A 28-year-old woman presents with recurrent syncope during exercise. ECG shows deep Q waves in leads II, III, and aVF with T-wave inversion. Echocardiogram reveals asymmetric septal hypertrophy. What is the most appropriate management?
Q32
A 45-year-old man presents with central chest pain radiating to his left arm and jaw. The pain started 2 hours ago and is described as crushing. His ECG shows ST elevation in leads II, III, and aVF. What is the most likely diagnosis?
Q33
A 66-year-old man attends cardiology clinic for cardiovascular risk assessment. He is asymptomatic with no history of cardiovascular disease. He has type 2 diabetes managed with metformin, hypertension treated with ramipril, and was diagnosed with chronic kidney disease stage 3a last year. He stopped smoking 5 years ago (30 pack-year history). His father died of myocardial infarction aged 58. Examination: BP 136/82 mmHg, BMI 29 kg/m². Blood tests show: total cholesterol 5.8 mmol/L, HDL 1.1 mmol/L, non-HDL 4.7 mmol/L, HbA1c 58 mmol/mol, eGFR 52 mL/min/1.73m². His QRISK3 score is calculated at 28%. What is the most appropriate management regarding cardiovascular risk reduction?
Q34
A 70-year-old man is admitted with acute pulmonary oedema. Echocardiography reveals severe aortic stenosis with aortic valve area 0.7 cm², mean gradient 48 mmHg, and LVEF 35%. He has severe symptoms (NYHA class III) with minimal exertion causing breathlessness. His past medical history includes previous stroke with full recovery, chronic kidney disease stage 3b (eGFR 38 mL/min/1.73m²), and chronic obstructive pulmonary disease with FEV1 45% predicted. He is 168 cm tall, weighs 58 kg, and has a calculated surgical risk (EuroSCORE II) of 18%. What is the most appropriate definitive management strategy?
Q35
A 53-year-old woman with exertional chest pain undergoes CT coronary angiography which shows 50% stenosis in the mid-left anterior descending artery. She has no other significant coronary disease. Her symptoms occur 2-3 times per week when walking uphill but resolve with rest after 3-4 minutes. She is a non-smoker with well-controlled hypertension on amlodipine. Her resting ECG is normal. What is the most appropriate initial anti-anginal medication to add for symptom control?
Q36
A 62-year-old man presents to the Emergency Department with 45 minutes of severe central chest pain and nausea. His initial ECG shows sinus rhythm with 2 mm ST-segment elevation in leads V1-V4. He receives aspirin 300 mg, ticagrelor 180 mg, and is transferred for primary PCI. Angiography reveals total occlusion of the proximal left anterior descending artery, which is successfully stented. Two days post-procedure, he develops sudden onset severe breathlessness and hypotension. Examination reveals BP 88/56 mmHg, heart rate 110 bpm, elevated JVP, and a new pansystolic murmur loudest at the left sternal edge. What is the most likely complication?
Q37
A 81-year-old woman presents with progressive breathlessness over 8 months. She can no longer climb stairs without stopping. Examination reveals BP 168/92 mmHg, heart rate 76 bpm regular, elevated JVP, bilateral basal fine inspiratory crackles, and mild ankle oedema. Heart sounds reveal a fourth heart sound. Echocardiography shows: LVEF 58%, left ventricular hypertrophy with normal wall motion, left atrial dilatation, E/e' ratio 18, and no significant valvular disease. NT-proBNP is 580 ng/L. What is the most likely diagnosis?
Q38
A 76-year-old man with permanent atrial fibrillation is taking apixaban 5 mg twice daily for stroke prevention. He presents to the Emergency Department following a fall with a large scalp laceration requiring suturing. His past medical history includes previous ischaemic stroke 3 years ago, hypertension, and type 2 diabetes. His current medications are apixaban, metformin, and amlodipine. He is haemodynamically stable. Blood tests show: haemoglobin 142 g/L, platelets 245 × 10⁹/L, creatinine 98 μmol/L (eGFR 64 mL/min/1.73m²). CT head shows no intracranial haemorrhage. The laceration is sutured successfully. What is the most appropriate management of his anticoagulation?
