AMC MCQ (CAT) emergency medicine questions

This man has signs of complete airway obstruction (unable to speak, cough, or breathe), which is a medical emergency requiring immediate physical intervention rather than reassurance. Australian Resuscitation Council guidelines recommend up to five sharp back blows first, with the patient leaning forward, followed by up to five chest thrusts if back blows are unsuccessful, alternating between the two. Abdominal thrusts are no longer first-line in Australian guidelines due to risk of internal injury, and are reserved for specific circumstances. Blind finger sweeps risk pushing the object further into the airway and are not recommended.

• B. Abdominal thrusts alone are not first-line in Australian Resuscitation Council guidelines; back blows are given first.
• C. Encouraging coughing is appropriate for partial obstruction with effective cough, not complete obstruction with no air movement.
• D. He is conscious with a perfusing rhythm; chest compressions are for cardiac arrest, not a conscious choking patient.
• E. Blind finger sweeps can push the foreign body further into the airway and risk injury; they are not recommended.

Ketamine is the preferred induction agent in haemodynamically unstable trauma patients because it maintains sympathetic tone and has minimal negative effects on blood pressure and cardiac output compared with other agents. Propofol and thiopentone cause significant dose-dependent vasodilation and myocardial depression, risking profound hypotension or cardiovascular collapse in a shocked patient. Midazolam, while used as an adjunct, is not a standard sole induction agent for RSI and can still contribute to hypotension. Morphine is an analgesic, not an induction agent, and causes histamine-mediated vasodilation.

• A. Propofol causes significant vasodilation and myocardial depression, risking severe hypotension in shock.
• B. Thiopentone causes profound vasodilation and myocardial depression, poorly tolerated in hypovolaemic shock.
• D. Morphine is an opioid analgesic, not an induction agent, and causes histamine release with vasodilation.
• E. Midazolam is not a standard primary RSI induction agent and can still worsen hypotension.

This is a 'can't intubate, can't oxygenate' scenario from angioedema causing complete supraglottic obstruction, which is a definitive indication for emergency cricothyroidotomy. The procedure bypasses the obstructed upper airway by creating a surgical airway through the cricothyroid membrane, below the level of obstruction. Further attempts at intubation or supraglottic devices are unlikely to succeed and waste critical time when the patient is hypoxic and deteriorating. Awake fibre-optic intubation is inappropriate in this emergency with an unco-operative, hypoxic patient and obscured anatomy.

• A. Repeated intubation attempts in a completely obscured airway waste time and will not succeed.
• B. She is already hypoxic and deteriorating; delaying for further medical therapy is unsafe when the airway is lost.
• D. Awake fibre-optic intubation requires patient cooperation and time, both unavailable in this emergency with an obscured airway.
• E. A laryngeal mask airway sits above the level of supraglottic obstruction and is unlikely to achieve ventilation here.

This patient has clinical signs of tension pneumothorax (hypotension, tracheal deviation, absent breath sounds, distended neck veins, hyperresonance), a life-threatening emergency requiring immediate decompression without waiting for imaging. Needle decompression is performed with a large-bore cannula in the second intercostal space at the midclavicular line on the affected side, converting the tension pneumothorax to a simple pneumothorax. This is a temporising measure and must be followed by formal intercostal catheter insertion. Imaging would cause a dangerous delay in a patient who is haemodynamically compromised.

• A. Fluid alone does not relieve the mechanical obstruction to venous return caused by tension pneumothorax.
• B. Formal intercostal catheter placement follows initial needle decompression but is not the first step in a crashing patient.
• C. Imaging causes a dangerous delay; tension pneumothorax is a clinical diagnosis requiring immediate decompression.
• D. Pericardiocentesis treats cardiac tamponade, not tension pneumothorax; the clinical picture here is pneumothorax, not tamponade.

The ATLS primary survey follows a strict ABCDE sequence to identify and treat the most immediately life-threatening problems first. Having confirmed the airway with cervical spine protection (A), the next step is to assess breathing and ventilation (B), including inspection, palpation, percussion and auscultation of the chest, before moving to circulation. Interventions for circulation (haemorrhage control, IV access) and disability or exposure (splinting fractures) occur later in the sequence. The secondary survey is only performed after the primary survey is complete and the patient is haemodynamically stabilised.

• A. Splinting the femur is part of the circulation/exposure assessment, which comes after breathing in the ABCDE sequence.
• B. Intravenous access and bloods are part of the circulation assessment, which follows breathing in the ABCDE sequence.
• C. The secondary survey is performed only after the primary survey is complete, not before breathing has been assessed.
• E. Scalp haemorrhage control is part of the circulation assessment, which comes after breathing in the ABCDE sequence.

This ECG describes ventricular fibrillation, a chaotic rhythm with no organised electrical activity, which is a shockable rhythm in cardiac arrest. The priority is immediate unsynchronised defibrillation, as early defibrillation is the single most important determinant of survival in VF arrest. Synchronised cardioversion is inappropriate because there is no organised QRS complex for the defibrillator to synchronise with. Amiodarone and adrenaline are given according to the ALS algorithm but only after initial defibrillation attempts, not instead of it.

• A. VF is a shockable rhythm; compressions alone without defibrillation delay the single most effective treatment.
• B. Amiodarone is given after the third shock in refractory VF, not as the initial action.
• C. Synchronised cardioversion requires an organised QRS complex to synchronise to, which is absent in ventricular fibrillation.
• E. Adrenaline is given after the second shock in the ALS algorithm, not before the first defibrillation attempt.

This patient's history of missed dialysis and the sine-wave ECG pattern are classic for severe hyperkalaemia, one of the 4H's reversible causes of cardiac arrest. Hyperkalaemia causes loss of P waves, widening of the QRS complex, and eventually a sine-wave pattern as potassium accumulates in renal failure without dialysis. Treatment includes calcium gluconate to stabilise the myocardium and insulin with glucose to shift potassium intracellularly, alongside continued resuscitation. The other reversible causes are not suggested by this specific history and ECG appearance.

