MST Week 2 (sports Injury) Flashcards
Define neuromuscular
Affecting or characteristic of both neural and muscular tissue
What are the signs of myasthenia gravis
Complaints of muscle weakness in an otherwise healthy and strong patient
Ptosis (droopy upper eyelid)
Cannot prolong muscle contraction
Symptoms progressing
What is myasthenia gravis
Disorder of neuromuscular transmission
Production of autoantibodies directed against the nicotinic AChR
Prevalence of about 1 in 10-20,000
Women affected about twice as often as men
Peak onset in women 2-3 decades, peak in men 5-6 decades
Key properties of synapses
Unidirectional
Irreversible delay
Chemical
How does an action potential in the motor neurone lead to contraction of the muscle fibre
1) action potential in motor neurone arrives at axon terminal
2) terminal membrane depolarises, volatge gated calcium channels open
3) calcium mediated exocytosis of acetylcholine (ACh) into extracellular space
4) interaction of ACh with nicotinic acetylcholine receptor
5) influx of sodium ions and efflux of potassium ions from muscle cell via nAChRs, generation of receptor potentials
6) if RGPs are sufficient to pass thereshold an action potential is generated
7) action potential propagates through muscle, which leads to release of calcium ions from sarcoplasmic reticulum leading to contraction of muscle
How does action potential lead to end plate potential
Open Ca2+ ion channel Ca2+ entry Exocytosis of ACh ACh binds to nicotinic receptor Conformational change Na+ influx and K+ efflux Depolarisation
End plate potential
How does an end plate potential lead to a contraction
Propagated action potential
Spreads in muscle
Contraction
How is myasthenia gravis treated
Increase the ACh levels at the neuromuscular junction.
What clinical use does neuromuscular blockade serve
Surgery
Prevents muscle contractions
Maintain muscle relaxation / paralysis without deep general anaesthesia
Cosmetic surgery
What does the patient experience during neuromuscular blockade
Slow methodical paralysis in skeletal muscle
Extrinsic muscles of eye first, then the small muscles of the face and hands followed by muscles of pharynx, respiratory muscles last
Individuals still experience pain
How can we block neuromuscular transmission
1) prevent synthesis (block Ch uptake)
2) prevent release (exocytosis)
3) block receptor activation (nicotinic receptor antagonists)
4) increase reuptake / inactivation
Clinical uses of Botox
Cervical dystonia - neuromuscular movement disorder involving the head and neck
Blepharospasm - involuntary contraction of the eye muscles
Severe primary axillary hyperhidrosis (excessive sweating)
What are the 2 classes of neuromuscular blockers
1) non-depolarising: nACh-R antagonists
2) depolarising nACh-R agonists
Features of non-depolarising blockers
- Occupy without stimulating post-synaptic nACh receptors
- additive effect of similar drugs
- block is competitive
- onset of action 3-5 min, duration typically 30+ min
- block not preceded by stimulation
Features of non-depolarising blockers
- during block, high freq stimulation causes tetanus with duration only slightly longer than a twitch
- block antagonised by agents that depolaris muscle membrane
- block antagonised by drugs that increase ACh release
- block reversed by anticholinesterases