500 SBAs in Clinical Medicine Flashcards
A 66-year-old woman complains of stiffness and weakness climbing stairs. She has a history of hypertension and diet-controlled type 2 diabetes. On examination, there is mild upper arm weakness, hip flexion is 4−/5 bilaterally, with bilateral wasting and flickers of fasciculations in the right quadriceps. Knee extension is 4/5.
Dorsiflexion and plantar flexion are strong. Brisk knee and ankle reflexes are
elicited, as well as a positive Hoffman’s and Babinski’s sign. Sensory examination and cranial nerves are normal. Her BM is 8.9, her pulse is regular and her blood pressure is 178/97. What is the most likely diagnosis?
A. Myasthenia gravis
B. Diabetic neuropathy
C. Myositis
D. Motor neurone disease
E. Multiple sclerosis (MS)
D
- Woman presents with upper (brisk reflexes, upgoing plantar) and lower (fasciculations) motor neurone signs
- Motor neurone disease presents with mixed upper and lower motor neurone signs and importantly no sensory involvement
- In this case there is involvement of two regions (arms and legs)
- Bulbar signs such as tongue wasting and fasciculation often help make the diagnosis
- Myositis affects the muscle resulting in:
- tenderness
- wasting
- fasciculation
- But no upper motor neurone signs
- Although patient is diabetic - neuropathies only result in lower motor neurone signs
- There may be motor and/or sensory.
- Typically, diabetes results in peripheral neuropathy - most commonly sensory
- Proximal distribution of weakness would be in keeping with myasthenia but not the UMN signs
- No mention of fatigability, which is a key feature
- MS in this age group is less common and an inflammatory disorder of the CNS would not result in LMN signs
A 23-year-old man is stabbed in the neck. Once stabilized, his MRI shows a right
hemisection of the cord at C6. What is the expected result of this injury?
A. Paralysed diaphragm
B. Absent sensation to temperature in the left hand
C. Paralysis of the left hand
D. Absent sensation to light touch in the left hand
E. Brisk right biceps reflex
B
- Hemisection of the cord ⇒ Brown-Sequard syndrome
- Results in ipsilatral paralysis and loss of light touch and vibration sensation and contralateral loss in pain and temperature below the point of the lesion
- Spinothalamic tracts cross at the level of the cord so sensation to pain and temperature would be lost in the contralateral limbs
- C3, C4 and C5 keep the diaphgram alive, so breathing should be preserved.
- Right corticospinal tract has been severed ⇒ right, ipsilateral hand would be paralysed as well as the right leg
- Left dorsal columns carry light touch fibers from the left limb
- They have been unaffected by the injury
- C6 is responsible for the biceps reflex and would be lost
- Reflexes distal to the lesion would be brisk
A 23-year-old woman complains that her right leg has become progressively stiff and clumsy over the last couple of weeks. She is worried as she has not been able to go to work for the last 4 days. On examination, tone is increased and there is a catch at the knee. She has six beats of clonus and an upgoing plantar. Power is reduced to 3-4/5 in the right leg flexors. There is no sensory involvement and the rest of the neurological exam is normal other than a pale disc on opthalmoscopy. On further questioning, she admits that she has had two episodes of blurred vision in her right eye in the last two years. Each lasted a couple of weeks from which she fully recovered. What is the most appropriate initial treatment?
A. A non-steroidal anti-inflammatory drug (NSAID)
B. Interferon-beta
C. Bed rest
D. Methotrexate
E. A course of oral steroids
E
- Subacute onset of upper motor neurone signs on a background of episodes of optic neuritis in a young woman makes relapsing-remitting MS the most likely diagnosis
- The diagnosis of MS hinges on the presence of multiple CNS lesions separated by time and space
- These manifest in either signs/symptoms or as enhancing white matter lesions on gadolinium-enhanced MRI
- There is no specific role for NSAIDs in MS
- Even if patient complained of pain it would be important to ensure its origin
- NSAIDs would not be appropriate for neuropathic pain
- Patient ⇒ eligible for disease-modifying drugs such as interferon beta or glatiramer acetate as she has a relapsing-remitting course and recent symptoms ==> this would not be the immediate treatment
- These drugs reduce the number of relapses experienced by one third over two years and are expensive
- Long term effects on morbidity remain unclear
- Bed rest alone is inappropriate as this patient would benefit from a course of steroids as she has disabling symptoms
- Oral steroids have been shown to be as effective as IV steroids although patients tend to admitted for IV treatment
- They reduce the length of relapse so the patient would recover quicker, but have no effect on number of relapses or accumulation of disability
- There is no evidence for methotrexate in relapsing-remitting MS
A 78 year old right-handed male collapses and is brought into accident and
emergency. He seems to follow clear one-step commands but he gets very frustrated as he cannot answer questions. He is unable to lift his right hand or leg. He has an irregularly irregular pulse and his blood pressure is 149/87. He takes only aspirin and frusemide. What is the most likely diagnosis?
