A 55-year-old woman with a documented allergy to peanuts accidentally consumes a food item containing peanut oil at a restaurant. Within 10 minutes, she develops generalized urticaria, lip swelling, wheeze, and feels dizzy. Her friend administers her adrenaline auto-injector (300 micrograms) intramuscularly to the anterolateral thigh. An ambulance arrives 8 minutes later. On examination, her blood pressure is 85/50 mmHg, heart rate 125 bpm, respiratory rate 30 breaths per minute with audible wheeze, and oxygen saturation 90% on room air. What is the primary mechanism by which adrenaline improves this patient's condition?
Q122
A 32-year-old woman collapses while attending a funeral. Witnesses report she became pale, felt hot, and then lost consciousness for approximately 20 seconds. She recovered quickly and feels well now but slightly embarrassed. She has no past medical history and takes no medications. Examination reveals blood pressure 120/75 mmHg, heart rate 70 bpm regular, no murmurs, clear lung fields, and normal neurological examination. Her ECG shows normal sinus rhythm with no abnormalities. What underlying pathophysiological mechanism best explains her episode?
Q123
A 45-year-old man presents to the Emergency Department with severe central chest pain radiating to his jaw, associated with sweating and nausea. His ECG shows ST-segment elevation of 3 mm in leads II, III, and aVF. His blood pressure is 125/80 mmHg, heart rate 85 bpm regular, and oxygen saturation 97% on room air. The nearest cardiac catheterization laboratory is 90 minutes away by ambulance. Which troponin level finding would you expect in this patient if measured immediately on arrival?
Q124
A 68-year-old man with a history of chronic obstructive pulmonary disease presents to the Emergency Department with a 48-hour history of fever, productive cough, and confusion. On examination, his temperature is 38.5°C, heart rate 110 bpm, blood pressure 95/60 mmHg, respiratory rate 28 breaths per minute, and oxygen saturation 89% on room air. Blood tests reveal lactate 3.2 mmol/L, creatinine 145 μmol/L, and white cell count 18 × 10⁹/L. What is the initial fluid resuscitation target in the management of this patient's sepsis?
Q125
A 51-year-old man is admitted with severe community-acquired pneumonia complicated by septic shock. He is intubated and ventilated on the Intensive Care Unit. Despite noradrenaline infusion at 0.4 micrograms/kg/min, his mean arterial pressure remains 58 mmHg (target ≥65 mmHg). He has received appropriate fluid resuscitation and is on hydrocortisone and broad-spectrum antibiotics. His central venous oxygen saturation (ScvO2) is 58% (target ≥70%). Echocardiography shows left ventricular ejection fraction of 35% (previously normal). What is the most appropriate additional intervention?
Q126
A 23-year-old woman collapses at a gym. Bystanders report she was exercising on a treadmill when she suddenly fell and lost consciousness. She had no warning symptoms. She regained consciousness after 60 seconds but was confused for several minutes. She has no significant medical history but mentions her brother died suddenly aged 19 during sport. Her initial observations and blood tests are normal. Her ECG shows sinus rhythm, rate 68/min, with deep T wave inversion in leads V1-V4 and a slightly prolonged QTc of 475 ms. What is the most likely underlying diagnosis?
Q127
A 67-year-old woman is admitted to the Emergency Department with suspected community-acquired pneumonia and sepsis. She receives 2 litres of intravenous crystalloid and broad-spectrum antibiotics. Despite fluid resuscitation, her blood pressure remains 82/50 mmHg with a lactate of 4.5 mmol/L. The decision is made to start noradrenaline. Her current blood tests show: sodium 136 mmol/L, potassium 5.2 mmol/L, creatinine 165 μmol/L (baseline 88 μmol/L), glucose 12.4 mmol/L. In addition to noradrenaline, which other intervention has been shown to reduce mortality in patients with septic shock according to recent evidence?
Q128
A 44-year-old man with no significant past medical history presents to the Emergency Department with 90 minutes of severe central chest pain. His ECG shows 4 mm ST-segment elevation in leads V2-V5. The nearest primary PCI centre is 90 minutes away by ambulance. He is haemodynamically stable. According to current guidelines, what is the most appropriate reperfusion strategy for this patient?
