Safe Prescribing — MCQs

A 61-year-old woman with type 2 diabetes is admitted with acute kidney injury secondary to dehydration. Her creatinine has risen from 95 μmol/L to 284 μmol/L. She is on insulin glargine 40 units at night and insulin aspart 12 units three times daily with meals. What is the most appropriate insulin adjustment during her acute illness?

Q53

A 58-year-old man with chronic atrial fibrillation on warfarin therapy requires antibiotic treatment for a lower respiratory tract infection. His INR has been stable at 2.4 for the past 6 months. Which antibiotic is most likely to significantly increase his INR and require closer monitoring?

Q54

A 65-year-old woman with atrial fibrillation is on warfarin with target INR 2-3. She has been stable for 2 years with INR checks every 10 weeks. She is prescribed a 7-day course of ciprofloxacin 500mg twice daily for a urinary tract infection. Her current INR is 2.4 measured 3 days ago. What is the most appropriate monitoring and management strategy?

Q55

A 73-year-old man with non-valvular atrial fibrillation (CHA₂DS₂-VASc score 5) is established on dabigatran 150mg twice daily. He requires urgent surgery for acute appendicitis within the next 6 hours. His last dose of dabigatran was 3 hours ago. His creatinine is 118 μmol/L (eGFR 52 ml/min/1.73m²). Laboratory tests show: APTT 46 seconds (normal 26-36), thrombin time >200 seconds (normal 15-19). What is the most appropriate management of his anticoagulation before proceeding to surgery?

Q56

A 44-year-old man with type 2 diabetes is on insulin glargine 48 units at bedtime and insulin lispro 12 units with each meal. Over the past month he has gained 6kg in weight and reports frequent hypoglycaemic episodes, particularly nocturnal. His home blood glucose diary shows: pre-breakfast 3.2-4.8 mmol/L, pre-lunch 8.2-11.4 mmol/L, pre-dinner 9.8-13.2 mmol/L, bedtime 6.8-8.4 mmol/L. His HbA1c is 64 mmol/mol (8.0%). Which insulin adjustment represents the best management approach?

Q57

A 58-year-old woman is commenced on enoxaparin 1.5mg/kg once daily for treatment of confirmed pulmonary embolism. Her weight is 112kg and her renal function shows: creatinine 102 μmol/L, eGFR 56 ml/min/1.73m². On day 3 of treatment, she develops new thrombocytopenia with platelet count dropping from 298×10⁹/L to 92×10⁹/L. She has no bleeding and is haemodynamically stable. What is the most appropriate immediate management?

Q58

A 69-year-old woman with mechanical mitral valve replacement (St Jude prosthesis) is established on warfarin with target INR 3.0-4.0. She is admitted with major gastrointestinal bleeding presenting with haematemesis and melaena. Her observations show: BP 88/52 mmHg, HR 118 bpm, temperature 36.8°C. Blood tests reveal: Hb 72 g/L, INR 3.6, creatinine 178 μmol/L. What is the most appropriate immediate management of her anticoagulation?

Q59

A 51-year-old man with type 1 diabetes for 25 years attends diabetes clinic. He has recurrent hypoglycaemia unawareness and experiences 3-4 episodes weekly of blood glucose <3.0 mmol/L, often without warning symptoms. He is on insulin degludec 32 units once daily and insulin aspart with meals. His HbA1c is 48 mmol/mol (6.5%). What is the most appropriate adjustment to his insulin regimen?

Q60

A 74-year-old man with permanent atrial fibrillation on apixaban 5mg twice daily is admitted with acute hip fracture requiring surgical fixation. His renal function shows: creatinine 156 μmol/L, eGFR 42 ml/min/1.73m². He weighs 58kg and is 168cm tall. Surgery is planned for the next morning. On admission his APTT is 38 seconds (normal 26-36 seconds). What is the most appropriate perioperative anticoagulation management?

Safe Prescribing UK Medical PG Practice Questions and MCQs

Question 51: A 70-year-old man with atrial fibrillation on rivaroxaban 20mg once daily develops infective endocarditis. Blood cultures grow Streptococcus viridans and transoesophageal echocardiography confirms a 12mm vegetation on the mitral valve. What is the most appropriate anticoagulation management?

