Safe Prescribing — MCQs
On this page
A 76-year-old woman with atrial fibrillation is on dabigatran 150mg twice daily. She is admitted with a large retroperitoneal haemorrhage. Her haemoglobin is 72 g/L (baseline 135 g/L), blood pressure 88/52 mmHg, and heart rate 118 bpm. She last took dabigatran 6 hours ago. Her renal function shows eGFR 42 ml/min/1.73m². What is the most appropriate specific reversal strategy for her anticoagulation?
A 43-year-old woman with newly diagnosed type 1 diabetes is being discharged on basal-bolus insulin therapy. She will use insulin degludec 22 units once daily and insulin aspart before each meal using a carbohydrate counting ratio of 1 unit per 10g carbohydrate. She asks about alcohol consumption. Which of the following represents the most appropriate advice regarding alcohol and insulin management?
A 68-year-old man with atrial fibrillation is established on apixaban 5mg twice daily. He develops cellulitis of his right leg and is prescribed flucloxacillin by his general practitioner. After 5 days of antibiotics, he presents with frank haematuria and bruising. His renal function shows eGFR has dropped from 65 ml/min/1.73m² to 38 ml/min/1.73m². What is the most appropriate immediate management of his anticoagulation?
A 55-year-old woman with type 2 diabetes is admitted with acute coronary syndrome. She is normally managed on metformin 1g twice daily, sitagliptin 100mg once daily, and insulin glargine 40 units at bedtime. Her admission glucose is 14.2 mmol/L and HbA1c is 68 mmol/mol. She is scheduled for coronary angiography with possible percutaneous coronary intervention later today. Which modification to her diabetes medications is most appropriate prior to the procedure?
A 47-year-old man with type 1 diabetes presents to the emergency department with a 2-day history of vomiting and diarrhoea. He has continued taking his usual insulin doses (insulin detemir 32 units twice daily and insulin aspart 10 units before meals) but has been unable to eat. His capillary blood glucose is 3.2 mmol/L and ketones are 0.4 mmol/L. What is the most appropriate immediate insulin management?
A 64-year-old woman with newly diagnosed atrial fibrillation and CHA₂DS₂-VASc score of 4 is being considered for anticoagulation. She has normal renal function (eGFR 78 ml/min/1.73m²) and no valvular heart disease. She expresses concern about the need for regular blood monitoring. Which of the following statements regarding direct oral anticoagulants (DOACs) versus warfarin is most accurate in this context?
A 52-year-old man with type 2 diabetes is established on a basal-bolus insulin regimen. He uses insulin glargine 24 units at bedtime and insulin lispro before meals. Which of the following statements best describes the pharmacokinetic profile of insulin lispro compared to regular human insulin?
A 66-year-old man with atrial fibrillation on warfarin therapy presents for routine INR monitoring. His target INR is 2-3. Today's INR is 2.4. He reports starting a course of antibiotics from his general practitioner 3 days ago for a chest infection. Which antibiotic is most likely to require increased frequency of INR monitoring due to significant interaction with warfarin?
A 49-year-old man with type 2 diabetes for 12 years is admitted with hypoglycaemia (blood glucose 2.1 mmol/L). He is conscious and able to swallow. His medications include insulin detemir 38 units at bedtime, insulin aspart 12 units with each meal, metformin 1g twice daily, and gliclazide 80mg twice daily. After initial treatment with oral glucose, his blood glucose stabilizes at 6.8 mmol/L. What is the most appropriate medication review to prevent recurrence?
A 58-year-old woman with rheumatoid arthritis has been taking methotrexate 20mg once weekly for 3 years with good disease control. She develops a severe chest infection and her GP prescribes co-amoxiclav. Three days later she is admitted with mouth ulcers, sore throat, fever, and lethargy. Blood tests show: WBC 1.8 × 10⁹/L (neutrophils 0.4 × 10⁹/L), Hb 102 g/L, platelets 98 × 10⁹/L. What is the most likely explanation for her presentation?
Safe Prescribing UK Medical PG Practice Questions and MCQs
Question 71: A 76-year-old woman with atrial fibrillation is on dabigatran 150mg twice daily. She is admitted with a large retroperitoneal haemorrhage. Her haemoglobin is 72 g/L (baseline 135 g/L), blood pressure 88/52 mmHg, and heart rate 118 bpm. She last took dabigatran 6 hours ago. Her renal function shows eGFR 42 ml/min/1.73m². What is the most appropriate specific reversal strategy for her anticoagulation?
