Safe Prescribing — MCQs
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A 66-year-old man with non-valvular atrial fibrillation (CHA₂DS₂-VASc score 4) is on edoxaban 60mg once daily. He develops progressive chronic kidney disease, and his most recent eGFR is 28 ml/min/1.73m². His weight is 72kg and he has no other comorbidities. What is the most appropriate adjustment to his anticoagulation?
A 41-year-old woman with type 1 diabetes on insulin pump therapy (continuous subcutaneous insulin infusion) is admitted with acute pyelonephritis. She is alert, tolerating oral fluids, and maintaining her oral intake. Her blood glucose is 14.2 mmol/L and capillary ketones are 0.8 mmol/L. What is the most appropriate insulin management during her admission?
A 73-year-old man with mechanical aortic valve replacement on warfarin (target INR 2.5-3.5) presents with melaena. His INR is 7.2 and haemoglobin is 74 g/L (baseline 135 g/L). He is haemodynamically stable (BP 128/76 mmHg, HR 88 bpm). Upper GI endoscopy is planned. What is the most appropriate immediate management of his anticoagulation?
A 55-year-old woman with type 2 diabetes is on a basal-bolus insulin regimen (insulin glargine 32 units at bedtime, insulin lispro 8 units with each meal). She is scheduled for elective laparoscopic cholecystectomy as the first case in the morning. What is the most appropriate perioperative insulin management?
A 68-year-old man with atrial fibrillation on apixaban 5mg twice daily requires emergency surgery for a perforated duodenal ulcer. His last dose of apixaban was 8 hours ago. His renal function is normal (eGFR 68 ml/min/1.73m²). What is the most appropriate approach to managing his anticoagulation perioperatively?
A 37-year-old woman with type 1 diabetes for 18 years is admitted with severe vomiting and abdominal pain. Her capillary blood glucose is 22.4 mmol/L and capillary ketones are 4.8 mmol/L. Arterial blood gas shows pH 7.24, bicarbonate 12 mmol/L. She is diagnosed with diabetic ketoacidosis. Her usual insulin is insulin aspart three times daily with meals and insulin glargine at bedtime. What is the most appropriate initial insulin management?
A 52-year-old woman with newly diagnosed deep vein thrombosis is commenced on rivaroxaban. She weighs 58kg and has normal renal function (eGFR 78 ml/min/1.73m²). She is also taking carbamazepine 400mg twice daily for epilepsy. What is the most appropriate anticoagulation regimen?
A 64-year-old man with atrial fibrillation is on rivaroxaban 20mg once daily. He develops acute bacterial meningitis and requires treatment with rifampicin. Understanding drug interactions with DOACs, what is the most appropriate management of his anticoagulation?
A 71-year-old woman with type 2 diabetes on insulin glargine 26 units at bedtime and metformin 1g twice daily presents with a painful diabetic foot ulcer. She is started on oral antibiotics but reports poor oral intake due to nausea. Her capillary blood glucose readings over the past 24 hours range from 4.2 to 6.8 mmol/L. What is the most appropriate approach to her insulin management?
A 46-year-old man with epilepsy is established on phenytoin 300mg daily. He attends for routine monitoring. His recent phenytoin level is 18 mg/L (therapeutic range 10-20 mg/L), but he reports mild ataxia and diplopia. What is the most appropriate explanation for these symptoms?
Safe Prescribing UK Medical PG Practice Questions and MCQs
Question 81: A 66-year-old man with non-valvular atrial fibrillation (CHA₂DS₂-VASc score 4) is on edoxaban 60mg once daily. He develops progressive chronic kidney disease, and his most recent eGFR is 28 ml/min/1.73m². His weight is 72kg and he has no other comorbidities. What is the most appropriate adjustment to his anticoagulation?