A. Switch to warfarin with target INR 2-3
B. Continue rivaroxaban 20mg once daily throughout treatment
C. Stop all anticoagulation until endocarditis is treated (Correct Answer)
D. Switch to therapeutic dose low molecular weight heparin
E. Reduce rivaroxaban to 15mg once daily

Explanation: ***Stop all anticoagulation until endocarditis is treated*** - In native valve **infective endocarditis (IE)**, the risk of **intracranial hemorrhage** from septic emboli or ruptured **mycotic aneurysms** outweighs the benefits of stroke prevention from atrial fibrillation. - Major guidelines recommend **discontinuing anticoagulation** in the acute phase of native valve IE because the vegetation remains friable and the risk of **hemorrhagic transformation** of an embolic stroke is high (up to 60%). *Switch to warfarin with target INR 2-3* - **Warfarin** is contraindicated in acute native valve endocarditis as it carries a high risk of **intramuscular or intracranial bleeding** during the unstable infectious period. - While warfarin is used for mechanical valves, this patient has **atrial fibrillation**, which does not justify the hemorrhagic risks during acute IE. *Continue rivaroxaban 20mg once daily throughout treatment* - **Rivaroxaban** (a DOAC) should not be continued because its anticoagulant effect is fixed and difficult to reverse quickly if a **haemorrhagic stroke** occurs. - **Direct Oral Anticoagulants** have no established safety profile in the setting of acute infective endocarditis and increase the risk of severe **embolic complications**. *Switch to therapeutic dose low molecular weight heparin* - Even though **LMWH** has a shorter half-life than some agents, **therapeutic doses** still significantly increase the risk of bleeding into septic brain infarcts. - LMWH or **unfractionated heparin** might only be considered in very specific scenarios involving mechanical valves, but it is not recommended for native valve IE in this patient. *Reduce rivaroxaban to 15mg once daily* - Reducing the dose of rivaroxaban does not mitigate the high risk of **septic embolism-induced bleeding** and remains clinically unsafe. - There is no evidence supporting **dose reduction** of DOACs as a strategy to manage the bleeding risks associated with **mitral valve vegetations**.

Question 52: A 61-year-old woman with type 2 diabetes is admitted with acute kidney injury secondary to dehydration. Her creatinine has risen from 95 μmol/L to 284 μmol/L. She is on insulin glargine 40 units at night and insulin aspart 12 units three times daily with meals. What is the most appropriate insulin adjustment during her acute illness?

A. Continue current insulin doses unchanged as diabetes management remains a priority
B. Reduce all insulin doses by 25% due to decreased renal clearance of insulin (Correct Answer)
C. Switch to a variable rate intravenous insulin infusion (VRIII) until renal function improves
D. Stop basal insulin but continue mealtime insulin at reduced doses
E. Increase insulin doses by 20% to account for stress hyperglycaemia

Explanation: ***Reduce all insulin doses by 25% due to decreased renal clearance of insulin*** - In **acute kidney injury (AKI)**, the kidneys' ability to degrade and clear insulin is significantly impaired, leading to a prolonged **half-life** and high risk of **hypoglycemia**. - Guidelines suggest a **dose reduction of 25-50%** when the eGFR or creatinine clearance drops significantly to ensure patient safety while maintaining glycemic control. *Continue current insulin doses unchanged as diabetes management remains a priority* - Maintaining the same dose in the setting of a **tripled creatinine** (95 to 284 μmol/L) would likely result in severe, life-threatening **hypoglycemia**. - While diabetes management is a priority, the **pharmacokinetics** of insulin are altered by renal failure, necessitating an immediate adjustment. *Switch to a variable rate intravenous insulin infusion (VRIII) until renal function improves* - A **VRIII** is typically reserved for patients who are **nil by mouth**, vomiting, or undergoing surgery, rather than for AKI alone. - If the patient is still eating and drinking, a **subcutaneous basal-bolus regimen** with dose adjustments is the preferred and safer management strategy. *Stop basal insulin but continue mealtime insulin at reduced doses* - Stopping **basal insulin** (Glargine) completely puts the patient at risk for **hyperglycemia** and potentially **diabetic ketoacidosis (DKA)** or ketosis, even in Type 2 diabetes. - A **basal-bolus** approach should be maintained to provide a steady physiological level of insulin, but at lower quantities. *Increase insulin doses by 20% to account for stress hyperglycaemia* - Although **stress hyperglycemia** occurs during acute illness, the effect of **reduced renal clearance** in AKI far outweighs the increase in insulin resistance. - Increasing the dose would dangerously exacerbate the risk of **hypoglycemic episodes** in a patient with reduced renal function.