- A. Administer prothrombin complex concentrate (PCC) 50 units/kg
- B. Administer intravenous vitamin K 10mg
- C. Administer idarucizumab 5g intravenously (Correct Answer)
- D. Arrange urgent haemodialysis to remove dabigatran
- E. Administer tranexamic acid 1g intravenously
Explanation: ***Administer idarucizumab 5g intravenously***- **Idarucizumab** is a specific monoclonal antibody fragment that binds directly to **dabigatran**, rapidly and completely reversing its anticoagulant effect.- This immediate reversal is critical for patients with **life-threatening bleeding**, such as a **retroperitoneal haemorrhage** causing hemodynamic instability. *Administer prothrombin complex concentrate (PCC) 50 units/kg*- **PCC** is primarily used to reverse the effects of **vitamin K antagonists** (e.g., warfarin) or, less effectively, Factor Xa inhibitors.- It is not the specific or most effective reversal agent for **dabigatran**, as its mechanism does not directly counteract dabigatran's action. *Administer intravenous vitamin K 10mg*- **Vitamin K** is administered to reverse the effects of **warfarin** by promoting the synthesis of vitamin K-dependent clotting factors.- It has no role in reversing **dabigatran**, which is a **direct thrombin inhibitor** and does not interact with the vitamin K pathway. *Arrange urgent haemodialysis to remove dabigatran*- While **dabigatran** is partially dialyzable due to its low protein binding, **haemodialysis** is a slow process.- It is not an appropriate immediate strategy for an **acute, life-threatening bleed** requiring rapid reversal of anticoagulation. *Administer tranexamic acid 1g intravenously*- **Tranexamic acid** is an **antifibrinolytic** agent that inhibits fibrinolysis, helping to stabilize clots.- It does not reverse the underlying **anticoagulant effect** of dabigatran and is therefore not a specific reversal strategy, although it may be used as adjunctive therapy.
Question 72: A 43-year-old woman with newly diagnosed type 1 diabetes is being discharged on basal-bolus insulin therapy. She will use insulin degludec 22 units once daily and insulin aspart before each meal using a carbohydrate counting ratio of 1 unit per 10g carbohydrate. She asks about alcohol consumption. Which of the following represents the most appropriate advice regarding alcohol and insulin management?
- A. Avoid alcohol completely as it unpredictably affects blood glucose levels
- B. Alcohol increases blood glucose, so increase mealtime insulin dose by 20% when drinking
- C. Alcohol can cause delayed hypoglycaemia, so reduce basal insulin dose on days when drinking
- D. Alcohol inhibits gluconeogenesis and can cause delayed hypoglycaemia for up to 24 hours; have carbohydrate snack before bed (Correct Answer)
- E. Alcohol has no effect on insulin requirements if consumed with food
Explanation: ***Alcohol inhibits gluconeogenesis and can cause delayed hypoglycaemia for up to 24 hours; have carbohydrate snack before bed*** - Alcohol consumption inhibits **hepatic gluconeogenesis**, which significantly increases the risk of **delayed hypoglycemia** long after the acute effects of the drink have worn off. - Patients on insulin should be advised to consume a **carbohydrate snack** before bed and never drink on an empty stomach to prevent nocturnal or next-day hypoglycemic episodes. *Avoid alcohol completely as it unpredictably affects blood glucose levels* - While alcohol does affect glucose levels, it is not necessary to **avoid it completely**; patients can drink in moderation if they follow safety precautions. - Complete avoidance is generally unrealistic for many patients and prevents them from learning how to manage **real-world scenarios** safely. *Alcohol increases blood glucose, so increase mealtime insulin dose by 20% when drinking* - Increasing insulin doses while drinking is dangerous because the predominant risk of alcohol in insulin-treated patients is **hypoglycemia**, not hyperglycemia. - Although sugary mixers may cause a transient rise, the metabolic effect of alcohol suppresses **liver glucose output**, making extra insulin a risk for severe reactions. *Alcohol can cause delayed hypoglycaemia, so reduce basal insulin dose on days when drinking* - Reducing the **basal insulin** (like degludec) is discouraged because it can lead to poor glycemic control and a risk of **diabetic ketoacidosis (DKA)**. - Management should focus on supplemental **carbohydrate intake** rather than adjusting the long-acting insulin dose which lasts for many hours beyond the metabolic window of the alcohol. *Alcohol has no effect on insulin requirements if consumed with food* - Even when consumed with food, alcohol still impairs the liver's ability to release glucose, potentially necessitating **less bolus insulin** or extra snacks. - Claiming it has **no effect** is medically inaccurate and dangerous, as it ignores the 24-hour window of increased **hypoglycemia risk**.
