Safe Prescribing — MCQs

A 51-year-old woman with type 1 diabetes is admitted with hyperemesis gravidarum at 8 weeks gestation. She is unable to tolerate oral intake. Her usual insulin regimen is insulin glargine 26 units at bedtime and insulin aspart 8 units before meals. Her admission blood glucose is 7.2 mmol/L, and ketones are 1.8 mmol/L. She is commenced on intravenous fluids. What is the most appropriate insulin management to prevent starvation ketosis while avoiding hypoglycaemia?

Q94

A 63-year-old man with chronic kidney disease stage 4 (eGFR 24 ml/min/1.73m²) develops acute deep vein thrombosis. He weighs 82kg. Low molecular weight heparin is prescribed. According to BNF guidance for patients with significant renal impairment requiring therapeutic anticoagulation with LMWH, what is the most appropriate monitoring strategy?

Q95

A 54-year-old woman with type 2 diabetes is on a basal-bolus insulin regimen consisting of insulin detemir 28 units twice daily and insulin aspart 10 units with meals. She is admitted with community-acquired pneumonia and started on clarithromycin. Over 48 hours, her blood glucose readings increase from typical range of 6-9 mmol/L to consistent readings of 14-18 mmol/L despite good oral intake. Which mechanism best explains this deterioration in glycaemic control?

Q96

A 77-year-old man with mechanical aortic valve replacement is established on warfarin with target INR 2.5-3.5. He develops epistaxis that is controlled with anterior nasal packing in the emergency department. His INR on arrival is 7.8 and haemoglobin is 118 g/L (baseline 135 g/L). He has no other sites of bleeding. What is the most appropriate management of his anticoagulation?

Q97

A 69-year-old woman with atrial fibrillation on edoxaban 60mg once daily is scheduled for colonoscopy with polypectomy in 5 days. She has normal renal function (eGFR 72 ml/min/1.73m²) and no other significant comorbidities. What is the most appropriate perioperative management of her anticoagulation according to current UK guidance?

Q98

A 48-year-old man with type 1 diabetes for 22 years presents to the emergency department with a 2-day history of vomiting and abdominal pain. His capillary blood glucose is 24.8 mmol/L, ketones 4.2 mmol/L, and arterial blood gas shows pH 7.21, bicarbonate 12 mmol/L. He is diagnosed with diabetic ketoacidosis. His usual insulin is insulin degludec 35 units once daily and insulin aspart with meals. What is the most appropriate initial insulin management?

Q99

A 56-year-old woman is commenced on dabigatran 150mg twice daily for stroke prevention in atrial fibrillation. She has a CHA₂DS₂-VASc score of 3. Her baseline renal function shows eGFR 68 ml/min/1.73m². According to MHRA and NICE guidance, what is the recommended frequency for monitoring renal function in this patient?

Q100

A 61-year-old man with type 2 diabetes on basal-bolus insulin therapy (insulin glargine 40 units at bedtime, insulin lispro 12 units with meals) is admitted with suspected stroke. His admission blood glucose is 3.8 mmol/L. CT brain confirms acute ischaemic stroke with no indication for thrombolysis. He is kept nil by mouth pending swallow assessment. What is the most appropriate immediate insulin management?

Safe Prescribing UK Medical PG Practice Questions and MCQs

Question 91: According to the Medicines and Healthcare products Regulatory Agency (MHRA) guidance on direct oral anticoagulants (DOACs), which parameter must be assessed before prescribing and monitored regularly during treatment?

A. Liver function tests only
B. International normalised ratio (INR)
C. Renal function (creatinine clearance or eGFR) (Correct Answer)
D. Activated partial thromboplastin time (APTT)
E. Anti-Xa levels