• A. Cardiac tamponade would suggest pulseless electrical activity with a history of pericardial effusion or trauma, not this ECG pattern.
• C. Hypothermia would show J waves (Osborn waves) and a history of cold exposure, neither present here.
• D. Hypoxia is not specifically suggested by this history or ECG pattern; there is no history of respiratory compromise.
• E. Tension pneumothorax would present with absent breath sounds and tracheal deviation, not a sine-wave ECG.

When primary PCI cannot be performed within 90-120 minutes of diagnosis (first medical contact), as in this case with an anticipated delay of over 2 hours to the catheterisation laboratory, fibrinolytic therapy should be given promptly unless contraindicated. Tenecteplase is a weight-adjusted bolus fibrinolytic suitable for rural and remote settings. Following fibrinolysis, the patient should still be transferred for early angiography (pharmacoinvasive strategy), ideally within 24 hours, or sooner if reperfusion fails. Delaying treatment for transfer increases myocardial loss and mortality.

• B. Dual antiplatelet therapy alone without reperfusion therapy leaves the occluded artery untreated for hours, causing avoidable myocardial damage.
• C. Waiting over 2 hours for PCI exceeds the guideline-recommended time window and worsens outcomes compared with immediate fibrinolysis.
• D. GTN does not achieve reperfusion and merely treats symptoms; it does not address the underlying coronary occlusion.
• E. Heparin alone without a fibrinolytic or timely PCI does not achieve reperfusion of the occluded artery.

Ischaemic stroke within the preceding 3 months is an absolute contraindication to fibrinolytic therapy because of the high risk of haemorrhagic transformation and intracranial haemorrhage. Fibrinolytics lyse clot indiscriminately, including any residual thrombus or fragile vessels at the recent infarct site in the brain. In this scenario, primary PCI should be pursued even with a longer transfer time, or the patient should be referred for urgent retrieval. Absolute contraindications take priority over the benefits of early reperfusion.

• A. Advanced age alone is not an absolute contraindication, though it increases bleeding risk and is factored into the overall risk-benefit assessment.
• B. A residual deficit from a stroke more than 3 months ago would not itself be an absolute contraindication; it is the recency of the stroke that matters here.
• C. The location of the infarct does not affect eligibility for fibrinolysis; it only affects the pattern of ECG changes and prognosis.
• D. A systolic blood pressure of 150 mmHg is below the threshold (generally over 180 mmHg systolic) that constitutes a relative contraindication.

Sudden tearing interscapular chest pain, a significant blood pressure differential between arms, asymmetric pulses, a new diastolic murmur of aortic regurgitation, and a widened mediastinum on chest X-ray together are classic for acute aortic dissection. The pulse and blood pressure discrepancy reflects involvement of the aortic arch branches, and the diastolic murmur suggests proximal extension causing aortic valve incompetence. This diagnosis is a surgical emergency requiring urgent CT aortography and cardiothoracic consultation, and beta-blockers for blood pressure control should be used cautiously, avoiding thrombolysis.

• A. STEMI typically presents with crushing substernal pain and ECG changes rather than tearing back pain with pulse and blood pressure asymmetry between limbs.
• C. Pulmonary embolism causes pleuritic chest pain and dyspnoea but does not explain the blood pressure differential, unequal pulses or diastolic murmur.
• D. Oesophageal rupture typically follows vomiting or instrumentation and presents with subcutaneous emphysema, not pulse and blood pressure discrepancy.
• E. Pneumothorax causes sudden dyspnoea and unilateral reduced breath sounds, not a tearing pain radiating to the back with pulse asymmetry.

This patient has atrial fibrillation with adverse features including hypotension, altered conscious state and signs of hypoperfusion, indicating haemodynamic instability. Unstable tachyarrhythmia with a pulse requires immediate synchronised cardioversion under sedation rather than pharmacological rate or rhythm control, which act too slowly to prevent deterioration or cardiac arrest. Synchronisation times the shock to the R wave to avoid inducing ventricular fibrillation. Delaying definitive treatment to trial medications in an unstable patient risks further haemodynamic collapse.

• A. Amiodarone takes too long to achieve rhythm control and is not appropriate as first-line therapy in an unstable patient requiring immediate intervention.
• B. Vagal manoeuvres are used for stable supraventricular tachycardia, not for atrial fibrillation with haemodynamic instability.
• C. Beta-blockers can worsen hypotension and act too slowly for a patient who is already haemodynamically unstable.
• E. Oral medications have delayed onset and are inappropriate for a patient with hypotension and altered conscious state.

In a haemodynamically stable patient with regular narrow-complex tachycardia unresponsive to vagal manoeuvres, intravenous adenosine is the first-line pharmacological treatment. Adenosine transiently blocks conduction through the atrioventricular node, interrupting the re-entry circuit responsible for most supraventricular tachycardias. It is given as a rapid bolus followed immediately by a saline flush because of its very short half-life of under 10 seconds, with the dose increased to 12 mg if the initial 6 mg dose is ineffective. Patients should be warned of transient flushing, chest tightness or a sense of impending doom.

• A. Digoxin has a slow onset of action and is not appropriate for acute termination of SVT in the emergency setting.
• B. Lignocaine is used for ventricular arrhythmias, not supraventricular tachycardia.
• D. Magnesium sulfate is used for torsades de pointes or refractory ventricular arrhythmias, not standard SVT.
• E. Oral verapamil has delayed onset and is unsuitable for acute termination; intravenous calcium channel blockers are a second-line option after adenosine.

Acute cardiogenic pulmonary oedema with significant respiratory distress and adequate blood pressure is managed with vasodilators such as glyceryl trinitrate to reduce preload and afterload, combined with non-invasive ventilation (continuous positive airway pressure or bilevel) to improve oxygenation, reduce work of breathing and decrease the need for intubation. Intravenous furosemide is also typically given to promote diuresis, but the fastest acting initial interventions are vasodilation and ventilatory support given the hypoxia and respiratory distress. This patient's blood pressure is adequate to tolerate nitrate therapy. Intubation is reserved for those failing non-invasive ventilation or with impending respiratory failure.

