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NM Blockers

PHAR 341

QuestionAnswer
Are motor axons myelinated? Yes
What NT is released at the NMJ? ACh
What receptor is activated during muscle contraction Nicotinic receptor
What does vesamicol do? Blocks ACh uptake into storage vesicles
What does hemicholinium do? Blocks uptake of choline into the presynaptic terminal
What do AChE inhibitors do? Inhibit the breakdown of ACh in the synaptic cleft
What does 4-AP do? increases the release of synaptic vesicles
What does black widow spider toxin do? Causes massive explosive release of ACh, emptying all vesicles and preventing them from refilling
What does botulinum do? Prevents the vesicular release of ACh at NMJ by cleaving docking proteins
What is the MoA of 4-AP? blocks nerve fibre K+ Channels and causes a prolonged AP which enhances release of ACh from the pre-synaptic terminal at the NMJ
What are the therapeutic uses of 4-AP? MS, MG, SC injury
What is botulinum toxin A also called? Botox
What is botulinum toxin B also called? Myobloc
What protein does Botulinum toxin A cleave? SNAP 25
What protein does Botulinum toxin B cleave? VAMP/Synaptobrevin
What are the therapeutic uses of Botulinum? Cosmetic, opthalmic, Face & neck spasms, hyperhidrosis, pain
Which patients are CI to using Botulinum? Those with NM disease, e.g. MG, MS
What is the most common SE of botulinum? unintended local weakness muscles near the site of injection
What are other SE of botulinum? Flu-like symptoms, anaphylaxis, excessive fatigue
Where are non-depolarizing NM blockers derived from? Curare
What is the MoA of non-depolarizing NM blockers? Competitively binds to the nicotinic receptor but does not produce a response
How can a non-depolarizing NM blocker be overcome? Increased concentrations of ACh
What is the order of paralysis? Eyelid, tongue, pharynx, jaw muscle, diaphragm, limbs, trunk, musculature
How does a depolarizing NM blocker work? Binds to and activates the receptor causing depolarization, uncoordinated fasciculating muscle contraction, maintained depolarization , muscle relaxation and desensitization of the nicotinic receptor
What are the therapeutic uses of NM blockers? Surgical muscle relaxation, electroconvulsive therapy, mechanical respiration, reduce/prevent muscle contraction
What are examples of non-depolarizing NM blockers? Tubocurarine, pancuronium, atacurium, alpha-bungarotoxin
What is an example of a depolarizing NM blocker? Succinylcholine
What are SE of tubocurarine? Histamine release (hypotension), increased salivation, autonomic gangion blockade, pooling of blood in extremities (vasodilation)
What are SE of Atacurium? slight histamine release (hypotension)
When is atacurium useful? In pts with liver/kidney dysfunction b/c it undergoes spontaneous hydrolysis
What are SE of pancuronium no histamine release or ganglion blockade
What are SE of alpha-bungarotoxin? Rapid paralysis of skeletal muscles, death due to respiratory failure
What are SE of succinylcholine? Arrhythmias (bradycardia), hyperkalemia, dose dependent alteration in CO, emesis, muscular pain, increased IOP
How is succinylcholine broken down? by blood pseudocholinesterases
Which has a higher affinity for receptors, ACh or succinylcholine? succinylcholine
When should succinylcholine be avoided? Fractures, glaucoma, paraplegia
What is the MoA of Dantrolene? reduces the release of Ca2+ from the SR and causing muscle relaxation
What are the SE of dantrolene? generalized muscle weakness, transient drowsiness (due to CNS penetration)
Who is at risk of idiosyncratic fatal hepatitis due to dantrolene? Females over the age of 35 taking dantrolene for more than 2 months
What are the therapeutic uses of Dantrolene? Malignant hyperthermia and spasicity
Created by: 517228175
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