Explanation: ***Renal function (creatinine clearance or eGFR)*** - **MHRA guidance** mandates that **renal function** must be assessed before starting **DOACs** and monitored at least **annually** because these drugs are renally cleared. - Dose adjustments are essential based on **creatinine clearance (CrCl)** to prevent drug accumulation and reduce the risk of **major bleeding** events. *Liver function tests only* - While **liver function** should be checked periodically for some agents, it is not the primary parameter used for **dose titrations** or mandatory routine monitoring under MHRA safety guidance. - **Renal function** is the more critical parameter as it directly dictates the safety threshold for continuing medication or reducing the dose. *International normalised ratio (INR)* - **INR** is used to monitor **warfarin** therapy but is not a reliable or required measure for monitoring the anticoagulant effect of **DOACs**. - One of the primary clinical advantages of **DOACs** is that they offer stable anticoagulation without the need for **routine coagulation monitoring**. *Activated partial thromboplastin time (APTT)* - **APTT** may be prolonged by some **DOACs** (particularly **dabigatran**), but it does not provide a linear or accurate measurement of the drug's therapeutic level. - This test is primarily used for monitoring **unfractionated heparin** and is not recommended for routine monitoring of **direct oral anticoagulants**. *Anti-Xa levels* - **Anti-Xa assays** can be used to measure the activity of Factor Xa inhibitors (like **rivaroxaban** or **apixaban**) in emergencies, but they are not used for **regular monitoring**. - MHRA focuses on **organ function** (renal) for routine safety monitoring rather than the drug's direct biochemical effect on the clotting cascade.

Question 92: A 59-year-old woman with ulcerative colitis is started on azathioprine 150mg once daily. According to current UK prescribing guidance, what is the recommended frequency for monitoring full blood count in the first 8 weeks of treatment?

A. Daily for the first week, then weekly
B. Weekly for the first 8 weeks (Correct Answer)
C. Fortnightly for the first 8 weeks
D. At baseline, 2 weeks, 4 weeks, then 8 weeks
E. At baseline, then monthly

Explanation: ***Weekly for the first 8 weeks***- According to current **UK prescribing guidance** and the **BNF**, patients starting **azathioprine** must have their **Full Blood Count (FBC)** monitored weekly for at least the first **8 weeks**.- This intensive monitoring is essential to detect early **myelosuppression** (bone marrow suppression), a common and serious dose-related side effect.*Daily for the first week, then weekly*- **Daily blood tests** are overly frequent and not required for routine initiation of azathioprine in an outpatient setting.- This level of monitoring is usually reserved for acute inpatient **haematological emergencies** or highly experimental protocols.*Fortnightly for the first 8 weeks*- **Fortnightly** (every 2 weeks) monitoring is insufficient during the high-risk initiation phase where **neutropenia** or **thrombocytopenia** can develop rapidly.- Guidelines only transition to less frequent intervals (e.g., every 3 months) after the initial stable period of **8 to 12 weeks**.*At baseline, 2 weeks, 4 weeks, then 8 weeks*- While it captures some early data points, this schedule misses the crucial **weekly requirement** mandated for safety during the first two months.- Adhering to this schedule would increase the clinical risk of missing a significant drop in **white cell count** between scheduled tests.*At baseline, then monthly*- **Monthly monitoring** is too infrequent for the initiation phase of **thiopurines** like azathioprine.- Monthly or three-monthly checks are only appropriate for patients who have already established a **stable dose** and demonstrated a consistent haematological profile.

Question 93: A 51-year-old woman with type 1 diabetes is admitted with hyperemesis gravidarum at 8 weeks gestation. She is unable to tolerate oral intake. Her usual insulin regimen is insulin glargine 26 units at bedtime and insulin aspart 8 units before meals. Her admission blood glucose is 7.2 mmol/L, and ketones are 1.8 mmol/L. She is commenced on intravenous fluids. What is the most appropriate insulin management to prevent starvation ketosis while avoiding hypoglycaemia?

A. Omit all insulin until she resumes oral intake, monitor ketones 4-hourly
B. Continue insulin glargine at usual dose, omit insulin aspart, add 10% glucose to intravenous fluids (Correct Answer)
C. Reduce insulin glargine to 13 units daily, omit insulin aspart, give correction doses for glucose >12 mmol/L
D. Commence variable rate intravenous insulin infusion with 5% glucose infusion
E. Continue insulin glargine 26 units, give insulin aspart 4 units every 6 hours regardless of oral intake