Question 73: A 68-year-old man with atrial fibrillation is established on apixaban 5mg twice daily. He develops cellulitis of his right leg and is prescribed flucloxacillin by his general practitioner. After 5 days of antibiotics, he presents with frank haematuria and bruising. His renal function shows eGFR has dropped from 65 ml/min/1.73m² to 38 ml/min/1.73m². What is the most appropriate immediate management of his anticoagulation?
- A. Continue apixaban 5mg twice daily and monitor renal function in 1 week
- B. Reduce apixaban to 2.5mg twice daily and recheck renal function in 48 hours
- C. Stop apixaban immediately, give prothrombin complex concentrate
- D. Stop apixaban temporarily until bleeding resolves and renal function stabilizes (Correct Answer)
- E. Switch to warfarin with target INR 2-3
Explanation: ***Stop apixaban temporarily until bleeding resolves and renal function stabilizes*** - The patient presents with **frank haematuria** and **bruising**, indicating **active bleeding** while on an anticoagulant. This, combined with a significant **acute kidney injury (AKI)** (eGFR dropped from 65 to 38), means apixaban clearance is impaired, increasing drug accumulation and bleeding risk. - Temporarily stopping **apixaban** is crucial to allow the drug to be cleared (half-life ~12 hours) and to allow time for the **bleeding** to resolve and **renal function** to recover and stabilize, at which point the need for anticoagulation can be reassessed. *Continue apixaban 5mg twice daily and monitor renal function in 1 week* - Continuing a full dose of **apixaban** in the presence of **frank haematuria** and an acute drop in **renal function** is unsafe and will exacerbate the bleeding risk and renal impairment due to drug accumulation. - Waiting one week to monitor renal function is too long given the acute nature of the **AKI** and active bleeding; immediate action and closer monitoring are required. *Reduce apixaban to 2.5mg twice daily and recheck renal function in 48 hours* - While apixaban dose reduction is indicated for certain renal impairment criteria (e.g., eGFR 15-50 ml/min with other factors), this is for stable conditions, not for managing **active bleeding** and **acute kidney injury**. - In the setting of ongoing bleeding and impaired drug clearance, a temporary **cessation of apixaban** is necessary rather than a mere dose reduction, as reduction may still allow for further accumulation and bleeding. *Stop apixaban immediately, give prothrombin complex concentrate* - Stopping apixaban immediately is correct, but administering **prothrombin complex concentrate (PCC)** or specific reversal agents (like Andexanet alfa for apixaban) is typically reserved for **severe or life-threatening bleeding** (e.g., intracranial hemorrhage, hemodynamic instability). - While haematuria is significant, the scenario doesn't describe a life-threatening bleed requiring immediate full reversal. The primary step for non-life-threatening but active bleeding is to stop the anticoagulant and support the patient. *Switch to warfarin with target INR 2-3* - Switching to **warfarin** is inappropriate in this acute setting, as warfarin has a slow onset of action and would not address the immediate issues of **active bleeding** and **acute kidney injury**. - Furthermore, managing **warfarin** in a patient with fluctuating **renal function** and potential drug-drug interactions (e.g., with antibiotics affecting gut flora) would be complex and delay resolution of the acute problem.
Question 74: A 55-year-old woman with type 2 diabetes is admitted with acute coronary syndrome. She is normally managed on metformin 1g twice daily, sitagliptin 100mg once daily, and insulin glargine 40 units at bedtime. Her admission glucose is 14.2 mmol/L and HbA1c is 68 mmol/mol. She is scheduled for coronary angiography with possible percutaneous coronary intervention later today. Which modification to her diabetes medications is most appropriate prior to the procedure?