Question 53: A 58-year-old man with chronic atrial fibrillation on warfarin therapy requires antibiotic treatment for a lower respiratory tract infection. His INR has been stable at 2.4 for the past 6 months. Which antibiotic is most likely to significantly increase his INR and require closer monitoring?

A. Amoxicillin
B. Clarithromycin (Correct Answer)
C. Doxycycline
D. Nitrofurantoin
E. Trimethoprim

Explanation: ***Clarithromycin***- **Clarithromycin** is a potent inhibitor of the **CYP450 system**, specifically **CYP3A4**, which reduces the metabolism of **warfarin** and leads to a significant increase in **INR**.- Co-prescribing this macrolide requires intensive **INR monitoring** and potential dose reduction to prevent life-threatening **bleeding complications**.*Amoxicillin*- **Amoxicillin** is generally considered safe with **warfarin** as it has minimal direct effect on **hepatic enzyme metabolism**.- While any broad-spectrum antibiotic can theoretically alter **gut flora** and reduce **Vitamin K synthesis**, the risk of significant INR elevation with this agent is very low.*Doxycycline*- **Doxycycline** can occasionally cause a mild increase in the anticoagulant effect of **warfarin**, but the interaction is usually less clinically significant than with macrolides.- It does not inhibit the primary **CYP enzymes** responsible for **warfarin metabolism** as strongly as clarithromycin does.*Nitrofurantoin*- **Nitrofurantoin** has no documented significant interaction with **warfarin** and is not associated with an increase in **INR**.- It is primarily used for **urinary tract infections** and is unsuitable for treating the lower respiratory tract infection described.*Trimethoprim*- **Trimethoprim** (and Co-trimoxazole) can increase the **INR** by inhibiting **CYP2C9**, the main enzyme for **S-warfarin**.- While it requires monitoring, the metabolic inhibition by **macrolides** like **clarithromycin** is a frequently tested high-risk interaction in safe prescribing.

Question 54: A 65-year-old woman with atrial fibrillation is on warfarin with target INR 2-3. She has been stable for 2 years with INR checks every 10 weeks. She is prescribed a 7-day course of ciprofloxacin 500mg twice daily for a urinary tract infection. Her current INR is 2.4 measured 3 days ago. What is the most appropriate monitoring and management strategy?

A. Continue warfarin at current dose, recheck INR in 10 weeks as scheduled
B. Reduce warfarin dose by 20% for the duration of antibiotic therapy, recheck INR in 1 week
C. Continue warfarin at current dose, check INR 3-5 days after starting ciprofloxacin (Correct Answer)
D. Temporarily switch from warfarin to low molecular weight heparin for the duration of antibiotic therapy
E. Increase frequency of INR monitoring to twice weekly but continue warfarin at current dose

