Neuromuscular Blocking Drugs Flashcards
What neuromuscular blocking drugs that we talk about target the CNS
Baclofen
Tizanidine
Diazepam
What neuromuscular blocking drugs target the actual muscle
Dantrolene
Why is it clinically necessary to block tranmission at the neuromuscular end plate of Ach
Needed for surgical relaxation, tracheal intubation, and control of ventilation
What is the process of Ach getting across the synapse
- AP sent down nerve, inside becomes more positive and causes Ca2+ channels to open
- Ca2+ comes in it becomes more positive, which activated the vesicles contains Ach and cause Ach to be released
- once ACh goes across synapse, it binds to the Na+ channels to open them (Nm is Na channel)
- Na+ influx into the muscle fiber
- small amount of K flux out of fiber
- this causes contraction
Ach receptor
2 alpha subunits that Ach has to bind
What are the two types of neuromuscular blocking drugs
- Non-depolarizing
2. Depolarizing
No depolarizing neuromuscular blocking drugs
Tubocurarine Atracurium Pancuronium Vecuronium Rocuronium Cisatracurium
MOA of nondepolarixing neuromuscular blocking drugs
Nicotinic antagonist-competitive antagonists, compete with Ach for receptor
- prevent action of Ach at NMJ.
- competitive blockers, can be overcome by increasing Ach
- bind to and block the Nm receptor, no Na can get in, cause relaxation
What is a nondepolarizing neuromuscular blocking drug reversed with
Achase inhibitor
What are the effects of nondepolarizing neuromuscular blocking drugs on the cardiac and smooth muscle
None because it only works on No receptors
CNS effects of nondepolarizing neuromuscular blocking drugs
None
Analgesia and sedation with nondepolarizing neuromuscular blocking drugs
They dont have these affects. Have to give these first before the nondepolarizing drug so the patient doesn’t feel pain
Clinical use for nondepolarixing neuromuscular blocking drugs
Used mainly in anesthesia protocols or in the ICU to afford muscle relaxation and or immobility
Atracurium
- nondepolarizing neuromuscular blocking drugs
- forms laudanosine, which can cause seizures
Cisatracurium
- Nondepolarizing neuromuscular blocking drug
- forms less laudanosine than atracurium
- one of the most commonly used muscle relaxants in clinical practice
What is the most commonly used muscle relaxant in clinical practice
Cisatracurium
What’s the difference between atracurium and cisatracurium
Cisatracurium does not produce as much laudanosine, which means less risk of seizures
Duration of action of nondepolarizing neuromuscular blocking drugs
- long acting ones are more potent and require low concentrations. Tubocurarine, pancuronium
- intermediate actions of vecuronium, rocuronium, atracurium, cisatracurium
- most are pretty short acting
Reversal of non-depolarizing agents
- neostigmine: Achase inhibitor, allows more Ache to be in the cleft to compete with drug
- sugammadex: encapsulates and binds with molecules of rocuronium or vecuronium, thereby rapidly reversing their neuromuscular blocking effect
Depolarizing (non-competitive) neuromuscular blocking drugs
Succinylcholine
What is succinylcholine
Depolarizing (non-competitive) neuromuscular blocking drug
-2 Ach stuck together
MOA of succinylcholine
Classic depolarizing agent
- stimulates all cholinergic receptors
- binds directly to the postsynaptic Ach receptors of the NMJ causing continuous stimulation of these receptors.
- leads to transient fasciculations followed by muscular paralysis
- composed of 2 Ach molecules
- STRONG ACH RECEPTOR AGONIST
- sustained depolarization and prevents muscle contraction
- acts like a nicotinic agonist and depolarizes the NMJ
What is succinylcholine broken down by
Pseudocholinesterase
What is a problem with succinylcholine?
Since it stays bound to the Nm receptor, the receptor stays open, allowing Na to go in and K to come out, too much K going out can cause hyperkalemia
-people need tested to make sure K levels are not increased
