PLAB 1 (UKMLA AKT) acute & emergency medicine questions

The rhythm described is ventricular fibrillation, a shockable rhythm. Resuscitation Council UK guidance is to deliver a single unsynchronised shock as soon as it is identified, then resume chest compressions immediately for 2 minutes without pausing to check for a pulse or rhythm change. Adrenaline is given after the third shock in shockable rhythms, not before the first. Amiodarone is given after the third shock if VF/VT persists.

• B. Atropine is used for symptomatic bradycardia, not for a shockable pulseless rhythm.
• C. Adrenaline in shockable rhythms is only given from the third shock onwards, not before the first shock.
• D. Synchronised cardioversion is used for an unstable patient with a pulse, not for pulseless VF.
• E. Amiodarone is given after the third shock if the rhythm remains shockable, not as the first action.

In non-shockable rhythms (asystole or pulseless electrical activity), adrenaline 1 mg IV is given as soon as intravenous access is achieved and then repeated every 3-5 minutes, which corresponds to alternate 2-minute CPR cycles. Adrenaline's alpha-adrenergic vasoconstrictor effect increases coronary and cerebral perfusion pressure during CPR. Giving it more frequently than every 3-5 minutes is not supported by guidelines and may worsen post-arrest myocardial dysfunction.

• A. Giving adrenaline every single 2-minute cycle is more frequent than recommended.
• B. Every 10 minutes is too infrequent and would reduce coronary perfusion pressure between doses.
• D. A single dose is insufficient; adrenaline is repeated throughout prolonged resuscitation.
• E. Adrenaline is used during the arrest itself to improve perfusion, not withheld until after ROSC.

The clinical findings of tracheal deviation away from the affected side, hyperresonant percussion, and absent breath sounds indicate a tension pneumothorax, a recognised complication of subclavian central line insertion. Air trapped in the pleural space under pressure shifts the mediastinum, kinks the great veins, and raises intrathoracic pressure, drastically reducing venous return to the heart and causing obstructive cardiac arrest. This is one of the 4 Ts (tension pneumothorax) that must be actively excluded and treated during resuscitation. Immediate needle decompression or thoracostomy is required.

• B. Local anaesthetic toxicity typically causes seizures and arrhythmias, not the examination findings described.
• C. Pulmonary embolism does not cause unilateral hyperresonance or tracheal deviation.
• D. There is no indication of large-volume cold fluid infusion causing hypothermia here.
• E. Tamponade would cause muffled heart sounds and raised JVP, not tracheal deviation or hyperresonance.

This patient has a narrow-complex tachycardia with adverse features: shock (hypotension), syncope risk (confusion), and signs of hypoperfusion. The Resuscitation Council UK peri-arrest tachycardia algorithm mandates synchronised cardioversion when adverse features are present, regardless of QRS width, after sedation or anaesthesia. Pharmacological measures are reserved for stable patients without adverse features. Delaying definitive treatment with drug trials in an unstable patient risks deterioration to cardiac arrest.

• A. Oral beta-blockade is far too slow and inappropriate in a haemodynamically unstable patient.
• C. Amiodarone is used in stable tachycardia or after failed cardioversion, not as first-line treatment for an unstable patient.
• D. Vagal manoeuvres are a first step in stable patients only, not appropriate when adverse features are present.
• E. Adenosine may be tried in a stable regular narrow-complex tachycardia but this patient is unstable with adverse features requiring cardioversion.

This patient has bradycardia with adverse features (hypotension, poor perfusion signs) due to complete heart block. The Resuscitation Council UK algorithm recommends atropine 500 micrograms IV as the first-line treatment, which can be repeated to a maximum of 3 mg. Atropine works by blocking vagal (parasympathetic) tone at the sinoatrial and atrioventricular nodes, increasing heart rate. If there is an unsatisfactory response or risk factors for asystole, transcutaneous pacing should be arranged while considering second-line drugs such as isoprenaline or adrenaline infusion.

• A. Adrenaline as an IV bolus is reserved for cardiac arrest, not first-line for a bradycardic patient with a pulse.
• B. Glycopyrronium is an antimuscarinic sometimes used but is not the Resuscitation Council UK first-line agent for unstable bradycardia.
• D. Amiodarone has no role in the management of bradycardia.
• E. Isoprenaline is a second-line agent used if atropine fails, not the initial choice.

Current post-resuscitation care guidance from Resuscitation Council UK emphasises avoiding hyperoxia, as excessive oxygen can worsen reperfusion injury through free radical formation. Oxygen should be titrated to maintain saturation at 94-98% once reliable monitoring is available. Targeted temperature management is still recommended for comatose survivors, but current guidance favours a target of around 32-36°C with active prevention of fever rather than mandatory deep cooling, and this patient's temperature is not yet addressed as the priority over correcting hyperoxia. Normocapnia and a mean arterial pressure sufficient to maintain organ perfusion (not hypotension) are also targeted.

• A. Temperature management is important but the immediate priority is correcting the hyperoxia from FiO2 of 1.0; a fixed target of exactly 32°C is not mandated and active cooling is not the first correction needed.
• B. Hypotension should be avoided; a mean arterial pressure adequate for organ and cerebral perfusion is targeted instead.
• D. Hyperventilation causing hypocapnia reduces cerebral blood flow and can worsen neurological outcome; normocapnia is the target.
• E. There is no indication of infection; prophylactic antibiotics are not routinely recommended.

All patients with suspected acute coronary syndrome should receive a loading dose of aspirin 300 mg as soon as possible, as it inhibits platelet aggregation and reduces mortality. Oxygen should only be given if oxygen saturation is below 94% (or below 88% in patients at risk of hypercapnic respiratory failure); this patient is saturating well on air, so routine oxygen is not indicated and may cause harm through hyperoxia-mediated vasoconstriction. Beta-blockers and anticoagulation decisions are made after cardiology-led risk stratification, not as the immediate first step. Imaging should not delay antiplatelet therapy and reperfusion planning.