• A. Beta-blockers are avoided in the acute decompensated phase as they can worsen cardiac output and are not first-line for immediate symptom relief.
• B. Intubation is reserved for patients failing non-invasive ventilation or in extremis; this patient should first be trialled on non-invasive support.
• C. Intravenous fluids would worsen volume overload and pulmonary oedema in this fluid-overloaded patient.
• D. Oral furosemide has delayed onset of action compared with intravenous administration and does not address the acute hypoxia requiring ventilatory support.

A silent chest indicates such severe airflow limitation that air movement is insufficient to generate breath sounds, and when combined with a rising PaCO2 and drowsiness it signals impending respiratory arrest from exhaustion. Normally, tachypnoea in asthma drives a low or normal PaCO2; a normal or rising PaCO2 in a severely distressed patient is a life-threatening sign requiring immediate ICU involvement and consideration of intubation. Tachycardia, hypoxia and tachypnoea alone are markers of severity but are seen in severe (non-life-threatening) asthma and do not by themselves mandate ICU referral. Drowsiness or confusion reflects hypercapnic narcosis and cerebral hypoxia, both markers of a peri-arrest state. Therapeutic Guidelines classify silent chest, cyanosis, bradycardia, hypotension, exhaustion and altered consciousness as life-threatening features.

• B. Hypoxia at this level indicates severity but is not as specific for imminent arrest as a silent chest with hypercapnia.
• C. Tachypnoea alone is a feature of severe, not necessarily life-threatening, asthma.
• D. Blood pressure is within normal range and does not indicate severity here.
• E. Tachycardia is expected with salbutamol use and hypoxia but is not itself an ICU-defining criterion.

Intravenous magnesium sulfate is recommended in Therapeutic Guidelines for patients with life-threatening or severe asthma not responding to initial nebulised bronchodilators and corticosteroids, typically given as 10 mmol (2.5 g) over 20 minutes. It acts as a smooth muscle relaxant by inhibiting calcium influx into bronchial smooth muscle cells, producing additional bronchodilation. Aminophylline is reserved for cases unresponsive to magnesium and standard therapy, usually with specialist input, due to its narrow therapeutic index. Ketamine and adrenaline infusions are not first-line add-on therapies outside peri-intubation or anaphylaxis contexts, and montelukast has no role in acute severe asthma.

• A. Montelukast is an oral maintenance agent with no role in acute severe exacerbations.
• B. Ketamine may be used for sedation during intubation but is not a standard bronchodilator escalation step.
• C. Adrenaline infusion is reserved for anaphylaxis or peri-arrest situations, not standard escalation in asthma.
• D. Aminophylline is used later if magnesium and standard therapy fail, given its toxicity risk.

Tension pneumothorax is a clinical diagnosis characterised by mediastinal shift causing tracheal deviation away from the affected side, obstructed venous return producing distended neck veins, and hypotension from reduced cardiac output, which together indicate haemodynamic compromise requiring immediate needle or finger thoracostomy decompression. Hyperresonance, absent breath sounds, pleuritic pain and reduced chest movement occur in both simple and tension pneumothorax and reflect the presence of air in the pleural space rather than the degree of mediastinal and circulatory compromise. Tension pneumothorax should not await chest X-ray confirmation because of the risk of cardiovascular collapse. Simple pneumothorax typically has stable vital signs and a midline trachea.

• A. Pleuritic pain is common to pneumothorax of any size and does not indicate tension.
• B. Absent breath sounds occur with any significant pneumothorax, simple or tension.
• C. Reduced chest movement reflects the presence of a pneumothorax but not specifically tension physiology.
• D. This occurs in any pneumothorax and does not indicate tension physiology.

The combination of progressive headache worse in the morning, nausea, altered cognition, and papilloedema on fundoscopy are classic red flags indicating raised intracranial pressure, most commonly from an intracranial mass lesion such as a tumour. This presentation mandates urgent neuroimaging, typically CT or MRI brain, to identify the underlying cause and guide further management, including neurosurgical referral if indicated. Papilloedema specifically reflects raised intracranial pressure transmitted along the optic nerve sheath and is never a feature of primary headache disorders. Delay in recognising these red flags can result in herniation and permanent neurological damage.

• A. Cluster headache causes unilateral periorbital pain with autonomic features, not papilloedema or progressive confusion.
• B. Medication overuse headache occurs with chronic analgesic use and does not produce papilloedema or cognitive changes.
• C. Giant cell arteritis typically presents with temporal tenderness, jaw claudication and visual loss from arteritic ischaemia, not papilloedema with morning headache.
• E. Tension-type headache does not cause papilloedema, morning predominance, or confusion.

This patient has clinical features highly suggestive of meningococcal meningitis, including fever, meningism and a non-blanching purpuric rash, a presentation requiring immediate empirical antibiotic therapy with intravenous ceftriaxone without delay for investigations. Lumbar puncture and neuroimaging should not delay antibiotic administration, as mortality increases with every hour of delayed treatment in bacterial meningitis, particularly with signs of sepsis such as this patient's tachycardia and relative hypotension. Blood cultures should be taken immediately before antibiotics if this can be done without delay, but antibiotics must not be withheld awaiting results. Dexamethasone may also be considered but is secondary to prompt antibiotic therapy.

• B. Benzylpenicillin alone does not provide adequate empirical cover and withholding further treatment pending cultures risks clinical deterioration.
• C. Performing CT brain before antibiotics causes unacceptable delay; antibiotics should not be withheld for imaging unless there are specific contraindications to immediate lumbar puncture, and even then antibiotics are given first.
• D. Oral antibiotics are inadequate for suspected bacterial meningitis with septic features and purpura; this requires immediate intravenous treatment and hospital admission.
• E. Waiting for lumbar puncture results before starting antibiotics causes dangerous treatment delay in a patient with signs of sepsis and purpura.

In a haemodynamically unstable trauma patient with suspected intra-abdominal injury, FAST scan is the investigation of choice because it can be performed rapidly at the bedside without interrupting resuscitation, identifying free intraperitoneal fluid suggestive of haemorrhage. A positive FAST scan in an unstable patient is an indication for emergency laparotomy rather than further imaging. CT scanning requires haemodynamic stability for safe transfer to the scanner and is inappropriate in a hypotensive patient who needs immediate source control. Diagnostic peritoneal lavage has largely been superseded by FAST and CT in modern trauma care.