Explanation: ***Continue warfarin at current dose, check INR 3-5 days after starting ciprofloxacin*** - **Ciprofloxacin** inhibits **CYP450 enzymes** (primarily CYP1A2 and CYP3A4) and reduces gut bacterial **Vitamin K** production, both of which potentiate the anticoagulant effect of **warfarin** and increase bleeding risk. - Maintaining the current warfarin dose while performing early **INR monitoring** (within 3-5 days of starting ciprofloxacin) is the most appropriate strategy to detect an elevated INR and adjust the dose if necessary. *Continue warfarin at current dose, recheck INR in 10 weeks as scheduled* - Waiting 10 weeks for an INR check is unsafe as **ciprofloxacin** can cause a rapid and significant increase in **INR** within the first week of therapy. - This approach fails to address a known **drug-drug interaction** and places the patient at high risk of **hemorrhagic complications**. *Reduce warfarin dose by 20% for the duration of antibiotic therapy, recheck INR in 1 week* - **Empirical dose reduction** is generally not recommended as the individual response to warfarin-antibiotic interactions is highly variable. - Reducing the dose without evidence of supratherapeutic INR could lead to an **under-therapeutic INR**, increasing the risk of **thromboembolism**. *Temporarily switch from warfarin to low molecular weight heparin for the duration of antibiotic therapy* - **Bridging therapy** with **LMWH** is typically reserved for procedures or conditions where oral anticoagulation is interrupted or contraindicated, not for managing a common **drug interaction** for a **UTI**. - This strategy is unnecessarily complex, more expensive, and less convenient than adjusting warfarin based on monitored INR. *Increase frequency of INR monitoring to twice weekly but continue warfarin at current dose* - Monitoring **INR twice weekly** for a short 7-day course of antibiotics is usually excessive and creates an unnecessary burden on the patient. - A single, well-timed INR check 3-5 days after starting the antibiotic is generally sufficient to assess the peak interaction effect and guide dose adjustments.

Question 55: A 73-year-old man with non-valvular atrial fibrillation (CHA₂DS₂-VASc score 5) is established on dabigatran 150mg twice daily. He requires urgent surgery for acute appendicitis within the next 6 hours. His last dose of dabigatran was 3 hours ago. His creatinine is 118 μmol/L (eGFR 52 ml/min/1.73m²). Laboratory tests show: APTT 46 seconds (normal 26-36), thrombin time >200 seconds (normal 15-19). What is the most appropriate management of his anticoagulation before proceeding to surgery?

A. Proceed to surgery without delay as the bleeding risk is acceptable with urgent surgery
B. Delay surgery for 12 hours to allow dabigatran clearance, then proceed without reversal
C. Administer prothrombin complex concentrate 50 units/kg immediately before surgery
D. Administer idarucizumab 5g intravenously as a specific reversal agent before surgery (Correct Answer)
E. Give activated charcoal 50g orally to reduce dabigatran absorption and delay surgery by 4 hours

Explanation: ***Administer idarucizumab 5g intravenously as a specific reversal agent before surgery*** - **Idarucizumab** is a specific monoclonal antibody fragment that provides immediate and complete reversal of **dabigatran** by binding to it with high affinity. - It is indicated for patients requiring **urgent surgery** or procedures where the bleeding risk is high, especially when lab tests like **thrombin time** are significantly prolonged. *Proceed to surgery without delay as the bleeding risk is acceptable with urgent surgery* - Proceeding without reversal is unsafe given the **thrombin time >200 seconds**, which indicates a high concentration of dabigatran in the system. - The **eGFR of 52 ml/min** and the recent dose (3 hours ago) mean the drug is likely at peak levels, posing a severe **haemorrhagic risk**. *Delay surgery for 12 hours to allow dabigatran clearance, then proceed without reversal* - With an **eGFR of 52 ml/min**, the half-life of dabigatran is approximately **15-18 hours**, meaning 12 hours is insufficient for complete clearance. - Clinical delay in **acute appendicitis** management increases the risk of **perforation** and peritonitis. *Administer prothrombin complex concentrate 50 units/kg immediately before surgery* - **Prothrombin complex concentrate (PCC)** is primarily used for the reversal of **Warfarin** or **Factor Xa inhibitors** (like Apixaban or Rivaroxaban). - PCC is not a specific reversal agent for **direct thrombin inhibitors** like dabigatran and is much less effective than **idarucizumab**. *Give activated charcoal 50g orally to reduce dabigatran absorption and delay surgery by 4 hours* - **Activated charcoal** is only effective if administered within **2 hours** of dabigatran ingestion; this patient took his dose 3 hours ago. - This intervention would not address the drug already absorbed into the **systemic circulation** or the immediate need for surgery.