Q129
A 63-year-old man is admitted to the Emergency Department with suspected sepsis secondary to cellulitis of his right leg. Initial observations: temperature 38.3°C, heart rate 95/min, blood pressure 125/75 mmHg, respiratory rate 20/min. Blood tests show: white cells 14.2 × 10⁹/L, lactate 1.8 mmol/L, creatinine 98 μmol/L. He is given intravenous flucloxacillin and 1 litre of intravenous fluids. Six hours later, he becomes increasingly confused and agitated. Repeat observations: temperature 39.1°C, heart rate 122/min, blood pressure 88/55 mmHg, respiratory rate 28/min, oxygen saturations 94% on air. Repeat lactate is 4.2 mmol/L. His urine output over 6 hours is 80 ml. What SOFA score change and qSOFA score would this patient have?
Q130
A 48-year-old woman is brought to the Emergency Department with altered consciousness. Her husband reports she developed throat tightness and difficulty breathing 20 minutes after taking ibuprofen for a headache. She has asthma usually well-controlled with salbutamol and beclomethasone inhalers. On examination: decreased consciousness (GCS 12), widespread wheeze, blood pressure 75/45 mmHg, heart rate 125/min, respiratory rate 32/min, oxygen saturations 88% on 15L oxygen via non-rebreathe mask. What should be the immediate priority in management?
Acute Medical Presentations UK Medical PG Practice Questions and MCQs
Question 121: A 55-year-old woman with a documented allergy to peanuts accidentally consumes a food item containing peanut oil at a restaurant. Within 10 minutes, she develops generalized urticaria, lip swelling, wheeze, and feels dizzy. Her friend administers her adrenaline auto-injector (300 micrograms) intramuscularly to the anterolateral thigh. An ambulance arrives 8 minutes later. On examination, her blood pressure is 85/50 mmHg, heart rate 125 bpm, respiratory rate 30 breaths per minute with audible wheeze, and oxygen saturation 90% on room air. What is the primary mechanism by which adrenaline improves this patient's condition?
A. Direct bronchodilation via beta-2 receptor agonism and prevention of further mediator release via alpha receptor activation on mast cells (Correct Answer)
B. Competitive inhibition of histamine at H1 receptors preventing further allergic cascade
C. Stabilization of mast cell membranes preventing further degranulation
D. Direct antagonism of leukotriene receptors reducing bronchoconstriction
E. Suppression of T-lymphocyte activation and cytokine release
Explanation: ***Direct bronchodilation via beta-2 receptor agonism and prevention of further mediator release via alpha receptor activation on mast cells***
- **Adrenaline** (epinephrine) is a physiological antagonist, rapidly reversing the effects of **anaphylaxis** by acting on alpha and beta adrenergic receptors.
- Its **beta-2 receptor agonism** causes immediate **bronchodilation**, relieving wheeze, and its **alpha-1 receptor agonism** leads to **vasoconstriction**, increasing **blood pressure** and reducing **angioedema**.
*Competitive inhibition of histamine at H1 receptors preventing further allergic cascade*
- This is the mechanism of **antihistamines**, which primarily alleviate **urticaria** and **pruritus** but do not treat life-threatening symptoms.
- Antihistamines are ineffective at reversing severe **bronchospasm** or **hypotension** seen in **anaphylaxis**.
*Stabilization of mast cell membranes preventing further degranulation*
- This describes the action of **mast cell stabilizers** (e.g., cromolyn sodium), which are used for **prophylaxis** of allergic reactions.
- These drugs have a slow onset and no role in the acute emergency management of established **anaphylaxis**.
*Direct antagonism of leukotriene receptors reducing bronchoconstriction*
- This is the mechanism of **leukotriene receptor antagonists** (e.g., montelukast), primarily used for **asthma** and allergic rhinitis management.
- **Leukotriene antagonists** do not provide the rapid, broad-spectrum effects on **blood pressure**, **bronchospasm**, and **edema** needed for **anaphylaxis**.