A. Left cortical infarct
B. Right internal capsule infarct
C. Left cortical haemorrhage
D. Left internal capsule haemorrhage
E. Brainstem haemorrhage
A
- Most likely suffered a left cortical infarct ⇒ probably as a result of an embolus secondary to atrial fibrillation
- Treatment with warfarin wouldhave reduced his annual risk of stroke from roughly 5 to 1 percent.
- A left sided infarct because of the contralateral (right) hemiparesis and dysphasia (involvement of the dominant cortex
- It is not a capsular or brainstem event as the patient has an expressive dysphasia which implies involvement of Broca’s area which is cortical
- It is more likely to be ischaemic than haemorrhagic
- Roughly 80% of strokes are infarcts, 20% are haemorrhagic and in this case there is a plausible embolic explanation coupled with only mild hypertension
- Haemorrhagic strokes tend to occur in younger patients with severe hypertension and a family history (pointing to an anatomical anomaly)
- However, the differentiation requires a CT scan
A 19-year-old woman collapses at a concert and is witnessed to have a tonic-clonic seizure lasting 2 minutes. When the paramedics arrive and ask her questions, she mumbles but no-one can understand what she is saying. Only when the paramedic applies pressure to her nailbed does she open her eyes and reach out with her other hand to rub her nail and then push him away. What is her Glasgow Coma Scale (GCS)?
A. 12
B. 11
C. 10
D. 9
E. 8
D
The GCS is frequently used to assess level of consciousness. The lowest
score is 3, the highest 15. A score of 8 or below is classified as coma. GCS
is assessed by evaluating eye (1–4), verbal (1–5) and motor (1–6) response.
Clinically, it is best to assess for the highest possible score and work down.
So, if a patient is not opening their eyes spontaneously, assess whether
they respond to verbal command and only then to pain. In this case, E = 2
(responds to pain), V = 2 (incomprehensible sounds), M = 5 (localizes to
pain), giving this patient a GCS of 9/15. It is important to carefully monitor
her GCS, like most measurements a trend is more useful than a one-off
assessment.
A 79-year-old man is admitted with left hemiparesis. CT reveals a middle cerebral artery infarct. What is his most significant risk factor for stroke?
A. Hypertension
B. Smoking
C. Family history
D. Diabetes
E. Cholesterol
A
The three most important risk factors for stroke are hypertension, hypertension and hypertension (A)! INTERSTROKE, a recent large case–control study evaluating risk factors for stroke, has shown that ten risk factors are associated with 90 per cent of the risk of stroke and that of these modifiable risk factors, hypertension is the most important for all stroke subtypes and is a particularly dangerous risk factor for intracerebral haemorrhage.
Other risk factors include smoking (B), lipids (E) and diabetes (D) which promote atherosclerosis. Poor diet, lack of regular activity and increased waist–hip ratio are as significant risk factors as smoking.
Unmodifiable risk factors include increasing age (by far the most significant), male sex, family history (C) and ethnicity (higher in Blacks and Asians). Patients in atrial fibrillation have an annual stroke risk of 5 per cent. This can be lowered to 1 per cent by anticoagulating with warfarin, aiming for an international normalized ratio (INR) of
between 2 and 3 (avoid confusion with aspirin which is an antiplatelet).
Stroke is the third most common cause of death in England (after heart
disease and cancer) and is more often disabling than fatal, so primary and
secondary prevention are crucial.
A 42-year-old woman presents with ataxia. Gadolinium-enhanced MRI reveals
multiple subcortical white matter lesions as well as enhancing lesions in the
cerrebellum and spinal cord. She is diagnosed with MS. Two months later she
develops optic neuritis. What feature is associated with a milder disease course?
A. Her age of 42
B. Her initial presentation of ataxia
C. Her female gender
D. The interval between the two episodes of two months
E. Her MRI scan appearance
C
In this woman’s case, all of the features except her gender (C) point to a
more aggressive disease course. Although it is close to impossible to
predict an individual patient’s outcome, features of a better prognosis
include onset under 25 years (A), optic neuritis or sensory, rather than
cerebellar symptoms on initial presentation (B), a long interval (>1 year)
between relapses (D) and few lesions on MRI (E). Full recovery from
relapses is also a positive feature. Progressive MS carries a poorer prognosis
compared to relapsing–remitting MS.