Question 56: A 44-year-old man with type 2 diabetes is on insulin glargine 48 units at bedtime and insulin lispro 12 units with each meal. Over the past month he has gained 6kg in weight and reports frequent hypoglycaemic episodes, particularly nocturnal. His home blood glucose diary shows: pre-breakfast 3.2-4.8 mmol/L, pre-lunch 8.2-11.4 mmol/L, pre-dinner 9.8-13.2 mmol/L, bedtime 6.8-8.4 mmol/L. His HbA1c is 64 mmol/mol (8.0%). Which insulin adjustment represents the best management approach?

A. Reduce insulin glargine to 38 units at bedtime and increase insulin lispro to 16 units with each meal
B. Continue insulin glargine at 48 units, reduce breakfast insulin lispro to 8 units, increase lunch and dinner insulin lispro to 16 units each
C. Reduce insulin glargine to 40 units and split the dose to twice daily administration to reduce nocturnal hypoglycaemia (Correct Answer)
D. Switch insulin glargine to morning administration and reduce dose to 40 units, increase all insulin lispro doses to 14 units
E. Reduce insulin glargine to 42 units at bedtime, maintain breakfast insulin lispro at 12 units, increase lunch and dinner insulin lispro to 14 units each

Explanation: ***Reduce insulin glargine to 40 units and split the dose to twice daily administration to reduce nocturnal hypoglycaemia*** - The current **insulin glargine** dose of 48 units at bedtime is causing **nocturnal hypoglycaemia** and very low **pre-breakfast glucose** levels (3.2-4.8 mmol/L), indicating an excessive basal effect during the night. - Reducing the total daily dose to 40 units and splitting it into **twice-daily administration** provides a more stable and consistent **basal insulin** profile, effectively reducing nocturnal lows and improving overall control without severe peaks. *Reduce insulin glargine to 38 units at bedtime and increase insulin lispro to 16 units with each meal* - While reducing the **basal insulin** dose is appropriate, a single large reduction to 38 units at bedtime may still leave the patient vulnerable to nocturnal lows or create a gap in **basal coverage** later in the 24-hour cycle. - Increasing all **insulin lispro** doses significantly, without addressing the timing of basal delivery, could lead to **daytime hypoglycaemia** and does not optimize the **basal insulin** profile to prevent nocturnal lows. *Continue insulin glargine at 48 units, reduce breakfast insulin lispro to 8 units, increase lunch and dinner insulin lispro to 16 units each* - Continuing **insulin glargine** at 48 units fails to address the core problem of **nocturnal hypoglycaemia** and low **pre-breakfast glucose** readings. - Although mealtime **lispro** adjustments are considered, the underlying excessive **basal insulin** dose will likely perpetuate the unsafe nocturnal pattern and contribute to the patient's weight gain. *Switch insulin glargine to morning administration and reduce dose to 40 units, increase all insulin lispro doses to 14 units* - Switching the entire **basal insulin** dose to morning administration may not provide adequate **basal coverage** during the later night and early morning hours, potentially leading to increased glucose levels before breakfast despite current lows. - While reducing the **glargine** dose is appropriate, increasing all **insulin lispro** doses without fine-tuning the **basal** timing could lead to inconsistent blood glucose control and further weight gain. *Reduce insulin glargine to 42 units at bedtime, maintain breakfast insulin lispro at 12 units, increase lunch and dinner insulin lispro to 14 units each* - A modest reduction of **insulin glargine** to 42 units may not be sufficient to completely eliminate the **frequent nocturnal hypoglycaemia** and significantly low **pre-breakfast glucose** readings (3.2 mmol/L). - While increasing lunch and dinner **insulin lispro** addresses daytime hyperglycemia, this option does not optimize the **basal insulin** profile for stable 24-hour coverage as effectively as splitting the dose to manage nocturnal risk.

Question 57: A 58-year-old woman is commenced on enoxaparin 1.5mg/kg once daily for treatment of confirmed pulmonary embolism. Her weight is 112kg and her renal function shows: creatinine 102 μmol/L, eGFR 56 ml/min/1.73m². On day 3 of treatment, she develops new thrombocytopenia with platelet count dropping from 298×10⁹/L to 92×10⁹/L. She has no bleeding and is haemodynamically stable. What is the most appropriate immediate management?