*Suppression of T-lymphocyte activation and cytokine release*
- This mechanism is characteristic of **corticosteroids** or immunosuppressants, which have a delayed onset of action.
- While corticosteroids may be given in **anaphylaxis** to prevent **biphasic reactions**, they do not provide immediate relief of acute **cardiovascular** or **respiratory** compromise.
Question 122: A 32-year-old woman collapses while attending a funeral. Witnesses report she became pale, felt hot, and then lost consciousness for approximately 20 seconds. She recovered quickly and feels well now but slightly embarrassed. She has no past medical history and takes no medications. Examination reveals blood pressure 120/75 mmHg, heart rate 70 bpm regular, no murmurs, clear lung fields, and normal neurological examination. Her ECG shows normal sinus rhythm with no abnormalities. What underlying pathophysiological mechanism best explains her episode?
A. Sudden reduction in cardiac output due to arrhythmia
B. Increased vagal tone leading to vasodilation and bradycardia (Correct Answer)
C. Hypoglycaemia causing cerebral hypoperfusion
D. Acute pulmonary embolism with transient haemodynamic compromise
E. Vertebrobasilar insufficiency with brainstem hypoperfusion
Explanation: ***Increased vagal tone leading to vasodilation and bradycardia***
- This patient presents with classic **vasovagal syncope**, the most common cause of syncope, often triggered by **emotional stress** or prolonged standing, as seen at a funeral.
- The pathophysiology involves a **reflex-mediated** surge in **parasympathetic activity** (vagal tone) causing **bradycardia** and a withdrawal of sympathetic tone causing **vasodilation**, leading to transient global cerebral hypoperfusion.
*Sudden reduction in cardiac output due to arrhythmia*
- Cardiac syncope typically occurs without a significant **prodrome** and often happens during exertion or while supine, which is not consistent with this presentation.
- The presence of a **normal ECG** and the absence of structural heart disease or palpitations make a primary **arrhythmia** unlikely in this clinical context.
*Hypoglycaemia causing cerebral hypoperfusion*
- **Hypoglycemia** typically presents with neuroglycopenic symptoms like confusion and tremors rather than a sudden, self-terminating loss of consciousness.
- Unlike syncope, which resolves within minutes, hypoglycemia does not resolve spontaneously without the administration of **glucose** or a source of carbohydrates.
*Acute pulmonary embolism with transient haemodynamic compromise*
- A **pulmonary embolism** severe enough to cause syncope would typically present with **tachycardia**, tachypnoea, or hypoxia during the physical examination.
- This patient's **normal vital signs**, clear lungs, and rapid recovery are inconsistent with the significant right heart strain required for a PE-induced collapse.
*Vertebrobasilar insufficiency with brainstem hypoperfusion*
- **Vertebrobasilar insufficiency** is very rare in a young patient without vascular risk factors and would usually present with focal **neurological deficits** like vertigo or diplopia.
- Syncope caused by vascular insufficiency requires significant **compromise of blood flow** to the reticular activating system, which is not suggested by this isolated episode.
Question 123: A 45-year-old man presents to the Emergency Department with severe central chest pain radiating to his jaw, associated with sweating and nausea. His ECG shows ST-segment elevation of 3 mm in leads II, III, and aVF. His blood pressure is 125/80 mmHg, heart rate 85 bpm regular, and oxygen saturation 97% on room air. The nearest cardiac catheterization laboratory is 90 minutes away by ambulance. Which troponin level finding would you expect in this patient if measured immediately on arrival?
A. Normal troponin level (Correct Answer)
B. Troponin level 10 times the upper reference limit
C. Troponin level 100 times the upper reference limit
D. Troponin level peaked and starting to decline
E. Troponin level at the upper reference limit
Explanation: ***Normal troponin level***
- In the hyperacute phase of a **ST-elevation myocardial infarction (STEMI)**, troponins are often within the normal range because they typically take **3 to 6 hours** to rise in the bloodstream.
- The diagnosis of STEMI is based on **clinical presentation** and **ECG findings** (ST elevation in leads II, III, and aVF); treatment such as reperfusion should never be delayed while waiting for biomarker results.