• A. CT requires patient transfer and takes time, which is unsafe in a haemodynamically unstable patient needing immediate assessment and likely surgery.
• C. Plain X-ray has poor sensitivity for intra-abdominal haemorrhage and is not appropriate for assessing internal bleeding.
• D. Observation is inappropriate in an unstable, hypotensive patient with signs of significant abdominal trauma requiring urgent assessment.
• E. Diagnostic peritoneal lavage is an invasive, time-consuming historical technique largely replaced by FAST in current trauma protocols.

This patient demonstrates ongoing haemorrhagic shock with hypotension, tachycardia and a positive FAST scan despite initial crystalloid resuscitation, meeting criteria for massive transfusion protocol activation. Massive transfusion protocols deliver red cells, fresh frozen plasma and platelets in fixed ratios early, correcting coagulopathy and avoiding dilutional effects from excessive crystalloid, which worsens outcomes in trauma haemorrhage. Current damage control resuscitation principles favour early balanced blood product transfusion over large-volume crystalloid in haemorrhagic shock. Delaying transfusion to await full cross-match is inappropriate in life-threatening haemorrhage, where group-specific or O-negative blood should be used immediately.

• A. A single unit of red cells is inadequate for this degree of shock and does not address the need for balanced component resuscitation.
• C. Further large-volume crystalloid worsens dilutional coagulopathy and delays definitive haemorrhage control; it is not appropriate in ongoing haemorrhagic shock.
• D. Waiting for fully cross-matched blood causes dangerous delay; emergency release blood should be used immediately in life-threatening haemorrhage.
• E. CT scanning before addressing ongoing haemorrhagic shock delays resuscitation and is unsafe in a haemodynamically unstable patient.

Naloxone has a short elimination half-life of roughly 30 to 90 minutes, whereas transdermal fentanyl and many other opioids continue to be absorbed or redistributed for several hours. As the naloxone effect wears off, the still-active opioid can re-sedate the patient, producing recurrent respiratory depression. This is why patients reversed with naloxone need extended monitoring, and why an infusion rather than repeated boluses alone may be required for long-acting opioids. Transdermal fentanyl is particularly prone to this because the patch continues to deliver drug from a subcutaneous depot even after removal.

• A. Naloxone-precipitated withdrawal causes agitation and autonomic arousal, not sedation.
• B. This is possible but far less likely than the known pharmacokinetic mismatch and is not the best explanation given the clinical context.
• C. There is no pharmacological mechanism by which naloxone triggers rebound absorption from a patch.
• E. Acute tolerance to naloxone itself is not a recognised clinical phenomenon over this timeframe.

Salicylates directly stimulate the medullary respiratory centre, causing a primary respiratory alkalosis (low PaCO2 with elevated pH), while simultaneously uncoupling oxidative phosphorylation and causing accumulation of organic acids, producing a primary metabolic acidosis (low bicarbonate). The classic early salicylate picture is this mixed disturbance, often with a near-normal or slightly alkalotic pH because the two processes partially offset each other. Renal compensation for a respiratory alkalosis takes days, far too slow to explain a reduced bicarbonate at 4 hours. Recognising this mixed pattern is important because progression to a dominant metabolic acidosis signals worsening toxicity and the need for urinary alkalinisation or haemodialysis.

• A. Renal compensation is far too slow to produce the low bicarbonate seen within hours of ingestion.
• C. The bicarbonate is reduced, not elevated, excluding a primary metabolic alkalosis.
• D. There is no evidence of metabolic alkalosis; the bicarbonate is low, not elevated.
• E. Respiratory compensation for a metabolic acidosis would lower CO2 but the pH here is elevated, not low as expected with an uncompensated primary metabolic acidosis.

Pressure immobilisation bandaging should be left in place until the patient is in a setting equipped to manage systemic envenomation, including antivenom and resuscitation facilities, because removal can cause a bolus of venom to enter the circulation. The bandage should then be removed and the patient observed with serial examination and repeat coagulation studies (INR, APTT, fibrinogen) over several hours, since venom effects may be delayed. Antivenom is given only if there is clinical or laboratory evidence of envenomation, such as coagulopathy, neurotoxicity, myotoxicity or significant local signs, not empirically in an asymptomatic patient with normal initial bloods. A venom detection kit on a bite-site swab or urine can help identify snake type if envenomation is confirmed.

• B. The patient cannot be safely discharged this early because systemic effects of envenomation can be delayed several hours.
• C. The bandage should be removed once appropriate facilities are available, not left indefinitely, and ongoing monitoring with coagulation studies is still required.
• D. Antivenom carries a risk of anaphylaxis and should not be given empirically without evidence of envenomation.
• E. Incision and suction are outdated and ineffective first aid measures that may increase local tissue damage and systemic absorption of venom.

This presentation of altered mental state with a core temperature above 40°C following exertion in hot conditions indicates exertional heat stroke, a medical emergency distinguished from heat exhaustion by the presence of central nervous system dysfunction. Management priority is rapid reduction of core temperature, ideally with cold water immersion or evaporative cooling with fanning plus misting, combined with intravenous fluid resuscitation to address hypotension and tachycardia from volume depletion and vasodilation. Rapid cooling to below 39°C within the first 30 to 60 minutes significantly reduces morbidity and mortality. Antipyretics such as paracetamol are ineffective in heat stroke because the hypothalamic set point is not raised, unlike in fever.

• A. Cooling should be rapid, not slow, because delay increases the risk of multiorgan damage.
• B. Dantrolene is used for malignant hyperthermia and neuroleptic malignant syndrome, not for exertional heat stroke.
• C. Oral rehydration and rest are appropriate for heat exhaustion without CNS dysfunction, but this patient's confusion indicates heat stroke requiring active cooling and intravenous fluids.
• E. Paracetamol targets hypothalamic set-point elevation in fever and has no role in heat stroke, where the set point is normal.