A. Continue enoxaparin and monitor platelets daily as this represents typical thrombocytopenia secondary to acute thrombosis
B. Discontinue enoxaparin immediately, send blood for heparin-induced thrombocytopenia antibodies, commence fondaparinux (Correct Answer)
C. Reduce enoxaparin dose by 50% and add aspirin 75mg once daily to maintain anticoagulation while investigating
D. Switch to unfractionated heparin infusion as this has lower risk of thrombocytopenia than LMWH
E. Discontinue enoxaparin, commence warfarin with target INR 2-3, give platelet transfusion if count falls below 50×10⁹/L

Explanation: ***Discontinue enoxaparin immediately, send blood for heparin-induced thrombocytopenia antibodies, commence fondaparinux*** - The patient's **platelet count drop of >50%** (from 298 to 92 × 10⁹/L) within 3 days of starting enoxaparin is highly suggestive of **Heparin-Induced Thrombocytopenia (HIT)**, especially given the timing. - Immediate management for suspected HIT involves stopping all heparin products (including LMWH) and initiating a **non-heparin anticoagulant** like **fondaparinux** to prevent **paradoxical thrombosis**, which is the primary danger. *Continue enoxaparin and monitor platelets daily as this represents typical thrombocytopenia secondary to acute thrombosis* - A **>50% drop in platelet count** is not a typical manifestation of acute thrombosis; it strongly indicates an **immune-mediated process** like HIT. - Continuing heparin in the setting of suspected HIT significantly increases the risk of **life-threatening thrombotic complications** (HIT with thrombosis, HITT). *Reduce enoxaparin dose by 50% and add aspirin 75mg once daily to maintain anticoagulation while investigating* - Dose reduction of enoxaparin is ineffective for HIT as even small amounts of heparin perpetuate the **antibody-mediated platelet activation** and immune response. - **Aspirin** is an antiplatelet agent and does not provide adequate anticoagulation for a confirmed pulmonary embolism, nor does it address the underlying pathophysiology of HIT. *Switch to unfractionated heparin infusion as this has lower risk of thrombocytopenia than LMWH* - This statement is incorrect; **Unfractionated Heparin (UFH)** actually carries a significantly **higher risk of HIT** compared to LMWH. - Antibodies in HIT (anti-PF4/heparin) generally **cross-react** with both LMWH and UFH, making switching to UFH ineffective and potentially harmful. *Discontinue enoxaparin, commence warfarin with target INR 2-3, give platelet transfusion if count falls below 50×10⁹/L* - Initiating **warfarin** as monotherapy in acute HIT is contraindicated due to the risk of precipitating **venous limb gangrene** and skin necrosis from rapid protein C depletion in an already prothrombotic state. - **Platelet transfusions** are generally *avoided* in HIT because they can exacerbate the prothrombotic state by providing more platelets for activation by the circulating antibodies, unless there is severe, life-threatening bleeding.

Question 58: A 69-year-old woman with mechanical mitral valve replacement (St Jude prosthesis) is established on warfarin with target INR 3.0-4.0. She is admitted with major gastrointestinal bleeding presenting with haematemesis and melaena. Her observations show: BP 88/52 mmHg, HR 118 bpm, temperature 36.8°C. Blood tests reveal: Hb 72 g/L, INR 3.6, creatinine 178 μmol/L. What is the most appropriate immediate management of her anticoagulation?

A. Withhold warfarin and give oral vitamin K 5mg, transfuse blood products as needed, restart warfarin when INR <2.0
B. Administer prothrombin complex concentrate 50 units/kg and intravenous vitamin K 5mg immediately (Correct Answer)
C. Give fresh frozen plasma 4 units and vitamin K 10mg intravenously, arrange urgent upper GI endoscopy
D. Withhold warfarin, give vitamin K 10mg orally, commence therapeutic dose low molecular weight heparin once haemodynamically stable
E. Administer tranexamic acid 1g intravenously and withhold warfarin for 48 hours until INR normalises