Explanation: ***Continue insulin glargine at usual dose, omit insulin aspart, add 10% glucose to intravenous fluids*** - In **Type 1 Diabetes**, basal insulin must never be omitted to prevent **diabetic ketoacidosis (DKA)**; adding **intravenous glucose** allows the basal insulin to suppress ketogenesis without causing hypoglycemia. - **Hyperemesis gravidarum** causes a starvation state; maintaining the usual **basal insulin** dose while providing carbohydrate substrate is the standard strategy for patients who are **nil by mouth**. *Omit all insulin until she resumes oral intake, monitor ketones 4-hourly* - Omitting insulin in a patient with **Type 1 Diabetes** will rapidly lead to **absolute insulin deficiency**, causing uncontrolled lipolysis and life-threatening **DKA**. - Safe management requires at least **basal insulin** cover regardless of oral intake to maintain metabolic stability. *Reduce insulin glargine to 13 units daily, omit insulin aspart, give correction doses for glucose >12 mmol/L* - Reducing the **basal insulin** dose significantly increases the risk of **ketosis** and development of DKA, especially as insulin requirements often rise in pregnancy. - Relying on **correction doses** is a reactive rather than proactive approach and fails to prevent the metabolic shift toward **ketone production**. *Commence variable rate intravenous insulin infusion with 5% glucose infusion* - While effective, a **Variable Rate Intravenous Insulin Infusion (VRIII)** is more invasive and complex than necessary if the patient's glucose is currently stable and they are not in established DKA. - This approach is typically reserved for prolonged periods of being **nil by mouth** or during active labor and delivery, rather than initial hyperemesis management. *Continue insulin glargine 26 units, give insulin aspart 4 units every 6 hours regardless of oral intake* - Administering **insulin aspart** (a rapid-acting analog) without concurrent carbohydrate intake significantly increases the risk of severe **iatrogenic hypoglycemia**. - **Prandial or bolus insulin** should generally only be given when there is a corresponding nutritional intake to cover.

Question 94: A 63-year-old man with chronic kidney disease stage 4 (eGFR 24 ml/min/1.73m²) develops acute deep vein thrombosis. He weighs 82kg. Low molecular weight heparin is prescribed. According to BNF guidance for patients with significant renal impairment requiring therapeutic anticoagulation with LMWH, what is the most appropriate monitoring strategy?

A. No monitoring required; use standard weight-based dosing throughout treatment
B. Monitor anti-Xa levels 3-4 hours post-dose, aiming for peak level 0.5-1.0 IU/ml (Correct Answer)
C. Monitor APTT daily, aiming for ratio 1.5-2.5 times control
D. Measure trough anti-Xa levels before next dose, aiming for level <0.2 IU/ml
E. Monitor anti-Xa levels 3-4 hours post-dose, aiming for peak level 1.0-2.0 IU/ml

Explanation: ***Monitor anti-Xa levels 3-4 hours post-dose, aiming for peak level 0.5-1.0 IU/ml*** - In patients with **renal impairment (eGFR <30)**, LMWH can accumulate; therefore, **anti-Xa levels** must be monitored to ensure safety and efficacy. - The **peak level** should be measured **3-4 hours post-dose**, with a target range of **0.5-1.0 IU/ml** for standard twice-daily therapeutic dosing. *No monitoring required; use standard weight-based dosing throughout treatment* - Standard dosing without monitoring is risky in **CKD stage 4** because LMWH is **renally cleared**, leading to an increased risk of **hemorrhage**. - Most guidelines and the **BNF** recommend either dose reduction or intense monitoring of **anti-Xa levels** in severe renal failure. *Monitor APTT daily, aiming for ratio 1.5-2.5 times control* - **APTT** is used to monitor **unfractionated heparin (UFH)**, not low molecular weight heparin (LMWH). - LMWH has a more predictable response but does not significantly prolong the **Activated Partial Thromboplastin Time**. *Measure trough anti-Xa levels before next dose, aiming for level <0.2 IU/ml* - Monitoring for LMWH is primarily based on **peak levels** to assess therapeutic efficacy and risk of toxicity. - **Trough levels** are not standard practice for routine LMWH monitoring, although they may occasionally be used to assess **accumulation** in complex cases. *Monitor anti-Xa levels 3-4 hours post-dose, aiming for peak level 1.0-2.0 IU/ml* - A peak range of **1.0-2.0 IU/ml** is generally the target for **once-daily** high-dose regimens, which are often avoided in renal impairment. - In significant renal impairment, **twice-daily** divided doses with a lower target peak (0.5-1.0 IU/ml) are preferred to minimize **bleeding risk**.