Moderate hypothermia (core temperature 28 to 32°C) with a perfusing rhythm is managed with gentle handling to avoid precipitating ventricular fibrillation, removal of wet clothing, insulation to prevent further heat loss, and external rewarming using warmed blankets, forced-air warming devices or chemical heat packs. Patients should be kept horizontal and movements minimised because rough handling or sudden posture changes can trigger malignant arrhythmias in a hypothermic, irritable myocardium. Warmed intravenous fluids (not cold) can be given to support circulation, but immersion in hot water is impractical and dangerous in the field due to risk of afterdrop and cardiovascular collapse. Core temperature and cardiac rhythm should be monitored continuously en route to hospital.

• A. Intravenous fluids given to a hypothermic patient should be warmed, not cold, to avoid worsening hypothermia.
• B. Immersion in hot water on scene is impractical, risks burns, and can cause dangerous afterdrop and cardiovascular collapse.
• D. Defibrillation is not indicated for sinus bradycardia; shockable rhythms in hypothermia are reserved for actual ventricular fibrillation or pulseless ventricular tachycardia.
• E. Vigorous limb massage can precipitate ventricular fibrillation by returning cold, acidotic peripheral blood to the core and is contraindicated.

Carbon monoxide poisoning should be suspected whenever a patient presents with headache, nausea or altered mentation after exposure to combustion sources such as generators, especially when multiple household members are affected simultaneously. Standard pulse oximetry is unreliable because it cannot distinguish carboxyhaemoglobin from oxyhaemoglobin and will show a falsely normal reading, as in this patient. The diagnosis is confirmed by measuring carboxyhaemoglobin level directly using co-oximetry on an arterial or venous blood gas sample. Hyperbaric oxygen therapy is considered for severe poisoning with loss of consciousness, significant neurological or cardiac findings, carboxyhaemoglobin level above around 25%, or pregnancy with carboxyhaemoglobin above about 20%, due to carbon monoxide's effect of displacing oxygen from haemoglobin and impairing cellular respiration.

• A. ECG may show ischaemic changes in severe cases but is not the confirmatory test for the diagnosis.
• B. Lactate may be elevated from tissue hypoxia but is nonspecific and does not confirm carbon monoxide poisoning.
• C. Standard pulse oximetry cannot differentiate carboxyhaemoglobin from oxyhaemoglobin and gives a falsely reassuring normal reading in carbon monoxide poisoning.
• D. Chest X-ray may show pulmonary oedema in severe poisoning but does not confirm the diagnosis of carbon monoxide exposure.

The combination of sudden severe abdominal and back pain, hypotension, and a pulsatile abdominal mass in an older patient with vascular risk factors such as smoking and hypertension is the classic triad of ruptured abdominal aortic aneurysm. This diagnosis is a surgical emergency requiring immediate resuscitation and urgent surgical or endovascular repair; in a haemodynamically unstable patient with this clinical picture, bedside ultrasound or immediate transfer to theatre takes priority over further imaging if the diagnosis is clinically clear. Risk factors include age over 65, male sex, smoking, hypertension and a family history of aneurysmal disease. Delay in recognition is a major cause of preventable death from this condition.

• A. A perforated peptic ulcer typically causes peritonism with a rigid abdomen rather than a pulsatile mass.
• B. Acute pancreatitis causes epigastric pain radiating to the back but does not produce a pulsatile abdominal mass.
• C. Renal colic causes severe flank pain but is not associated with hypotension or a pulsatile mass.
• E. Mesenteric ischaemia causes severe pain often out of proportion to examination findings but does not produce a pulsatile mass.

The classic history of periumbilical pain migrating to the right iliac fossa, accompanied by anorexia, low-grade fever, localised peritonism at McBurney's point, a positive Rovsing's sign, and a neutrophilic leukocytosis is the typical clinical picture of acute appendicitis. A negative beta-hCG excludes ectopic pregnancy, and the absence of vaginal discharge or bleeding makes pelvic inflammatory disease and ruptured ovarian cyst less likely, though these remain important differentials in women of reproductive age with RIF pain. Diagnosis is primarily clinical, supported by inflammatory markers, with imaging such as ultrasound or CT reserved for atypical presentations or diagnostic uncertainty. Timely surgical referral for appendicectomy is important to reduce the risk of perforation.

• A. A ruptured ovarian cyst typically causes sudden onset pain at the time of rupture, often mid-cycle, without the classic migratory pattern or marked leukocytosis seen here.
• B. Mesenteric adenitis is a diagnosis of exclusion typically seen in children or adolescents following a viral illness, and does not typically produce Rovsing's sign or this degree of leukocytosis.
• C. A negative beta-hCG excludes ectopic pregnancy as the cause of this presentation.
• E. Pelvic inflammatory disease typically presents with vaginal discharge, cervical motion tenderness and bilateral adnexal tenderness, none of which are described here.

Sudden severe testicular pain with a high, horizontally lying testis, absent cremasteric reflex, and no relief with elevation (negative Prehn's sign) are classic features of testicular torsion, a surgical emergency. The absence of fever and normal urinalysis argue against an infective cause such as epididymo-orchitis. Testicular torsion requires immediate urological referral for surgical exploration and detorsion, ideally within 4-6 hours of symptom onset to preserve testicular viability, as salvage rates fall sharply beyond this window.

• A. Varicocele presents as a chronic, dull, dragging scrotal ache rather than acute severe pain.
• B. Epididymo-orchitis typically causes gradual onset pain with fever and pyuria, and pain is often relieved by scrotal elevation.
• C. Torsion of the appendix testis causes a more localised, less severe pain with a palpable tender nodule and preserved cremasteric reflex.
• D. An incarcerated hernia usually presents with a groin mass and bowel obstruction features rather than isolated testicular signs.

This patient meets qSOFA criteria (altered mentation, respiratory rate ≥22/min, systolic blood pressure ≤100 mmHg) and has a likely catheter-associated urinary source of sepsis. The Sepsis Six bundle mandates that blood cultures be taken and empirical broad-spectrum intravenous antibiotics be administered within one hour of recognition, alongside oxygen, intravenous fluids, lactate measurement and urine output monitoring. Delaying antibiotics for imaging or oral therapy increases mortality, as each hour of delay in sepsis is associated with worse outcomes.