*Troponin level 10 times the upper reference limit*
- A level this significantly elevated reflects substantial myocardial necrosis that typically occurs **12 to 24 hours** after the onset of symptoms.
- High-sensitivity assays may show early rises, but a **10-fold increase** is unlikely in a patient presenting immediately to the Emergency Department.
*Troponin level 100 times the upper reference limit*
- Such extreme elevations are characteristic of the **peak phase** of a large myocardial infarction, usually seen reached near the **24-hour mark**.
- This level is not biologically plausible in the earliest stages of chest pain when the patient first arrives at the hospital.
*Troponin level peaked and starting to decline*
- Cardiac troponins (I and T) stay elevated for **7 to 14 days**; a declining level would indicate an event that occurred several days prior.
- Since the patient is currently experiencing **acute severe chest pain**, they are in the initial phase of the injury, not the recovery phase.
*Troponin level at the upper reference limit*
- While a minor rise may be detected with **high-sensitivity assays**, most patients presenting hyperacutely will still have levels below the **99th percentile URL**.
- Relying on a borderline value at the reference limit would be inaccurate for diagnosis compared to the **diagnostic ECG changes** already present.
Question 124: A 68-year-old man with a history of chronic obstructive pulmonary disease presents to the Emergency Department with a 48-hour history of fever, productive cough, and confusion. On examination, his temperature is 38.5°C, heart rate 110 bpm, blood pressure 95/60 mmHg, respiratory rate 28 breaths per minute, and oxygen saturation 89% on room air. Blood tests reveal lactate 3.2 mmol/L, creatinine 145 μmol/L, and white cell count 18 × 10⁹/L. What is the initial fluid resuscitation target in the management of this patient's sepsis?
A. 500 mL crystalloid over 30 minutes (Correct Answer)
B. 250 mL crystalloid over 15 minutes
C. 500 mL colloid over 60 minutes
D. 1000 mL crystalloid over 1 hour
E. 2000 mL crystalloid over 24 hours
Explanation: ***500 mL crystalloid over 30 minutes***
- According to **UK Sepsis Trust** and **NICE guidelines**, the standard initial bolus for an adult with sepsis and hypotension is **500 mL of crystalloid**.
- This patient shows signs of **septic shock** (hypotension and lactate >2 mmol/L), necessitating rapid yet controlled fluid resuscitation to restore **tissue perfusion**.
*250 mL crystalloid over 15 minutes*
- This volume is typically reserved for patients with a known history of **heart failure** or **severe renal failure** to minimize the risk of fluid overload.
- While the patient has COPD, the standard starting bolus remains higher unless there is clinical evidence of **pulmonary edema**.
*500 mL colloid over 60 minutes*
- **Crystalloids** (like 0.9% Saline or Hartmann’s) are the preferred fluid for initial resuscitation over **colloids**, which show no survival benefit and may increase risk.
- A 60-minute duration is too slow for a patient presenting with **hypotension** and elevated **lactate**.
*1000 mL crystalloid over 1 hour*
- While older guidelines suggested aggressive large-volume loading, current practice favors **smaller boluses** (500 mL) followed by frequent clinical reassessment.
- Large volumes (30mL/kg) are still used but should be delivered in incremental stages to prevent **iatrogenic fluid overload**.
*2000 mL crystalloid over 24 hours*
- This rate represents **maintenance fluid** requirements rather than the urgent **resuscitative bolus** needed for sepsis management.
- Delaying significant fluid administration over 24 hours would fail to address the patient's immediate **circulatory collapse**.
Question 125: A 51-year-old man is admitted with severe community-acquired pneumonia complicated by septic shock. He is intubated and ventilated on the Intensive Care Unit. Despite noradrenaline infusion at 0.4 micrograms/kg/min, his mean arterial pressure remains 58 mmHg (target ≥65 mmHg). He has received appropriate fluid resuscitation and is on hydrocortisone and broad-spectrum antibiotics. His central venous oxygen saturation (ScvO2) is 58% (target ≥70%). Echocardiography shows left ventricular ejection fraction of 35% (previously normal). What is the most appropriate additional intervention?