Question 95: A 54-year-old woman with type 2 diabetes is on a basal-bolus insulin regimen consisting of insulin detemir 28 units twice daily and insulin aspart 10 units with meals. She is admitted with community-acquired pneumonia and started on clarithromycin. Over 48 hours, her blood glucose readings increase from typical range of 6-9 mmol/L to consistent readings of 14-18 mmol/L despite good oral intake. Which mechanism best explains this deterioration in glycaemic control?

A. Clarithromycin-induced reduction in insulin absorption from subcutaneous sites
B. Increased insulin resistance secondary to acute infection and inflammatory response (Correct Answer)
C. Drug interaction between clarithromycin and insulin causing enhanced insulin clearance
D. Clarithromycin-induced pancreatitis reducing endogenous insulin secretion
E. Impaired glucose renal excretion due to clarithromycin nephrotoxicity

Explanation: ***Increased insulin resistance secondary to acute infection and inflammatory response*** - Acute illness, such as **pneumonia**, triggers the release of **counter-regulatory hormones** (e.g., cortisol, catecholamines, glucagon) and **pro-inflammatory cytokines** (e.g., TNF-α, IL-6). - These substances significantly increase **insulin resistance** in peripheral tissues and stimulate **hepatic glucose production**, leading to marked hyperglycaemia despite the usual insulin doses. *Clarithromycin-induced reduction in insulin absorption from subcutaneous sites* - Macrolide antibiotics like **clarithromycin** have no known pharmacological effect on the **subcutaneous absorption** kinetics of insulin analogues. - The deterioration in glycaemic control is primarily driven by the systemic **inflammatory state** of pneumonia, not a drug-delivery failure. *Drug interaction between clarithromycin and insulin causing enhanced insulin clearance* - There is no direct **pharmacokinetic interaction** between clarithromycin and insulin; insulin is primarily cleared by **proteolysis** in the liver and kidneys. - While clarithromycin inhibits **CYP3A4**, this enzyme system is not involved in the metabolism or clearance of exogenous insulin. *Clarithromycin-induced pancreatitis reducing endogenous insulin secretion* - While some drugs can cause **acute pancreatitis**, clarithromycin is not a classic causative agent, and the patient presents with **pneumonia**, not symptoms like epigastric pain. - In Type 2 diabetes patients on a **basal-bolus regimen**, the primary driver of acute hyperglycaemia during infection is **peripheral insulin resistance**, not a sudden loss of residual beta-cell function. *Impaired glucose renal excretion due to clarithromycin nephrotoxicity* - **Clarithromycin** is not typically associated with significant **nephrotoxicity** or alterations in the renal threshold for glucose. - Renal glucose excretion is a compensatory mechanism; impairing it would not be the primary driver of such a marked **glycaemic rise** during an acute infection.

Question 96: A 77-year-old man with mechanical aortic valve replacement is established on warfarin with target INR 2.5-3.5. He develops epistaxis that is controlled with anterior nasal packing in the emergency department. His INR on arrival is 7.8 and haemoglobin is 118 g/L (baseline 135 g/L). He has no other sites of bleeding. What is the most appropriate management of his anticoagulation?

A. Give oral vitamin K 5mg, withhold warfarin, and recheck INR in 24 hours
B. Give intravenous vitamin K 1mg, withhold warfarin, and recheck INR in 6-12 hours (Correct Answer)
C. Give prothrombin complex concentrate and intravenous vitamin K 5mg immediately
D. Withhold warfarin only and recheck INR daily until <5.0
E. Give fresh frozen plasma 15 ml/kg and oral vitamin K 10mg