Q39
A 45-year-old woman of African-Caribbean origin presents to her GP with elevated blood pressure. She has had three clinic readings over 4 months averaging 154/96 mmHg. Ambulatory blood pressure monitoring confirms an average of 152/94 mmHg. She has no other medical history, takes no regular medications, and does not smoke. Her BMI is 24 kg/m². Blood tests show: sodium 139 mmol/L, potassium 4.1 mmol/L, creatinine 76 μmol/L (eGFR >90 mL/min/1.73m²), HbA1c 36 mmol/mol, total cholesterol 4.8 mmol/L. Urinalysis shows no protein. ECG and fundoscopy are normal. What is the most appropriate first-line antihypertensive medication?
Q40
A 58-year-old man with stable angina is commenced on sublingual glyceryl trinitrate (GTN) spray for symptom relief. He experiences exertional chest tightness approximately 3 times per week, which resolves after 2-3 minutes of rest. He asks how the GTN spray works to relieve his symptoms. Which of the following best describes the primary mechanism of action of GTN in relieving anginal chest pain?
Cardiology UK Medical PG Practice Questions and MCQs
Question 31: A 28-year-old woman presents with recurrent syncope during exercise. ECG shows deep Q waves in leads II, III, and aVF with T-wave inversion. Echocardiogram reveals asymmetric septal hypertrophy. What is the most appropriate management?
A. Beta-blockers
B. ACE inhibitors
C. Implantable cardioverter defibrillator (Correct Answer)
D. Septal myectomy
E. Heart transplantation
Explanation: ***Implantable cardioverter defibrillator*** - Recurrent syncope during exercise in a patient with **Hypertrophic Cardiomyopathy (HCM)**, evidenced by **asymmetric septal hypertrophy**, is a critical high-risk factor for **sudden cardiac death (SCD)** due to ventricular arrhythmias. - The presence of syncope (a major high-risk feature) mandates the placement of an **ICD** for primary prevention of fatal arrhythmias, as it directly addresses the life-threatening risk.*Beta-blockers* - These are standard first-line medical therapy for reducing symptoms (angina, dyspnea) in HCM by decreasing heart rate and contractility, thereby alleviating dynamic **left ventricular outflow tract (LVOT) obstruction**. - However, beta-blockers alone are not sufficient to prevent **SCD** in a high-risk patient presenting with documented syncope, making an ICD more appropriate for this specific presentation.*ACE inhibitors* - **ACE inhibitors** and other vasodilators generally reduce systemic vascular resistance and preload, which can decrease ventricular filling and worsen the dynamic **LVOT obstruction** in HCM. - Therefore, these medications are typically avoided or used with great caution in patients with obstructive HCM, as they can exacerbate symptoms like syncope.*Septal myectomy* - This is an invasive surgical procedure indicated for severe, persistent symptoms related to significant **LVOT obstruction** (>50 mmHg) that are refractory to maximum medical therapy (e.g., beta-blockers). - While it addresses the obstruction, it is not the immediate, lifesaving intervention required to mitigate the high risk of **SCD** signaled by the patient's syncope; an ICD directly protects against fatal arrhythmias.*Heart transplantation* - This is reserved for patients with end-stage HCM who develop refractory, debilitating **NYHA Class III/IV heart failure** or severe arrhythmias despite all other medical and device interventions. - Given the patient's age and primary presentation centering on SCD risk rather than end-stage failure, transplantation is too aggressive and not indicated for initial management.
Question 32: A 45-year-old man presents with central chest pain radiating to his left arm and jaw. The pain started 2 hours ago and is described as crushing. His ECG shows ST elevation in leads II, III, and aVF. What is the most likely diagnosis?