A 71-year-old man with atrial fibrillation is seen in clinic following an episode of
syncope. He describes getting a poor night’s sleep and, as he got out of bed in the morning, feeling dizzy for a couple of seconds before the lights dimmed around him. He was woken a couple of seconds later by his wife who had witnessed the event. She says he went pale and fell to the floor and his arms and legs jerked. After waking, he was shaken but was ‘back to normal’ a few minutes after the event. His medication includes aspirin, atenolol and frusemide. What is the most likely diagnosis?
A. Vasovagal syncope
B. Orthostatic hypotension
C. Cardiogenic syncope
D. Transient ischaemic attack (TIA)
E. Seizure
B
This man most likely experienced an episode of orthostatic or postural
hypotension (B) where syncope occurs as a result of reduced cerebral
perfusion as the patient moves from lying to standing. Symptoms are
similar to vasovagal in that the patient may become pale and describe ‘the
lights or sound dimming’. Perfusion is restored after the patient collapses
and unconsciousness lasts no more than seconds or a couple of minutes
with full recovery. However, vasovagal epsiodes (A) can be brought on by
sleep or food deprivation, hot or emotional environments, Valsalva
manoeuvre (such as straining) and are not as closely related to position.
Syncope while lying down is more suggestive of cardiac syncope or seizure
activity. It is important to rule out cardiac causes of syncope (C) which
may be heralded by chest pain or palpitations. Arrhythmias or aortic
stenosis may be the underlying cause. TIAs (D) are a very rare cause of
syncope. Seizures (E) may be triggered by lack of sleep. They may be
heralded by an aura, typically visual or olfactory. There may be urinary
incontinence, tonic-clonic movements, tongue-biting and cyanosis during the event. However, jerky movements may occur in syncope of any cause.
This alone does not equate to a seizure.
A 41-year-old man complains of terrible headache. It started an hour ago, without warning, while stressed at work. It affects the right side of his head. He scores it ‘11/10’ in severity. When asked, he agrees that light does bother him a little. He had a similar episode six months ago, experiencing very similar headaches over 2 weeks which resolved spontaneously. On observation, he looks quite distressed and prefers to pace up and down, unable to sit still. What is the diagnosis?
A. Subarachnoid haemorrhage
B. Tension headache
C. Intracerebral haemorrhage
D. Migraine
E. Cluster headache
E
Cluster headache (E) is more common in men and is classically excruciating,
unilateral headache associated with autonomic features such as miosis,
ptosis, conjunctival injection, tearing, sensation of nasal congestion and
facial flushing.
Timing is important, headaches occur in clusters of multiple
episodes over a couple of weeks, then resolve spontaneously only to
reoccur months to years later.
They are not associated with aura or signs of raised intracranial pressure.
Although the headache is severe and of acute onset in this instance, with possible photophobia, there is nothing in the stem to suggest raised intracranial pressure, such as papilloedema, nausea and vomiting or meningism, such as nuchal rigidity (A).
More importantly, he has had similar episodes in the past. The timing and mautonomic symptoms point to cluster headache.
Tension headache (B) is classically associated with stress, reported as a tight band around the head and is much more benign.
Intracranial haemorrhage (C), depending on location, is likely to cause focal signs or, especially if posterior fossa, signs of raised intracranial pressure and coning. Hypertension is an important risk factor.
Migraine (D) classically is heralded by an aura and is associated with nausea and vomiting with osmo- (smell), phono- (sound) and photophobia. Patients prefer to curl up in a dark, quiet room, whereas patients with cluster headache feel the need to move around.
A 49-year-old man complains of sudden onset, painless unilateral visual loss
lasting about a minute. He describes ‘a black curtain coming down’. His blood
pressure is 158/90, heart rate 73 bpm. There is an audible bruit on auscultation of his neck. His past medical history is insignificant other than deep vein thrombosis of his right leg ten years ago. The most likely diagnosis is:
A. Retinal vein thrombosis
B. Retinal artery occlusion
C. Amaurosis fugax
D. Optic neuritis
E. Acute angle glaucoma
C
This man gives a classical description of amaurosis fugax (C), painless,
unilateral visual loss of short duration described as ‘a black curtain
descending’, caused by retinal artery emboli, with a likely cardiac source
as a consequence of atrial fibrillation.
Retinal artery (B) and vein (A) occlusion are also painless and of sudden
onset, but they typically occur in older patients and result in prolonged
visual loss. Amaurosis fugax may herald retinal artery occlusion which is
confirmed on ophthalmoscopy showing oedema and a cherry red macula. It
is also a complication of giant cell (temporal) arteritis.