- A. Continue edoxaban 60mg once daily as dose reduction is only needed below eGFR 15 ml/min/1.73m²
- B. Reduce edoxaban dose to 30mg once daily (Correct Answer)
- C. Switch to apixaban 2.5mg twice daily as it is safer in renal impairment
- D. Switch to warfarin as DOACs should be avoided in CKD stage 4
- E. Stop anticoagulation as bleeding risk outweighs stroke risk at this level of renal function
Explanation: ***Reduce edoxaban dose to 30mg once daily*** - For patients with **non-valvular atrial fibrillation**, the standard dose of **edoxaban** (60mg) must be reduced to **30mg once daily** if the **creatinine clearance (or eGFR)** is between **15-50 ml/min**. - This patient's **eGFR of 28 ml/min/1.73m²** falls within this range, necessitating a dose reduction to maintain therapeutic levels and minimize **bleeding risk**. *Continue edoxaban 60mg once daily as dose reduction is only needed below eGFR 15 ml/min/1.73m²* - Maintaining the full **60mg dose** in the presence of **moderate renal impairment** (eGFR 28 ml/min) significantly increases the risk of **drug accumulation** and **major bleeding**. - **Edoxaban** dose reduction is required for an eGFR of **15-50 ml/min**, not just below 15 ml/min, where it is contraindicated. *Switch to apixaban 2.5mg twice daily as it is safer in renal impairment* - **Apixaban** dose reduction to 2.5mg twice daily is indicated only if the patient meets at least two of the following: **age ≥80 years**, **weight ≤60 kg**, or **serum creatinine ≥1.5 mg/dL**. - This patient (age 66, weight 72kg, eGFR 28 ml/min) does not meet these specific criteria, making a switch unnecessary when **edoxaban** can be appropriately adjusted. *Switch to warfarin as DOACs should be avoided in CKD stage 4* - **DOACs** are generally preferred over **warfarin** for non-valvular AF, even in **CKD stage 4** (eGFR 15-29 ml/min), provided accurate **dose adjustments** are made. - **Warfarin** is typically reserved for patients with specific conditions like **mechanical heart valves** or when eGFR is below 15 ml/min (End-Stage Renal Disease). *Stop anticoagulation as bleeding risk outweighs stroke risk at this level of renal function* - A **CHA₂DS₂-VASc score of 4** indicates a **high annual stroke risk** (~4%) that generally outweighs the bleeding risk in patients with stable CKD, making continued anticoagulation crucial. - **Chronic kidney disease** is an independent risk factor for both **stroke and bleeding**, necessitating careful **anticoagulation dose management** rather than cessation.
Question 82: A 41-year-old woman with type 1 diabetes on insulin pump therapy (continuous subcutaneous insulin infusion) is admitted with acute pyelonephritis. She is alert, tolerating oral fluids, and maintaining her oral intake. Her blood glucose is 14.2 mmol/L and capillary ketones are 0.8 mmol/L. What is the most appropriate insulin management during her admission?