A. Anterior STEMI
B. Inferior STEMI (Correct Answer)
C. Lateral STEMI
D. Posterior STEMI
E. Unstable angina
Explanation: ***Inferior STEMI***- **ST elevation** in leads **II, III, and aVF** specifically indicates myocardial infarction of the **inferior wall** of the left ventricle. This finding, combined with classic chest pain, is diagnostic of an **Inferior STEMI**.- The occlusion responsible for an inferior STEMI most commonly involves the **right coronary artery (RCA)**, especially its proximal or mid segments, or less commonly, a dominant left circumflex artery (LCX).*Anterior STEMI*- **Anterior STEMI** is characterized by **ST elevation** in the precordial leads, typically **V1 through V4**.- This type of myocardial infarction is primarily caused by an occlusion of the **left anterior descending (LAD) artery**.*Lateral STEMI*- A **lateral STEMI** is identified by **ST elevation** in leads **I, aVL, V5, and V6**.- This usually signifies an occlusion of the **left circumflex artery (LCX)** or a diagonal branch of the LAD.*Posterior STEMI*- A **posterior STEMI** is suggested by **ST depression** and prominent R waves in leads **V1-V3** (reciprocal changes).- Definitive diagnosis often requires obtaining posterior ECG leads (**V7, V8, V9**) to visualize **ST elevation** directly.*Unstable angina*- **Unstable angina** presents with acute ischemic chest pain but *lacks* persistent **ST elevation** on the electrocardiogram.- While cardiac biomarkers may be elevated or normal, the absence of **ST elevation** on ECG differentiates it from a STEMI, which necessitates immediate reperfusion.
Question 33: A 66-year-old man attends cardiology clinic for cardiovascular risk assessment. He is asymptomatic with no history of cardiovascular disease. He has type 2 diabetes managed with metformin, hypertension treated with ramipril, and was diagnosed with chronic kidney disease stage 3a last year. He stopped smoking 5 years ago (30 pack-year history). His father died of myocardial infarction aged 58. Examination: BP 136/82 mmHg, BMI 29 kg/m². Blood tests show: total cholesterol 5.8 mmol/L, HDL 1.1 mmol/L, non-HDL 4.7 mmol/L, HbA1c 58 mmol/mol, eGFR 52 mL/min/1.73m². His QRISK3 score is calculated at 28%. What is the most appropriate management regarding cardiovascular risk reduction?
A. Commence atorvastatin 20 mg once daily and recheck lipids in 3 months (Correct Answer)
B. Commence atorvastatin 80 mg once daily without need for routine lipid monitoring
C. Advise lifestyle modifications only as QRISK3 is below treatment threshold
D. Commence atorvastatin 40 mg and aspirin 75 mg daily
E. Arrange CT coronary angiography before starting any medication
Explanation: ***Commence atorvastatin 20 mg once daily and recheck lipids in 3 months***- This patient has multiple significant cardiovascular risk factors (Type 2 diabetes, hypertension, CKD stage 3a, 30 pack-year smoking history, family history of early MI, and a calculated **QRISK3 score of 28%**). For **primary prevention**, **NICE guidelines** recommend starting a **high-intensity statin** such as **atorvastatin 20 mg** in patients with a QRISK3 score ≥ 10% or with type 2 diabetes. A **repeat lipid profile** is required after 3 months to ensure a **>40% reduction in non-HDL cholesterol** has been achieved and to guide dose adjustments.*Commence atorvastatin 80 mg once daily without need for routine lipid monitoring*- **Atorvastatin 80 mg** is typically reserved for **secondary prevention** in patients with established cardiovascular disease or if lower doses fail to achieve lipid targets, not usually as an initial dose for primary prevention.- **Routine lipid monitoring** at 3 months is **essential** after initiating statin therapy to assess treatment efficacy and guide potential dose titration.*Advise lifestyle modifications only as QRISK3 is below treatment threshold*- The threshold for pharmacological intervention for primary prevention is a **QRISK3 score of 10% or greater**; this patient's score of **28%** is significantly higher and also has type 2 diabetes.