Explanation: ***Administer prothrombin complex concentrate 50 units/kg and intravenous vitamin K 5mg immediately*** - In the presence of **major/life-threatening bleeding** (haematemesis with tachycardia and hypotension), **Prothrombin Complex Concentrate (PCC)** is the gold standard for immediate reversal of warfarin-induced coagulopathy. - **Intravenous Vitamin K** is required alongside PCC to sustain the reversal once the exogenous clotting factors are metabolised. *Withhold warfarin and give oral vitamin K 5mg, transfuse blood products as needed, restart warfarin when INR <2.0* - **Oral vitamin K** has a slow onset of action (6–24 hours), which is clinically inappropriate and dangerous in the context of **haemodynamic instability**. - While blood products like RBCs are needed for her **Hb of 72 g/L**, they do not address the underlying coagulopathy required to stop the active bleeding. *Give fresh frozen plasma 4 units and vitamin K 10mg intravenously, arrange urgent upper GI endoscopy* - **Fresh Frozen Plasma (FFP)** is no longer first-line because it requires large volumes (risk of **fluid overload**), needs time to thaw, and provides less reliable factor concentration than PCC. - Management must prioritize **haemostatic correction** with PCC before invasive procedures like endoscopy are performed in an unstable patient. *Withhold warfarin, give vitamin K 10mg orally, commence therapeutic dose low molecular weight heparin once haemodynamically stable* - **Low Molecular Weight Heparin (LMWH)** is contraindicated during active, major bleeding and could worsen the patient's prognosis. - Switching to LMWH is a strategy for long-term management of **mechanical valves**, but the immediate priority here is emergency **reversal of anticoagulation**. *Administer tranexamic acid 1g intravenously and withhold warfarin for 48 hours until INR normalises* - **Tranexamic acid** is an antifibrinolytic and does not directly reverse the **Vitamin K antagonist** effect of warfarin. - Simply withholding warfarin and waiting 48 hours is insufficient, as the patient is currently in **haemorrhagic shock** and requires replacement of factors II, VII, IX, and X.

Question 59: A 51-year-old man with type 1 diabetes for 25 years attends diabetes clinic. He has recurrent hypoglycaemia unawareness and experiences 3-4 episodes weekly of blood glucose <3.0 mmol/L, often without warning symptoms. He is on insulin degludec 32 units once daily and insulin aspart with meals. His HbA1c is 48 mmol/mol (6.5%). What is the most appropriate adjustment to his insulin regimen?

A. Reduce insulin degludec to 26 units and accept higher HbA1c target of 53-58 mmol/mol (7-7.5%) to minimise hypoglycaemia (Correct Answer)
B. Switch from insulin degludec to insulin glargine which has lower risk of nocturnal hypoglycaemia
C. Add acarbose to slow carbohydrate absorption and reduce post-prandial insulin requirements
D. Increase insulin degludec to 38 units to reduce counter-regulatory hormone surges causing rebound hypoglycaemia
E. Switch to insulin pump therapy (continuous subcutaneous insulin infusion) as this is contraindicated with impaired awareness

Explanation: ***Reduce insulin degludec to 26 units and accept higher HbA1c target of 53-58 mmol/mol (7-7.5%) to minimise hypoglycaemia*** - The patient has **hypoglycaemia unawareness** and frequent episodes, indicating that the current HbA1c of 6.5% is achieved at the cost of dangerous **iatrogenic hypoglycaemia**. - Scrupulous avoidance of low blood glucose for several weeks can help **restore warning symptoms**; therefore, reducing the basal dose and relaxing targets is the first-line management. *Switch from insulin degludec to insulin glargine which has lower risk of nocturnal hypoglycaemia* - **Insulin degludec** is an ultra-long-acting analogue that generally has a **lower or similar risk** of nocturnal hypoglycaemia compared to standard glargine (U100). - Switching to glargine would not address the primary issue of **over-insulinisation** and the need for a higher glycaemic target. *Add acarbose to slow carbohydrate absorption and reduce post-prandial insulin requirements* - **Acarbose** is an alpha-glucosidase inhibitor primarily used in Type 2 Diabetes and is not a standard treatment for **hypoglycaemia unawareness** in Type 1 Diabetes. - If a patient on acarbose develops hypoglycaemia, they must be treated with **pure glucose (dextrose)** because the drug prevents the breakdown of complex sugars. *Increase insulin degludec to 38 units to reduce counter-regulatory hormone surges causing rebound hypoglycaemia* - Increasing the insulin dose in a patient already experiencing 3-4 hypoglycaemic episodes per week is **dangerous** and will exacerbate the risk of a fatal event. - "Rebound" effects (like the **Somogyi phenomenon**) are managed by reducing the preceding insulin dose, not increasing it. *Switch to insulin pump therapy (continuous subcutaneous insulin infusion) as this is contraindicated with impaired awareness* - **Insulin pump therapy** is actually **indicated** (not contraindicated) by NICE for patients with disabling hypoglycaemia or impaired awareness despite optimized MDIs. - While a pump may be a future step, the statement incorrectly claims it is contraindicated, and the immediate priority is **dose adjustment**.

