Professional and Linguistic Assessments Board Exam

The best answer to the question is 'Hypoxaemia due to COPD' because the clinical presentation and history of the patient strongly suggest this as the underlying cause of cyanosis. Cyanosis is a bluish discolouration of the skin and mucous membranes due to an increased concentration of deoxygenated haemoglobin in the blood. In this case, the patient has a history of chronic obstructive pulmonary disease (COPD), which is a well-known cause of hypoxaemia. COPD leads to airflow limitation and impaired gas exchange, resulting in reduced oxygen levels in the blood. The patient's low oxygen saturation of 88% on room air is indicative of hypoxaemia. Additionally, the chest X-ray showing hyperinflation of the lungs is consistent with COPD, further supporting the diagnosis. The patient's symptoms of shortness of breath, tachycardia, and increased respiratory rate are also typical of hypoxaemia. Therefore, hypoxaemia due to COPD is the most likely cause of the cyanosis observed in this patient.

The other options are less likely to be the cause of the patient's cyanosis for several reasons. 'Methaemoglobinaemia' is a condition where there is an abnormal amount of methaemoglobin in the blood, which can cause cyanosis. However, it is not typically associated with COPD and would require a specific exposure or genetic predisposition, which is not mentioned in the patient's history. 'Peripheral vasoconstriction' can cause cyanosis by reducing blood flow to the extremities, but it would not explain the low oxygen saturation or the respiratory symptoms. 'Carbon monoxide poisoning' leads to a cherry-red discolouration rather than a bluish one and is associated with normal oxygen saturation readings due to the binding of carbon monoxide to haemoglobin, which is not consistent with the patient's presentation. 'Anaemia' can cause pallor and fatigue but does not typically cause cyanosis unless it is severe, and even then, it would not explain the low oxygen saturation seen in this patient. Therefore, these options do not align with the clinical findings and history as well as hypoxaemia due to COPD does.

Administering high-flow oxygen is the most appropriate initial management step for this patient because he presents with acute hypoxaemia, as indicated by his oxygen saturation of 88% on room air. In emergency medicine, ensuring adequate oxygenation is a priority, especially in cases of sudden onset breathlessness where hypoxia is evident. High-flow oxygen therapy can rapidly increase the oxygen saturation levels, thereby alleviating symptoms of breathlessness and preventing further complications such as hypoxic damage to vital organs. The patient's history of smoking and hypertension, along with the acute presentation, suggests a possible pulmonary embolism or acute exacerbation of chronic obstructive pulmonary disease (COPD), both of which can cause significant hypoxaemia. Immediate oxygen therapy is crucial in stabilising the patient while further diagnostic evaluations are conducted to determine the underlying cause of his symptoms. High-flow oxygen is a non-invasive, readily available intervention that can be administered quickly in the emergency setting, making it the best initial step in managing this patient's acute respiratory distress.

Performing an immediate chest CT scan, while useful for diagnosing conditions like pulmonary embolism, is not the best initial management step because it does not address the patient's immediate hypoxaemia. Starting antibiotics is inappropriate as there is no evidence of infection, such as fever or productive cough, in the patient's presentation. Administering a bronchodilator may be considered if there is a suspicion of an acute asthma attack or COPD exacerbation, but the primary concern here is the low oxygen saturation, which needs to be corrected first. Prescribing diuretics would be more appropriate if there were signs of fluid overload or heart failure, such as peripheral oedema or elevated jugular venous pressure, which are not present in this case. Therefore, while these options may be relevant in specific contexts or as part of a broader management plan, they do not address the immediate need to correct the patient's hypoxaemia.

In the context of a high-speed road traffic accident, the mechanism of injury and clinical findings suggest a significant risk of cervical spine injury. The patient presents with mild tenderness in the cervical spine, which raises the suspicion of potential cervical spine trauma. A CT scan of the cervical spine is the most appropriate imaging study in this scenario because it provides a detailed and rapid assessment of bony structures, allowing for the identification of fractures or dislocations that might not be visible on plain X-rays. CT scans are highly sensitive and specific for detecting cervical spine injuries, making them the preferred choice in trauma settings where a cervical spine injury is suspected. Given the patient's presentation and the need for a thorough evaluation to rule out any serious injury, a CT scan of the cervical spine is the best option to ensure accurate diagnosis and appropriate management.