- While **lifestyle modifications** are important, they are **insufficient** as the sole management for a patient with such a high calculated risk and existing comorbidities, who clearly needs statin therapy.*Commence atorvastatin 40 mg and aspirin 75 mg daily*- **Aspirin** is generally **not recommended** for the **primary prevention** of cardiovascular disease due to the increased risk of bleeding (e.g., gastrointestinal hemorrhage) outweighing the benefits in asymptomatic individuals.- The standard initial dose for primary prevention with atorvastatin is **20 mg**, with 40 mg usually considered if the initial 20 mg fails to meet the target non-HDL reduction.*Arrange CT coronary angiography before starting any medication*- **CT coronary angiography** is typically indicated for investigating **new-onset chest pain** suspected to be angina, not for asymptomatic individuals with clear indications for statin therapy based on validated risk scores.- In this asymptomatic patient with a high **QRISK3 score of 28%** and significant risk factors, initiating statin therapy is the appropriate first step for risk reduction, without needing further imaging before commencing treatment.
Question 34: A 70-year-old man is admitted with acute pulmonary oedema. Echocardiography reveals severe aortic stenosis with aortic valve area 0.7 cm², mean gradient 48 mmHg, and LVEF 35%. He has severe symptoms (NYHA class III) with minimal exertion causing breathlessness. His past medical history includes previous stroke with full recovery, chronic kidney disease stage 3b (eGFR 38 mL/min/1.73m²), and chronic obstructive pulmonary disease with FEV1 45% predicted. He is 168 cm tall, weighs 58 kg, and has a calculated surgical risk (EuroSCORE II) of 18%. What is the most appropriate definitive management strategy?
A. Transcatheter aortic valve implantation (TAVI) (Correct Answer)
B. Balloon aortic valvuloplasty as definitive treatment
C. Medical management with diuretics and ACE inhibitors only
D. Urgent coronary artery bypass grafting with valve replacement
E. Surgical aortic valve replacement
Explanation: ***Transcatheter aortic valve implantation (TAVI)***
- This patient has **symptomatic severe aortic stenosis** (NYHA class III, AVA 0.7 cm², mean gradient 48 mmHg) and numerous comorbidities including **CKD stage 3b**, **COPD**, and reduced **LVEF (35%)**, resulting in a very high surgical risk (EuroSCORE II 18%).
- **TAVI** is the recommended definitive treatment for high-risk or inoperable patients with severe, symptomatic aortic stenosis, significantly improving prognosis compared to medical management.
*Balloon aortic valvuloplasty as definitive treatment*
- This procedure offers only temporary symptomatic relief and is associated with very high rates of **restenosis** within 6-12 months.
- It is typically used as a **bridge to TAVI/SAVR** in hemodynamically unstable patients or for palliative purposes, not as a definitive long-term solution.
*Medical management with diuretics and ACE inhibitors only*
- Medical management alone does not address the underlying **mechanical obstruction** of severe aortic stenosis and has been shown to have poor long-term outcomes, with a 50% mortality rate at 2 years for **symptomatic severe AS**.
- While **diuretics** can alleviate acute pulmonary edema, they do not alter the progression of the valvular disease or improve survival in severe, symptomatic cases.
*Urgent coronary artery bypass grafting with valve replacement*
- There is no mention of significant **coronary artery disease** requiring **CABG** in the patient's presentation.
- Adding **CABG** to valve replacement would significantly increase the complexity and **operative risk** for an already high-risk patient, without clear indication.
*Surgical aortic valve replacement*
- Although **surgical aortic valve replacement (SAVR)** is a definitive treatment, this patient's **high surgical risk profile** (EuroSCORE II 18%) and multiple comorbidities (age 70, previous stroke, CKD, COPD, low LVEF) make SAVR a less favorable option.