- A. Continue insulin pump therapy with increased basal and bolus rates to account for infection (Correct Answer)
- B. Discontinue pump and convert to variable rate intravenous insulin infusion
- C. Discontinue pump and convert to basal-bolus subcutaneous insulin regimen
- D. Continue pump but add supplementary subcutaneous rapid-acting insulin for correction
- E. Continue pump unchanged as ketones are not significantly elevated
Explanation: ***Continue insulin pump therapy with increased basal and bolus rates to account for infection***- Patients on **continuous subcutaneous insulin infusion (CSII)** should continue their therapy during illness if they are **alert**, tolerating oral intake, and able to **self-manage** the device.- Acute infection increases **insulin resistance** and counter-regulatory hormones, necessitating an **increase in basal and bolus rates** to maintain glycemic control and prevent ketoacidosis.*Discontinue pump and convert to variable rate intravenous insulin infusion*- **Variable rate intravenous insulin infusion (VRIII)** is only indicated if the patient is **vomiting**, unable to eat, has a reduced level of consciousness, or is undergoing **major surgery**.- This patient is alert and tolerating fluids, so transitioning to intravenous therapy unnecessarily complicates management and increases the risk of **glycemic instability**.*Discontinue pump and convert to basal-bolus subcutaneous insulin regimen*- Switching to a **basal-bolus regimen** is unnecessary when the patient's existing pump therapy is effective and they are capable of managing it.- Disrupting established **pump therapy** can be distressing for the patient and often leads to poorer control during the transition period.*Continue pump but add supplementary subcutaneous rapid-acting insulin for correction*- Giving separate injections while the pump is running increases the risk of **insulin stacking**, which can lead to severe **hypoglycemia**.- Dose adjustments for hyperglycemia should be managed through the **pump's bolus calculator** or by temporary basal rate increases rather than supplementary injections.*Continue pump unchanged as ketones are not significantly elevated*- Leaving the pump rates unchanged during an infection is inappropriate because **pro-inflammatory cytokines** elevate blood glucose regardless of ketone levels.- A **blood glucose of 14.2 mmol/L** and the presence of ketones (0.8 mmol/L) indicate that current insulin delivery is insufficient to meet the body's **increased metabolic demands**.
Question 83: A 73-year-old man with mechanical aortic valve replacement on warfarin (target INR 2.5-3.5) presents with melaena. His INR is 7.2 and haemoglobin is 74 g/L (baseline 135 g/L). He is haemodynamically stable (BP 128/76 mmHg, HR 88 bpm). Upper GI endoscopy is planned. What is the most appropriate immediate management of his anticoagulation?
- A. Stop warfarin and give oral vitamin K 1-3mg; repeat INR in 24 hours
- B. Stop warfarin, give intravenous vitamin K 5mg, and arrange urgent endoscopy once INR normalises (Correct Answer)
- C. Stop warfarin, give prothrombin complex concentrate and intravenous vitamin K 5mg for immediate reversal
- D. Stop warfarin and arrange urgent endoscopy without reversal as he is haemodynamically stable
- E. Continue warfarin at reduced dose as cessation risks valve thrombosis
Explanation: ***Stop warfarin, give intravenous vitamin K 5mg, and arrange urgent endoscopy once INR normalises*** - The patient has **major bleeding** (melaena with significant haemoglobin drop) but is **haemodynamically stable**, making intravenous vitamin K the appropriate choice for rapid reversal (within 6-12 hours). - Reversing the INR to a safer level before endoscopy is crucial to minimize the risk of **procedural bleeding**, while avoiding the immediate and complete reversal of PCC which carries a higher **thromboembolic risk** for mechanical valves. *Stop warfarin and give oral vitamin K 1-3mg; repeat INR in 24 hours* - **Oral vitamin K** has a slower onset of action and is typically used for **non-bleeding** or **minor bleeding** scenarios with elevated INR, not active melaena with a significant Hb drop. - Waiting 24 hours to recheck INR is too long for a patient with **active gastrointestinal bleeding** and an INR of 7.2, as this delays necessary intervention and increases bleeding risk. *Stop warfarin, give prothrombin complex concentrate and intravenous vitamin K 5mg for immediate reversal* - **Prothrombin complex concentrate (PCC)** provides immediate reversal but carries a higher risk of **thromboembolic events**, particularly with mechanical heart valves. - PCC is generally reserved for **life-threatening bleeding** or intracranial hemorrhage. Since the patient is **haemodynamically stable**, the immediate thrombotic risks of PCC outweigh its benefit in this specific context. *Stop warfarin and arrange urgent endoscopy without reversal as he is haemodynamically stable* - Performing an **endoscopy** with an INR of 7.2 carries an unacceptably high risk of **uncontrolled bleeding**, especially if therapeutic interventions like biopsy or cautery are required. - While currently stable, the significant **haemoglobin drop** indicates serious bleeding that necessitates correction of the coagulopathy before any invasive procedure. *Continue warfarin at reduced dose as cessation risks valve thrombosis* - Continuing **warfarin** in a patient with an INR of 7.2 and active **melaena** is contraindicated, as it will exacerbate bleeding and could lead to a life-threatening hemorrhage. - The immediate risk of severe bleeding from over-anticoagulation far outweighs the theoretical risk of **valve thrombosis** from temporary warfarin cessation in this acute situation.
