Formative Qs Flashcards
An 82 year old woman has had decline in her memory, concentration and physical function. This has happened in an episodic fashion. She had sudden onset of difficulty planning and organising her affairs 3 months ago. She is an ex-smoker and has hypertension and peripheral vascular disease.
She has a broad based gait and increased tone in her right leg and arm with hyper-reflexia. Her Montreal Cognitive Assessment Score is 22/30.
Investigations:
MR scan brain: multiple white matter hyperintensities in both hemispheres
What is the most likely diagnosis?
Vascular dementia
A 30 year old man has three months of generalised fatigue and a number of syncopal episodes.
He has areas of hyperpigmentation on his face, neck and back of his hands. His BP is 122/80 mmHg lying and 92/60 mmHg on standing.
Investigations
Sodium 130 mmol/L (135-145)
Potassium 5.7 mmol/L (3.5-5.0)
Urea 6.4 mmol/L (3.0-7.0)
Creatinine 77 µmol/L (60-110)
Deficiency of which hormone is most likely to explain the hyperkalaemia?
Aldosterone
This patient has clinical features of Addison’s disease (fatigue, hyperpigmentation, postural hypotension
with syncope, hyponatraemia with hyperkalamia). The resultant hypoaldosteronism with Addison’s is associated with
hyperkalaemia due to fact that a major function of aldosterone is to increase urinary potassium excretion.
A 30 year old woman has three months of generalised headache which tend to be worse in the morning and occasional episodes of transient visual loss especially when she bends forwards.
Her blood pressure is 130/90 mmHg. Her BMI is 32. Her fundoscopy shows bilateral papilloedema.
Investigations
CT scan head: normal
What is the most likely diagnosis?
Benign intracranial hypertension/ Raised intracranial pressure
The clinical presentation is typical of idiopathic intracranial hypertension. A disease that is most common in
women of child-bearing age and is associated with obesity. The presence of pappilloedema points to raised intracranial
pressure. The diagnosis would be conrmed by measuring CSF pressure by a lumbar puncture.
A 50 year old man has six months of tingling and burning sensation in his feet. He has a 30 year history of type 1 diabetes mellitus. He has diabetic retinopathy.
He has reduced sensation to light touch and pinprick to just above the ankles in both legs with reduced joint position sense at the big toes.
He has a small ulcer under the left first metatarsal.
What is the most likely diagnosis?
Diabetic neuropathy
Brisk reexes are one of the key signs of upper motor neuron lesions. They may take a few days to begin to
become brisk however – in parallel with the increase in tone.
Answer: C. Neuromuscular junction weakness classically is fatiguable, due to depletion in the available
acetylcholine neurotransmitters with repeated muscle usage; this can be demonstrated in the clinical examination, with
weakness emerging on repeated muscle exertion (e.g. sustained upgaze for 1 minute, or pumping the arm up and down
10x).
Spasticity is a sign of upper motor neuron pathology. Sensory loss implies involvement of sensory pathways, and the
neuromuscular junction is unrelated to sensory information. Fasciculations are a sign of lower motor neuron pathology
(reecting denervation of muscles). Decreased deep tendon reexes are seen in lower motor neuron pathology – in
neuromuscular junction disorders the reexes are usually normal.
His GCS score is 11/15 E3 V4 M4 The GCS is scored out of 15. The lowest score possible is 3. A
coma is dened as a GCS of 8 or below.
The described scenario – lightheadedness and nausea followed by a transient loss of consciousness, pallor,
sweating, spontaneous recovery within a few minutes, and post-event fatigue – is classic for a vasovagal response. The
event’s context (long-haul ight, prolonged seating, and prior similar episode while standing for an extended period in a
queue) further supports this diagnosis.
This patient is suffering from a Bell’s palsy which involves the facial nerve (cranial nerve VII). This involves
weakness on one side of the face. The forehead is bilaterally innervated and so if the lesion is centrally (ie stroke) then
there would be weakness of one side of the face but with forehead sparing.
If the lesion was lower, for instance in
the thoracic cord, we wouldn’t expect to see the sensory and motor changes in the hands.
This patient has presented with classic cerebellar signs (ataxia, broad-based gait, nystagmus and poor
coordination).
The patient’s symptoms of severe, recurrent headaches around the right eye, lasting for approximately 45
minutes and associated with watering of the right eye, suggest the most likely diagnosis is cluster headaches.
Cluster headaches are a type of primary headache disorder characterized by recurrent, severe, unilateral headaches
typically located around or behind one eye. The pain is often described as sharp, burning, or piercing, and is often
accompanied by symptoms such as watering of the eye, nasal congestion or runny nose, and eyelid drooping on the
affected side. The headaches often wake the person from sleep and typically occur in clusters or cycles, with several
headaches per day or per week for weeks to months, followed by remission periods.
The headache pattern described, with severe unilateral eye pain, with no neurological symptoms between episodes, is
consistent with the typical presentation of cluster headaches. Additionally, the timing of the headache attacks, being
more common in the night time and waking the patient from sleep, is also consistent with cluster headaches.
Imaging studies such as CT or MRI are not usually necessary for diagnosis, however, if the diagnosis is uncertain an MRI
can be used to rule out structural lesions or other causes of the symptoms.
The frontal lobe is responsible for control of behaviour and personality, judgement, and executive
functioning. Sensory perception is processed in the parietal lobes. Spatial orientation is mediated by the parietal and
occipital lobes. Visual processing is mediated by the occipital lobs. Body temperature is mediated by the hypothalamus.
Acromegaly is caused by excess growth hormone (GH), often due to a pituitary adenoma. Characteristic
features include enlarged hands and feet, facial changes, and soft tissue overgrowth. Carpal tunnel syndrome is
commonly associated with acromegaly due to increased soft tissue and bone growth leading to nerve compression.