- Current guidelines recommend **TAVI** over SAVR for patients with severe symptomatic AS who are at high surgical risk, especially those with a **EuroSCORE II > 8-10%**.
Question 35: A 53-year-old woman with exertional chest pain undergoes CT coronary angiography which shows 50% stenosis in the mid-left anterior descending artery. She has no other significant coronary disease. Her symptoms occur 2-3 times per week when walking uphill but resolve with rest after 3-4 minutes. She is a non-smoker with well-controlled hypertension on amlodipine. Her resting ECG is normal. What is the most appropriate initial anti-anginal medication to add for symptom control?
A. Bisoprolol 2.5 mg once daily (Correct Answer)
B. Isosorbide mononitrate 30 mg twice daily
C. Ivabradine 5 mg twice daily
D. Nicorandil 10 mg twice daily
E. Ranolazine 375 mg twice daily
Explanation: ***Bisoprolol 2.5 mg once daily***
- **NICE guidelines** recommend either a **beta-blocker** or a calcium channel blocker as first-line treatment for **stable angina**; since she is already on amlodipine (a calcium channel blocker), adding a beta-blocker is the correct next step.
- Bisoprolol reduces **myocardial oxygen demand** by decreasing heart rate and contractility, making it highly effective for preventing **exertional symptoms**.
*Isosorbide mononitrate 30 mg twice daily*
- **Long-acting nitrates** are considered **second-line** therapies, typically used if first-line agents are contraindicated or insufficient for symptom control.
- Potential issues such as **nitrate tolerance** and headaches often make them less preferable than starting a beta-blocker as initial add-on therapy.
*Ivabradine 5 mg twice daily*
- This medication is reserved for patients in **sinus rhythm** who cannot tolerate beta-blockers or remain symptomatic with a heart rate **>70 bpm** despite optimal beta-blocker therapy.
- It specifically inhibits the **If current** in the SA node but does not offer the broader cardiovascular protection or first-line status of beta-blockers.
*Nicorandil 10 mg twice daily*
- Nicorandil acts as both a **potassium-channel activator** and a nitrate, but it is classified as a **second-line** add-on treatment.
- It is generally used when patients remain symptomatic on **dual therapy** or have contraindications to standard first-line medications.
*Ranolazine 375 mg twice daily*
- Ranolazine inhibits the **late sodium current** and is used as an adjunctive treatment for angina that is not controlled by other agents.
- Like nicorandil, it is an **alternative second-line** option and is not the appropriate initial step following a calcium channel blocker.
Question 36: A 62-year-old man presents to the Emergency Department with 45 minutes of severe central chest pain and nausea. His initial ECG shows sinus rhythm with 2 mm ST-segment elevation in leads V1-V4. He receives aspirin 300 mg, ticagrelor 180 mg, and is transferred for primary PCI. Angiography reveals total occlusion of the proximal left anterior descending artery, which is successfully stented. Two days post-procedure, he develops sudden onset severe breathlessness and hypotension. Examination reveals BP 88/56 mmHg, heart rate 110 bpm, elevated JVP, and a new pansystolic murmur loudest at the left sternal edge. What is the most likely complication?