Question 84: A 55-year-old woman with type 2 diabetes is on a basal-bolus insulin regimen (insulin glargine 32 units at bedtime, insulin lispro 8 units with each meal). She is scheduled for elective laparoscopic cholecystectomy as the first case in the morning. What is the most appropriate perioperative insulin management?
- A. Omit morning rapid-acting insulin, give usual basal insulin, convert to variable rate intravenous insulin infusion perioperatively (Correct Answer)
- B. Omit all insulin on the day of surgery and commence sliding scale when blood glucose exceeds 12 mmol/L
- C. Give 50% of usual basal insulin on morning of surgery, omit rapid-acting insulin, start variable rate insulin infusion
- D. Continue all usual insulin doses and schedule surgery after lunch
- E. Give usual basal insulin the night before but omit morning dose, commence intravenous insulin at induction
Explanation: ***Omit morning rapid-acting insulin, give usual basal insulin, convert to variable rate intravenous insulin infusion perioperatively***- For a patient on a **basal-bolus** regimen, the **basal insulin** (glargine) should be continued to provide background coverage and prevent **ketoacidosis** while nil by mouth.- **Rapid-acting insulin** (lispro) is omitted because the patient will not be consuming a meal, and a **Variable Rate Intravenous Insulin Infusion (VRIII)** ensures precise glucose control during the surgical stress response.*Omit all insulin on the day of surgery and commence sliding scale when blood glucose exceeds 12 mmol/L*- Omitting all insulin is dangerous as it can lead to **hyperglycemia** and life-threatening **diabetic ketoacidosis (DKA)**, even in Type 2 diabetics under stress.- Waiting for glucose to exceed 12 mmol/L before acting is reactive rather than **proactive management**, leading to poor glycemic control during surgery.*Give 50% of usual basal insulin on morning of surgery, omit rapid-acting insulin, start variable rate insulin infusion*- Cutting the **basal dose by 50%** is generally unnecessary for patients with stable Type 2 diabetes and may result in inadequate background insulin levels.- Current guidelines recommend continuing the **full dose** of long-acting analogues like glargine to maintain metabolic stability and prevent hyperglycemia.*Continue all usual insulin doses and schedule surgery after lunch*- Continuing **bolus insulin** doses while the patient is fasting for surgery would cause severe **hypoglycemia** due to lack of carbohydrate intake.- Delaying surgery until after lunch is inappropriate for **pre-operative fasting protocols** and disrupts efficient theatre scheduling for elective cases.*Give usual basal insulin the night before but omit morning dose, commence intravenous insulin at induction*- The **morning dose** of basal insulin should not be omitted if it is usually taken then, as continuous basal coverage is essential to prevent metabolic decompensation, especially during surgical stress.- Waiting until **anaesthetic induction** to start insulin management may be too late to control the elevation in blood glucose caused by the **surgical stress response**, leading to hyperglycemia before surgery even begins.
Question 85: A 68-year-old man with atrial fibrillation on apixaban 5mg twice daily requires emergency surgery for a perforated duodenal ulcer. His last dose of apixaban was 8 hours ago. His renal function is normal (eGFR 68 ml/min/1.73m²). What is the most appropriate approach to managing his anticoagulation perioperatively?
