Safe Prescribing — MCQs
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A 71-year-old man with atrial fibrillation has been on warfarin for 4 years with stable INR control. He is admitted with an acute ischaemic stroke. CT head shows no haemorrhage. His INR on admission is 2.4 (target 2-3) and his NIHSS score is 16. He is outside the thrombolysis window. What is the most appropriate management of his anticoagulation?
A 34-year-old woman with type 1 diabetes on insulin pump therapy presents to the emergency department with nausea, vomiting, and abdominal pain. Her capillary blood glucose is 24.5 mmol/L and blood ketones are 4.8 mmol/L. Her insulin pump is functioning normally. She is diagnosed with diabetic ketoacidosis. What is the most appropriate initial insulin management?
A 52-year-old man with rheumatoid arthritis has been stable on methotrexate 20mg weekly for 18 months. He develops an acute chest infection with productive cough and fever. His blood tests show: WCC 3.2 × 10⁹/L, neutrophils 1.1 × 10⁹/L, platelets 145 × 10⁹/L. What is the most appropriate immediate management of his methotrexate therapy?
A 66-year-old woman with atrial fibrillation is established on apixaban 5mg twice daily. She develops acute pyelonephritis and requires antibiotic therapy. Her renal function shows eGFR of 42 ml/min/1.73m². Which antibiotic should be prescribed with particular caution due to potential interaction increasing apixaban levels?
A 58-year-old man with type 2 diabetes is prescribed insulin aspart. He asks about the appropriate timing of administration relative to meals. What is the recommended timing for administering rapid-acting insulin analogues such as insulin aspart?
According to the Medicines and Healthcare products Regulatory Agency (MHRA) guidance, what is the recommended minimum interval between switching from warfarin to a direct oral anticoagulant (DOAC) such as apixaban in a patient with atrial fibrillation?
A 45-year-old woman with newly diagnosed psoriatic arthritis is prescribed methotrexate 15mg once weekly. According to the British National Formulary, which day of the week should folic acid supplementation be avoided to ensure optimal efficacy of methotrexate therapy?
A 77-year-old man with atrial fibrillation and chronic kidney disease stage 3b (eGFR 38 ml/min/1.73m²) is on apixaban 2.5mg twice daily. He weighs 73kg, is 178cm tall, and is 78 years old. His creatinine is 156 μmol/L. On medication review, you calculate his CHA₂DS₂-VASc score as 4 and HAS-BLED score as 3. His apixaban dose was reduced based on meeting dose reduction criteria. However, on careful review, what is the most appropriate action?
A 54-year-old woman with type 1 diabetes for 28 years presents with recurrent severe hypoglycaemic episodes, including two requiring emergency services in the past 3 months. She has hypoglycaemia unawareness and takes insulin degludec 32 units once daily and insulin aspart before meals. Her HbA1c is 48 mmol/mol. Continuous glucose monitoring shows significant glycaemic variability with frequent hypoglycaemic episodes, particularly nocturnal. What is the most appropriate next step in her management?
A 69-year-old man on rivaroxaban 20mg once daily for atrial fibrillation (CHA₂DS₂-VASc score 4) undergoes routine blood tests. Results show: eGFR 28 ml/min/1.73m² (previously 45 ml/min/1.73m² six months ago), creatinine 198 μmol/L. He has no bleeding and is otherwise well. What is the most appropriate management of his anticoagulation?
Safe Prescribing UK Medical PG Practice Questions and MCQs
Question 131: A 71-year-old man with atrial fibrillation has been on warfarin for 4 years with stable INR control. He is admitted with an acute ischaemic stroke. CT head shows no haemorrhage. His INR on admission is 2.4 (target 2-3) and his NIHSS score is 16. He is outside the thrombolysis window. What is the most appropriate management of his anticoagulation?