- A. Continue all medications as normal and check glucose 2 hours post-procedure
- B. Omit metformin on the day of procedure and for 48 hours afterwards, continue other medications (Correct Answer)
- C. Stop insulin and metformin, continue sitagliptin only
- D. Stop all oral medications, convert to variable rate intravenous insulin infusion
- E. Continue metformin and insulin, omit sitagliptin on day of procedure
Explanation: ***Omit metformin on the day of procedure and for 48 hours afterwards, continue other medications***- **Metformin** should be withheld during procedures involving **iodinated contrast media** to prevent the risk of **lactic acidosis** if contrast-induced nephropathy occurs.- **Insulin glargine** (basal insulin) and **sitagliptin** (DPP-4 inhibitor) are typically continued to maintain glycemic control with a low risk of hypoglycemia.*Continue all medications as normal and check glucose 2 hours post-procedure*- Continuing **metformin** during **coronary angiography** is unsafe due to the potential for acute kidney injury and associated toxic accumulation of the drug.- Monitoring glucose alone does not address the physiological risks associated with **contrast media** and metformin interaction.*Stop insulin and metformin, continue sitagliptin only*- Stopping **basal insulin** (glargine) in a patient with type 2 diabetes managed on insulin can lead to severe **hyperglycemia** or ketoacidosis during the stress of a procedure.- **Metformin** must be stopped, but the omission of insulin is clinically inappropriate for maintaining stable peri-operative glucose levels.*Stop all oral medications, convert to variable rate intravenous insulin infusion*- A **variable rate intravenous insulin infusion (VRIII)** is generally reserved for patients with poor glycemic control who are fasting for long periods or are hemodynamically unstable.- This patient is undergoing a discrete procedure and can be managed by omitting **metformin** while continuing other medications to maintain safety.*Continue metformin and insulin, omit sitagliptin on day of procedure*- This approach is incorrect as it fails to address the high-risk medication, **metformin**, which is the priority for omission before **contrast exposure**.- Omission of **sitagliptin** is unnecessary as it does not carry the same systemic risks as metformin in the context of **angiography**.
Question 75: A 47-year-old man with type 1 diabetes presents to the emergency department with a 2-day history of vomiting and diarrhoea. He has continued taking his usual insulin doses (insulin detemir 32 units twice daily and insulin aspart 10 units before meals) but has been unable to eat. His capillary blood glucose is 3.2 mmol/L and ketones are 0.4 mmol/L. What is the most appropriate immediate insulin management?
- A. Continue basal insulin at current dose but omit all bolus insulin until eating normally
- B. Reduce both basal and bolus insulin by 50% until symptoms resolve
- C. Stop all insulin until the patient can tolerate oral intake
- D. Continue basal insulin and give small doses of rapid-acting insulin with glucose drinks (Correct Answer)
- E. Switch to variable rate intravenous insulin infusion
Explanation: ***Continue basal insulin and give small doses of rapid-acting insulin with glucose drinks*** - In **Type 1 Diabetes**, **basal insulin** must **never be stopped** during illness to prevent the rapid development of **diabetic ketoacidosis (DKA)**. - This approach aligns with "sick day rules" for managing illness: treating **hypoglycemia** with **glucose-containing drinks** while providing sufficient insulin to prevent **ketone production** and cover consumed carbohydrates. *Continue basal insulin at current dose but omit all bolus insulin until eating normally* - While **basal insulin** is crucial, omitting all **bolus insulin** when consuming glucose-containing fluids to manage hypoglycemia can lead to **hyperglycemia** and risk of **ketosis**. - Patients should be advised to take **small, adjusted bolus doses** of rapid-acting insulin to cover the carbohydrates from **liquid intake**. *Reduce both basal and bolus insulin by 50% until symptoms resolve* - A fixed **50% reduction** is an arbitrary and potentially insufficient adjustment, as illness can increase **insulin resistance** due to **stress hormones**, thus increasing insulin requirements. - Insulin adjustments during illness should be **dynamic** and guided by frequent **blood glucose** and **ketone monitoring**, rather than a blanket reduction. *Stop all insulin until the patient can tolerate oral intake* - Stopping all insulin is extremely dangerous for **Type 1 diabetics** and will rapidly lead to severe **diabetic ketoacidosis (DKA)** within hours, as the body cannot produce its own insulin. - Even without solid food intake, **basal insulin** is essential to regulate endogenous glucose production and prevent severe **lipolysis** and **ketogenesis**. *Switch to variable rate intravenous insulin infusion* - **Variable rate intravenous insulin infusion (VRIII)** is typically reserved for more severe conditions, such as persistent or uncontrollable vomiting, severe **DKA**, surgical procedures, or prolonged inability to tolerate oral intake. - For a patient who can potentially manage oral intake of glucose drinks and whose ketones are only slightly elevated, initial management typically involves **sick day rules** and close monitoring rather than immediate intravenous therapy.