• A. His oxygen saturation is 97%, so supplemental oxygen is not indicated and may be harmful.
• C. Anticoagulation is part of definitive ACS management but aspirin loading takes priority immediately.
• D. Beta-blockade is not the immediate priority and requires assessment for contraindications first.
• E. Imaging must not delay time-critical antiplatelet therapy in suspected STEMI.

Inferior STEMI (ST elevation in II, III, aVF) is frequently associated with right ventricular infarction due to shared blood supply from the right coronary artery. The right ventricle in this setting is preload-dependent, so nitrates, which cause venodilation and reduce venous return, can precipitate profound hypotension. The combination of hypotension, raised JVP and clear lung fields after nitrate administration in an inferior MI is the classic clue. Nitrates should therefore be avoided or used with extreme caution in suspected right ventricular infarction, and management instead focuses on fluid loading to maintain right-sided filling pressures.

• B. Reinfarction would not characteristically follow immediately after a vasodilator with a clear chest and raised JVP.
• C. Pulmonary oedema would cause crackles and a clear chest makes this unlikely.
• D. Tamponade typically develops over time with muffled heart sounds and distant heart sounds, not immediately after nitrate administration.
• E. There is no rash, bronchospasm or angioedema to suggest anaphylaxis.

Ventricular septal rupture typically presents three to five days post-MI with a new harsh pansystolic murmur loudest at the lower left sternal edge, often with a palpable thrill, and causes acute biventricular failure from left-to-right shunting. Papillary muscle rupture instead causes acute severe mitral regurgitation with a murmur radiating to the axilla and pulmonary oedema, but typically without a thrill and with the murmur loudest at the apex. The thrill and sternal edge location point to a septal rather than valvular lesion. Diagnosis is confirmed with urgent echocardiography and management requires emergency surgical referral.

• A. Pericarditis causes a friction rub, not a pansystolic murmur with a thrill, and does not typically cause this degree of hypotension.
• B. Free wall rupture usually presents with sudden cardiac tamponade and electromechanical dissociation rather than a new murmur.
• C. There is no fever or other feature of infective endocarditis described.
• E. Papillary muscle rupture produces an apical murmur radiating to the axilla, not one loudest at the lower sternal edge with a thrill.

Acute pulmonary oedema is managed by sitting the patient upright to reduce venous return and work of breathing, giving oxygen to correct hypoxia (saturation below 94%), and giving intravenous loop diuretic such as furosemide to promote diuresis and venodilation. A nitrate infusion can be considered in patients with adequate blood pressure, which this patient has. Intravenous fluids would worsen pulmonary congestion and are contraindicated. Non-invasive ventilation is reserved for patients failing to respond to initial medical therapy or with persistent hypoxia or acidosis, not as a substitute for diuretic treatment.

• A. Non-invasive ventilation is used for patients not responding to initial medical treatment, not as first-line instead of diuretics.
• B. Intravenous fluids would worsen pulmonary oedema in a fluid-overloaded patient.
• D. Oral diuretics act too slowly and outpatient review is inappropriate for this acute presentation.
• E. Lying flat increases venous return and worsens breathlessness; fluids are also contraindicated.

Cardiac tamponade presents with Beck's triad of hypotension, raised jugular venous pressure, and muffled heart sounds, along with pulsus paradoxus, an exaggerated fall in systolic blood pressure of more than 10 mmHg on inspiration, as described here. Malignant pericardial effusion is a common cause in patients with lung cancer. Diagnosis is confirmed with echocardiography showing pericardial effusion with diastolic collapse of the right ventricle, and treatment is urgent pericardiocentesis. Tension pneumothorax causes tracheal deviation and unilateral absent breath sounds rather than muffled heart sounds, and constrictive pericarditis presents more chronically with Kussmaul's sign rather than pulsus paradoxus.

• A. Asthma causes wheeze and does not produce Beck's triad or pulsus paradoxus of this degree.
• B. Constrictive pericarditis typically causes Kussmaul's sign, a rise in JVP on inspiration, rather than pulsus paradoxus, and progresses more chronically.
• C. Tension pneumothorax presents with unilateral absent breath sounds and tracheal deviation, not muffled heart sounds with pulsus paradoxus.
• D. Massive PE causes hypotension and raised JVP but does not typically cause muffled heart sounds or marked pulsus paradoxus.

This patient meets criteria for sepsis with a likely urinary source, hypotension, tachycardia, tachypnoea and a raised lactate indicating tissue hypoperfusion. The Sepsis Six bundle should be completed within one hour: give oxygen if needed, take blood cultures, measure lactate, give intravenous broad-spectrum antibiotics, give intravenous fluids, and monitor urine output. Antibiotics must not be delayed for culture results, imaging, or oral administration, as delay increases mortality. Vasopressors are reserved for patients not responding to adequate fluid resuscitation and are usually started in a critical care setting rather than a general ward.

• B. Vasopressors are considered after fluid resuscitation has failed and require critical care monitoring, not as an immediate first step on a general ward.
• C. Imaging should not delay time-critical antibiotic administration in sepsis.
• D. Antibiotics must be given empirically within one hour and must not wait for culture results.
• E. Oral antibiotics are inadequate for this unwell, hypotensive patient who needs intravenous treatment.