- A. Continue warfarin unchanged and monitor INR daily
- B. Withhold warfarin for 7 days then restart when neurologically stable
- C. Immediately reverse anticoagulation with vitamin K and prothrombin complex concentrate
- D. Switch immediately to low molecular weight heparin for 14 days
- E. Withhold warfarin for 14 days then restart after repeat CT excludes haemorrhagic transformation (Correct Answer)
Explanation: ***Withhold warfarin for 14 days then restart after repeat CT excludes haemorrhagic transformation***- For patients with **severe ischaemic stroke** (indicated by an **NIHSS score of 16**), current guidelines generally recommend delaying anticoagulation for **14 days** to minimize the risk of haemorrhagic transformation.- Repeat imaging is essential before restarting to ensure there is no **haemorrhagic transformation**, which is a high risk in large infarcts regardless of the therapeutic INR.*Continue warfarin unchanged and monitor INR daily*- Continuing full anticoagulation in the acute phase of a **large ischaemic stroke** significantly increases the risk of symptomatic **intracranial haemorrhage** into the infarcted tissue.- Current clinical guidelines recommend a temporary interruption of therapy even if the patient was previously stable and within the **therapeutic range**.*Withhold warfarin for 7 days then restart when neurologically stable*- While some guidelines suggest a 3 to 7-day delay for **minor strokes** or TIAs, a 7-day window is considered too short for a **severe stroke** (NIHSS > 15).- Severity of the stroke, as measured by the **NIHSS score**, dictates the length of the delay; a longer period is required for larger areas of brain tissue damage.*Immediately reverse anticoagulation with vitamin K and prothrombin complex concentrate*- Acute reversal with **PCC and Vitamin K** is indicated for **haemorrhagic strokes** or life-threatening bleeding, not for an acute ischaemic stroke.- Reversing anticoagulation unnecessarily in a patient with **atrial fibrillation** may increase the risk of further **thromboembolic events** unnecessarily.*Switch immediately to low molecular weight heparin for 14 days*- Starting **LMWH** would still provide full systemic anticoagulation, which carries the same high risk of **haemorrhagic transformation** as warfarin in the acute setting.- Heparin is not recommended as a bridge or acute treatment for **ischaemic stroke** prevention immediately following the event due to the bleeding risk.
Question 132: A 34-year-old woman with type 1 diabetes on insulin pump therapy presents to the emergency department with nausea, vomiting, and abdominal pain. Her capillary blood glucose is 24.5 mmol/L and blood ketones are 4.8 mmol/L. Her insulin pump is functioning normally. She is diagnosed with diabetic ketoacidosis. What is the most appropriate initial insulin management?
- A. Continue the insulin pump at current basal rate and add intravenous variable rate insulin infusion
- B. Discontinue the insulin pump completely and start intravenous variable rate insulin infusion (Correct Answer)
- C. Increase the pump basal rate by 20% and add correction boluses
- D. Continue the pump and administer intramuscular insulin instead of intravenous
- E. Continue the pump unchanged and give subcutaneous rapid-acting insulin boluses
Explanation: ***Discontinue the insulin pump completely and start intravenous variable rate insulin infusion*** - In the management of **Diabetic Ketoacidosis (DKA)**, standard protocols require the transition to **Fixed Rate Intravenous Insulin Infusion (FRIII)** or Variable Rate (VRIII) to ensure reliable insulin delivery and rapid titration. - Continuing the pump during severe DKA is avoided because **subcutaneous absorption** can be unpredictable due to dehydration and poor peripheral perfusion, making IV the preferred route. *Continue the insulin pump at current basal rate and add intravenous variable rate insulin infusion* - Running both systems simultaneously increases the risk of **insulin stacking**, which can lead to severe **hypoglycemia** as the ketoacidosis resolves. - Standard guidelines recommend that all **subcutaneous insulin** (except long-acting analogs in some protocols) be stopped while an IV insulin infusion is active. *Increase the pump basal rate by 20% and add correction boluses* - This approach is inappropriate for established **DKA** as it relies on subcutaneous delivery which is too slow and unreliable for metabolic emergency stabilization. - Pump failure (e.g., infusion set blockage) is a common cause of DKA in pump users, so relying on the same device for rescue therapy is **clinically unsafe**. *Continue the pump and administer intramuscular insulin instead of intravenous* - **Intramuscular insulin** is not the standard of care for DKA management in a hospital setting when **intravenous access** is available. - **Intravenous insulin** has a much shorter half-life and allows for the immediate adjustment of rates needed to suppress **ketogenesis** and stabilize blood glucose. *Continue the pump unchanged and give subcutaneous rapid-acting insulin boluses* - Subcutaneous boluses are insufficient to clear **ketonemia** and correct the severe metabolic acidosis associated with a blood ketone level of **4.8 mmol/L**. - Management must focus on systemic volume expansion and **IV insulin** to halt the production of fatty acids and ketones at the liver.