A. Acute mitral regurgitation due to papillary muscle rupture
B. Ventricular septal defect (Correct Answer)
C. Left ventricular free wall rupture
D. Acute stent thrombosis
E. Right ventricular infarction
Explanation: ***Ventricular septal defect***- This patient's presentation of sudden hemodynamic collapse and a new **pansystolic murmur** loudest at the **left sternal edge** following an **anterior STEMI** is pathognomonic for a ventricular septal defect (VSD).- VSD typically occurs within 3-5 days of a large myocardial infarction due to **septal wall necrosis**, leading to a left-to-right shunt and **cardiogenic shock**.*Acute mitral regurgitation due to papillary muscle rupture*- While it presents with a pansystolic murmur and shock, the murmur is typically loudest at the **cardiac apex** and radiates to the **axilla**.- This complication is more commonly associated with **inferior wall MIs** due to the single blood supply (PDA) of the **posteromedial papillary muscle**.*Left ventricular free wall rupture*- This usually results in sudden cardiovascular collapse with **electromechanical dissociation (PEA)** and signs of **cardiac tamponade** (muffled heart sounds).- It is often rapidly fatal and does not typically present with a loud, distinct **pansystolic murmur**.*Acute stent thrombosis*- Typically presents with a recurrence of **crushing chest pain** and new **ST-segment elevation** in the originally affected leads.- While it can cause hypotension and heart failure, it would not explain the sudden development of a new **mechanical murmur**.*Right ventricular infarction*- Classically presents with the triad of **hypotension**, **elevated JVP**, and **clear lung fields**, but is almost exclusively seen in **inferior STEMIs** (RCA occlusion).- This condition does not produce a **pansystolic murmur**; such a murmur would only appear if a VSD or tricuspid regurgitation happened concurrently.
Question 37: A 81-year-old woman presents with progressive breathlessness over 8 months. She can no longer climb stairs without stopping. Examination reveals BP 168/92 mmHg, heart rate 76 bpm regular, elevated JVP, bilateral basal fine inspiratory crackles, and mild ankle oedema. Heart sounds reveal a fourth heart sound. Echocardiography shows: LVEF 58%, left ventricular hypertrophy with normal wall motion, left atrial dilatation, E/e' ratio 18, and no significant valvular disease. NT-proBNP is 580 ng/L. What is the most likely diagnosis?
A. Heart failure with preserved ejection fraction (Correct Answer)
B. Pulmonary fibrosis with cor pulmonale
C. Aortic stenosis with preserved LV function
D. Restrictive cardiomyopathy
E. Hypertensive crisis with pulmonary oedema
Explanation: ***Heart failure with preserved ejection fraction***- The patient presents with classic signs and symptoms of heart failure (breathlessness, elevated JVP, crackles, oedema) coupled with a **preserved left ventricular ejection fraction (LVEF 58%)** and elevated **NT-proBNP**.- Key echocardiographic findings, including **left ventricular hypertrophy**, **left atrial dilatation**, an elevated **E/e' ratio of 18** (indicating increased LV filling pressures), and a **fourth heart sound**, all strongly point to significant **diastolic dysfunction**, which is the hallmark of HFpEF.*Pulmonary fibrosis with cor pulmonale*- While basal crackles are present, these are usually **"velcro-like"** in pulmonary fibrosis, and there's no primary evidence of significant interstitial lung disease.- **Cor pulmonale** involves right ventricular dysfunction secondary to lung disease, whereas the echocardiogram clearly shows **left ventricular hypertrophy** and signs of **left-sided diastolic dysfunction**, not primarily right heart strain from lung pathology.*Aortic stenosis with preserved LV function*- The echocardiography report explicitly states **"no significant valvular disease"**, which directly excludes hemodynamically significant aortic stenosis as the cause.- Aortic stenosis typically presents with a characteristic **systolic ejection murmur** best heard at the right upper sternal border, often radiating to the carotids, which was not described.*Restrictive cardiomyopathy*- While it causes **diastolic dysfunction** and can mimic HFpEF, it is less common than HFpEF in an elderly patient with long-standing hypertension and LVH.- Restrictive cardiomyopathy often involves specific patterns (e.g., **myocardial amyloidosis**) and may present with more prominent or earlier **right-sided heart failure** symptoms.*Hypertensive crisis with pulmonary oedema*- A **hypertensive crisis** is defined by a significantly higher blood pressure (typically >180/120 mmHg) and is characterized by an **acute, sudden onset** of symptoms.- This patient's symptoms have been **progressive over 8 months**, which is a chronic presentation inconsistent with an acute hypertensive emergency.
