Muscle relaxants Flashcards
Mechanism of skeletal muscle contraction
initiation of impulse, release of acetylcholine, activation of nicotinic receptor at motor end plate, opening of ion channel, passage of Na depolarization of end plate, muscle contraction
Drug targets
neuromuscular blocking agents interfere with process of signal conduction, also by blocking muscle contraction even if the signal to contract is propogated along the neuron
Skeletal muscle reflex arc
increase in Ca causes muscle contraction, signal carried from spinal cord to muscle (efferent neurons), muscles to spinal cord (afferent neurons)
GABA
gamma aminobutyric acid inhibitory neurotransmitter in CNS that bind to GABA receptors and decrease efferent firing- stops reflex arc to prevent inappropriate contractions
Muscle spasm
a sudden, involuntary muscle contraction, initiated by trauma, tonic or clonic, painful (spasm-pain-spasm etc)
Chronic muscle spasms can result in
muscle atrophy
Muscle spasticity
increased muscle tone or contraction, stiff awkward movements, caused by nerve damage in CNS, usually permanent (cerebral palsy), not disease but a process
Skeletal muscle relaxants are used to
decrease muscle spasms or spasticity, selective for skeletal muscles
Central acting muscle relaxants mostly work by
decreasing signalling from the efferent neurons as opposed to directly inhibiting contraction
Skeletal muscle relaxant drugs
Baclofen (Lioresal), Cyclobensaprine (Flexeril), Carisoprodol (Soma), Metaxalone (Skelaxin), Methocarbamol (Robaxin), Chlorzoxazone (Parafon Forte), Dantrolene (Dantrium), Orphenadrine (Norflex)
Baclofen (Lioresal) MOA
centrally acting GABA agonist on efferent neurons, inhibits transmission of reflexes at spinal cord level, relieving muscle spasticity, also inhibits substance P in spinal cord
Baclofen (Lioresal) clinical uses
spasticity, migraine prevention, MS, spinal cord injury, usually long term
Baclofen (Lioresal) ADRs
CNS related, drowsiness, sedation, muscle weakness, hypotension, HA, *less sedating than others
Baclofen (Lioresal) boxed warning
severe withdrawal from abrupt d/c, causes altered mental status and rebound spasticity
Baclofen (Lioresal) Pearls (5)
TID, PO, can be given intrathecal route for spinal cord injury, MS, degenerative myelopathy, CA; caution with seizure pts, older drug
Cyclobenzaprine (Flexeril) MOA
centrally-acting, structurally and pharmacologically very similar to TCAs, reduces tonic somatic motor activity
Cyclobenzaprine (Flexeril) Clinical uses
muscle spasms associated w/ muscle injury or strain, short term use only, also good for low back spasms
Cyclobenzaprine (Flexeril) ADRs
drowsiness, dizziness, sedation, anticholinergic (no BPH, glaucoma, Alzheimer’s)
Cyclobenzaprine (Flexeril) Pearls (4)
Only PO, immediate release or long acting (TID/daily), not for use in MS or cerebral palsy, caution in elderly, MAOI pts, or liver failure
Tizanidine (Zanaflex) MOA
alpha agonist, similar to clonidine, bu not lipophilic enough to penetrate BBB, causes presynaptic inhibition of motor neurons
Tizanidine (Zanaflex) clinical uses
PO and BID-TID, spasticity, unlabeled for tension HA, acute low back pain
Tizanidine (Zanaflex) ADRs
drowsiness, hypotension, dry mouth, constipation
Carisoprodol (Soma) MOA
not sure, but is CNS depressant, sedating/anxiolytic properties resulting in muscle relaxation
Carisoprodol (Soma) clinical uses
Acute management of musculoskeletal pain (2-3 weeks)
Carisoprodol (Soma) ADRs
drowsiness, sedation!!, dizziness
Carisoprodol (Soma) Pearls (6)
QID, PO only, result in addiction, caution in elderly/ pt with drug abuse, abrupt d/c= withdrawal, DEA controlled
Metaxalone (Skelaxin) MOA
not sure, but CNS depressant, breaks spasm-pain cycle, no direct effect on skeletal muscle
Metaxalone (Skelaxin) clinical use
muscle spasms/discomfort
Metaxalone (Skelaxin) ADRs
CNS depression, dizziness, drowsiness, sedation
Metaxalone (Skelaxin) pearls (4)
TID-QID, only PO, caution in renal AND hepatic failure, elderly, pts taking other sedatives and pt with anemia
Methocarbamol (Robaxin) MOA
CNS depression
Methocarbamol (Robaxin) ADRs
bradycardia
Methocarbamol (Robaxin) Pearls (6)
IV, PO, IM, IV contra in renal insufficiency, caution in pt with seizure disorders, usually for long-term
Dantrolene (Dantrium) MOA
unique in that it is not central acting, acts directly on skeletal muscle, interfering w/ excitation/contraction coupling to produce relaxation, decr amt of Ca released
Dantrolen (Dantrium) clinical use
acute management of malignant hyperthermia, neuroleptic malignant syndrome (short-term), and cerebral palsy or MS (long-term), Rare, IV and PO
Dantrolen (Dantrium) ADRs
euphoria, muscle weakness, drowsiness/sedation, hepatotoxic w/ chronic use
Other skeletal muscle relaxants
Chlorozoxazone (Parafon Forte) PO only and Orphenadrine (Norflex)- centrally acting, euphorigenic and analgesic properties
Neuromuscular blockers types
depolarizing (Succinylcholine, (Anectine)) and non-depolarizing (Pancuronium, Vecuronium (Norcuron), Rocuronium (Zemuron), Cisatracurium (Nimbex), Atracurium
NMBs cause
system-wide paralysis, are selective for skeletal muscle not smooth muscle
Succinylcholine (Anectine) MOA
depolarizing, acetylcholine agonist, binds nicotinic receptors to open the channels and cause immediate depolarization, leave channels open and unable to contract muscle
Succinylcholine (Anectine) clinical use
1x IVP dose for intubations, very fast onset, short duration
Succinylcholine (Anectine) ADRs
hyperkalemia, bradycardia, malignant hyperthermia
Non-depolarizing NMBs MOA
compete with acetylcholine at the nicotinic receptor sites of neuromuscular junction, will not see initial muscle contraction
Non-depolarizing NMBs clinical uses
intubation, and continuous paralysis in critically ill, paralysis during surgical procedures, in ICU for pts whose respiratory fnc is not improving while on mechaniclal ventilation
Non-depolarizing NMBs ADRs
hypotension, hyperkalemia (mostly in pts with burns, nerve damage, crush injuries, head injuries), CNS stimulation(Rocuronium), tachy (Pancuronium)
Non-depolarizing NMBs Pearls (6)
monitor with train of four (2/4), all given parenterally, short T1/2, always via continuous infusion, relative quick onset, not for combative or agitated pts
Rocuronium (Zemuron) Pearls (3)
fastest onset, avoid in liver failure, DOC in pt w/ renal failure
Vecuronium/Pancuronium avoid in
pt with renal failure
Which has active metabolites that make DOA variable
Vecuronium
Cisatracurium (Nimbex) pearls
$$$, unique metabolism (Hoffman eilimination) that results in spontaneous breakdown of drug
NMB consideration
T1/2 and duration dictate how that are used, do not use in management of seizures, reversed with acetylcholinesterase inhibitors (Physostigmine, neostigmine), always ensure pt is properly sedated w/ ample analgesia, high risk med!