Question 133: A 52-year-old man with rheumatoid arthritis has been stable on methotrexate 20mg weekly for 18 months. He develops an acute chest infection with productive cough and fever. His blood tests show: WCC 3.2 × 10⁹/L, neutrophils 1.1 × 10⁹/L, platelets 145 × 10⁹/L. What is the most appropriate immediate management of his methotrexate therapy?
- A. Continue methotrexate at the same dose and monitor weekly
- B. Reduce methotrexate dose to 10mg weekly until infection resolves
- C. Withhold methotrexate temporarily until infection resolves and blood counts recover (Correct Answer)
- D. Switch to subcutaneous methotrexate to improve bioavailability
- E. Add folinic acid rescue therapy while continuing methotrexate
Explanation: ***Withhold methotrexate temporarily until infection resolves and blood counts recover***- Immediate cessation of **methotrexate** is required due to the presence of both **neutropenia** (neutrophils 1.1 × 10⁹/L, below the < 1.5 × 10⁹/L threshold) and an **active infection**, which significantly increases the risk of **sepsis**.- **Methotrexate** is a folate antagonist that can cause **bone marrow suppression**; withholding it allows the marrow to recover and the immune system to effectively combat the bacterial load.*Continue methotrexate at the same dose and monitor weekly*- Continuing methotrexate therapy in the face of **neutropenia** and infection presents an unacceptable risk for **life-threatening sepsis** and worsening infection.- Weekly monitoring is insufficient for an acute drop in **white cell counts** coupled with symptomatic clinical deterioration and infection.*Reduce methotrexate dose to 10mg weekly until infection resolves*- Dose reduction is inappropriate when **cytopenia** is already present; the drug must be stopped entirely to permit rapid **neutrophil recovery**.- Even a lower dose maintains **immunosuppression**, which would interfere with the body's ability to clear the **acute chest infection**.*Switch to subcutaneous methotrexate to improve bioavailability*- Increasing bioavailability by switching to subcutaneous administration would likely worsen **methotrexate toxicity** and potentially exacerbate the suppression of the **haematopoietic system**.- Subcutaneous administration is primarily used to bypass **gastrointestinal side effects** or improve absorption, not to manage **hematologic complications** or infections.*Add folinic acid rescue therapy while continuing methotrexate*- **Folinic acid (leucovorin)** rescue is typically reserved for high-dose oncology regimens, specific toxicity, or acute **methotrexate overdose**, rather than managing infection-related neutropenia.- Adding folinic acid while continuing the drug does not adequately address the immediate danger posed by the patient's **low neutrophil count** and active infection.
Question 134: A 66-year-old woman with atrial fibrillation is established on apixaban 5mg twice daily. She develops acute pyelonephritis and requires antibiotic therapy. Her renal function shows eGFR of 42 ml/min/1.73m². Which antibiotic should be prescribed with particular caution due to potential interaction increasing apixaban levels?