- A. Proceed to surgery immediately; apixaban effect is minimal at 8 hours
- B. Delay surgery for 24 hours after last apixaban dose to minimise bleeding risk
- C. Administer idarucizumab to reverse anticoagulation before surgery
- D. Proceed to surgery and consider prothrombin complex concentrate (PCC) if significant bleeding occurs (Correct Answer)
- E. Give vitamin K 10mg intravenously before proceeding to surgery
Explanation: ***Proceed to surgery and consider prothrombin complex concentrate (PCC) if significant bleeding occurs*** - A **perforated duodenal ulcer** is a life-threatening emergency requiring immediate surgical intervention; delaying surgery to allow for apixaban washout is not an option. - Although **andexanet alfa** is the specific reversal agent for Factor Xa inhibitors, **four-factor Prothrombin Complex Concentrate (PCC)** is a widely available and recommended option to manage severe or life-threatening bleeding in patients on apixaban when specific agents are unavailable or in an emergency setting. *Proceed to surgery immediately; apixaban effect is minimal at 8 hours* - Apixaban has a half-life of approximately **12 hours**, meaning a substantial anticoagulant effect is still present 8 hours after the last dose, not a minimal one. - While surgery must proceed immediately due to the emergency, the surgical team must be prepared for **increased bleeding risk** and have strategies in place to manage it. *Delay surgery for 24 hours after last apixaban dose to minimise bleeding risk* - Delaying surgery for a **perforated viscus** will significantly increase the risk of **peritonitis, sepsis, and mortality**. - The recommended 24-48 hour interruption for apixaban before surgery is appropriate for **elective procedures**, not for urgent or emergent interventions. *Administer idarucizumab to reverse anticoagulation before surgery* - **Idarucizumab** is the specific reversal agent for **dabigatran**, a direct thrombin inhibitor. - It is completely ineffective against **apixaban**, which is a direct Factor Xa inhibitor, and thus would provide no benefit. *Give vitamin K 10mg intravenously before proceeding to surgery* - **Vitamin K** is used to reverse the anticoagulant effects of **warfarin** by increasing the synthesis of Vitamin K-dependent clotting factors. - It has no mechanism of action or effect on **Direct Oral Anticoagulants (DOACs)** like apixaban, which directly inhibit specific clotting factors.
Question 86: A 37-year-old woman with type 1 diabetes for 18 years is admitted with severe vomiting and abdominal pain. Her capillary blood glucose is 22.4 mmol/L and capillary ketones are 4.8 mmol/L. Arterial blood gas shows pH 7.24, bicarbonate 12 mmol/L. She is diagnosed with diabetic ketoacidosis. Her usual insulin is insulin aspart three times daily with meals and insulin glargine at bedtime. What is the most appropriate initial insulin management?
- A. Continue her usual basal-bolus regimen and add intravenous insulin infusion
- B. Stop all subcutaneous insulin and commence fixed-rate intravenous insulin infusion at 0.1 units/kg/hour
- C. Stop rapid-acting insulin, continue basal insulin, and start fixed-rate intravenous insulin infusion (Correct Answer)
- D. Double her usual insulin doses and administer subcutaneously
- E. Give stat dose of 10 units rapid-acting insulin subcutaneously then reassess
Explanation: ***Stop rapid-acting insulin, continue basal insulin, and start fixed-rate intravenous insulin infusion***- Current guidelines recommend commencing a **fixed-rate intravenous insulin infusion (FRIII)** at 0.1 units/kg/hour to manage acute DKA effectively, allowing precise titration.- **Basal insulin** (e.g., glargine) should be continued to provide a background level of insulin, preventing **rebound hyperglycemia** and ketosis when the IV infusion is eventually discontinued or transitioning to subcutaneous insulin.*Continue her usual basal-bolus regimen and add intravenous insulin infusion*- Continuing **rapid-acting mealtime insulin** (aspart) is inappropriate as the patient is symptomatic with vomiting and likely **nil by mouth (NBM)**.