Explanation: ***Give intravenous vitamin K 1mg, withhold warfarin, and recheck INR in 6-12 hours***- For an **INR between 5.0 and 8.0 with minor bleeding** (like controlled epistaxis), guidelines recommend **intravenous vitamin K** due to its more predictable and rapid onset compared to the oral route.- A low dose of **1mg** is preferred in patients with **mechanical heart valves** to avoid complete reversal of anticoagulation, which would increase the risk of **valve thrombosis**.*Give oral vitamin K 5mg, withhold warfarin, and recheck INR in 24 hours*- **Oral vitamin K** has a slower onset of action than the intravenous route, making it less suitable when there is active, albeit minor, bleeding.- A **5mg dose** is excessively high for this clinical scenario and risks making the patient resistant to warfarin for several days.*Give prothrombin complex concentrate and intravenous vitamin K 5mg immediately*- **Prothrombin complex concentrate (PCC)** is reserved for **major bleeding** (life-threatening or into critical organs) or an INR > 8.0 with specific risk factors.- This patient's bleeding is **clinically controlled** with packing and his hemoglobin drop is modest, so high-dose reversal is not indicated.*Withhold warfarin only and recheck INR daily until <5.0*- Simply **withholding warfarin** is insufficient management for a patient with an **INR > 5.0 who is experiencing active bleeding**.- Active bleeding requires pharmacological intervention with **Vitamin K** to speed up the synthesis of clotting factors and ensure patient safety.*Give fresh frozen plasma 15 ml/kg and oral vitamin K 10mg*- **Fresh frozen plasma (FFP)** is inferior to PCC for warfarin reversal; it requires large volumes and takes longer to administer and work.- A **10mg dose of vitamin K** would cause prolonged resistance to warfarin, which is dangerous for a patient requiring lifelong anticoagulation for a **mechanical aortic valve**.

Question 97: A 69-year-old woman with atrial fibrillation on edoxaban 60mg once daily is scheduled for colonoscopy with polypectomy in 5 days. She has normal renal function (eGFR 72 ml/min/1.73m²) and no other significant comorbidities. What is the most appropriate perioperative management of her anticoagulation according to current UK guidance?

A. Omit edoxaban on the morning of the procedure, resume normal dose 6 hours post-procedure if haemostasis achieved (Correct Answer)
B. Stop edoxaban 48 hours before procedure, resume 24 hours post-procedure
C. Stop edoxaban 24 hours before procedure, bridge with LMWH, resume edoxaban 48 hours post-procedure
D. Continue edoxaban without interruption as colonoscopy is low bleeding risk
E. Stop edoxaban 72 hours before procedure, resume normal dose 12 hours post-procedure

Explanation: ***Omit edoxaban on the morning of the procedure, resume normal dose 6 hours post-procedure if haemostasis achieved***- For DOACs like **edoxaban** in patients with a normal **eGFR**, omitting the dose on the day of a **moderate bleeding risk** procedure (such as polypectomy) is generally sufficient due to its short half-life.- Post-procedure resumption at **6 hours** is appropriate once **primary haemostasis** is confirmed, balancing the risk of stroke against the risk of post-polypectomy bleeding.*Stop edoxaban 48 hours before procedure, resume 24 hours post-procedure*- A **48-hour cessation** is typically reserved for patients with **impaired renal function** or those undergoing very **high-risk surgery**, which does not apply here.- Resuming at 24 hours is unnecessarily cautious if **haemostasis** is achieved earlier, potentially increasing the **thromboembolic risk** for a patient with atrial fibrillation.*Stop edoxaban 24 hours before procedure, bridge with LMWH, resume edoxaban 48 hours post-procedure*- **Bridging with LMWH** is not recommended for **DOACs** because of their rapid onset and offset of action; it increases **bleeding risk** without benefit.- Resuming at **48 hours** is a delayed reintroduction for a standard colonoscopy with polypectomy, leaving the patient under-anticoagulated and at risk for **atrial fibrillation-related stroke**.*Continue edoxaban without interruption as colonoscopy is low bleeding risk*- While a diagnostic colonoscopy is low risk, a **polypectomy** is classified as a **moderate bleeding risk** procedure requiring temporary cessation of anticoagulants.- Continuing anticoagulation during an invasive procedure with a moderate bleeding risk significantly increases the risk of **uncontrolled gastrointestinal bleeding**.*Stop edoxaban 72 hours before procedure, resume normal dose 12 hours post-procedure*- A **72-hour cessation** is excessive for edoxaban in a patient with an **eGFR of 72**, as the drug is mostly cleared within 24-48 hours.- This prolonged interruption creates an unnecessary and extended **prothrombotic window** for a patient already categorized as needing anticoagulation for atrial fibrillation.