A. Increase noradrenaline to maximum dose before adding second agent
B. Add vasopressin as second-line vasopressor
C. Add dobutamine to improve cardiac output and oxygen delivery (Correct Answer)
D. Administer further fluid bolus of 1 litre crystalloid
E. Add milrinone for inotropic support
Explanation: ***Add dobutamine to improve cardiac output and oxygen delivery***
- This patient exhibits **septic cardiomyopathy** (reduced LVEF 35%) and low **ScvO2 (58%)**, indicating inadequate oxygen delivery despite fluid resuscitation and vasopressors.
- **Dobutamine** is the first-line inotrope recommended by the **Surviving Sepsis Campaign** to increase cardiac output and improve tissue perfusion in this clinical scenario.
*Increase noradrenaline to maximum dose before adding second agent*
- Escalating **noradrenaline** without addressing the underlying **low cardiac output** increases the risk of excessive vasoconstriction and end-organ ischemia.
- Higher doses of vasopressors will not improve the **ScvO2**, which is low due to poor pump function rather than just low mean arterial pressure.
*Add vasopressin as second-line vasopressor*
- **Vasopressin** is primarily used to reduce noradrenaline requirements or reach MAP targets through peripheral vasoconstriction.
- It has no **inotropic properties** and will not improve the reduced **LVEF** or the low oxygen delivery indicated by the ScvO2.
*Administer further fluid bolus of 1 litre crystalloid*
- The prompt states the patient has received **appropriate fluid resuscitation**; excessive fluid can lead to **pulmonary edema** and worsened gas exchange in pneumonia.
- Given the **reduced LVEF**, the patient is unlikely to be fluid-responsive and requires inotropic support rather than volume expansion.
*Add milrinone for inotropic support*
- **Milrinone** is a phosphodiesterase inhibitor that causes significant **vasodilation**, which can worsen hypotension in a patient already in septic shock.
- Due to its long half-life and risk of **refractory hypotension**, it is generally considered second-line to **dobutamine** in acute sepsis management.
Question 126: A 23-year-old woman collapses at a gym. Bystanders report she was exercising on a treadmill when she suddenly fell and lost consciousness. She had no warning symptoms. She regained consciousness after 60 seconds but was confused for several minutes. She has no significant medical history but mentions her brother died suddenly aged 19 during sport. Her initial observations and blood tests are normal. Her ECG shows sinus rhythm, rate 68/min, with deep T wave inversion in leads V1-V4 and a slightly prolonged QTc of 475 ms. What is the most likely underlying diagnosis?
A. Long QT syndrome type 1
B. Hypertrophic cardiomyopathy (Correct Answer)
C. Brugada syndrome
D. Arrhythmogenic right ventricular cardiomyopathy
E. Catecholaminergic polymorphic ventricular tachycardia
Explanation: ***Hypertrophic cardiomyopathy***
- The patient's presentation of **exercise-induced syncope**, a **family history of sudden cardiac death** in a young relative, and characteristic **deep T-wave inversion in leads V1-V4** are classic features, particularly suggesting apical HCM.
- This condition is a leading cause of **sudden cardiac death (SCD)** in young athletes and can be diagnosed by ECG findings consistent with ventricular hypertrophy and **repolarization abnormalities**, even with a slightly prolonged QTc.
*Long QT syndrome type 1*
- While **LQTS type 1** is known to cause syncope during exercise, especially with adrenergic stress, the specific ECG finding of **deep T-wave inversions in V1-V4** is not characteristic of LQTS, which primarily involves a prolonged QT interval with specific T-wave morphology depending on the type.
- Although the QTc is slightly prolonged at 475 ms, it is less striking than the T-wave inversions, and the strong family history of SCD during sport, combined with the ECG morphology, points more towards a structural heart disease.
*Brugada syndrome*
- **Brugada syndrome** is characterized by distinctive **coved ST-segment elevation** in leads V1-V3 with an inverted T-wave, a pattern not described in this patient's ECG.
- Syncope or arrhythmias in Brugada syndrome typically occur at **rest or during sleep**, rather than during strenuous exercise like treadmill activity.