In anaphylaxis, intramuscular adrenaline 500 micrograms (0.5 mL of 1:1000) is given into the anterolateral thigh, as this site has good vascularity for rapid absorption. If there is no improvement, the same dose can be repeated after five minutes, and this patient is now six minutes from her first dose with ongoing hypotension and wheeze. Intravenous adrenaline is only given by those experienced in its use, usually in a critical care setting with cardiac monitoring, because of the risk of arrhythmia. Subcutaneous administration has slower and less reliable absorption than intramuscular injection, and the deltoid is not the recommended site due to its smaller muscle bulk.

• A. Subcutaneous injection has slower, less predictable absorption than intramuscular injection in anaphylaxis.
• B. Intravenous adrenaline carries a high risk of arrhythmia and is reserved for specialists in a monitored critical care setting, not routine second dosing.
• C. Doses should be repeated every five minutes if there is no improvement, not delayed to ten minutes.
• E. The anterolateral thigh, not the deltoid, is the recommended injection site due to better absorption.

Anaphylaxis can recur as a biphasic reaction, typically within 4 to 12 hours of the initial event, even after apparently complete resolution with treatment. Resuscitation Council UK guidance recommends a minimum observation period, usually 6 to 12 hours depending on severity, response to treatment and risk factors (asthma, previous biphasic reaction, poor access to further care), before safe discharge. Patients with severe reactions, those requiring more than one dose of adrenaline, or those with reactions of unclear cause warrant the longer end of this observation window. All patients should be discharged with an adrenaline auto-injector, a written management plan and referral to allergy services.

• B. ICU admission for 48 hours is unnecessary once the patient is stable and not in keeping with guidance.
• C. Immediate discharge risks missing a biphasic reaction, which can occur several hours later.
• D. Steroids alone without an observation period do not reliably prevent or detect a biphasic reaction.
• E. One hour is too short to reliably exclude a biphasic reaction.

In acute severe or life-threatening asthma not responding to initial bronchodilators, inhaled corticosteroids and steroids, British Thoracic Society/SIGN guidance recommends a single dose of IV magnesium sulphate 1.2-2 g infused over 20 minutes as the next step. It acts as a bronchial smooth muscle relaxant and has a favourable safety profile compared with aminophylline. IV aminophylline is reserved for cases that fail to respond to magnesium and should only be given after discussion with a senior clinician, as it carries a narrow therapeutic index and significant arrhythmia risk. Intubation is reserved for true respiratory failure or exhaustion, which is not yet present here.

• A. Aminophylline is considered after magnesium sulphate has failed and requires senior input given its narrow therapeutic index.
• B. Repeating steroid without escalating bronchodilator therapy is not the recommended next step at this stage.
• C. Montelukast has no established role in the acute management of severe asthma exacerbations.
• D. Intubation is premature; the patient is not exhausted, drowsy or in respiratory failure.

Tension pneumothorax is a clinical diagnosis based on respiratory distress, hypotension, tracheal deviation away from the affected side, absent breath sounds and hyperresonance on the affected side. Resuscitation Council UK and ATLS guidance state that treatment must not be delayed for imaging; needle decompression (or finger thoracostomy where trained) should be performed immediately in the second intercostal space, mid-clavicular line, on the affected side. A chest drain is then inserted to definitively manage the pneumothorax after decompression. Waiting for imaging in a haemodynamically unstable patient with these signs risks cardiac arrest.

• B. CT is far too slow and the patient is unstable; this is a clinical diagnosis requiring immediate action.
• C. Imaging delays life-saving treatment in a clinically obvious tension pneumothorax with haemodynamic compromise.
• D. A formal chest drain can follow but needle decompression should not be omitted as the immediate first step in a crashing patient.
• E. Echocardiography does not address the immediate life threat and delays treatment.

In chronic hypercapnic respiratory failure, as seen in long-standing COPD, some patients rely on hypoxia rather than hypercapnia as their main respiratory drive because they have become relatively insensitive to carbon dioxide. Administering uncontrolled high-flow oxygen removes this hypoxic drive, reducing ventilation and worsening carbon dioxide retention and respiratory acidosis, as reflected in this patient's markedly raised PaCO2 and low pH. Worsening of ventilation-perfusion mismatch (via loss of hypoxic pulmonary vasoconstriction) also contributes. NICE and BTS guidance recommend titrating oxygen to a target saturation of 88-92% in patients with COPD or risk factors for hypercapnic respiratory failure, using a Venturi mask and adjusting according to arterial blood gases.

• A. Oxygen therapy does not acutely raise pulmonary artery pressure in this context.
• B. Suppression of erythropoietin is a chronic effect unrelated to the acute ventilatory deterioration seen here.
• D. Oxygen does not cause bronchoconstriction; the problem relates to ventilatory drive and V/Q mismatch, not airway calibre.
• E. There is no hypersensitivity mechanism involved in oxygen-induced hypercapnia.

Massive pulmonary embolism causing haemodynamic instability or cardiac arrest, with a strong clinical suspicion supported by echocardiographic evidence of right ventricular strain, is an indication for immediate thrombolysis even without confirmatory CTPA, as per Resuscitation Council UK and European Society of Cardiology guidance. Alteplase breaks down the thrombus, rapidly reducing pulmonary vascular obstruction and right ventricular strain, and should not be delayed for imaging in this life-threatening situation. Anticoagulation alone with heparin does not actively dissolve the existing clot and is insufficient for a haemodynamically unstable or peri-arrest patient. Surgical embolectomy is reserved for cases where thrombolysis is contraindicated or has failed.

• B. An IVC filter prevents further emboli from the legs but does nothing for the existing life-threatening embolus.
• C. Surgical embolectomy is reserved for when thrombolysis is contraindicated or ineffective, and is not immediately available in an arrest situation.
• D. Heparin prevents further clot formation but does not dissolve the existing obstructive thrombus causing haemodynamic collapse.
• E. Unfractionated heparin alone does not address the acute haemodynamic compromise from a large clot burden.