- A. Amoxicillin
- B. Nitrofurantoin
- C. Trimethoprim
- D. Clarithromycin (Correct Answer)
- E. Cefalexin
Explanation: ***Clarithromycin***- **Clarithromycin** is a potent inhibitor of both **CYP3A4** and **P-glycoprotein (P-gp)**, which are the primary pathways responsible for the metabolism and transport of apixaban.- Concurrent use significantly increases **apixaban plasma concentrations**, raising the risk of major **bleeding**, especially in patients with existing **renal impairment** (eGFR < 50 ml/min).*Amoxicillin*- **Amoxicillin** is a penicillin-based antibiotic that does not inhibit **CYP3A4** or **P-gp** enzymes.- It has no clinically significant **pharmacokinetic interaction** with apixaban and is generally safe to prescribe for susceptible infections.*Nitrofurantoin*- **Nitrofurantoin** is primarily excreted renally and acts locally in the bladder; it does not interfere with the **metabolic pathways** of DOACs like apixaban.- Notably, it is often avoided in **pyelonephritis** due to poor tissue penetration and should be used with caution when **eGFR** is low, but not due to drug interactions.*Trimethoprim*- **Trimethoprim** does not have a major affect on the **CYP450 system**, specifically the 3A4 isoform relevant to apixaban.- While it can increase levels of drugs like **methotrexate** or **phenytoin**, it does not increase the risk of bleeding when combined with **apixaban**.*Cefalexin*- **Cefalexin** is a first-generation cephalosporin that lacks the **enzyme inhibition** properties required to alter apixaban levels.- It is considered a relatively safe alternative for **urinary tract infections** in patients taking oral anticoagulants.
Question 135: A 58-year-old man with type 2 diabetes is prescribed insulin aspart. He asks about the appropriate timing of administration relative to meals. What is the recommended timing for administering rapid-acting insulin analogues such as insulin aspart?
- A. 15-30 minutes before meals
- B. 30-45 minutes before meals
- C. Immediately before meals or within 5-15 minutes of starting a meal (Correct Answer)
- D. Immediately after completing the meal
- E. At bedtime, regardless of meal timing
Explanation: ***Immediately before meals or within 5-15 minutes of starting a meal*** - **Rapid-acting insulin analogues** like **aspart**, **lispro**, and **glulisine** have a very fast onset of action (10-20 minutes), making them ideal for managing **postprandial glucose** peaks. - Administering them just before or at the start of eating ensures that the insulin's **peak effect** (1-3 hours) aligns precisely with the absorption of carbohydrates from the meal. *30-45 minutes before meals* - This timing is specific to **Regular (Short-acting) human insulin**, which requires more time to dissociate from hexamers into monomers for absorption. - Giving **aspart** this early would significantly increase the risk of **pre-meal hypoglycemia** because its action begins much faster than regular insulin. *15-30 minutes before meals* - While closer to the correct window, this is generally too early for **rapid-acting analogues** and may lead to a mismatch between glucose entry and insulin action. - Standardization for these medications emphasizes **immediate administration** to optimize safety and patient compliance with meal routines. *Immediately after completing the meal* - Post-meal dosing is generally reserved for patients with **gastroparesis** or unpredictable intake, such as **young children** or the elderly. - For most adults, waiting until after the meal leads to **postprandial hyperglycemia** because the blood glucose rises faster than the insulin can take effect. *At bedtime, regardless of meal timing* - **Intermediate-acting (NPH)** or **long-acting (glargine, detemir)** insulins are administered at bedtime to provide **basal coverage** throughout the night. - **Rapid-acting insulin** is strictly for **bolus (mealtime) coverage** or correction; using it at bedtime without food would cause severe **nocturnal hypoglycemia**.
Question 136: According to the Medicines and Healthcare products Regulatory Agency (MHRA) guidance, what is the recommended minimum interval between switching from warfarin to a direct oral anticoagulant (DOAC) such as apixaban in a patient with atrial fibrillation?
- A. Start DOAC when INR falls below 3.0
- B. Start DOAC when INR falls below 2.5
- C. Start DOAC when INR falls below 2.0 (Correct Answer)
- D. Start DOAC when INR falls below 1.5
- E. Start DOAC immediately and stop warfarin
Explanation: ***Start DOAC when INR falls below 2.0***- According to **MHRA guidance**, warfarin should be discontinued and the **DOAC** initiated once the **INR** is less than **2.0** to ensure a safe transition.- This threshold minimizes the **bleeding risk** that would occur from the overlapping pharmacological effects of both **anticoagulants**.*Start DOAC when INR falls below 3.0*- An **INR of 3.0** indicates that the patient is still significantly anticoagulated by **warfarin**, leading to an unsafe overlap.- Initiating a **DOAC** at this level markedly increases the risk of **major hemorrhage** due to supra-therapeutic anticoagulation.*Start DOAC when INR falls below 2.5*- While the target range for many conditions is 2.0–3.0, 2.5 is still high enough to cause **excessive anticoagulation** when combined with a new agent.- Most clinical guidelines and the **MHRA** specifically mandate waiting for the **INR** to drop further to prioritize **patient safety**.*Start DOAC when INR falls below 1.5*- Waiting for the **INR** to fall below **1.5** is unnecessary and may leave the patient at an increased risk of **thromboembolic events** (like stroke in AF).- The pharmacological transition is considered safe and effective at the **2.0 threshold**, making a lower target inefficient.*Start DOAC immediately and stop warfarin*- Immediate initiation without monitoring the **washout of warfarin** is dangerous because warfarin has a **long half-life**.- This approach results in a period of **dual anticoagulation**, significantly raising the risk of **life-threatening bleeding**.