*Arrhythmogenic right ventricular cardiomyopathy*
- While ARVC can cause sudden cardiac death in young individuals and may show **T-wave inversions in V1-V3** (often associated with epsilon waves), the prominent deep T-wave inversions extending to V4, combined with exercise-induced syncope, are more indicative of **hypertrophic cardiomyopathy**, especially apical forms.
- ARVC primarily affects the **right ventricle**, leading to fibrofatty replacement, and often presents with ventricular tachycardias of LBBB morphology.
*Catecholaminergic polymorphic ventricular tachycardia*
- CPVT is a primary electrical disorder where the **resting ECG is typically normal**, meaning it would not show baseline findings like deep T-wave inversions or QTc prolongation.
- While it causes **exercise-induced syncope** due to polymorphic or bidirectional ventricular tachycardia, the diagnostic ECG features are absent at rest, making it a less likely explanation for the described baseline ECG.
Question 127: A 67-year-old woman is admitted to the Emergency Department with suspected community-acquired pneumonia and sepsis. She receives 2 litres of intravenous crystalloid and broad-spectrum antibiotics. Despite fluid resuscitation, her blood pressure remains 82/50 mmHg with a lactate of 4.5 mmol/L. The decision is made to start noradrenaline. Her current blood tests show: sodium 136 mmol/L, potassium 5.2 mmol/L, creatinine 165 μmol/L (baseline 88 μmol/L), glucose 12.4 mmol/L. In addition to noradrenaline, which other intervention has been shown to reduce mortality in patients with septic shock according to recent evidence?
A. Early initiation of renal replacement therapy
B. Administration of hydrocortisone 50 mg intravenously four times daily (Correct Answer)
C. Tight glycaemic control targeting glucose 4-6 mmol/L with insulin
D. Administration of sodium bicarbonate for acidosis
E. High-dose thiamine supplementation
Explanation: ***Administration of hydrocortisone 50 mg intravenously four times daily***
- Low-dose **corticosteroids** are indicated in **septic shock** that is unresponsive to fluid resuscitation and **vasopressors** (noradrenaline).
- Recent trials (e.g., APROCCHSS) suggest that hydrocortisone can accelerate **shock reversal** and may provide a **mortality benefit** in severe cases by improving vascular sensitivity to catecholamines.
*Early initiation of renal replacement therapy*
- Major trials, such as **STARRT-AKI**, have shown that early initiation of **RRT** does not improve survival compared to a standard, delayed approach based on urgent indications.
- It is generally reserved for patients with life-threatening complications of **AKI** rather than being used as a primary treatment for sepsis-induced acidosis or uremia.
*Tight glycaemic control targeting glucose 4-6 mmol/L with insulin*
- High-intensity insulin therapy (targeting 4-6 mmol/L) is associated with an increased risk of **severe hypoglycemia** and higher mortality rates (**NICE-SUGAR trial**).
- Current guidelines recommend a more moderate target range for **glucose control**, typically between **6-10 mmol/L** or <10 mmol/L.
*Administration of sodium bicarbonate for acidosis*
- The use of **sodium bicarbonate** for metabolic acidosis in sepsis has not demonstrated a general reduction in mortality or vasopressor requirements.
- It is usually only considered in cases of extreme **metabolic acidosis** where the pH levels fall below **7.2 or 7.15** to mitigate myocardial depression.
*High-dose thiamine supplementation*
- While thiamine is essential for aerobic metabolism, routine supplementation in all **septic shock** patients lacks robust evidence for reducing mortality.
- It is primarily indicated in patients with suspected **thiamine deficiency**, such as those with chronic alcohol use or severe malnutrition, rather than as a universal sepsis intervention.
Question 128: A 44-year-old man with no significant past medical history presents to the Emergency Department with 90 minutes of severe central chest pain. His ECG shows 4 mm ST-segment elevation in leads V2-V5. The nearest primary PCI centre is 90 minutes away by ambulance. He is haemodynamically stable. According to current guidelines, what is the most appropriate reperfusion strategy for this patient?
