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26 Cards in this Set

  • Front
  • Back
Neuromuscular Blocking Drugs do what? and how is this accomplished?
Neuromuscular-blocking drugs block neuromuscular transmission at the neuromuscular junction, causing paralysis of the affected skeletal muscles. This is accomplished either by acting presynaptically via the inhibition of acetylcholine (ACh) synthesis or release, or by acting postsynaptically at the acetylcholine receptor.
Clinically how are NMBDs used and what should be available during their use?
Clinically, neuromuscular block is used as an adjunct to anesthesia to induce paralysis, so that surgery can be carried out with less complications. Because neuromuscular block may paralyze muscles required for breathing, mechanical ventilation should be available to maintain adequate respiration.
What are the two classes of NMBDs?
Depolarizing and non-depolarizing (competitive)
How do non-deplarizing NMBDs work?
All of these agents act as competitive antagonists against ACh at the site of postsynaptic ACh receptors.

This drug needs to block about 70-80% of the Ach receptors for neuromuscular conduction to fail, and hence, for effective blockade to occur. At this stage, EPPs (end-plate potentials) can still be detected, but are too small the reach the threshold potential needed for activation of muscle fiber contraction.
How do depolarizing NMBDs work?
Depolarizing blocking agents work by depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine. However, these agents are resistant to degradation by acetylcholinesterase, and can persistently depolarize the muscle fibers as opposed to the transient depolarization by ACh which is rapidly degraded. Initially, they cause muscular fasciculations (muscle twitches) while they are depolarizing the muscle fibers. Eventually, after sufficient depolarization has occurred, the muscle is no longer responsive to ACh released by the motoneurons. Hence, full neuromuscular block has been achieved.
Inhibition of acetylcholinesterase, the enzyme responsible for degrading acetylcholine, will cause ACh to have the same effect as these agents.
What is the main difference between depolarizing and non-depolarizing NMBDs?
The main difference is in the reversal of these two types of neuromuscular-blocking drugs. Non-depolarizing blockers are reversed by anticholinesterase drugs. Since they are competitive antagonists at the ACh receptor so can be reversed by increases in ACh. The depolarizing blockers already have ACh-like actions, so these agents will have prolonged effect under the influence of anticholinesterase.
What side effects do NMBDs cause in the body?
Since these drugs may cause paralysis of the diaphragm, mechanical ventilation should be at hand to provide respiration.

Additionally, these drugs may exhibit cardiovascular effects, since they are not fully selective for the nicotinic receptor and hence may have effects on muscarinic receptors (PMID 2682131). If muscarinic receptors of the autonomic ganglia or adrenal medulla are blocked, these drugs may cause hypotension and tachycardia. Additionally, neuromuscular blockers may facilitate histamine release, which causes hypotension, flushing, and tachycardia.

In depolarizing the musculature, suxamethonium may trigger the release of large amounts of potassium from muscle fibers. This puts the patient at risk for life-threatening complications, such as hypokalemia and cardiac arrhythmias.
What are the two primary targets of NMBDs used in clinical anesthesia?
Acetylcholinesterase and AChR
All NMBDs are what?
antagonist ofthe AChR
Name the depolarizing NMBDs.
Name the non-depolarizing NMBDs.
pancuronium, vecuronium, rocuronium, d-tubocurarine, cisatracurium, mivacurium
Non-depolarizing NMBDs are often divided into two chemical classes, which are...
aminosteroid derivatives and benzylisoquinolines
Name the aminosteroid derivatives.
pancuronium, vecuronium, rocuronium
Name the benzylisoquinolines
d-tubocurarine, cisatracurium, mivacurium
Short acting NMBDs.
Short acting NMBDs.
Intermediate acting NMBDs.
vecuronium, rocuronium, cisatricurium
long acting NMBDs.
d-tubocurarine, pancuronium
Depolarizing blockade occurs when...
a drug mimics the action of the NT ACh. SCh, like ACh, binds and activates the AChR, which leads to depolarization of the endplate and adjacent muscle membrane. B/C SCh is not degraded as quickly as ACh, persistant endplate depolarization inhibits the inward flow of sodium ions, and there is accommodation or inexcitability of the perijunctional muscle membrane. Inactivation of sodium channels explains how muscle relaxation can occur in the presence of an endplate potential sufficient to trigger an action potential.
Depolarizing blockade is characterized by...
*muscle fasciculation followed by relaxation
*absence of fade after tetanic or TOF stimulation
*absence of posttetanic potentiation
*potentiation of the block by anticholinesterases
*Antagonism of the block by nondepolarizing relaxants
Non depolarizing blockade is characterized by...
*absence of fasciculations
*fade during tetanic and TOf stimulation
*Antagonism of block by depolarizing agents and anticholinesterases
*Potentiation of block by other nondepolarizing agents
Recovery from a depolarizing block occurs...
in 10 to 15 min, except in patient with inhibited or atypical plasma cholinesterases
Recovery from a nondepolarizing block occurs when... how can this be accelerated?
drug diffuse from their sites of action, acc. by administering agents that inhibit acetylcholinesterases (anticholinesterases)
Name the anticholinesterases.
edrophonium, neostigmine, and pyridostigmine
How do anticholinesterases work and where are their effects.
work by increasing ACh, and they have muscurinic and nitotinic effects
Muscurinic effects are... but can by minimized how?
salivation, bradycardia, tearing, miosis, and bronchoconstriction
*minimized by administration of antimuscurinic drugs such as atropine and glycopyrolate before the anticholinesterase