In any trauma patient with a potential cervical spine injury, the jaw thrust combined with manual in-line stabilisation is the preferred first manoeuvre to open the airway because it avoids extending or moving the neck. Head tilt–chin lift is reserved for non-trauma patients where cervical injury is not a concern. Airway adjuncts such as oropharyngeal or nasopharyngeal airways may be used subsequently once the airway is opened, and intubation is considered if the airway cannot be maintained, but the first action is the safe manual manoeuvre.

• A. Head tilt–chin lift extends the neck and risks worsening a cervical spine injury.
• B. An airway adjunct alone does not address the obstructed airway and should follow, not replace, the opening manoeuvre.
• D. Same reasoning as the nasopharyngeal airway; it does not substitute for first opening the airway safely.
• E. Intubation without first attempting basic airway manoeuvres and with no assessment is premature and not the immediate first step.

The ABCDE sequence in the primary survey exists because airway obstruction kills faster than breathing problems, which kill faster than circulatory compromise, which kills faster than a neurological or disability issue, and so on. Addressing problems in this order ensures the most rapidly fatal threats are treated first, even if other injuries are also present. Only once each step is assessed and stabilised does the team proceed to the secondary survey for detailed examination and history-taking. This logic underpins all ATLS teaching and prioritisation in trauma.

• A. While documentation matters, this is not the clinical rationale for the sequence.
• B. History-taking is part of the secondary survey and is deliberately deferred until life threats are excluded or treated.
• C. Imaging is adjunct to, not a substitute for, the clinical primary survey and does not dictate its order.
• E. Total time in the department is not the rationale; patient survival through correct prioritisation is.

Flail chest occurs when multiple adjacent ribs are fractured in at least two places, creating a free-floating segment that moves paradoxically inward on inspiration and outward on expiration due to the negative intrathoracic pressure acting on the unstable segment. The central trachea and equal, bilateral breath sounds argue against tension pneumothorax or massive haemothorax, which typically cause tracheal deviation and unilateral signs. The underlying pulmonary contusion, rather than the paradoxical movement itself, is usually responsible for the hypoxia seen in flail chest.

• A. Tension pneumothorax causes tracheal deviation away from the affected side and unilaterally absent breath sounds, not present here.
• B. Massive haemothorax causes dullness to percussion and reduced breath sounds on the affected side with a central or shifted trachea depending on severity, not paradoxical chest wall movement.
• D. Simple pneumothorax does not produce paradoxical chest wall movement and breath sounds are typically reduced unilaterally.
• E. Cardiac tamponade presents with muffled heart sounds, raised jugular venous pressure and hypotension (Beck's triad), not paradoxical chest wall movement.

Tranexamic acid is an antifibrinolytic that inhibits the conversion of plasminogen to plasmin, reducing clot breakdown, and has been shown in the CRASH-2 trial to reduce mortality in trauma patients with significant haemorrhage when given early, ideally within 3 hours of injury. It is recommended as part of major haemorrhage protocols alongside blood product transfusion, typically as a loading dose followed by an infusion. Giving it later than 3 hours after injury may be harmful. It is not a substitute for blood products but complements them in control of traumatic haemorrhage.

• A. Recombinant factor VIIa is not recommended as a routine first-line agent in trauma haemorrhage protocols due to limited mortality benefit and thrombotic risk.
• B. Desmopressin is used in mild haemophilia A or von Willebrand disease, not standard major trauma haemorrhage.
• D. Vitamin K reverses warfarin-induced coagulopathy over hours to days and has no role in acute traumatic haemorrhage without anticoagulant use.
• E. Protamine sulfate reverses heparin anticoagulation and has no role in haemorrhagic shock from trauma in a patient not on heparin.

This patient meets low-risk criteria from validated clinical decision tools such as the Canadian C-Spine Rule: he is alert, has no neurological deficit, no midline tenderness, no distracting injury, is not intoxicated, and can actively rotate his neck 45 degrees in each direction without pain. In such patients, the cervical spine can be clinically cleared and the collar safely removed without the need for imaging. Imaging is reserved for patients who do not meet these low-risk criteria or who have a high-risk factor such as age over 65 years or a dangerous mechanism of injury.

• A. Observation and prolonged immobilisation are unnecessary once the spine is clinically cleared.
• B. Plain X-rays are not required when the clinical decision rule allows safe clearance without imaging.
• C. A soft collar provides no meaningful immobilisation and is not indicated once the spine has been clinically cleared.
• E. CT imaging is unnecessary radiation exposure in a patient who meets clinical clearance criteria.

A lucid interval followed by rapid deterioration after a focal temporal blow is classic for extradural (epidural) haematoma, caused by rupture of the middle meningeal artery, often associated with a temporal bone fracture. CT shows a biconvex (lentiform) hyperdense collection that does not cross suture lines. The dilated pupil reflects uncal herniation compressing the third cranial nerve on the same side as the clot. Subdural haematoma typically follows a more gradual course, especially in older or atrophic brains, and appears crescentic on CT.

• A. Subarachnoid haemorrhage classically presents with sudden severe headache rather than a lucid interval after trauma.
• B. Diffuse axonal injury usually causes immediate, prolonged loss of consciousness without a lucid interval.
• D. Subdural bleeds are usually from bridging vein tears, develop more gradually, and appear crescent-shaped, not lentiform; the lucid interval is less typical.
• E. Contusions cause more localised, patchy injury and do not typically produce this rapid lucid-interval deterioration.

Eye opening to pain scores 2, inappropriate words (confused speech that does not form sensible sentences) scores 3, and withdrawal from pain scores 4, giving a total GCS of 2 + 3 + 4 = 9. The GCS is scored out of 15 across three domains: eye opening (1-4), verbal response (1-5), and motor response (1-6), and a total score of 8 or below defines a comatose state requiring airway protection.