A. Immediate transfer for primary PCI regardless of time delay
B. Administer thrombolysis immediately and transfer after treatment (Correct Answer)
C. Administer thrombolysis only if chest pain persists after medical therapy
D. Observe with medical therapy as symptom onset >60 minutes ago
E. Arrange urgent coronary angiography within 24 hours without immediate reperfusion
Explanation: ***Administer thrombolysis immediately and transfer after treatment*** - If the predicted time from **STEMI diagnosis** to primary **PCI** exceeds **120 minutes**, immediate **fibrinolysis** (thrombolysis) is indicated unless contraindicated. - Given the 90-minute transport time plus additional door-to-balloon delays, the total time would exceed the therapeutic window, making a **pharmaco-invasive strategy** more appropriate.*Immediate transfer for primary PCI regardless of time delay* - Primary PCI is superior to fibrinolysis only if it can be performed within **120 minutes** of the time fibrinolysis could have been started. - A total delay exceeding the recommended window increases **myocardial necrosis** and mortality compared to prompt fibrinolysis.*Administer thrombolysis only if chest pain persists after medical therapy* - Fibrinolysis is a time-critical **reperfusion therapy**, not a rescue medication for failed medical therapy like nitrates or morphine. - Delaying fibrinolysis to wait for symptom resolution leads to worse clinical outcomes and increased **infarct size**.*Observe with medical therapy as symptom onset >60 minutes ago* - Reperfusion therapy is indicated for all patients with STEMI who present within **12 hours** of symptom onset; the window has not closed at 60 minutes. - Observing the patient without active reperfusion for an **anterior STEMI** carries a high risk of **heart failure** and cardiogenic shock.*Arrange urgent coronary angiography within 24 hours without immediate reperfusion* - Urgent angiography within 24 hours is appropriate for high-risk **NSTEMI**, but persistent ST-elevation requires **immediate reperfusion** to open the occluded artery. - Delaying intervention by 24 hours without first achieving reperfusion via fibrinolysis results in preventable **myocardial damage** and increased mortality.
Question 129: A 63-year-old man is admitted to the Emergency Department with suspected sepsis secondary to cellulitis of his right leg. Initial observations: temperature 38.3°C, heart rate 95/min, blood pressure 125/75 mmHg, respiratory rate 20/min. Blood tests show: white cells 14.2 × 10⁹/L, lactate 1.8 mmol/L, creatinine 98 μmol/L. He is given intravenous flucloxacillin and 1 litre of intravenous fluids. Six hours later, he becomes increasingly confused and agitated. Repeat observations: temperature 39.1°C, heart rate 122/min, blood pressure 88/55 mmHg, respiratory rate 28/min, oxygen saturations 94% on air. Repeat lactate is 4.2 mmol/L. His urine output over 6 hours is 80 ml. What SOFA score change and qSOFA score would this patient have?
A. SOFA score increase of 1 point, qSOFA score 2
B. SOFA score increase of 2 points, qSOFA score 3 (Correct Answer)
C. SOFA score increase of 3 points, qSOFA score 2
D. SOFA score increase of 4 points, qSOFA score 3
E. SOFA score increase of 2 points, qSOFA score 2
Explanation: ***SOFA score increase of 2 points, qSOFA score 3***
- The **qSOFA** score is 3, based on the presence of **altered mental status** (confusion/agitation), **respiratory rate ≥22/min** (28/min), and **systolic blood pressure ≤100 mmHg** (88 mmHg).
- The **SOFA score** increase is 2 points, reflecting new organ dysfunction from a baseline of 0: **cardiovascular dysfunction** (MAP 66 mmHg <70 mmHg = 1 point) and **renal dysfunction** (urine output 80 ml/6hr = 320 ml/24hr, which is <500 ml/day = 1 point).
*SOFA score increase of 1 point, qSOFA score 2*
- This option incorrectly calculates the **qSOFA** score, as the patient meets all three criteria (altered mental status, tachypnoea, and hypotension), not just two.
- An increase of only 1 point in the **SOFA score** would not meet the diagnostic criteria for sepsis-related organ dysfunction according to Sepsis-3 guidelines, which require an increase of ≥2 points.
*SOFA score increase of 3 points, qSOFA score 2*
- This option underestimates the **qSOFA** score; the patient clearly exhibits all three positive criteria: altered mentation, tachypnoea (RR 28), and hypotension (SBP 88).