Question 137: A 45-year-old woman with newly diagnosed psoriatic arthritis is prescribed methotrexate 15mg once weekly. According to the British National Formulary, which day of the week should folic acid supplementation be avoided to ensure optimal efficacy of methotrexate therapy?
- A. The day before methotrexate administration
- B. The same day as methotrexate administration (Correct Answer)
- C. The day after methotrexate administration
- D. Two days after methotrexate administration
- E. Three days after methotrexate administration
Explanation: ***The same day as methotrexate administration*** - **Methotrexate** is a **dihydrofolate reductase inhibitor**; taking folic acid on the same day can theoretically provide a substrate that competes with the drug, potentially reducing its **therapeutic efficacy**. - The **BNF** and clinical guidelines recommend omitting folic acid on the day of methotrexate to ensure maximal suppression of the **folate metabolic pathway** in target cells. *The day before methotrexate administration* - Taking folic acid 24 hours prior to the dose does not interfere with the **pharmacokinetics** or the peak activity of methotrexate. - It helps maintain **tissue folate stores**, reducing the risk of side effects like **mucositis** and bone marrow suppression. *The day after methotrexate administration* - This is the most common clinical practice, known as a **"folate rescue,"** usually occurring at least **24 hours after** the methotrexate dose. - Taking it at this interval helps mitigate **gastrointestinal toxicity** and hepatotoxicity without compromising the drug's immunosuppressive action. *Two days after methotrexate administration* - Folic acid administration 48 hours post-dose is safe and keeps the supplement well outside the **peak concentration window** of methotrexate. - Clinical protocols vary (e.g., 5mg weekly vs. daily except on drug day), but this delay poses no risk to **drug efficacy**. *Three days after methotrexate administration* - Supplementing later in the week remains effective for preventing **folate deficiency** symptoms caused by chronic methotrexate use. - The primary concern is simply avoiding the **same-day co-administration**, so any day sufficiently distal to the dose is acceptable.
Question 138: A 77-year-old man with atrial fibrillation and chronic kidney disease stage 3b (eGFR 38 ml/min/1.73m²) is on apixaban 2.5mg twice daily. He weighs 73kg, is 178cm tall, and is 78 years old. His creatinine is 156 μmol/L. On medication review, you calculate his CHA₂DS₂-VASc score as 4 and HAS-BLED score as 3. His apixaban dose was reduced based on meeting dose reduction criteria. However, on careful review, what is the most appropriate action?