Question 76: A 64-year-old woman with newly diagnosed atrial fibrillation and CHA₂DS₂-VASc score of 4 is being considered for anticoagulation. She has normal renal function (eGFR 78 ml/min/1.73m²) and no valvular heart disease. She expresses concern about the need for regular blood monitoring. Which of the following statements regarding direct oral anticoagulants (DOACs) versus warfarin is most accurate in this context?
- A. DOACs require monthly INR monitoring but have fewer dietary restrictions than warfarin
- B. DOACs do not require routine coagulation monitoring and have predictable pharmacokinetics (Correct Answer)
- C. DOACs require weekly monitoring of anti-Xa levels for the first 3 months
- D. DOACs have similar monitoring requirements to warfarin but shorter half-lives
- E. DOACs require monthly renal function testing but no coagulation monitoring
Explanation: ***DOACs do not require routine coagulation monitoring and have predictable pharmacokinetics*** - **DOACs** provide a consistent anticoagulant response due to their **predictable pharmacokinetics**, which eliminates the need for routine **INR** or coagulation monitoring. - They are often preferred for patients with **non-valvular atrial fibrillation** who desire convenience and lack of **dietary restrictions** compared to warfarin. *DOACs require monthly INR monitoring but have fewer dietary restrictions than warfarin* - **INR monitoring** is specific to **Warfarin** (Vitamin K Antagonist) therapy to ensure the patient remains within the **therapeutic range**. - While DOACs do have fewer **dietary restrictions**, they do not use INR as a measurement of their therapeutic effect. *DOACs require weekly monitoring of anti-Xa levels for the first 3 months* - Routine monitoring of **anti-Xa levels** is not recommended for patients on DOACs such as **Apixaban** or **Rivaroxaban**. - Measurement of drug levels is only typically considered in **emergency situations**, such as major bleeding or prior to urgent surgery. *DOACs have similar monitoring requirements to warfarin but shorter half-lives* - The primary advantage of DOACs is that they have **significantly fewer monitoring requirements** compared to the frequent blood tests needed for warfarin. - While they do generally have **shorter half-lives**, their monitoring protocols are entirely distinct from the **INR-based** approach used for warfarin. *DOACs require monthly renal function testing but no coagulation monitoring* - While DOACs do require **renal function monitoring** because they are renally excreted, **monthly testing** is unnecessary for a patient with an **eGFR of 78**. - Guidelines generally recommend checking renal function at **initiation** and then **annually**, unless the patient is elderly or has known **chronic kidney disease**.
Question 77: A 52-year-old man with type 2 diabetes is established on a basal-bolus insulin regimen. He uses insulin glargine 24 units at bedtime and insulin lispro before meals. Which of the following statements best describes the pharmacokinetic profile of insulin lispro compared to regular human insulin?
- A. Insulin lispro has a delayed onset of action of 60 minutes and duration of 6-8 hours
- B. Insulin lispro has an onset of action within 15 minutes and duration of 2-5 hours (Correct Answer)
- C. Insulin lispro has an onset of action of 30 minutes and duration of 8-10 hours
- D. Insulin lispro has an onset of action within 15 minutes and duration of 12-24 hours
- E. Insulin lispro has an onset of action of 45 minutes and duration of 4-6 hours
Explanation: ***Insulin lispro has an onset of action within 15 minutes and duration of 2-5 hours***- **Insulin lispro** is a **rapid-acting insulin analogue** designed to mimic the physiological postprandial insulin spike, starting to work within **15 minutes**.- Its shorter duration of **2-5 hours** reduces the risk of **late postprandial hypoglycemia** compared to regular human insulin.*Insulin lispro has a delayed onset of action of 60 minutes and duration of 6-8 hours*- This profile more closely resembles **regular (short-acting) human insulin**, which requires administration 30-60 minutes before meals.- **Insulin lispro** is specifically engineered to avoid this delay by preventing the formation of **hexamers**, allowing for faster absorption.*Insulin lispro has an onset of action of 30 minutes and duration of 8-10 hours*- An onset of 30 minutes is characteristic of **regular insulin**, but a duration of 8-10 hours is unusually long for any bolus insulin.- **Rapid-acting analogues** like lispro are cleared more quickly from the circulation, typically lasting no more than **5 hours**.*Insulin lispro has an onset of action within 15 minutes and duration of 12-24 hours*- While the onset matches lispro, a **12-24 hour duration** is characteristic of **long-acting basal insulins** like **glargine** or **detemir**.- Using a bolus insulin with such a long duration would lead to cumulative and dangerous **hypoglycemia** if dosed with every meal.*Insulin lispro has an onset of action of 45 minutes and duration of 4-6 hours*- An onset of 45 minutes is too slow for **lispro** and would not provide adequate coverage for immediate **postprandial glucose excursions**.- **Lispro** is intended for injection immediately before or even just after a meal due to its much faster **15-minute onset**.
