a cofactor for **alkaline phosphatase**, which helps keep pyrophosphate soluble.- While associated with CPPD, **hypercalcaemia** remains a more frequent and classic biochemical screening target in initial presentations.*Hypophosphataemia*- This is incorrect as the actual association is with **hypophosphatasia**, a rare metabolic disorder affecting phosphate metabolism.- **Low phosphate** itself is not a primary driver of CPPD; instead, imbalances in **pyrophosphate** levels within the joint space are the critical factor.
Question 99: A 52-year-old woman with newly diagnosed rheumatoid arthritis is being considered for disease-modifying antirheumatic drug (DMARD) therapy. She has active disease with a DAS28 score of 5.2 and has no contraindications to treatment. According to current UK guidelines, what is the most appropriate first-line DMARD therapy?
- A. Methotrexate monotherapy (Correct Answer)
- B. Hydroxychloroquine monotherapy
- C. Sulfasalazine monotherapy
- D. Combination therapy with methotrexate, hydroxychloroquine, and sulfasalazine
- E. Adalimumab (TNF inhibitor)
Explanation: ***Methotrexate monotherapy*** - Current **NICE/UK guidelines** (NG100) recommend starting with **conventional synthetic DMARD monotherapy**, with **methotrexate** being the preferred first-line choice due to its high efficacy and safety profile in active RA. - It should be initiated and titrated to an optimal dose (e.g., up to **25mg weekly**) to achieve the treatment target of remission or low disease activity, especially with a high **DAS28 score of 5.2**. *Hydroxychloroquine monotherapy* - While a DMARD, hydroxychloroquine is generally considered **less potent** than methotrexate and is typically reserved for **mild rheumatoid arthritis** or as part of combination therapy. - It has a slower onset of action and is less effective at preventing **joint erosion** compared to methotrexate, making it unsuitable for active disease with a high DAS28 score. *Sulfasalazine monotherapy* - Sulfasalazine is an alternative conventional DMARD, but it is often considered **less effective** than methotrexate for inducing rapid remission in patients with active, newly diagnosed RA. - It is a suitable first-line option if **methotrexate is contraindicated** or poorly tolerated, but the patient in the scenario has no contraindications. *Combination therapy with methotrexate, hydroxychloroquine, and sulfasalazine* - While combination DMARD therapy was once a common initial strategy, **current UK guidelines** (NICE NG100, 2018) recommend starting with **monotherapy** to reduce initial toxicity and simplify treatment. - Intensified treatment with combination DMARDs or biologics is reserved for patients who do not achieve treatment targets on **optimal monotherapy**. *Adalimumab (TNF inhibitor)* - **Biological DMARDs** like adalimumab are not first-line therapies for newly diagnosed rheumatoid arthritis according to UK guidelines. - Their use is restricted to patients who have had an **inadequate response** to at least two conventional synthetic DMARDs (including methotrexate) and who have persistently **high disease activity** (e.g., DAS28 > 5.1).
Question 100: A 72-year-old man with metastatic lung cancer develops acute shortness of breath. CT pulmonary angiogram confirms bilateral pulmonary emboli. His platelet count is 45 × 10⁹/L, haemoglobin 88 g/L, creatinine 145 µmol/L (eGFR 38 mL/min/1.73m²). He is haemodynamically stable. What is the most appropriate anticoagulation approach?
- A. Treatment dose low molecular weight heparin (Correct Answer)
- B. Reduced dose apixaban 2.5mg twice daily
- C. Therapeutic dose unfractionated heparin infusion
- D. Inferior vena cava filter insertion without anticoagulation
- E. Treatment dose rivaroxaban 15mg twice daily for 3 weeks then 20mg daily
Explanation: ***Treatment dose low molecular weight heparin*** - **Low molecular weight heparin (LMWH)** is the preferred initial choice for **cancer-associated thrombosis (CAT)**, balancing efficacy and bleeding risk. - Although the patient has **thrombocytopenia** (platelet count 45 × 10⁹/L) and renal impairment (eGFR 38 mL/min/1.73m²), LMWH can be dose-adjusted based on weight and renal function, offering more control than fixed-dose DOACs in this setting. *Reduced dose apixaban 2.5mg twice daily* - This is an **inadequate dose** for the acute treatment of pulmonary embolism; the standard initial dose for PE is 10mg twice daily for 7 days. - Apixaban 2.5mg twice daily is primarily used for **secondary prevention** after the initial treatment phase or for stroke prevention in non-valvular atrial fibrillation. *Therapeutic dose unfractionated heparin infusion* - **Unfractionated heparin (UFH)** is typically reserved for patients who are **haemodynamically unstable** or have severe renal failure (eGFR <30 mL/min/1.73m²) due to its short half-life and reversibility. - It requires **frequent activated partial thromboplastin time (aPTT) monitoring** and carries a higher risk of **heparin-induced thrombocytopenia (HIT)** compared to LMWH. *Inferior vena cava filter insertion without anticoagulation* - **IVC filters** are generally indicated only when anticoagulation is **absolutely contraindicated**, such as in cases of active major bleeding. - The patient's platelet count of 45 × 10⁹/L and stable condition do not constitute an absolute contraindication to anticoagulation, and filters have potential complications without treating the underlying thrombotic state. *Treatment dose rivaroxaban 15mg twice daily for 3 weeks then 20mg daily* - While **DOACs** are an option for CAT, **rivaroxaban** is often associated with a higher risk of **gastrointestinal bleeding**, especially in patients with metastatic lung cancer or active GI malignancy. - The patient's **thrombocytopenia** (45 × 10⁹/L) and moderate renal impairment make the fixed-dose regimen of rivaroxaban less flexible and potentially riskier than the dose-adjustable LMWH.
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