Miscellaneous Quiz / Muscle Relaxants and Anti-Spasmotics

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QUIZ: Can you name the Muscle Relaxants and Anti-Spasmotics?

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SE: Drowsiness (transient), seizure in epileptics
Botulinum Toxin A (Botox) class
Use: As effective spasmolytics as diazepam - no sedation. Does not reduce muscle strength like dantrolene
Use: Opthalmic use & local muscle spasm. Also for more generalized spastic disorders d/t neuro injury (e.g. one limb post stroke) & cosmetic applications
SE: Drowsiness, hypotension
Turbocurarine class
Interactions: NM block is enhanced by gen anesthetics, local anesthetics, antiarrhythmic drugs, some antibiotics (aminoglycosides).
P-kinetics: Plasma cholinesterase: rapid inactivation (10-20 min). Note less PC in pts w/ renal failure
Gabapentin class
SE: Muscle weakness and sedation
Use: Malignant hyperthermia, triggered by gen anesthesia, NM blockers in pts w/ hered defects in Ca sequesteration -> sudden & prolonged release of Ca -> massive muscle contraction
P-kinetics: Long duration - 60 mins
Use: Cause paralysis during sx & ICU. Used for control of ventilat (elim. chest wall resistance) & tx of convulstions & seizures (no central effect).
SE: Vagolytic - tachycardia (may be useful in kids who tend to be bradycardic). No histamine release
P-kinetics: Fastest onset - 1 min. Shortest DOA: 5-10 mins. Very rapid hydrolysis by plasma cholinesterase; prolonged in pts w/ abnormal ACh. Two Phases
P-kinetics: Renal: slow elimination: long (60 mins) duration.
Reversal: Cholinesterase inhibitors - antagonizing ACh-esterase -> increased ACh at NMJ
SE: Bronchospasm & hypotension (attenuated by premedication w/ antihistamine). Histamine release
Doxacurium class
Methocarbamol class
Pancuronium class
SE: jaw rigidity, hyperkalemia (burn pts, nerve damage, head injury pts... denervation -> upregulation of extrajunctional receptors... poss -> cardiac arrest), myalgia
P-kinetics: Short duration - 15 mins
MOA: Agonist of nicotinic receptor (relatively resistant to degradation) -> excessive channel opening & muscle fatigue. Essentially blockade from excess stimulation
MOA: Increase (inhibitory) internuncial interneuron activity
MOA: Inhibition of glutaminergic transmission in the CNS
Cistatracurium class
P-kinetics: After IV admin during anesthesia --> skeletal muscle weakness --> flaccid --> inexcitable to stimulus. Sensitivity of muscles: Facial, foot, and hand >>> abd, trunk, di
Phase I cont. -> paralysis of arm, neck, leg muscles -> facial & pharyngeal muscles -> resp muscles. More slowly metabolized than ACh -> membrane remains depolarized, no 'repriming
P-kinetics: PO - rapidly absorbed, t1/2 = 4 hrs, BID. Intrathecal for severe spasticity & muscle pain
P-kinetics: Single injection works for weeks to months
Pipecuronium class
P-kinetics: Spontaneous breakdown - Hoffman elim: 20-35 min. Breakdown product, laudanosine, crosses BBB -> seizure w/ pronlonged use. Isomer w/ advantagous properties: cis-atracur
Atracurium class
Baclofen class
Mivacurium class
Tizanidine class
Metaxalone class
P-kinetics: All must be given IV. Quaternary amine- no access to CNS. Once injected rapid distrib. Vol of distrib similar to blood volume. Highly charged prevents membrane crossing
Rocuronium class
Interactions: Low dose nondepolarizing NM blockers antagonize succs-induced fasciculations & post-op pain.
SE: Less histamine release so less CV effects
Phase II cont. Late in phase II becomes similar to blockade w/ nondepolarizing drugs, reversible by ACh inhibitors. Use w/ caution in kids
Metocurine class
MOA: Related to TCAs. Interferes w/ polysynaptic reflexes in the brainstem that maintain skeletal muscle tone.
MOA: Competitive antagonist of Ach (low doses) -> surmountable blockade by tetanic stimulation and cholinesterase inhibitors. High doses block poorly.
Use: Sensitivity to NM blockers is increased in myasthenia gravis & older age AND is decreased in burn pts.
Phase I cont.. unresponsive to subsequent stimulus; augmented (NOT reversed) by ACh inhibitors.
Dizaepam class
MOA: Decrease Ia fiber activity. GABA-B agonist. Metabotropic receptor activation, increase gK+ -> hyperpolarization -> decrease in excitatory NT release in stretch reflex arc.
SE: Sedation, antimusc effects (dry mouth), fatigue, asthenia, nausea, constipation, dyspepsia, taste changes, blurred vision, HA, nervousness, confusion, transient visual hallucin
Chlorphenesin class
SE: Arrhythmias (w/ halothane); brady (alleviated w/ co-admin of Atropine); histamine release, increased IOP, transient dilation of choroidal vessels or myofibrils contraction
MOA: Decrease excitation-contraction coupling -> reduced skeletal muscle strength. Binds to the 'ryanodine' Ca channel in the SR, inhibits the release of (activator) Ca from the SR
Phase II: desensitizing: endplate depolarization decreases; membrane repolarizes, but cannot produce generalized depolarization
Riluzole class
Phase I - depolarizing: same effects as Ach but last longer. Generalized disorganized contraction of motor units (muscle fasciculation) over chest, abd; weakened by gen anesthesia
MOA: Prevents release of ACh from vesicles
Use: Prototype for acute, temporary muscle spasm caused by trauma or strain. Ineffective in cerebral palsy & SC injury.
P-kinetics: Hepatic: faster elimination (20-35 mins). Eliminated 70-90% via biliary excretion. Metabolic accumulation w/ extended use
Botulinum Toxin B (Myobloc) class
Carisoprodol class
P-kinetics: Onset 1-2 mins (fastest on non-depolarizing)
Vecuronium class
MOA: Congener of clonidine - central effects not fully known. Spasmolytic effect d/t reinforcement of both presynaptic & postsynaptic inhibition of the motor neuron in the cord
SE: rhabdomyolysis (poss w/ myoglobinuria), prolonged paralysis in pts w/ cholinesterase def, increased intragastric pressure (emesis), assoc w/ acute onset of malignant hypothermi
Use: Comparable in efficacy to diazepam, baclofen, dantrolene in several types of spasticity
Use: May be useful in spasm of MS pt
Dantrolene class
Use: ALS-induced spasm
Orphenadrine class
Succinylcholine class

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