Question 78: A 66-year-old man with atrial fibrillation on warfarin therapy presents for routine INR monitoring. His target INR is 2-3. Today's INR is 2.4. He reports starting a course of antibiotics from his general practitioner 3 days ago for a chest infection. Which antibiotic is most likely to require increased frequency of INR monitoring due to significant interaction with warfarin?
- A. Amoxicillin
- B. Doxycycline
- C. Clarithromycin (Correct Answer)
- D. Penicillin V
- E. Azithromycin
Explanation: ***Clarithromycin*** - **Clarithromycin** is a potent inhibitor of the **CYP3A4** enzyme, which significantly reduces the metabolism of **warfarin**, leading to a dangerous rise in **INR** levels. - Due to this high-risk interaction, clinical guidelines mandate **increased frequency of INR monitoring** (typically within 3-5 days) to prevent spontaneous bleeding. *Amoxicillin* - While broad-spectrum antibiotics can theoretically alter **gut flora** and reduce vitamin K synthesis, **Amoxicillin** has a relatively low risk of significant warfarin interaction. - It does not inhibit the **cytochrome P450** system, making it a safer profile compared to macrolides, though routine caution is still advised. *Doxycycline* - **Doxycycline** can occasionally enhance the effect of warfarin by interfering with **prothrombin activity**, but the effect is generally less predictable and potent than enzyme inhibitors. - It is not considered a primary **CYP450 inhibitor**, so it rarely necessitates the same level of urgent monitoring as clarithromycin. *Penicillin V* - **Penicillin V** has no major pharmacokinetic interaction with warfarin as it does not interfere with its metabolic pathways in the **liver**. - It is frequently chosen for infections in anticoagulated patients because it is unlikely to cause a clinically significant **INR deviation**. *Azithromycin* - Although a macrolide, **Azithromycin** is unique because it does not significantly inhibit **CYP3A4**, resulting in a much lower risk of interaction than clarithromycin or erythromycin. - While caution is still recommended, it is generally preferred over other macrolides for patients on **warfarin therapy**.
Question 79: A 49-year-old man with type 2 diabetes for 12 years is admitted with hypoglycaemia (blood glucose 2.1 mmol/L). He is conscious and able to swallow. His medications include insulin detemir 38 units at bedtime, insulin aspart 12 units with each meal, metformin 1g twice daily, and gliclazide 80mg twice daily. After initial treatment with oral glucose, his blood glucose stabilizes at 6.8 mmol/L. What is the most appropriate medication review to prevent recurrence?