• A. Outpatient management is inappropriate given hypotension and altered mental state indicating sepsis requiring hospital-based urgent treatment.
• B. Scoring tools support recognition but should not delay treatment once sepsis is clinically apparent.
• C. Oral antibiotics and delayed review are inadequate for a patient with signs of septic shock requiring immediate intravenous therapy.
• E. Awaiting chest X-ray results delays time-critical antibiotic administration and is not part of the Sepsis Six priority actions.

Noradrenaline (norepinephrine) is the first-line vasopressor for septic shock that is refractory to adequate fluid resuscitation, as recommended by Therapeutic Guidelines and international sepsis guidelines. Its potent alpha-1 adrenergic activity produces vasoconstriction that restores mean arterial pressure with relatively modest increases in heart rate and myocardial oxygen demand compared with other agents. Dopamine is no longer recommended due to higher rates of arrhythmia and mortality. Vasopressin or adrenaline may be added as second-line agents if blood pressure targets are not met on noradrenaline alone.

• A. Dobutamine is an inotrope used for myocardial dysfunction, not as primary vasopressor therapy for septic shock.
• B. Vasopressin is used as an adjunct to noradrenaline, not as sole first-line therapy.
• C. Adrenaline is reserved as a second-line agent or for refractory shock due to greater arrhythmogenic and metabolic side effects.
• E. Dopamine is associated with increased arrhythmias and mortality compared with noradrenaline and is not first-line.

This patient has febrile neutropenia, defined as fever with an absolute neutrophil count below 0.5 × 10^9/L, which is a medical emergency due to the risk of rapidly progressive sepsis from a diminished immune response. Therapeutic Guidelines recommend empirical broad-spectrum intravenous antibiotic therapy with a antipseudomonal beta-lactam such as piperacillin-tazobactam, commenced immediately after blood cultures are taken and within one hour of presentation, without waiting for culture or imaging results. This covers likely Gram-negative and Gram-positive pathogens until an organism is identified or the neutrophil count recovers.

• A. Oral antibiotics and delayed outpatient review are inappropriate for febrile neutropenia, which requires immediate intravenous therapy and inpatient assessment.
• B. Withholding antibiotics pending results risks rapid deterioration and is contrary to the one-hour treatment target for febrile neutropenia.
• C. Oral ciprofloxacin alone provides inadequate broad-spectrum cover and delayed review is unsafe in this high-risk setting.
• E. Vancomycin alone does not provide adequate Gram-negative cover and is only added to a beta-lactam if specific indications such as line infection or haemodynamic instability are present.

This child shows signs of decompensated shock (tachycardia, delayed capillary refill, hypotension) requiring urgent fluid resuscitation. The standard paediatric fluid bolus for shock is 10 mL/kg of an isotonic crystalloid such as 0.9% sodium chloride, given rapidly over 10-15 minutes. For an 18 kg child, this equals 180 mL. The response to the bolus should be reassessed and repeated if shock persists, with escalation of care considered after 40 mL/kg.

• B. This is 1 mL/kg, far too small a volume to correct shock.
• C. This is 20 mL/kg, exceeding the standard initial bolus volume and risking fluid overload before reassessment.
• D. Hypotonic dextrose-containing fluids are inappropriate for resuscitation and risk hyponatraemia.
• E. This is 5 mL/kg, which is insufficient for a child in decompensated shock.

This child has moderate croup (stridor and recession at rest but no agitation, cyanosis or significant distress), which according to Therapeutic Guidelines warrants a single dose of oral dexamethasone (0.15-0.6 mg/kg, typically 0.6 mg/kg) to reduce airway oedema via its anti-inflammatory glucocorticoid effect. Nebulised adrenaline is reserved for severe croup with marked stridor, recession, agitation or reduced consciousness. Most children with mild to moderate croup can be managed as outpatients after steroid administration and a period of observation. Chest X-ray is not routinely required as croup is a clinical diagnosis.

• A. ICU admission is not indicated for moderate croup without signs of severe respiratory distress or impending respiratory failure.
• B. Oral dexamethasone is preferred over nebulised budesonide when the child can tolerate oral medication, as it is equally effective and easier to administer.
• C. Croup is a clinical diagnosis based on history and examination; imaging is unnecessary and may distress the child.
• D. Nebulised adrenaline is reserved for severe croup with significant respiratory distress, agitation or hypoxia, not moderate croup.

The combination of a spiral femoral fracture in a pre-mobile infant, bruising of different ages suggesting repeated trauma, a torn frenulum (associated with forced feeding or object insertion), and a mechanism inconsistent with the developmental stage and injury pattern (a short fall rarely causes spiral femoral fractures) is highly suspicious for non-accidental injury. Spiral fractures result from torsional force, which is not typically generated by a simple fall. Multiple injuries of differing ages and implausible mechanisms are classic red flags requiring urgent child protection notification and skeletal survey. AMC candidates must recognise these injury patterns and the legal duty to report suspected child abuse.

• A. Osteogenesis imperfecta would not explain the frenulum tear or bruising of varying ages and is not supported by other features such as blue sclerae or family history.
• B. A fall from 30 cm in a non-mobile infant is an implausible mechanism for a spiral femoral fracture.
• C. A birth-related fracture would have presented in the neonatal period with swelling, not months later, and does not explain the bruising or frenulum tear.
• E. Rickets causes bowing deformities and growth plate changes rather than acute spiral fractures, and does not explain the other findings.

This patient has severe hyperkalaemia with classic ECG changes (peaked T waves, widened QRS, absent P waves) indicating membrane instability and imminent risk of ventricular arrhythmia or asystole. Intravenous calcium gluconate is the first-line emergency treatment; it works by raising the threshold potential at the cardiac cell membrane, counteracting the effect of hyperkalaemia on membrane excitability, without actually lowering the serum potassium concentration. This buys time while insulin with dextrose (which shifts potassium intracellularly via stimulation of the sodium-potassium ATPase pump) and other potassium-lowering measures take effect.