Question 98: A 48-year-old man with type 1 diabetes for 22 years presents to the emergency department with a 2-day history of vomiting and abdominal pain. His capillary blood glucose is 24.8 mmol/L, ketones 4.2 mmol/L, and arterial blood gas shows pH 7.21, bicarbonate 12 mmol/L. He is diagnosed with diabetic ketoacidosis. His usual insulin is insulin degludec 35 units once daily and insulin aspart with meals. What is the most appropriate initial insulin management?

A. Continue insulin degludec at usual dose and commence fixed-rate intravenous insulin infusion at 0.1 units/kg/hour (Correct Answer)
B. Omit insulin degludec and commence variable rate intravenous insulin infusion based on hourly blood glucose
C. Double the dose of insulin degludec and give boluses of insulin aspart every 2 hours
D. Continue insulin degludec and give boluses of intravenous insulin 10 units hourly
E. Omit all subcutaneous insulin and commence fixed-rate intravenous insulin infusion at 0.05 units/kg/hour

Explanation: ***Continue insulin degludec at usual dose and commence fixed-rate intravenous insulin infusion at 0.1 units/kg/hour*** - Guidelines recommend continuing **long-acting basal insulin** (like degludec) alongside iv insulin to prevent **rebound ketosis** and facilitate the transition back to subcutaneous insulin. - A **fixed-rate intravenous insulin infusion (FRIII)** at **0.1 units/kg/hour** is the standard protocol to reliably suppress **ketogenesis** and clear ketones. *Omit insulin degludec and commence variable rate intravenous insulin infusion based on hourly blood glucose* - **Variable rate intravenous insulin infusion (VRIII)** is used for glycaemic control in stable patients, not for the acute management of **ketosis** in DKA. - Omitting the basal insulin analogue can lead to a baseline insulin deficit, increasing the risk of **hyperglycaemia** when the infusion is eventually discontinued. *Double the dose of insulin degludec and give boluses of insulin aspart every 2 hours* - DKA is a medical emergency that requires **intravenous insulin** for rapid onset and precise titration; subcutaneous boluses are too slow and unpredictable. - Doubling the **basal dose** is inappropriate and increases the risk of delayed **hypoglycaemia** once the acute metabolic storm has resolved. *Continue insulin degludec and give boluses of intravenous insulin 10 units hourly* - **Hourly intravenous boluses** provide fluctuating insulin levels rather than the steady-state concentration needed to effectively suppress **lipolysis**. - Modern protocols have replaced bolus therapy with **continuous infusion (FRIII)** to ensure a more stable and safe reduction in ketones. *Omit all subcutaneous insulin and commence fixed-rate intravenous insulin infusion at 0.05 units/kg/hour* - Omitting the **basal analogue** is contrary to current best practice for patients already established on long-acting insulin regimens. - A rate of **0.05 units/kg/hour** is generally insufficient for adult DKA management and is typically reserved for specialized cases like **pregnancy** or extreme sensitivity.

Question 99: A 56-year-old woman is commenced on dabigatran 150mg twice daily for stroke prevention in atrial fibrillation. She has a CHA₂DS₂-VASc score of 3. Her baseline renal function shows eGFR 68 ml/min/1.73m². According to MHRA and NICE guidance, what is the recommended frequency for monitoring renal function in this patient?

A. Monthly for the first 3 months, then 3-monthly thereafter
B. Annually, or more frequently if clinically indicated (Correct Answer)
C. At baseline only, then if clinical deterioration occurs
D. 3-monthly for the first year, then 6-monthly thereafter
E. 6-monthly indefinitely