- Using both IV insulin and subcutaneous bolus insulin simultaneously increases the risk of unpredictable and dangerous **hypoglycemia** and makes insulin titration challenging.*Stop all subcutaneous insulin and commence fixed-rate intravenous insulin infusion at 0.1 units/kg/hour*- While FRIII is the standard of care for DKA, stopping **basal insulin** is an outdated practice that can lead to a gap in insulin coverage and complicate the transition back to subcutaneous therapy.- Maintaining the long-acting insulin during the acute phase ensures better **glycemic stability** and prevents a sudden drop in insulin levels once the IV infusion is tapered.*Double her usual insulin doses and administer subcutaneously*- **Subcutaneous insulin** is unreliable for treating severe DKA due to poor peripheral perfusion, especially in dehydrated patients, and does not allow for the rapid and precise titration provided by the **intravenous route**.- Simply doubling the dose does not address the underlying pathophysiology of DKA, which requires a controlled **fixed-rate infusion** to suppress ketogenesis and manage hyperglycemia.*Give stat dose of 10 units rapid-acting insulin subcutaneously then reassess*- A stat dose of subcutaneous insulin is insufficient and delays the initiation of the necessary **weight-based IV insulin infusion**, which is critical for rapid correction of DKA.- This approach fails to address the systemic emergency of DKA, including the severe **metabolic acidosis** and electrolyte disturbances that require continuous and controlled insulin administration.
Question 87: A 52-year-old woman with newly diagnosed deep vein thrombosis is commenced on rivaroxaban. She weighs 58kg and has normal renal function (eGFR 78 ml/min/1.73m²). She is also taking carbamazepine 400mg twice daily for epilepsy. What is the most appropriate anticoagulation regimen?
- A. Rivaroxaban 15mg twice daily for 21 days, then 20mg once daily
- B. Rivaroxaban 15mg twice daily for 21 days, then 15mg once daily due to weight <60kg
- C. Switch to apixaban as it has less drug interaction with carbamazepine
- D. Continue rivaroxaban but avoid concurrent use; seek alternative anticoagulation (Correct Answer)
- E. Rivaroxaban 20mg twice daily for 21 days to compensate for enzyme induction
Explanation: ***Continue rivaroxaban but avoid concurrent use; seek alternative anticoagulation***- **Carbamazepine** is a potent **CYP3A4** and **P-glycoprotein inducer**, which significantly reduces the plasma concentration of **Direct Oral Anticoagulants (DOACs)** like rivaroxaban.- Because the reduction in efficacy increases the risk of **thromboembolism** and cannot be reliably monitored, DOACs should be avoided in favor of agents like **warfarin** (where the interaction can be managed via **INR monitoring**) or LMWH.*Rivaroxaban 15mg twice daily for 21 days, then 20mg once daily*- While this is the standard loading and maintenance dose for acute **DVT**, it is inappropriate here due to the severe drug-drug interaction with **carbamazepine**.- Using standard dosing in the presence of a strong inducer leads to **subtherapeutic levels** and potential treatment failure.*Rivaroxaban 15mg twice daily for 21 days, then 15mg once daily due to weight <60kg*- Dose reduction for **weight <60kg** is specifically indicated for **apixaban** (if other criteria are met) or **edoxaban**, but is not the standard protocol for rivaroxaban in DVT treatment.- Reducing the dose further in a patient taking an **enzyme inducer** would dangerously exacerbate the risk of recurrent thrombosis.*Switch to apixaban as it has less drug interaction with carbamazepine*- All currently available DOACs, including **apixaban**, are substrates of **P-gp** and **CYP3A4**, meaning they are all significantly affected by carbamazepine.- Switching from one DOAC to another does not resolve the interaction; an alternative class like **VKA (warfarin)** is required.*Rivaroxaban 20mg twice daily for 21 days to compensate for enzyme induction*- Increasing the DOAC dose to compensate for induction is not clinically validated, as the degree of **metabolic induction** varies widely between individuals.- There is no routine way to monitor the **anticoagulant effect** of rivaroxaban to ensure a higher dose is safe or sufficient.