- A. Reduce insulin detemir dose by 20% as basal insulin is likely cause of overnight hypoglycaemia
- B. Discontinue gliclazide as sulfonylureas add limited benefit to insulin therapy and increase hypoglycaemia risk substantially (Correct Answer)
- C. Reduce all insulin doses by 10% and continue all oral medications
- D. Discontinue metformin as it can potentiate insulin action and cause hypoglycaemia
- E. Switch gliclazide to a DPP-4 inhibitor as they have lower hypoglycaemia risk
Explanation: ***Discontinue gliclazide as sulfonylureas add limited benefit to insulin therapy and increase hypoglycaemia risk substantially***- **Sulfonylureas** stimulate endogenous insulin secretion, which offers minimal cumulative benefit once a patient is established on a full **basal-bolus insulin** regimen.- Discontinuing this class significantly reduces the risk of **recurrent hypoglycaemia** and rationalizes treatment by removing unnecessary polypharmacy.*Reduce insulin detemir dose by 20% as basal insulin is likely cause of overnight hypoglycaemia*- While adjusting basal insulin may be necessary later, the **priority** is removing a drug class (Sulfonylurea) that is generally redundant once insulin is optimized.- The question does not specify the timing of the event; solely reducing insulin without addressing **gliclazide** leaves the patient at continued risk.*Reduce all insulin doses by 10% and continue all oral medications*- Simply reducing insulin doses is a reactive measure that fails to address the underlying **安全 risk** posed by combining secretagogues with exogenous insulin.- Continuing **sulfonylureas** alongside intensive insulin therapy is generally discouraged due to the high risk/low benefit ratio.*Discontinue metformin as it can potentiate insulin action and cause hypoglycaemia*- **Metformin** works by improving insulin sensitivity and inhibiting gluconeogenesis; it does not typically cause hypoglycaemia as single therapy.- Metformin should be **continued** in most type 2 diabetics on insulin because it provides cardiovascular benefits and helps limit weight gain.*Switch gliclazide to a DPP-4 inhibitor as they have lower hypoglycaemia risk*- While **DPP-4 inhibitors** have a lower hypoglycaemia profile, most patients on a basal-bolus regimen do not require additional agents beyond metformin.- Adding another agent instead of **rationalizing therapy** adds unnecessary cost and complexity without clear clinical benefit for this patient.
Question 80: A 58-year-old woman with rheumatoid arthritis has been taking methotrexate 20mg once weekly for 3 years with good disease control. She develops a severe chest infection and her GP prescribes co-amoxiclav. Three days later she is admitted with mouth ulcers, sore throat, fever, and lethargy. Blood tests show: WBC 1.8 × 10⁹/L (neutrophils 0.4 × 10⁹/L), Hb 102 g/L, platelets 98 × 10⁹/L. What is the most likely explanation for her presentation?
- A. Coincidental viral infection causing transient bone marrow suppression
- B. Co-amoxiclav has displaced methotrexate from protein binding sites, increasing free drug concentration and toxicity
- C. The patient has inadvertently taken methotrexate daily instead of weekly during her illness (Correct Answer)
- D. Co-amoxiclav has reduced renal excretion of methotrexate, leading to accumulation and toxicity
- E. Rheumatoid arthritis disease flare has caused reactive bone marrow suppression
Explanation: ***The patient has inadvertently taken methotrexate daily instead of weekly during her illness***- Inadvertent **daily administration** of methotrexate is a major cause of severe **pancytopenia** and **mucositis** (mouth ulcers, sore throat), as it inhibits dihydrofolate reductase and prevents DNA synthesis in rapidly dividing cells.- High-risk prescribing errors often occur during acute illnesses when patients become confused about **weekly dosing schedules**, leading to life-threatening **bone marrow suppression**.*Coincidental viral infection causing transient bone marrow suppression*- While some viruses (like Parvovirus B19) can cause marrow suppression, they typically cause a **pure red cell aplasia** rather than global pancytopenia with severe mucositis as seen here.- The temporal relationship with an acute illness and long-term **methotrexate** use makes drug toxicity a much more probable cause for these symptoms.*Co-amoxiclav has displaced methotrexate from protein binding sites, increasing free drug concentration and toxicity*- Methotrexate is significantly bound to **albumin**, but protein displacement by co-amoxiclav is not a clinically significant mechanism for acute, severe **methotrexate toxicity** at this dosage.- Drug interactions based on protein binding are generally less dangerous than those affecting **renal excretion** or metabolic pathways for methotrexate.*Co-amoxiclav has reduced renal excretion of methotrexate, leading to accumulation and toxicity*- While some antibiotics like **Trimethoprim** or **Penicillins** can compete for **renal tubular secretion** of methotrexate, this interaction is rarely severe enough to cause rapid-onset, profound pancytopenia and mucositis at low rheumatological doses of methotrexate.- Clinical guidelines suggest this interaction is more relevant with **high-dose methotrexate** used in oncology or in patients with underlying **renal impairment**.*Rheumatoid arthritis disease flare has caused reactive bone marrow suppression*- A rheumatoid flare usually causes **anemia of chronic disease** (normocytic/microcytic) and sometimes **thrombocytosis**, rather than profound **neutropenia** and **thrombocytopenia**.- Systemic features like severe **mouth ulcers** and **pancytopenia** are highly characteristic of methotrexate toxicity, not typically a direct manifestation of an RA flare itself.
Practice by Chapter
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free