- A. Continue apixaban 2.5mg twice daily as the dose reduction is appropriate
- B. Increase apixaban to 5mg twice daily as he does not meet the criteria for dose reduction (Correct Answer)
- C. Switch to rivaroxaban 15mg once daily as this is more appropriate for his renal function
- D. Switch to warfarin as apixaban dosing is too complex in renal impairment
- E. Continue current dose but add low-dose aspirin for additional thromboembolic protection
Explanation: ***Increase apixaban to 5mg twice daily as he does not meet the criteria for dose reduction***- Apixaban dose reduction (2.5mg BD) for atrial fibrillation requires meeting at least **two out of three** criteria: Age **≥80 years**, Weight **≤60kg**, or Serum Creatinine **≥133 μmol/L**.- This patient only meets **one criterion** (Creatinine 156 μmol/L); since he is **78 years old** and weighs **73kg**, the standard **5mg twice daily** dose is required for effective stroke prevention.*Continue apixaban 2.5mg twice daily as the dose reduction is appropriate*- This is incorrect because providing a reduced dose when not indicated leads to **suboptimal anticoagulation** and an increased risk of **ischemic stroke**.- A common clinical error is reducing the dose based on **renal impairment alone**, but apixaban specifically requires the "two-out-of-three" rule for dose reduction.*Switch to rivaroxaban 15mg once daily as this is more appropriate for his renal function*- While **Rivaroxaban 15mg** once daily is an alternative for patients with a CrCl of 15-49 ml/min, there is no clinical indication to switch if **Apixaban** can be correctly dosed and is tolerated.- **Apixaban** is often preferred in renal impairment (CKD stage 3) due to a potentially lower rate of **major bleeding** compared to other DOACs.*Switch to warfarin as apixaban dosing is too complex in renal impairment*- **DOACs** like apixaban are generally preferred over **Warfarin** in non-valvular AF due to a better safety profile, fewer drug-drug interactions, and no need for routine **INR monitoring**.- Apixaban is safely used in **CKD stage 3b** as long as the dosing criteria are followed correctly; its dosing is not overly complex for this patient.*Continue current dose but add low-dose aspirin for additional thromboembolic protection*- Adding **Aspirin** to an anticoagulant in the absence of a specific indication (e.g., recent acute coronary syndrome/stent) significantly increases **bleeding risk** without providing additional stroke prevention benefit in AF.- The priority is to optimize the **anticoagulant dose** (apixaban 5mg BD) to ensure adequate stroke prevention.
Question 139: A 54-year-old woman with type 1 diabetes for 28 years presents with recurrent severe hypoglycaemic episodes, including two requiring emergency services in the past 3 months. She has hypoglycaemia unawareness and takes insulin degludec 32 units once daily and insulin aspart before meals. Her HbA1c is 48 mmol/mol. Continuous glucose monitoring shows significant glycaemic variability with frequent hypoglycaemic episodes, particularly nocturnal. What is the most appropriate next step in her management?
- A. Reduce insulin degludec to 24 units and accept higher HbA1c target of 58-64 mmol/mol
- B. Switch to continuous subcutaneous insulin infusion (insulin pump) therapy
- C. Refer urgently to specialist diabetes centre for assessment for islet cell or pancreas transplantation (Correct Answer)
- D. Add a GLP-1 receptor agonist to reduce insulin requirements and hypoglycaemia risk
- E. Switch from insulin degludec to NPH insulin to allow more dose flexibility
Explanation: ***Refer urgently to specialist diabetes centre for assessment for islet cell or pancreas transplantation*** - This patient, with long-standing Type 1 diabetes, **hypoglycaemia unawareness**, and recurrent **severe hypoglycaemic episodes** (requiring emergency services) despite optimal basal-bolus insulin and **continuous glucose monitoring (CGM)**, meets the criteria for transplantation assessment. - When life-threatening **glycaemic variability** and severe hypoglycaemia persist despite advanced medical management, **pancreas or islet cell transplantation** offers the best chance for cure or significant improvement in glycaemic control and resolution of hypoglycaemia unawareness.*Reduce insulin degludec to 24 units and accept higher HbA1c target of 58-64 mmol/mol* - While accepting a higher **HbA1c target** can reduce hypoglycaemia risk and help restore **hypoglycaemia awareness**, this standalone measure is insufficient for a patient experiencing such severe and recurrent life-threatening episodes. - This approach might only partially mitigate the risk and could lead to **hyperglycaemia** without addressing the underlying failure of **counterregulatory responses** to hypoglycaemia.*Switch to continuous subcutaneous insulin infusion (insulin pump) therapy* - **Insulin pump therapy (CSII)** offers more precise and flexible insulin delivery, but this patient is already using modern analogue insulins (degludec, aspart) and **CGM**, yet still experiences severe episodes. - Given the severity (emergency services required twice in 3 months) and the failure of current advanced management, a pump alone is unlikely to provide the necessary level of control, and the patient has likely progressed beyond this as the primary next step.*Add a GLP-1 receptor agonist to reduce insulin requirements and hypoglycaemia risk* - **GLP-1 receptor agonists** are primarily indicated for Type 2 diabetes and are not routinely licensed or recommended for Type 1 diabetes, nor are they effective in addressing the lack of **glucagon response** in hypoglycaemia unawareness. - Adding such an agent could potentially complicate glycaemic control by slowing gastric emptying and increasing the risk of **gastrointestinal side effects** without offering significant protection against severe hypoglycaemia.*Switch from insulin degludec to NPH insulin to allow more dose flexibility* - **Insulin degludec** is a modern **ultra-long-acting insulin analogue** known for its very flat profile and low **intra-individual variability**, which significantly reduces the risk of nocturnal hypoglycaemia. - Switching to **NPH insulin**, an intermediate-acting human insulin with a pronounced peak and higher variability, would likely *increase* the risk of **nocturnal hypoglycaemia** and further destabilize glycaemic control, making the patient's condition worse.