Question 88: A 64-year-old man with atrial fibrillation is on rivaroxaban 20mg once daily. He develops acute bacterial meningitis and requires treatment with rifampicin. Understanding drug interactions with DOACs, what is the most appropriate management of his anticoagulation?
- A. Continue rivaroxaban at current dose as no significant interaction exists
- B. Increase rivaroxaban dose to 30mg once daily to compensate for reduced levels
- C. Switch to warfarin and monitor INR closely during rifampicin treatment (Correct Answer)
- D. Stop anticoagulation temporarily until rifampicin course is completed
- E. Switch to dabigatran as it is not affected by rifampicin
Explanation: ***Switch to warfarin and monitor INR closely during rifampicin treatment*** - **Rifampicin** is a potent inducer of **P-glycoprotein (P-gp)** and **CYP3A4**, which significantly reduces the plasma concentration of **rivaroxaban**, leading to a sub-therapeutic effect and increased **stroke risk**. - Unlike DOACs, the effect of rifampicin on **warfarin** metabolism can be safely managed because the anticoagulant effect is easily measurable via **INR monitoring**, allowing for precise dose adjustments. *Continue rivaroxaban at current dose as no significant interaction exists* - A major interaction exists; **rifampicin** can reduce **rivaroxaban** levels by up to 50% by inducing **P-gp** and **CYP3A4**, making it highly likely the patient will be under-anticoagulated. - Modern guidelines explicitly recommend avoiding the co-administration of **DOACs** with potent **enzyme inducers** like rifampicin due to the risk of **thromboembolism**. *Increase rivaroxaban dose to 30mg once daily to compensate for reduced levels* - There is no clinical evidence or licensed protocol for **dose-escalation** of rivaroxaban to overcome drug-drug interactions with potent inducers. - Increasing the dose without the ability to monitor **therapeutic drug levels** (unlike **INR** for **warfarin**) puts the patient at an unquantified risk of either **thrombosis** due to inadequate levels or **bleeding** from unpredictable high levels. *Stop anticoagulation temporarily until rifampicin course is completed* - This patient has **atrial fibrillation** and is at significant risk of a **thromboembolic stroke** if anticoagulation is discontinued, especially during an acute illness like **meningitis** which can increase hypercoagulability. - Temporary cessation is only appropriate for high-risk surgical procedures and is not a valid strategy for managing long-term **drug interactions** where anticoagulation is still required. *Switch to dabigatran as it is not affected by rifampicin* - This is incorrect as **dabigatran** is a major substrate of the **P-glycoprotein** efflux transporter, which is strongly induced by **rifampicin**. - Concurrent use of **rifampicin** and **dabigatran** results in a marked decrease in **dabigatran exposure**, similar to the effect seen with factor Xa inhibitors like rivaroxaban, leading to a loss of anticoagulation.
Question 89: A 71-year-old woman with type 2 diabetes on insulin glargine 26 units at bedtime and metformin 1g twice daily presents with a painful diabetic foot ulcer. She is started on oral antibiotics but reports poor oral intake due to nausea. Her capillary blood glucose readings over the past 24 hours range from 4.2 to 6.8 mmol/L. What is the most appropriate approach to her insulin management?