Retinal haemorrhages and cotton wool spots are typically seen in retinal vein occlusion. Optic neuritis (D) is associated with MS and patients complain of painful, blurred
vision.
Acute angle glaucoma (E), again seen in older patients, presents with
painful, blurred vision. Patients describe ‘seeing haloes around things’.
A 77-year-old woman is admitted to hospital with a urinary tract infection. She
receives antibiotics and seems to be responding well. On the fourth day she is eating her lunch when she suddenly drops her fork. She calls for the nurse who notices the left side of her face is drooping. What is the best next course of action?
A. CT head
B. Thrombolysis
C. MRI head
D. Aspirin
E. Place nil by mouth
E
This patient has suffered a stroke. This is a medical emergency. As she is
within the 3-hour window for thrombolysis (B), she must be assessed immediately. However, thrombolysis is only useful in ischaemic stroke and can severely worsen haemorrhagic stroke.
It is impossible to clinically tell the difference with certainty; she therefore warrants urgent imaging.
Haemorrhages are much easier to detect on CT (A) as blood shows up white (hyperdense), plus there is easier access to CT unlike MRI (C) which is not always available. If thrombolysis is contraindicated, 300 mg of aspirin (D) is given in the case of ischaemic stroke.
Option (E), however, is the most appropriate next step as removing her lunch is a quick, simple intervention that may prevent the complication of aspiration pneumonia.
The nurse can then call the doctors or put out a thrombolysis call.
A 71-year-old right-handed male is brought in by ambulance at 17:50 having
suffered a collapse. His wife came home to find him on the floor unable to move his right arm or leg and unable to speak. Her call to the ambulance was logged at 17:30. He has a past medical history of well-controlled hypertension, ischaemic heart disease and atrial fibrillation for which he is on warfarin. He had a hernia repair three months ago and his brother had a ‘bleed in the brain’ at the age of 67. What is the absolute contraindication to thrombolysis in this male?
A. Family history of haemorrhagic stroke
B. History of recent surgery
C. Time of onset
D. Current haemorrhagic stroke
E. Warfarin treatment
C
This man presents with a stroke. It is clinically impossible to tell with
certainty whether it is ischaemic or haemorrhagic (D) which is why he needs
a CT to differentiate between the two.
However, the time of onset is unclear and therefore it is not possible to determine whether he is outside the 3-hour time window for thrombolysis (C).
Neither warfarin treatment (E) nor family history of haemorrhagic stroke (A) are absolute contraindications although they would be taken into consideration. INR should be <1.7.
The absolute contraindications for thrombolysis are: onset of symptoms more than 3
hours ago, seizures at presentation, uncontrolled blood pressure (over
180/110), previous intracranial bleed, lumbar puncture in the last week,
ischaemic stroke or head injury in the last three months, active bleeding (not
menstruation), surgery (B) or major trauma (including CPR) within the last
2 weeks or non-compressible arterial puncture within the last week.
A 69-year-old man presents to clinic with a six-month history of progressive lower back pain which radiates down to his buttock. He found the pain was exacerbated while taking his daily morning walk and noticed that it eased going uphill but worsened downhill. He stopped his daily walks as a result and he now walks only slowly to the shops when he needs to, taking breaks to sit down and ease the pain. He has a history of hypertension, diabetes and prostatic hyperplasia. What is the diagnosis?
A. Peripheral vascular disease
B. Osteoporotic fracture
C. Spinal stenosis
D. Sciatica
E. Metastatic bone disease
C
- Good history of spinal claudication evidenced in this patient history ==> lower back pain and sciatica on walking
- Pain worsens when the spine is extended (walking, especially downhill and improves when flexed going uphill or sitting)
- Caused by narrowing of the spinal canal as a result of spondylosis (degenerative disease)
- Intermittent claudication from peripheral vascular disease can be similar in timing, worse on walking and relieved by rest but the pain comes from ischaemic muscles, typically calf or buttock and has no relation to the incline
- There is nothing to suggest osteoporotic fracture and in addition his sex iss protective for osteoperosis
- Sciatica presents as sharp pain shooting down the posterior leg and occur as a result of impingement of the nerve root forming the sciatic nerve
- It is a symptom rather than a diagnosis
- Metastatic bone disease could result in spinal stenosis or sciatica but in itself does not explain the patient’s exact symptoms and there is nothing to suggest malignancy in the stem such as constitutional symptoms or a nodular prostate
A 31-year-old woman presents to accident and emergency with progressive
difficulty walking associated with lower back pain. A few days ago she was tripping over things, now she has difficulty climbing stairs. She describes tingling and numbness in both hands which moved up to her elbows, she is unable to write. On examination, cranial nerves are intact but there is absent sensation to vibration and pin prick in her upper limbs to the elbow and lower limbs to the hip. Power is 3/5 in the ankles and 4−/5 at the hip with absent reflexes and mute plantars. Her blood pressure is 124/85, pulse 68 and sats 98 per cent on air. She has a past medical history of type I diabetes and recently recovered from an episode of food poisoning a month or two ago. What is the diagnosis?