Question 140: A 69-year-old man on rivaroxaban 20mg once daily for atrial fibrillation (CHA₂DS₂-VASc score 4) undergoes routine blood tests. Results show: eGFR 28 ml/min/1.73m² (previously 45 ml/min/1.73m² six months ago), creatinine 198 μmol/L. He has no bleeding and is otherwise well. What is the most appropriate management of his anticoagulation?
- A. Continue rivaroxaban 20mg once daily; dose reduction not required until eGFR <15 ml/min/1.73m²
- B. Reduce rivaroxaban dose to 15mg once daily and monitor renal function closely (Correct Answer)
- C. Switch to apixaban 2.5mg twice daily as it is safer in renal impairment
- D. Switch to warfarin with target INR 2-3 as DOACs are contraindicated in CKD stage 4
- E. Stop anticoagulation due to increased bleeding risk; start aspirin 75mg once daily
Explanation: ***Reduce rivaroxaban dose to 15mg once daily and monitor renal function closely***- For patients with atrial fibrillation and an **eGFR between 15-49 ml/min/1.73m²**, the licensed dose of **rivaroxaban** is reduced from 20mg to **15mg once daily** to prevent accumulation and bleeding.- This patient’s eGFR has declined to **28 ml/min/1.73m² (CKD stage 4)**, making the standard 20mg dose inappropriate and requiring closer monitoring of renal status.*Continue rivaroxaban 20mg once daily; dose reduction not required until eGFR <15 ml/min/1.73m²*- Maintaining the 20mg dose at an eGFR of 28 ml/min/1.73m² ignores established **renal dosing guidelines** and increases the patient's risk of **major hemorrhage**.- Dose reduction must occur when the **CrCl or eGFR falls below 50 ml/min**, not just when reaching end-stage renal disease.*Switch to apixaban 2.5mg twice daily as it is safer in renal impairment*- **Apixaban 2.5mg** twice daily is indicated only if the patient meets at least two criteria: **age ≥80**, **weight ≤60kg**, or **creatinine ≥133 μmol/L**; this patient only meets the creatinine criterion.- While apixaban has less renal clearance than rivaroxaban, a switch is not mandatory if the current agent can be correctly **dose-adjusted**.*Switch to warfarin with target INR 2-3 as DOACs are contraindicated in CKD stage 4*- DOACs like rivaroxaban and apixaban are **not contraindicated in CKD stage 4** (eGFR 15-29 ml/min); they are generally only contraindicated when **eGFR falls below 15 ml/min**.- Warfarin is an alternative for advanced CKD, but it requires frequent **monitoring** and is not the immediate required step given the license for dose-adjusted DOACs.*Stop anticoagulation due to increased bleeding risk; start aspirin 75mg once daily*- With a **CHA₂DS₂-VASc score of 4**, the patient is at high risk for **ischemic stroke**, and stopping anticoagulation would be hazardous.- **Aspirin monotherapy** is no longer recommended for stroke prevention in atrial fibrillation as it is significantly less effective than anticoagulants and still carries a bleeding risk.
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