- A. Continue current insulin dose unchanged as infection increases insulin requirements
- B. Reduce insulin glargine to 50% of usual dose due to reduced oral intake and risk of hypoglycaemia (Correct Answer)
- C. Stop insulin temporarily until oral intake improves
- D. Switch to sliding scale insulin until the acute illness resolves
- E. Increase insulin dose by 20% to account for infection-related insulin resistance
Explanation: ***Reduce insulin glargine to 50% of usual dose due to reduced oral intake and risk of hypoglycaemia***- Although infection usually increases insulin resistance, the patient's **poor oral intake** and current glucose levels (4.2-6.8 mmol/L) create a significant risk of **hypoglycaemia**.- A **50% dose reduction** of basal insulin is a safe strategy to prevent low blood sugar while maintaining a baseline metabolic requirement during acute illness.*Continue current insulin dose unchanged as infection increases insulin requirements*- While **systemic infection** increases metabolic demands, this patient is already at the lower end of the target range (**4.2 mmol/L**) while eating poorly.- Continuing the full dose of **26 units** without adequate carbohydrate intake would likely result in symptomatic hypoglycemia.*Stop insulin temporarily until oral intake improves*- Basal insulin should **never be stopped** in patients who require it, as a complete lack of insulin can lead to **metabolic decompensation** or ketoacidosis.- Even during fasting, the body requires **basal insulin** to suppress hepatic glucose production and ketogenesis.*Switch to sliding scale insulin until the acute illness resolves*- **Sliding scale insulin** as a monotherapy is generally discouraged because it is reactive rather than proactive, leading to **glycaemic variability**.- It is typically reserved for specialized inpatient settings or **perioperative care**, not as a substitute for appropriate basal insulin adjustment in this scenario.*Increase insulin dose by 20% to account for infection-related insulin resistance*- Increasing the dose is dangerous here because the patient's blood glucose is already **near-normal**, indicating that her current intake cannot sustain more insulin.- While **sick day rules** often suggest increasing doses for hyperglycemia during infection, they mandate a **dose reduction** if blood glucose levels are low or if intake is severely restricted.
Question 90: A 46-year-old man with epilepsy is established on phenytoin 300mg daily. He attends for routine monitoring. His recent phenytoin level is 18 mg/L (therapeutic range 10-20 mg/L), but he reports mild ataxia and diplopia. What is the most appropriate explanation for these symptoms?
- A. These symptoms are unrelated to phenytoin as the level is therapeutic
- B. Phenytoin exhibits zero-order kinetics, so small dose increases can cause disproportionate rises in plasma concentration
- C. The symptoms suggest phenytoin resistance requiring dose escalation
- D. A drug interaction has reduced phenytoin protein binding, increasing free fraction despite therapeutic total level (Correct Answer)
- E. The laboratory reference range is incorrect for this patient
Explanation: ***A drug interaction has reduced phenytoin protein binding, increasing free fraction despite therapeutic total level*** - Phenytoin is highly **protein-bound** (approx. 90%), and standard lab assays measure the **total phenytoin** (bound + unbound) rather than the active free fraction. - Clinical toxicity (e.g., **ataxia**, **diplopia**) can occur within the therapeutic total range if the **unbound (free) fraction** increases due to hypoalbuminemia or displacement by other drugs like **valproate**. *These symptoms are unrelated to phenytoin as the level is therapeutic* - Symptoms like **nystagmus**, **ataxia**, and **diplopia** are hallmark signs of phenytoin toxicity regardless of the reported total plasma level. - Relying solely on **total drug levels** is dangerous when clinical signs of toxicity are present, as individual patient physiology varies. *Phenytoin exhibits zero-order kinetics, so small dose increases can cause disproportionate rises in plasma concentration* - While it is true that phenytoin follows **zero-order (saturation) kinetics**, this would typically result in a high **total level** on the lab report. - In this scenario, the total level is still **within the normal range**, making protein displacement a more likely explanation for current toxicity. *The symptoms suggest phenytoin resistance requiring dose escalation* - These symptoms represent neurological **toxicity**, not treatment failure or resistance to the antiepileptics drugs. - Increasing the dose in a patient already experiencing **ataxia** would exacerbate the toxicity and risk severe **cerebellar dysfunction**. *The laboratory reference range is incorrect for this patient* - The standard therapeutic range (10-20 mg/L) is generally valid for most patients, but lab values must always be interpreted in a **clinical context**. - The issue is not the reference range itself, but the failure to account for the **biologically active free drug fraction** which is not routinely measured.
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