Question 38: A 76-year-old man with permanent atrial fibrillation is taking apixaban 5 mg twice daily for stroke prevention. He presents to the Emergency Department following a fall with a large scalp laceration requiring suturing. His past medical history includes previous ischaemic stroke 3 years ago, hypertension, and type 2 diabetes. His current medications are apixaban, metformin, and amlodipine. He is haemodynamically stable. Blood tests show: haemoglobin 142 g/L, platelets 245 × 10⁹/L, creatinine 98 μmol/L (eGFR 64 mL/min/1.73m²). CT head shows no intracranial haemorrhage. The laceration is sutured successfully. What is the most appropriate management of his anticoagulation?
A. Stop apixaban permanently and switch to aspirin 75 mg daily
B. Omit next dose of apixaban, restart after 48 hours if no bleeding complications
C. Continue apixaban at current dose without interruption (Correct Answer)
D. Reduce apixaban to 2.5 mg twice daily permanently
E. Stop apixaban for 1 week then recommence at reduced dose
Explanation: ***Continue apixaban at current dose without interruption***- In patients with **minor bleeding** that is successfully controlled with local measures (like suturing), **anticoagulation** should generally be continued without interruption.- This patient has a high **CHA₂DS₂-VASc score** (age ≥75, history of stroke, hypertension, diabetes), meaning the risk of a **thromboembolic event** from stopping apixaban outweighs the risk of re-bleeding from a managed scalp wound.*Stop apixaban permanently and switch to aspirin 75 mg daily*- Aspirin is significantly less effective than **DOACs** for stroke prevention in **atrial fibrillation** and offers no substantial reduction in major bleeding risk compared to apixaban.- Stopping therapy entirely after a minor trauma would leave this high-risk patient unprotected against a **recurrent ischaemic stroke**.*Omit next dose of apixaban, restart after 48 hours if no bleeding complications*- Brief interruption is typically reserved for **major surgery** or uncontrolled clinically significant bleeding; it is unnecessary for a successfully sutured **scalp laceration**.- Unnecessary omission of doses creates a **pro-thrombotic window** in a patient who has already suffered a previous stroke.*Reduce apixaban to 2.5 mg twice daily permanently*- Dose reduction criteria for **apixaban** require at least two of the following: age ≥80 years, weight ≤60 kg, or **creatinine ≥133 μmol/L**; this patient meets none of these.- Under-dosing anticoagulation in a high-risk patient is dangerous and results in inadequate **stroke prophylaxis**.*Stop apixaban for 1 week then recommence at reduced dose*- A one-week interruption is far too long for a minor trauma and significantly increases the risk of **cardioembolic stroke**.- There is no clinical indication for a **reduced dose** as his renal function (eGFR 64) and age do not meet the prescribing criteria for 2.5 mg twice daily.
Question 39: A 45-year-old woman of African-Caribbean origin presents to her GP with elevated blood pressure. She has had three clinic readings over 4 months averaging 154/96 mmHg. Ambulatory blood pressure monitoring confirms an average of 152/94 mmHg. She has no other medical history, takes no regular medications, and does not smoke. Her BMI is 24 kg/m². Blood tests show: sodium 139 mmol/L, potassium 4.1 mmol/L, creatinine 76 μmol/L (eGFR >90 mL/min/1.73m²), HbA1c 36 mmol/mol, total cholesterol 4.8 mmol/L. Urinalysis shows no protein. ECG and fundoscopy are normal. What is the most appropriate first-line antihypertensive medication?
A. Ramipril 2.5 mg once daily
B. Amlodipine 5 mg once daily (Correct Answer)
C. Bendroflumethiazide 2.5 mg once daily
D. Atenolol 50 mg once daily
E. Losartan 25 mg once daily
Explanation: ***Amlodipine 5 mg once daily***
- According to **NICE guidelines**, patients of **African or Caribbean family origin** of any age should be started on a **calcium channel blocker (CCB)** as first-line treatment.