• B. This describes the mechanism of resonium (sodium polystyrene sulfonate), which has a slow onset and is not used for acute cardioprotection.
• C. This describes the mechanism of cation exchange resins, which act too slowly to be useful in acute life-threatening hyperkalaemia.
• D. This describes the mechanism of agents such as fludrocortisone or loop diuretics, which act more slowly and are not the first-line emergency treatment.
• E. This describes the mechanism of insulin with dextrose, not calcium gluconate, which is the immediate membrane-stabilising treatment.

This man has an inferior ST-elevation myocardial infarction and requires urgent reperfusion therapy. In a remote setting without on-site percutaneous coronary intervention capability, the appropriate next step is to contact the regional retrieval service (such as the Careflight or Royal Flying Doctor Service coordination centre) for urgent aeromedical evacuation, while initiating guideline-directed therapy (aspirin, antiplatelet therapy, and thrombolysis if transfer will be delayed beyond guideline-recommended time to percutaneous coronary intervention) under remote telehealth medical support. Equity of access to timely cardiac care is a key consideration for Aboriginal and Torres Strait Islander patients in remote communities, and retrieval services are structured to coordinate this urgently. Standard protocols in the Northern Territory allow remote area nurses to initiate time-critical treatment under medical officer telephone orders as part of the retrieval process, rather than waiting for family or in-person authorisation.

• A. Thrombolysis should proceed under remote telehealth medical direction as part of retrieval coordination, not be contingent on finding a doctor independently of the retrieval process.
• B. Emergency life-saving treatment should not be delayed for family consent in a time-critical, capable adult who can give his own consent for treatment.
• D. A 600 km road transfer would cause dangerous delay in reperfusion for a time-critical STEMI compared with aeromedical evacuation.
• E. Overnight observation would cause a dangerous delay in treating a life-threatening STEMI.

In adult patients without dependent children, disclosure of intimate partner violence should be handled by validating the disclosure, performing a careful risk and safety assessment (including immediate safety that night), and offering referral to specialist domestic violence support services and safety planning resources. Reporting to police is not mandatory for a competent adult who declines it, respecting her autonomy, although she should be informed of the option to report and supported if she changes her mind. Clinicians should document findings and disclosures carefully as this may be important for future legal processes.

• B. Competent adults without dependent children have the right to decline police involvement in Australia; reporting is not mandatory in this situation.
• C. Contacting the perpetrator breaches confidentiality and could place the patient at greater risk of harm.
• D. Discharging without offering referral and safety planning fails to address her stated fear and ongoing risk.
• E. Mandatory reporting to child protection applies when children are involved or at risk; this patient has no children and this is not the appropriate pathway.

This patient has acute severe behavioural disturbance with failed de-escalation and immediate danger to himself and others, meeting criteria for emergency pharmacological sedation. Intramuscular droperidol is a commonly used first-line agent for rapid sedation in this setting due to its reliable onset and favourable safety profile, and it can be administered under emergency provisions in state mental health or guardianship legislation that permit treatment without full consent when there is immediate risk of serious harm, with retrospective documentation and review. Physical restraint without sedation increases the risk of physical harm and should be minimised and used only as a last resort alongside, not instead of, pharmacological management. Formal certification processes should follow, not precede, emergency treatment when there is immediate danger.

• A. Oral medication requires patient cooperation, which is not present here, and leaving him unsupervised in a waiting area does not address the immediate safety risk.
• B. Restraint alone without sedation increases risk of injury to the patient and staff and does not address the underlying agitation.
• C. Watchful waiting is inappropriate when there is immediate danger to the patient and staff; it risks injury and delays necessary care.
• D. Emergency legislation permits immediate treatment for imminent risk to safety before formal paperwork is completed, with documentation to follow.

A negative FAST in a haemodynamically unstable trauma patient with a pelvic fracture points to the pelvis as the source of bleeding, usually from venous plexus or arterial injury. Once a binder and initial resuscitation fail to restore stability, the patient needs blood product resuscitation (massive transfusion protocol) and definitive haemorrhage control, which is angioembolisation if interventional radiology is available or surgical pelvic packing/external fixation if not. Delaying for CT in a persistently unstable patient risks deterioration and death; CT is appropriate only once the patient is stabilised or in those who are haemodynamically normal. Ongoing crystalloid without blood products risks dilutional coagulopathy and does not address the underlying bleeding source.

• A. A suprapubic catheter does not address haemorrhage and risks injury if there is a concomitant bladder or urethral injury from the pelvic fracture.
• C. Diagnostic peritoneal lavage is obsolete and not indicated when FAST has already excluded intraperitoneal fluid.
• D. A second binder does not provide additional haemorrhage control once a correctly applied binder has failed and may worsen soft tissue injury.
• E. CT is contraindicated in a haemodynamically unstable patient who needs immediate haemorrhage control, not a diagnostic delay.

Flail chest occurs when three or more adjacent ribs are fractured in two or more places, creating a free-floating segment that moves paradoxically with respiration due to loss of continuity with the thoracic cage. The underlying pulmonary contusion, evident here as crackles and hypoxia, is usually the main driver of respiratory failure rather than the mechanical flail segment itself. Management involves adequate analgesia, oxygen, and often positive pressure ventilation if respiratory failure develops, as the lung parenchymal injury worsens over the first 24-48 hours. Diagnosis is clinical, based on paradoxical chest wall movement, and supported by chest X-ray or CT showing multiple rib fractures.

• A. Massive haemothorax presents with dullness to percussion and signs of hypovolaemic shock, not the described paradoxical segment movement.
• B. Diaphragmatic rupture typically presents with bowel sounds in the chest or abnormal nasogastric tube position on imaging, not paradoxical chest wall motion.
• C. A simple pneumothorax does not cause paradoxical chest wall movement or the palpable multiple rib fracture segment described.
• E. Tension pneumothorax presents with tracheal deviation, absent breath sounds, hyper-resonance and hypotension from mediastinal shift, not paradoxical chest wall movement.