An X-ray of the chest, while useful for assessing rib fractures or pneumothorax, does not provide adequate information about the cervical spine, which is the area of concern given the patient's symptoms and mechanism of injury. An MRI of the brain, although useful for evaluating brain injuries, is not indicated here as the patient is alert and oriented with a Glasgow Coma Scale score of 15, suggesting no immediate intracranial concerns. An ultrasound of the abdomen is not necessary in this case as the FAST scan was negative for free fluid, indicating no significant intra-abdominal injury. An ECG is not relevant to the primary concern of cervical spine injury and is more appropriate for assessing cardiac issues, which are not indicated by the patient's presentation. Therefore, these options do not address the specific clinical question of potential cervical spine injury following a high-speed accident.

Huntington's disease is the most likely diagnosis for this patient due to several key features presented in the clinical scenario. The patient exhibits involuntary, jerky, and irregular movements affecting the face and upper limbs, which are characteristic of chorea, a hallmark of Huntington's disease. The progression of symptoms over six months, along with the exacerbation of movements with stress and fatigue, aligns with the typical presentation of this neurodegenerative disorder. Additionally, the presence of a family history of a similar condition, with the patient's father being diagnosed with a neurological disorder in his late 50s, strongly suggests a hereditary component. Huntington's disease is an autosomal dominant disorder, meaning that it often presents in multiple generations within a family. The age of onset in the late 50s is also consistent with Huntington's disease, which typically manifests in mid-adulthood. The absence of cognitive decline at this stage does not rule out Huntington's disease, as cognitive symptoms can develop later in the disease course. Furthermore, the lack of significant muscle weakness or sensory loss helps differentiate Huntington's disease from other neurological disorders that might present with similar symptoms.

Parkinson's disease is characterised by tremors, rigidity, bradykinesia, and postural instability, which differ from the jerky, irregular movements seen in this patient. The absence of these cardinal symptoms and the presence of a family history of a similar condition make Parkinson's disease less likely. Essential tremor typically presents with rhythmic tremors, often affecting the hands and head, and does not usually involve the irregular, non-rhythmic movements described in this case. Additionally, essential tremor is not typically associated with a family history of neurological disorders presenting in the late 50s. Multiple sclerosis can present with a wide range of neurological symptoms, but the lack of sensory loss, muscle weakness, and other neurological deficits makes it an unlikely diagnosis. Moreover, multiple sclerosis does not typically present with a strong family history of similar conditions. Myasthenia gravis is characterised by muscle weakness that worsens with activity and improves with rest, which is not consistent with the involuntary movements described. The absence of muscle weakness and the presence of a family history further rule out myasthenia gravis as a likely diagnosis.

The best answer for the clinical presentation described is lumbar disc herniation. This condition is characterised by the displacement of disc material beyond the intervertebral disc space, which can compress adjacent nerve roots. The patient's symptoms, including lower back pain radiating down the left leg, numbness in the left foot, and difficulty lifting the foot, are indicative of radiculopathy, commonly associated with lumbar disc herniation. The reduced power in dorsiflexion of the left foot and decreased sensation in the left L5 dermatome suggest involvement of the L5 nerve root, which is frequently affected in lumbar disc herniation. Additionally, the positive straight leg raise test is a classic sign of nerve root irritation due to disc herniation. The absence of systemic symptoms such as fever or weight loss further supports this diagnosis, as these would be more suggestive of an infectious or neoplastic process.

Lumbar spinal stenosis typically presents with bilateral leg pain, numbness, and weakness, often exacerbated by walking and relieved by sitting, known as neurogenic claudication. The unilateral nature of the symptoms and the acute onset in this patient make lumbar spinal stenosis less likely. Spondylolisthesis involves the anterior displacement of a vertebra and can cause back pain and radiculopathy, but it is more common in younger individuals or those with a history of trauma or repetitive stress, which this patient does not report. Facet joint arthritis usually causes localised back pain without significant radicular symptoms, and the absence of significant trauma or degenerative changes in the history makes this diagnosis less probable. Ankylosing spondylitis is a chronic inflammatory condition that presents with back pain and stiffness, particularly in the morning, and is associated with systemic symptoms and a younger age of onset. The patient's age and the acute radicular symptoms do not align with ankylosing spondylitis.