• A. This would correspond to a lower motor or verbal score than described, for example if the verbal response were only incomprehensible sounds.
• B. This total would require spontaneous eye opening or a higher verbal/motor score than described.
• D. This total would require either localising to pain or a higher verbal score than inappropriate words.
• E. This total would require localising to pain (motor score 5) rather than simple withdrawal.

Cushing's triad (hypertension, bradycardia, and irregular respiration) reflects the body's attempt to preserve cerebral perfusion pressure (CPP = mean arterial pressure minus intracranial pressure) as intracranial pressure rises. The resulting hypertension stimulates baroreceptors, causing reflex vagally-mediated bradycardia, while brainstem compression produces irregular, often Cheyne-Stokes-like breathing. This triad is a late and ominous sign of critically raised intracranial pressure and impending herniation. It should prompt urgent senior review and measures to reduce intracranial pressure.

• A. The sympathetic response here is driven specifically by rising intracranial pressure reducing cerebral perfusion, not an independent process.
• B. ADH excess would cause fluid retention and hyponatraemia, not this acute haemodynamic triad.
• C. The nerve is not being directly compressed by the tumour; the bradycardia is a baroreceptor-mediated reflex to the rise in blood pressure.
• E. Hydrocephalus raises intracranial pressure, which reduces cerebral perfusion; the bradycardia is reflex, not a direct effect of reduced flow on the heart.

Intravenous thrombolysis with alteplase is indicated in acute ischaemic stroke within 4.5 hours of clearly established symptom onset, provided haemorrhage has been excluded on CT. Blood pressure must be controlled to below 185/110 mmHg before and during treatment because uncontrolled hypertension increases the risk of haemorrhagic transformation. Severe thrombocytopenia and other coagulopathies are contraindications, but a platelet count above 50 x 10^9/L is not itself a required threshold to achieve. Hypoglycaemia, not hyperglycaemia above 10 mmol/L, is a relevant exclusion because it can mimic stroke.

• A. Treatment should be given as soon as possible within the window; delaying needlessly reduces the benefit of thrombolysis, as efficacy falls with time.
• B. Thrombocytopenia below roughly 100 x 10^9/L is a caution, but there is no requirement to confirm a specific level above 50 x 10^9/L before treating; severely low platelets are simply a contraindication.
• C. CT angiography may guide decisions about thrombectomy but is not required before giving alteplase once haemorrhage is excluded and the patient is within the window.
• E. Hyperglycaemia is not a standard pre-thrombolysis check; it is hypoglycaemia that can mimic stroke and must be excluded.

When CT head is normal but clinical suspicion of subarachnoid haemorrhage remains high (thunderclap headache reaching maximum intensity within seconds), a lumbar puncture should be performed, ideally at least 12 hours after symptom onset, to allow red blood cell breakdown products to produce detectable xanthochromia and distinguish true subarachnoid haemorrhage from a traumatic tap. Modern CT within 6 hours of onset has very high sensitivity, but current guidance still recommends LP if CT is normal and suspicion persists beyond the early window or testing was delayed. Discharge without further investigation risks missing a life-threatening haemorrhage.

• A. Repeating CT does not reliably improve sensitivity enough to exclude subarachnoid haemorrhage; LP remains the next step.
• B. MRI is not the standard next investigation after a normal CT in this context; LP for xanthochromia is more appropriate and accessible.
• C. CT angiography is used to locate an aneurysm once subarachnoid haemorrhage is confirmed, not as the next diagnostic step after a normal plain CT.
• E. A thunderclap headache cannot be safely discharged without further investigation to exclude subarachnoid haemorrhage.

Diabetic ketoacidosis is diagnosed by the triad of hyperglycaemia (capillary glucose above 11 mmol/L or known diabetes), ketosis (blood ketones 3 mmol/L or more, or significant ketonuria), and acidosis (venous pH below 7.3 or bicarbonate below 15 mmol/L). This patient already has hyperglycaemia and acidosis, so blood ketones at or above this threshold complete the diagnostic criteria per the Joint British Diabetes Societies guideline. Blood ketone measurement is preferred over urine dipstick because it is more sensitive and allows monitoring of treatment response. Hyponatraemia, high osmolality, hyperkalaemia and oliguria are common associated findings but are not part of the core diagnostic triad.

• A. Hyponatraemia is common in DKA but not one of the three diagnostic criteria.
• C. High osmolality is a diagnostic feature of hyperosmolar hyperglycaemic state, not a required DKA criterion.
• D. Oliguria reflects dehydration severity but is not a diagnostic criterion for DKA.
• E. Hyperkalaemia often occurs in DKA but is not part of the diagnostic triad.

Once initial fluid resuscitation has begun, a fixed rate intravenous insulin infusion (0.1 units/kg/hour) should be started to switch off ketogenesis and correct acidosis. Insulin is not given as a single bolus in DKA because it causes a rapid shift of potassium into cells, risking dangerous hypokalaemia and rebound hyperglycaemia once the bolus wears off. Potassium replacement is only added once the level is known and only if it falls within the correct range, not automatically. Bicarbonate is not routinely used, as it worsens intracellular acidosis and paradoxical CNS acidosis; the acidosis corrects with fluids and insulin. Insulin should not be delayed, as it is essential to stop ongoing ketone production.

• B. A bolus dose causes rapid potassium shifts and is not used in DKA protocols; a continuous fixed rate infusion is correct.
• C. Bicarbonate is not routinely given in DKA and may worsen outcomes.
• D. Potassium should only be added according to the measured serum level, not automatically regardless of value.
• E. Insulin should not be withheld; it is started promptly alongside fluids, with potassium monitored and replaced as needed.