Question 60: A 74-year-old man with permanent atrial fibrillation on apixaban 5mg twice daily is admitted with acute hip fracture requiring surgical fixation. His renal function shows: creatinine 156 μmol/L, eGFR 42 ml/min/1.73m². He weighs 58kg and is 168cm tall. Surgery is planned for the next morning. On admission his APTT is 38 seconds (normal 26-36 seconds). What is the most appropriate perioperative anticoagulation management?

A. Continue apixaban 5mg twice daily throughout as it is needed for stroke prevention
B. Omit apixaban on the day of surgery, restart 5mg twice daily 48 hours post-operatively if haemostasis achieved (Correct Answer)
C. Stop apixaban now, give low molecular weight heparin bridging at treatment dose until 12 hours before surgery
D. Reduce apixaban to 2.5mg twice daily perioperatively due to renal impairment and bleeding risk
E. Discontinue apixaban, give prothrombin complex concentrate pre-operatively, restart apixaban 7 days post-surgery

Explanation: ***Omit apixaban on the day of surgery, restart 5mg twice daily 48 hours post-operatively if haemostasis achieved*** - For **urgent surgery** with a **high bleeding risk** like hip fixation, the DOAC should be held to ensure at least a 24-hour gap from the last dose to minimize perioperative bleeding. - The 5mg dose is correct because the patient only meets two criteria for dose reduction (**weight ≤60kg** and **creatinine ≥133 μmol/L**) but not the necessary two out of three (age ≥80, weight ≤60kg, creatinine ≥133 μmol/L) as he is 74 (under 80). *Continue apixaban 5mg twice daily throughout as it is needed for stroke prevention* - Continuing a **direct oral anticoagulant (DOAC)** during major surgery poses an unacceptable **bleeding risk**, especially for procedures involving bone. - **Periprocedural management** of DOACs requires a temporary interruption to ensure safe surgical hemostasis. *Stop apixaban now, give low molecular weight heparin bridging at treatment dose until 12 hours before surgery* - **Heparin bridging** is generally not recommended for DOACs due to their predictable and rapid onset and offset of action. - Bridging significantly increases the **risk of bleeding** without providing a clear benefit in preventing thromboembolism compared to simple interruption. *Reduce apixaban to 2.5mg twice daily perioperatively due to renal impairment and bleeding risk* - Dose reduction to 2.5mg twice daily is indicated for long-term therapy only if **two of three** criteria are met: **age ≥80**, **weight ≤60kg**, or **creatinine ≥133 μmol/L**; perioperative management focuses on interruption rather than reduction. - Reducing the dose does not provide sufficient **hemostatic safety** for major surgery compared to omitting the dose entirely. *Discontinue apixaban, give prothrombin complex concentrate pre-operatively, restart apixaban 7 days post-surgery* - **Prothrombin complex concentrate (PCC)** or specific reversal agents are reserved for **emergency surgery** (within 6 hours) or life-threatening bleeds, not scheduled semi-urgent cases. - Restarting anticoagulation as late as 7 days post-surgery would excessively increase the risk of **venous thromboembolism (VTE)** and stroke in a patient with **atrial fibrillation**.

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