Neuropathy & neuromuscular junction flashcards
18 high-yield MRCP Part 1 cards from the Intellect Medicos Neurology course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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What is the most common infective trigger of Guillain-Barré syndrome?
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Campylobacter jejuni.
Why? Molecular mimicry produces antibodies against gangliosides on peripheral nerves. A preceding diarrhoeal illness is also a poor prognostic sign.
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What is the classic CSF finding in Guillain-Barré syndrome?
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Albuminocytological dissociation: raised protein with a normal cell count.
Why? Inflamed nerve roots leak protein without a cellular response. Nerve conduction studies confirm demyelination.
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What is the disease-modifying treatment for Guillain-Barré syndrome?
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IV immunoglobulin or plasma exchange.
Why? Both speed recovery when given early.
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In Guillain-Barré syndrome, monitor FVC: consider ICU admission if FVC falls below ______ and intubation below 15 mL/kg.
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20 mL/kg
Why? Respiratory muscle weakness can progress quickly. Oxygen saturation drops late, so serial FVC is the key bedside monitor.
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In Guillain-Barré syndrome, monitor FVC: consider ICU admission if FVC falls below 20 mL/kg and intubation below ______.
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15 mL/kg
Why? Respiratory muscle weakness can progress quickly. Oxygen saturation drops late, so serial FVC is the key bedside monitor.
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What is the first-line diagnostic blood test for myasthenia gravis?
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Anti-acetylcholine receptor (AChR) antibodies.
Why? Positive in most generalised myasthenia. If negative, test anti-MuSK (often prominent bulbar weakness) and anti-LRP4.
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What is the first-line symptomatic drug for myasthenia gravis, and its mechanism?
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Pyridostigmine, an acetylcholinesterase inhibitor.
Why? It increases acetylcholine at the neuromuscular junction. Steroids, azathioprine or mycophenolate are added for immunosuppression.
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Name four drugs that can worsen myasthenia gravis.
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Any four: aminoglycosides (gentamicin), macrolides, quinolones, tetracyclines, beta-blockers, lithium, phenytoin, penicillamine, procainamide/quinidine, magnesium.
Why? These drugs impair neuromuscular transmission and can trigger a myasthenic crisis.
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What is the treatment of myasthenic crisis?
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IV immunoglobulin or plasma exchange, with respiratory support (monitor FVC; ventilate if needed).
Why? Crisis means respiratory or bulbar failure. Rapid immunotherapy reverses it within days. Infection is the most common trigger.
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What is the first-line symptomatic drug for Lambert-Eaton myasthenic syndrome, and how does it work?
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Amifampridine (3,4-diaminopyridine). It blocks presynaptic potassium channels, prolonging depolarisation and increasing acetylcholine release.
Why? LEMS is caused by antibodies against presynaptic voltage-gated calcium channels, so less ACh is released.
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What is the mechanism of riluzole in motor neurone disease, and what is its benefit?
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Reduces glutamate release. Prolongs survival by about 2-3 months.
Why? Glutamate excitotoxicity is thought to contribute to motor neurone death. Non-invasive ventilation gives a larger survival gain.
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Name four drugs that cause peripheral neuropathy.
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Any four: amiodarone, isoniazid, vincristine, nitrofurantoin, metronidazole, phenytoin, tricyclics.
Why? These are frequently tested causes of a drug-induced, mostly sensory, length-dependent neuropathy.
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Ophthalmoplegia, ataxia and areflexia after a diarrhoeal illness: which antibody is typical?
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Anti-GQ1b (Miller Fisher syndrome).
Why? Miller Fisher is a GBS variant that often starts with the eye muscles, with little limb weakness.
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A symmetrical demyelinating neuropathy has progressed for more than 8 weeks, with raised CSF protein. What is the diagnosis and first-line treatment?
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CIDP; corticosteroids or IVIG (plasma exchange is an alternative).
Why? CIDP is a chronic relative of GBS that needs long-term immunotherapy. Unlike GBS, it responds to steroids.
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Myasthenia gravis has just been diagnosed. Which imaging is needed, and why?
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CT chest, to look for a thymoma or thymic hyperplasia.
Why? Thymectomy is indicated for thymoma and is often offered in generalised AChR-antibody-positive MG.
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Which repetitive nerve stimulation finding is typical of Lambert-Eaton myasthenic syndrome?
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An incremental response (facilitation) with high-frequency stimulation or after brief exercise.
Why? Repeated activity lets calcium build up in the nerve terminal, so more acetylcholine is released. Myasthenia gravis shows a decrement instead.
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An injecting drug user develops diplopia, fixed dilated pupils, dysphagia and a descending symmetrical flaccid paralysis. Sensation is normal. What is the diagnosis and the specific treatment?
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Wound botulism; botulinum antitoxin, with respiratory support.
Why? Botulinum toxin blocks acetylcholine release at the neuromuscular junction. CSF is normal.
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What are the first-line drug options for painful diabetic peripheral neuropathy (NICE)?
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Amitriptyline, duloxetine, gabapentin or pregabalin.
Why? Start one; if it fails or is not tolerated, switch to another of the four. Tramadol is only for short-term rescue.