- **Amlodipine** is a preferred CCB that effectively lowers blood pressure in this demographic by reducing peripheral vascular resistance.
*Ramipril 2.5 mg once daily*
- This **ACE inhibitor** is typically first-line for patients **under 55 years** who are not of African or Caribbean origin.
- ACE inhibitors are known to be **less effective as monotherapy** in black patients due to lower plasma **renin levels**.
*Bendroflumethiazide 2.5 mg once daily*
- While a **thiazide-like diuretic** is an acceptable first-line alternative for this demographic, it is usually reserved for cases where CCBs are **not tolerated** or if there is evidence of heart failure.
- **Indapamide or chlortalidone** are now preferred over bendroflumethiazide when a diuretic is initiated for primary hypertension.
*Atenolol 50 mg once daily*
- **Beta-blockers** are not recommended as first-line therapy for hypertension unless the patient has specific indications like **atrial fibrillation** or heart failure.
- They are generally less effective at preventing stroke than other antihypertensive classes and can adversely affect **glucose metabolism**.
*Losartan 25 mg once daily*
- Like ACE inhibitors, **Angiotensin II Receptor Blockers (ARBs)** are less effective in patients of **African-Caribbean origin** as monotherapy.
- Losartan would typically be introduced at **Step 2** of the treatment algorithm in combination with a CCB for this specific patient group.
Question 40: A 58-year-old man with stable angina is commenced on sublingual glyceryl trinitrate (GTN) spray for symptom relief. He experiences exertional chest tightness approximately 3 times per week, which resolves after 2-3 minutes of rest. He asks how the GTN spray works to relieve his symptoms. Which of the following best describes the primary mechanism of action of GTN in relieving anginal chest pain?
A. Increases myocardial oxygen supply by coronary vasodilation
B. Reduces myocardial oxygen demand through venodilation and reduced preload (Correct Answer)
C. Improves coronary blood flow by reducing blood viscosity
D. Reduces myocardial oxygen demand through negative chronotropic effect
E. Inhibits platelet aggregation preventing acute thrombosis
Explanation: ***Reduces myocardial oxygen demand through venodilation and reduced preload***- Glyceryl trinitrate (GTN) primarily acts as a **nitric oxide donor**, leading to significant **venodilation**, which increases venous capacitance.- This **venodilation** effectively reduces **venous return** to the heart, decreasing **preload** and subsequently lowering **myocardial wall tension** and **myocardial oxygen demand**, thereby relieving angina.*Increases myocardial oxygen supply by coronary vasodilation*- While GTN can cause some **coronary vasodilation**, especially in larger epicardial vessels, its ability to significantly increase blood flow to ischemic areas with fixed **atherosclerotic stenoses** is limited.- The primary benefit in stable angina comes from reducing the heart's workload (demand), not from a major increase in **oxygen supply**.*Improves coronary blood flow by reducing blood viscosity*- GTN does not have any known effect on **blood viscosity** or its components, such as hematocrit or plasma proteins.- Modifying **blood viscosity** is not a mechanism employed by nitrates to relieve anginal symptoms.*Reduces myocardial oxygen demand through negative chronotropic effect*- GTN does not possess **negative chronotropic properties**; it does not directly slow the heart rate.- In fact, the systemic vasodilation and subsequent drop in blood pressure can sometimes induce a **reflex tachycardia**, which would increase, not decrease, oxygen demand.*Inhibits platelet aggregation preventing acute thrombosis*- GTN is not an **antiplatelet agent** and does not inhibit platelet aggregation or play a direct role in preventing **thrombosis**.- Medications like **aspirin** or **clopidogrel** are used for antiplatelet effects, which differ from the acute symptomatic relief provided by GTN.