A. MS
B. Guillain–Barré syndrome (GBS)
C. Myasthenia gravis
D. Diabetic neuropathy
E. Infective neuropathy
B
This woman presents with an ascending polyneuropathy. Her symptoms start distally and progress proximally, giving a glove and stocking distribution. Both sensory and motor neurones are involved. This is consistent with Guillain–Barré (B), an inflammatory disorder of the peripheral nerves often preceded by an infection such as campylobacter gastreoenteritis.
Multiple sclerosis (A) is an inflammatory disorder of the central nervous system resulting in upper motor neurone signs – this patient’s reflexes are absent.
Myasthenia gravis (C) is a disorder of the neuromuscular junction and although it results in lower motor neurone signs, there is no sensory involvement and the weakness is greater in proximal muscles and commonly involves the cranial nerves resulting in droopy eyelids, difficulty speaking and swallowing.
A key feature isfatigability as the stores of acetylcholine are used up. Although this
woman is diabetic and has a polyneuropathy, her symptoms progress too
quickly.
Diabetic neuropathy (D) takes time to develop and, although there are different types, most commonly results in a distal sensory neuropathy of the feet.
Vibration and pain are most affected which is why they may have a stomping gait and develop ulcers. Infective neuropathies (E) include Lyme disease from ticks and leprosy which is uncommon in developed countries and she has no history of travel.
A left-handed 79-year-old man presents with a troublesome resting tremor of his left hand. The tremor is evident in his writing. He has also noticed his writing is smaller than it used to be. He complains he has difficulty turning in bed to get comfortable and his wife complains that he sometimes kicks her in the middle of the night. When he gets out of bed in the morning he feels a little woozy, but this resolves after a while. On examination, he blinks about three times a minute and his face does not show much emotion. Glabelar tap is positive. He has a slow, shuffling gait. He has difficulty stopping, starting and turning. He holds his feet slightly apart to steady himself. When you pull him backwards, he is unable to right himself and stumbles back. Which of the signs and symptoms is not commonly associated with parkinsonism?
A. Postural instability
B. Rapid eye movement (REM) sleep disturbance
C. Hypomimia
D. Broad-based gait
E. Autonomic instability
D
This man presents with many symptoms of parkinsonism. However, the parkinsonian gait is typically narrow-based, not broad (D).
Parkinson’s is a disease of dopaminergic neurone loss in the nigrostriatal pathways and
results in the triad of bradykinesia, rigidity and tremor. A fourth sign to look out for is postural instability (A).
This can be elicited by asking the patient to steady himself and pulling him backwards. During REM sleep (B), the brain is active but muscles are paralysed (thus associated with dreaming).
In Parkinson’s disease (PD), muscles may be active allowing patients to act out their dreams, resulting in kicking, yelling, etc. Hypomimia (C) is the technical term for mask-like facies or reduced facial expression.
Symptoms of autonomic dysfunction (E) are common and include constipation, postural hypotension and sexual dysfunction. Very prominent autonomic symptoms may suggest Shy–Drager’s, a type of multiple system atrophy (which in turn is one of the Parkinson’s plus syndroms.)
A 33-year-old woman attends her six-month follow-up appointment for headache. They are migrainous in nature but whereas she used to have them every few months, over the last three months she has experienced a chronic daily headache which varies in location and can be anywhere from 3–7/10 severity. Her last migraine with aura was two months ago. She takes co-codamol qds and ibuprofen tds. What is the best medical management?
A. Stop all medication
B. Start paracetamol
C. Start sumatriptan
D. Start propranolol
E. Continue current medication
A
- This woman has developed analgesia (rebound) headache as result of over-using co-codamol and ibuprofen.
- Starting paracetamol would result in overdose as it is already contained in co-codamol.
- The treatment is to withdraw analgesics which initially will worsen the headache - patient should be prepared for this) but in the long run will alleviate it.
- It is not advisable for headache patients to take simple analgesia more than 2 days a week
- Once she is off the analgesia, it will be easier to discern the effect of her migraines
- She may require abortive sumatriptan to be taken as soon as the headache starts or prophylactic beta blockers taken daily
- Continuing her current medication will not improve matters