Cerebral oedema is a feared complication of DKA treatment, occurring most often in children and young adults, typically within the first 4 to 12 hours of treatment. It presents with headache, declining consciousness, and signs of raised intracranial pressure such as bradycardia and hypertension (Cushing's reflex), sometimes with papilloedema or abnormal pupillary responses. It is thought to result from rapid shifts in osmolality, particularly from overly rapid fluid administration or correction of glucose. Suspected cerebral oedema requires urgent senior review, hypertonic saline or mannitol, and restriction of fluid rate. Younger patients are at particularly high risk and require careful monitoring of neurological status throughout DKA treatment.

• B. Hypoglycaemia would cause tachycardia and sweating rather than bradycardia and hypertension, and typically improves rather than worsens with glucose correction.
• C. Pulmonary oedema would present with respiratory distress and hypoxia rather than headache and falling heart rate.
• D. Aspiration pneumonia would present with respiratory signs such as crackles, fever and hypoxia, not this neurological picture.
• E. Acute kidney injury does not explain this pattern of headache, bradycardia and hypertension.

In a conscious patient with hypoglycaemia who is unable or unwilling to safely take oral fluids but can still cooperate somewhat, buccal glucose gel (such as GlucoGel) rubbed into the inside of the cheek is the recommended first step, as it does not require swallowing and reduces aspiration risk. Oral drinks are appropriate only if the patient is fully cooperative and able to swallow safely. Intramuscular glucagon or intravenous glucose are reserved for patients who are unconscious, having seizures, or are too uncooperative for buccal gel to be effective. Withholding treatment is inappropriate given the significant hypoglycaemia and risk of neurological injury.

• A. An oral sugary drink risks aspiration since the patient is uncooperative and refusing to eat or drink.
• B. Withholding treatment is inappropriate; significant hypoglycaemia requires prompt correction.
• D. Glucagon is used when the patient is unconscious or buccal gel has failed, not as the first choice in a cooperative conscious patient.
• E. Intravenous glucose is used for unconscious patients or when other routes are unavailable, not as first line here.

A paracetamol level taken between 4 and 15 hours post-ingestion that lies on or above the treatment line on the nomogram is an indication to start acetylcysteine immediately, regardless of symptoms. Treatment should not be delayed while awaiting further levels once the level is above the line, because hepatotoxicity risk is time-dependent and early NAC administration (ideally within 8 hours of ingestion) is most effective at preventing liver injury. Waiting or repeating the level would waste time within the critical treatment window.

• A. Delaying treatment to repeat the level risks missing the optimal window for hepatoprotection.
• B. Oral methionine is a less reliable alternative used only when intravenous acetylcysteine is unavailable or refused.
• C. Activated charcoal is only useful within 1 hour of a large ingestion and does not replace NAC once the level is above the treatment line.
• D. Discharge is inappropriate given a toxic paracetamol level requiring immediate antidote therapy.

Most paracetamol is safely metabolised by glucuronidation and sulfation, but a small fraction is oxidised by cytochrome P450 (mainly CYP2E1) to the highly reactive and hepatotoxic metabolite N-acetyl-p-benzoquinone imine (NAPQI). Normally, NAPQI is rapidly inactivated by conjugation with glutathione. In overdose, glutathione stores become depleted, allowing NAPQI to accumulate and bind covalently to hepatocyte proteins, causing centrilobular necrosis. Acetylcysteine acts as a glutathione precursor, replenishing glutathione stores so that NAPQI can continue to be detoxified.

• A. Acetylcysteine does not inhibit CYP enzymes or affect gastrointestinal absorption of paracetamol.
• B. Glucuronidation is a normal baseline pathway and is not induced by acetylcysteine; it is overwhelmed in overdose, not enhanced by treatment.
• C. Acetylcysteine does not bind paracetamol directly; its action is intracellular, via glutathione repletion.
• D. Acetylcysteine does not act by promoting renal clearance of paracetamol.

Naloxone is a competitive opioid receptor antagonist with a relatively short half-life (around 60–90 minutes), which is frequently shorter than that of the opioid causing toxicity, especially longer-acting opioids or large heroin doses. As the naloxone effect wears off before the opioid has been cleared, respiratory depression can recur, a phenomenon called re-narcotisation. This is why patients given naloxone need close monitoring and often repeat doses or an infusion, rather than a single dose and discharge.

• A. Acute tolerance to naloxone after a single dose does not occur and is not a recognised phenomenon.
• C. Opioid withdrawal would present with agitation, dilated pupils, diarrhoea and tachycardia, not recurrent respiratory depression.
• D. Naloxone-induced pulmonary oedema is a rare recognised complication but presents with hypoxia and crackles, not isolated recurrent sedation and bradypnoea.
• E. The initial dose produced an adequate response; the issue is duration of action, not initial dose size.

Flumazenil is a benzodiazepine receptor antagonist that can be used for isolated benzodiazepine overdose causing significant respiratory depression, but it is contraindicated when there is co-ingestion of a pro-convulsant drug such as a tricyclic antidepressant. In mixed overdoses, reversing the benzodiazepine's anticonvulsant effect can precipitate seizures or arrhythmias that the benzodiazepine was partially protecting against, and the widened QRS here indicates significant tricyclic cardiotoxicity. Management should instead focus on airway support, monitoring and treatment of the tricyclic toxicity (such as sodium bicarbonate if arrhythmia or severe QRS widening develops).