Compartment syndrome is a clinical diagnosis suggested by pain out of proportion to injury, pain on passive stretch, paraesthesia, and a tense swollen compartment; pulses and capillary refill are often preserved until late, so their presence does not exclude the diagnosis. The first step is to remove all external constricting factors, including casts and tight dressings, to relieve any extrinsic pressure contributing to compartment pressure. If symptoms persist after this, urgent fasciotomy is required, as delay beyond 6-8 hours leads to irreversible muscle and nerve necrosis. Elevating the limb above heart level can reduce arterial perfusion pressure and worsen ischaemia, so the limb should be kept at heart level.

• A. MRI is not indicated and the delay risks irreversible muscle necrosis; compartment syndrome is a clinical diagnosis requiring immediate action.
• B. Increasing opioid analgesia masks the clinical signs needed to monitor for compartment syndrome and delays definitive treatment, risking irreversible damage.
• C. Elevation above heart level reduces perfusion pressure to the compartment and can worsen ischaemia; compression bandaging would further increase compartment pressure.
• D. Duplex ultrasound for DVT does not address the clinical picture of compartment syndrome and delays time-critical treatment.

Basilar skull fracture is suggested by the triad of Battle's sign (bruising over the mastoid process from extravasation of blood along the posterior auricular region), periorbital ecchymosis (racoon eyes) without direct orbital trauma, and cerebrospinal fluid rhinorrhoea or otorrhoea from a dural tear. Glucose-positive clear fluid from the nose supports CSF rather than mucus, as CSF contains glucose unlike typical nasal secretions. Management includes CT brain and skull base imaging, avoidance of nasogastric tubes and nasal packing, and neurosurgical consultation given the risk of meningitis and need to assess for an underlying dural defect. These patients require admission for observation given the risk of intracranial injury.

• A. An orbital blow-out fracture typically follows direct trauma to the eye and does not explain mastoid bruising or CSF leakage from the nose.
• B. A simple nasal bone fracture does not cause mastoid bruising, periorbital ecchymosis away from the nose, or CSF rhinorrhoea.
• C. Allergic rhinitis does not cause bruising over the mastoid processes or periorbital region, nor would the fluid test positive for glucose.
• E. Scalp haematoma alone does not account for Battle's sign, racoon eyes, or glucose-positive nasal fluid indicating a dural tear.

This is a tetanus-prone wound given the contamination with soil, presence of devitalised tissue, and puncture mechanism, which favours anaerobic conditions for Clostridium tetani. The patient's immunisation history is uncertain and his last dose was more than 15 years ago, which the Australian Immunisation Handbook classifies as an incomplete or uncertain history for a tetanus-prone wound, warranting both a tetanus toxoid-containing vaccine to boost active immunity and tetanus immunoglobulin to provide immediate passive protection while active immunity develops. Tetanus immunoglobulin provides preformed antibody for immediate neutralisation of toxin, whereas the vaccine stimulates the patient's own antibody response over 1-2 weeks. Antibiotics such as metronidazole are not a substitute for tetanus immunoglobulin or vaccination in wound management.

• A. Antibiotics do not provide specific protection against tetanus toxin and are not a recommended substitute for immunoglobulin or vaccination.
• B. Immunoglobulin alone is inadequate since his immunisation status is uncertain and a booster vaccine dose is also needed to ensure ongoing active immunity.
• C. Vaccine alone is insufficient for a tetanus-prone wound in a patient with an uncertain or incomplete immunisation history; immunoglobulin is also required for immediate passive protection.
• D. Tetanus-prone, contaminated puncture wounds require prophylaxis regardless of wound age; waiting or omitting prophylaxis risks clinical tetanus.

The Australasian paracetamol nomogram is used for single acute ingestions where the timing of ingestion is known, with blood taken no earlier than 4 hours post-ingestion to allow for absorption and distribution. A level plotting on or above the treatment line indicates a significant risk of hepatotoxicity and is an indication to commence intravenous N-acetylcysteine without delay, as NAC is most effective when started within 8 hours of ingestion. Waiting for a repeat level beyond 8 hours risks missing the window of maximum hepatoprotective benefit. Activated charcoal may be considered if presentation is within 1-2 hours of a large ingestion, but it does not replace NAC once the nomogram indicates treatment is required.

• B. Activated charcoal alone is inadequate once the level is above the treatment line; NAC is required regardless of charcoal administration, and charcoal is only useful if given early after ingestion.
• C. Discharge is inappropriate given a level above the treatment line, which carries a real risk of hepatotoxicity requiring treatment now, not just outpatient monitoring.
• D. Delaying treatment pending a repeat level risks missing the 8-hour window for optimal NAC efficacy when the current level already indicates treatment is required.
• E. Naloxone reverses opioid toxicity and has no role in paracetamol overdose management.

Tricyclic antidepressants block fast voltage-gated sodium channels in cardiac myocytes, slowing phase 0 depolarisation and widening the QRS complex, which predisposes to ventricular arrhythmias and hypotension. Sodium bicarbonate works through two mechanisms: the increased extracellular sodium concentration helps overcome the sodium channel blockade by increasing the sodium gradient driving depolarisation, and the resulting alkalosis reduces the affinity of the tricyclic antidepressant for the sodium channel. The combined effect narrows the QRS complex and improves blood pressure, and bicarbonate is indicated for a QRS duration greater than 100 milliseconds, ventricular arrhythmias, or hypotension in TCA overdose. Urinary alkalinisation plays no meaningful role in TCA elimination since tricyclics are highly protein-bound and extensively tissue-distributed, not renally cleared in a pH-dependent manner.

• A. Tricyclic antidepressants are not renally eliminated in a pH-dependent fashion, so urinary alkalinisation does not meaningfully enhance their clearance.
• C. Sodium bicarbonate does not chelate or bind the tricyclic antidepressant molecule directly; its effect is through sodium channel and pH-mediated mechanisms.
• D. Sodium bicarbonate does not act at muscarinic receptors; the anticholinergic effects of tricyclics are unrelated to bicarbonate's mechanism of action.
• E. Sodium bicarbonate has no significant effect on hepatic cytochrome P450 enzyme activity or tricyclic antidepressant metabolism.