Explanation: ***Annually, or more frequently if clinically indicated*** - For patients on **DOACs** with an **eGFR >60 ml/min/1.73m²**, MHRA and NICE guidelines recommend **renal function monitoring** at least once every 12 months. - This frequency ensures the **dosage** remains appropriate as renal function naturally declines with age or due to **intercurrent illness**. *Monthly for the first 3 months, then 3-monthly thereafter* - This intensive monitoring schedule is not required by standard guidelines for a patient with relatively **preserved renal function** (eGFR 68). - Such frequent testing is excessive and typically reserved for clinical trials or patients with **unstable renal status**. *At baseline only, then if clinical deterioration occurs* - Relying only on **baseline results** is unsafe, as **dabigatran** is highly dependent on **renal excretion** (approximately 80%). - Undetected declines in renal function can lead to **drug accumulation** and a significantly increased **risk of major bleeding**. *3-monthly for the first year, then 6-monthly thereafter* - This schedule is more aligned with patients who have **moderate renal impairment** (CrCl <60 ml/min). - For a patient with an **eGFR of 68**, this represents unnecessary healthcare utilization according to current **NICE guidance**. *6-monthly indefinitely* - While safer than annual monitoring, this is not the **standard minimum recommendation** for someone with an **eGFR above 60**. - A **6-monthly** frequency (or the "eGFR divided by 10" rule) is generally applied strictly when the eGFR falls below **60 ml/min/1.73m²**.

Question 100: A 61-year-old man with type 2 diabetes on basal-bolus insulin therapy (insulin glargine 40 units at bedtime, insulin lispro 12 units with meals) is admitted with suspected stroke. His admission blood glucose is 3.8 mmol/L. CT brain confirms acute ischaemic stroke with no indication for thrombolysis. He is kept nil by mouth pending swallow assessment. What is the most appropriate immediate insulin management?

A. Continue insulin glargine 40 units, omit insulin lispro, commence 10% glucose infusion, and monitor blood glucose 4-6 hourly (Correct Answer)
B. Omit all insulin, commence variable rate intravenous insulin infusion with glucose-potassium-insulin regime
C. Reduce insulin glargine to 20 units, omit insulin lispro, and monitor blood glucose 2-hourly
D. Continue insulin glargine 40 units, omit insulin lispro, and give correction doses of rapid-acting insulin for glucose >12 mmol/L
E. Omit insulin glargine, commence variable rate intravenous insulin infusion only, without glucose supplementation

Explanation: ***Continue insulin glargine 40 units, omit insulin lispro, commence 10% glucose infusion, and monitor blood glucose 4-6 hourly*** - In patients with **Type 2 Diabetes** who are **nil by mouth**, the **basal insulin** (glargine) should be continued at the full dose to prevent rebound hyperglycaemia. - Because the patient is not eating and has a baseline low glucose (3.8 mmol/L), **10% glucose infusion** is necessary to prevent further **hypoglycaemia** while omitting meal-time boluses. *Omit all insulin, commence variable rate intravenous insulin infusion with glucose-potassium-insulin regime* - A **Variable Rate Intravenous Insulin Infusion (VRIII)** is generally reserved for patients where subcutaneous management is unsafe or in **Type 1 Diabetes** with prolonged fasting. - It is unnecessarily complex and carries a higher risk of **iatrogenic delivery errors** for a Type 2 diabetic patient awaiting a simple swallow assessment. *Reduce insulin glargine to 20 units, omit insulin lispro, and monitor blood glucose 2-hourly* - Reducing the **basal insulin dose** by half is likely to lead to significant **rebound hyperglycaemia**, which is detrimental to neural recovery post-stroke. - Maintaining established basal insulin provides more stable glycaemic control than arbitrary dose reduction when used alongside **dextrose support**. *Continue insulin glargine 40 units, omit insulin lispro, and give correction doses of rapid-acting insulin for glucose >12 mmol/L* - This approach fails to address the patient's current **hypoglycaemia (3.8 mmol/L)** and the lack of carbohydrate intake while **nil by mouth**. - Relying solely on **sliding scale/correction doses** leads to erratic blood glucose fluctuations rather than the steady state required in **acute ischaemic stroke**. *Omit insulin glargine, commence variable rate intravenous insulin infusion only, without glucose supplementation* - Stopping **basal insulin** without providing an alternative source of insulin or glucose is dangerous and can lead to **ketosis** or severe hyperglycaemia. - Providing an **insulin infusion without glucose** in a patient with a blood sugar of 3.8 mmol/L would cause life-threatening **severe hypoglycaemia**.

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