• A. Naloxone has no role as there is no evidence of opioid toxicity, and combining with flumazenil does not address the tricyclic risk.
• C. Increasing the flumazenil dose would increase, not mitigate, the risk of seizures in this contraindicated situation.
• D. Giving flumazenil here risks precipitating seizures due to the tricyclic co-ingestion; it is not first-line in this context.
• E. Waiting until unresponsive to painful stimuli does not remove the underlying contraindication; the risk is present regardless of depth of sedation.

Salicylate toxicity classically produces a mixed acid-base disturbance: salicylates directly stimulate the medullary respiratory centre causing hyperventilation and a primary respiratory alkalosis (low PaCO2, raised pH), while simultaneously uncoupling oxidative phosphorylation in mitochondria, which generates excess organic acids and causes a primary metabolic acidosis (low bicarbonate). In this case, the near-normal pH despite a low bicarbonate and low PaCO2 reflects these two opposing processes occurring together, a hallmark of salicylate poisoning, especially in adults. In children, the metabolic acidosis often predominates earlier.

• A. The lactate is only mildly elevated and the respiratory alkalosis component (low PaCO2 with high-normal pH) would not be explained by lactic acidosis alone.
• B. A low bicarbonate of 16 mmol/L shows there is also a significant metabolic acidosis component, not pure respiratory alkalosis.
• D. The blood gas shows acidaemia tendency with low bicarbonate, not an alkalotic picture, and vomiting alone would not explain the markedly low PaCO2.
• E. Salicylate toxicity causes early hyperventilation and respiratory alkalosis, not respiratory depression or acidosis, except in very severe late poisoning.

Tricyclic antidepressants block cardiac fast sodium channels, producing QRS widening, a dominant R wave in aVR, and ventricular arrhythmias; this cardiotoxicity is classically treated with intravenous sodium bicarbonate. Bicarbonate works by increasing extracellular sodium concentration and alkalinising the blood, both of which help overcome the sodium channel blockade and reduce the tricyclic's binding affinity to the channel, narrowing the QRS and reducing arrhythmia risk. A target arterial pH of around 7.45–7.55 is often used to guide bicarbonate therapy in severe toxicity.

• A. Adenosine is used for supraventricular tachycardias with a normal QRS and has no role in broad complex tachycardia from sodium channel blockade.
• B. Flecainide is itself a sodium channel blocker and would worsen tricyclic-induced cardiotoxicity.
• C. Digoxin does not address the sodium channel blockade and carries arrhythmia risk of its own in this unstable patient.
• E. Verapamil is a calcium channel blocker that can worsen hypotension and has no role in reversing sodium channel blockade.

Standard two-wavelength pulse oximeters cannot differentiate carboxyhaemoglobin from oxyhaemoglobin because both absorb light at similar wavelengths, so the device reports a falsely normal or near-normal saturation even when functional oxygen-carrying capacity is markedly reduced. This is why a normal pulse oximetry reading does not exclude carbon monoxide poisoning, and diagnosis requires measuring carboxyhaemoglobin directly, typically by co-oximetry on an arterial or venous blood gas sample. Suspected cases should be treated with high-flow 100% oxygen via a tight-fitting mask regardless of the oximetry reading, which accelerates dissociation of carbon monoxide from haemoglobin.

• A. There is no indication of shivering or motion artefact in this scenario, and this is not the recognised mechanism of the oximetry discrepancy.
• B. Carbon monoxide binds avidly to haemoglobin (forming carboxyhaemoglobin) as well as myoglobin, and it is the haemoglobin binding that causes the oximetry inaccuracy.
• C. The oximetry artefact in carbon monoxide poisoning results from spectral overlap of carboxyhaemoglobin and oxyhaemoglobin, not from vasodilation affecting peripheral perfusion.
• D. A normal oximetry reading is expected in carbon monoxide poisoning and does not exclude the diagnosis; carboxyhaemoglobin level must be measured directly.

Following an anaphylactic reaction, patients should be discharged with two adrenaline auto-injectors and given practical training in when and how to use them, as food allergy reactions can recur unpredictably on re-exposure and may be more severe. Referral to a specialist allergy clinic is recommended for all patients with anaphylaxis to confirm the trigger, provide an individualised management plan, and consider further allergen testing in the appropriate setting rather than acutely in the emergency department. A written emergency action plan and education on allergen avoidance should also be provided.

• B. Skin prick testing is performed in a controlled allergy clinic setting, not acutely in the emergency department, due to the small risk of triggering another reaction.
• C. A course of steroids and no follow-up does not address future risk of recurrence or provide emergency treatment for a subsequent reaction.
• D. Avoidance advice alone is insufficient; patients need access to emergency adrenaline for future accidental exposures.
• E. Antihistamines alone do not treat anaphylaxis and an auto-injector should be provided given the risk of a future severe reaction.

The Parkland formula is 4 mL × body weight (kg) × %body surface area burned, with half of the total given in the first 8 hours from the time of injury. Both upper limbs (9% each = 18%) plus the anterior trunk (18%) gives a total burn surface area of 36%. Total 24-hour fluid = 4 × 70 × 36 = 10,080 mL, so half (5040 mL) is given over the first 8 hours. Timing is calculated from the time of the burn, not from arrival in hospital, which is a common error.

• A. This is the total 24-hour volume, not the first 8-hour volume.
• C. This is more than the correct 8-hour volume and does not match the formula calculation.
• D. This equals a quarter of the 24-hour total, not the correct first-8-hour half.
• E. This is only one-eighth of the 24-hour total and is far too low.

J waves (Osborn waves) are positive deflections at the junction of the QRS complex and ST segment and are classically seen in moderate to severe hypothermia, typically below 32°C. They occur due to altered myocardial repolarisation in the cold myocardium and tend to resolve with rewarming. Other ECG changes in hypothermia include bradycardia, prolonged PR, QRS and QT intervals, and atrial fibrillation. Recognising J waves helps confirm hypothermia as the cause of altered consciousness or arrhythmia rather than a primary cardiac event.