- While a 3-point SOFA increase is possible, the provided clinical features for cardiovascular and renal dysfunction sum to a 2-point increase based on standard SOFA criteria.
*SOFA score increase of 4 points, qSOFA score 3*
- While the **qSOFA** score of 3 is correctly identified, a **SOFA score** increase of 4 points usually implies more severe multi-organ failure involving additional systems like coagulation or hepatic function, which are not indicated by the data.
- Based on the observed hypotension and oliguria alone, the SOFA increase is 2 points, meeting the threshold for sepsis diagnosis.
*SOFA score increase of 2 points, qSOFA score 2*
- This option correctly identifies the **SOFA score increase** but incorrectly calculates the **qSOFA** score.
- The patient's **qSOFA** is 3, as all three criteria (altered mental status, respiratory rate ≥22/min, and systolic blood pressure ≤100 mmHg) are clearly present.
Question 130: A 48-year-old woman is brought to the Emergency Department with altered consciousness. Her husband reports she developed throat tightness and difficulty breathing 20 minutes after taking ibuprofen for a headache. She has asthma usually well-controlled with salbutamol and beclomethasone inhalers. On examination: decreased consciousness (GCS 12), widespread wheeze, blood pressure 75/45 mmHg, heart rate 125/min, respiratory rate 32/min, oxygen saturations 88% on 15L oxygen via non-rebreathe mask. What should be the immediate priority in management?
A. Secure airway with endotracheal intubation before other interventions
B. Administer intramuscular adrenaline 0.5 mg immediately (Correct Answer)
C. Give intravenous hydrocortisone 200 mg first
D. Commence rapid fluid resuscitation with 2 litres crystalloid
E. Nebulize salbutamol 5 mg and reassess
Explanation: ***Administer intramuscular adrenaline 0.5 mg immediately***- This patient presents with life-threatening **anaphylaxis** characterized by rapid onset of **throat tightness**, **difficulty breathing**, widespread **wheeze**, **hypotension** (75/45 mmHg), and altered consciousness following **ibuprofen** ingestion. **Intramuscular (IM) adrenaline** is the critical first-line treatment for severe anaphylaxis.- **Adrenaline** acts rapidly via **alpha-1 receptors** to cause **vasoconstriction** (reversing hypotension) and **beta-2 receptors** to cause **bronchodilation**, reduce laryngeal edema, and stabilize mast cells, directly addressing all major systemic manifestations.*Secure airway with endotracheal intubation before other interventions*- While airway compromise is present (GCS 12, throat tightness), **IM adrenaline** often rapidly reduces **laryngeal edema** and **bronchospasm**, potentially improving the airway without immediate intubation or making it safer if still required.- Attempting immediate **endotracheal intubation** can be technically very challenging in a patient with severe airway swelling and can dangerously delay the administration of the life-saving adrenaline.*Give intravenous hydrocortisone 200 mg first*- **Corticosteroids** like hydrocortisone have a **slow onset of action** (several hours) and are primarily used to prevent **protracted** or **biphasic reactions** rather than treating acute anaphylactic symptoms.- Their administration should **never delay** the immediate and essential use of **adrenaline** in a patient with acute circulatory or respiratory compromise.*Commence rapid fluid resuscitation with 2 litres crystalloid*- Fluid resuscitation is an important adjunctive treatment for managing the **hypotension** (distributive shock) seen in anaphylaxis, but it does not address the concurrent **bronchospasm** or **laryngeal edema**.- **IM adrenaline** must be given first or at least concurrently, as it directly reverses the underlying pathophysiology of vasodilation and bronchoconstriction.*Nebulize salbutamol 5 mg and reassess*- **Salbutamol** (a beta-2 agonist) primarily treats **bronchospasm** and will not address the critical **hypotension**, **laryngeal edema**, or systemic mast cell activation characteristic of severe anaphylaxis.- Relying solely on nebulized salbutamol and reassessment would dangerously delay the administration of **adrenaline**, which is the only medication that comprehensively treats all life-threatening aspects of anaphylaxis.