• A. Diffuse ST elevation with reciprocal aVR depression suggests pericarditis, not hypothermia.
• B. A sawtooth pattern describes atrial flutter, which is not the classic hypothermia finding.
• C. Delta waves are seen in Wolff-Parkinson-White syndrome, not hypothermia.
• E. T wave inversion with QT prolongation is nonspecific and not the hallmark hypothermia change.

Heat stroke is defined by core temperature above 40°C with central nervous system dysfunction, and it is a medical emergency requiring immediate aggressive cooling to reduce mortality. Cold water immersion is the most effective method, but evaporative cooling with tepid water and fanning, combined with ice packs to the groin, neck and axillae, is a practical alternative in hospital. Antipyretics such as paracetamol act on the hypothalamic set point and are ineffective because heat stroke is a failure of thermoregulation rather than a pyrogen-mediated fever. Intravenous fluids and supportive care are also given, but rapid physical cooling is the priority intervention.

• B. Dantrolene is used for malignant hyperthermia and neuroleptic malignant syndrome, not exertional heat stroke.
• C. Chlorpromazine is not indicated and can impair sweating and thermoregulation, worsening hyperthermia.
• D. Paracetamol targets the hypothalamic set point and does not work in heat stroke, where the problem is thermoregulatory failure, not fever.
• E. Hydrocortisone has no established role in the emergency management of heat stroke.

Chronic alcohol use enhances GABA-mediated inhibition and suppresses NMDA-mediated excitation, and the brain adapts by down-regulating GABA receptors and up-regulating NMDA receptors. Sudden cessation removes the GABAergic depressant effect, leaving the adapted hyperexcitable NMDA system unopposed, producing autonomic hyperactivity, tremor, agitation and hallucinations. This neuroadaptive process explains why delirium tremens typically peaks 48-72 hours after the last drink, matching this patient's day 3 presentation. Chlordiazepoxide, a long-acting benzodiazepine, is used to substitute for alcohol's GABA effect and allow gradual, safer withdrawal.

• B. There is no indication here of chronic liver disease or decompensation to suggest hepatic encephalopathy.
• C. Thiamine deficiency causes Wernicke's encephalopathy with ophthalmoplegia, ataxia and confusion, not the agitation and hallucinations of delirium tremens.
• D. Acetaldehyde accumulation occurs with disulfiram use and alcohol co-ingestion, causing flushing and vomiting, not this withdrawal picture.
• E. There is no evidence of excessive water intake or measured hyponatraemia in this scenario.

Sudden severe central abdominal pain radiating to the back, hypotension, tachycardia and a pulsatile expansile epigastric mass in an older patient with vascular risk factors are classic features of a ruptured abdominal aortic aneurysm. An expansile mass (one that pushes the examiner's hands apart) distinguishes a true aneurysm from a pulsatile but non-expansile mass that merely transmits pulsation from an adjacent structure. This is a surgical emergency requiring immediate senior surgical and vascular input, with resuscitation guided by permissive hypotension rather than aggressive fluid loading. Delay in recognition is a major cause of preventable death.

• A. Pancreatitis typically causes epigastric pain radiating to the back but does not produce a pulsatile expansile mass or this degree of haemodynamic collapse at onset.
• B. Perforated duodenal ulcer classically causes sudden severe pain with a rigid, board-like abdomen rather than a pulsatile mass.
• C. Renal colic causes severe loin-to-groin pain but does not cause hypotension or a pulsatile abdominal mass.
• E. Mesenteric ischaemia typically presents with pain disproportionate to examination findings but without a pulsatile mass.

In a haemodynamically unstable patient with clinical features of ruptured abdominal aortic aneurysm, the diagnosis is made clinically and the priority is immediate transfer to theatre for emergency repair, since further imaging delays life-saving surgery. Fluid resuscitation should follow a permissive hypotension strategy, giving the minimum volume needed to maintain a palpable radial pulse or systolic blood pressure around 80-90 mmHg, because aggressive normalisation of blood pressure can increase bleeding by disrupting the tamponading clot. CT angiography is only appropriate if the patient is haemodynamically stable enough to tolerate the delay. This approach follows standard vascular surgery and resuscitation principles for exsanguinating haemorrhage.

• A. Restoring blood pressure to normal with aggressive fluids can dislodge the clot tamponading the rupture and worsen haemorrhage.
• C. CT delays definitive treatment in an unstable patient and risks death during transfer to the scanner.
• D. Bedside ultrasound may support the diagnosis but should not delay transfer to theatre in a clinically obvious unstable rupture.
• E. Tranexamic acid has no proven role in ruptured AAA and observing for 30 minutes delays essential surgery.

Acute delirium in a hospitalised elderly patient is most often caused by a reversible precipitant, and urinary retention is strongly suggested here by the palpable bladder and failure to void for 10 hours. The correct approach is to identify and treat the underlying cause first rather than simply sedating the agitation, as sedatives can worsen confusion and increase falls risk in older patients. A bladder scan confirms retention, and catheterisation relieves the obstruction, which often resolves the delirium. NICE guidance on delirium emphasises a thorough search for precipitating factors such as infection, constipation, pain, medication and urinary retention before considering pharmacological management of agitation.

• A. Benzodiazepines should be avoided where possible in elderly delirium and do not address the underlying cause; they can worsen confusion.
• B. Psychiatric assessment is not the immediate priority when a readily reversible physical cause is evident.
• D. A CT head is not indicated without focal neurology or head injury, and the clinical picture already points to a reversible cause.
• E. There is no evidence of infection such as fever or focal signs to justify empirical antibiotics as the immediate priority.