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97 Cards in this Set
- Front
- Back
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how do neuromuscular blockers work?
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block the cholinergic transmission between somatic motor nerve endings and the nicotninc receptors on the end plate of skeletal muscle
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what is the most important application of neuromuscular blockers?
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surgical relaxation, especially for intra-abdominal and intrathoracic procedures
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what use do neuromuscular blockers have in terms of ventilation?
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eliminate chest wall resistance and ineffective spontaneous ventilation so it can be used for critically ill patients with ventilator failure
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when is mechanical ventilation required?
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when a full dose of neuromuscular blockers is used
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how do neuromuscular blockers treat convulsions?
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attenuate or eliminate the peripheral manifestations of convulsions
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what will neuromuscular blockers not do?
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cross the BBB
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what is the MOA of nondepolarizing neuromuscular blockers?
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pure competitive agonists that occupy the nicotinic receptor to block Ach from gaining access
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how can the effect of nondepolarizing neuromuscular blockers be overcome?
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ACE inhibitor to increase the amount of Ach available in the synaptic cleft
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how long is the onset of action for nondepolarizing neuromuscular blockers?
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short (1-6mins)
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which nondepolarizing neuromuscular blockers will have a slightly longer duration of action?
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those eliminated by the kidney
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what can inhaled anesthetics do?
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strongly potentiate and prolong the neuromuscular blockade
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what is an example of a neuromuscular anesthetic?
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isolurane
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what will prolong the relaxation caused by nondepolarizing neuromuscular blockers? (2)
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aminoglycoside antibiotics
antiarrhythmic agents |
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what is atracurium?
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a nondepolarizing neuromuscular blockers
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what is cistracurium?
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a nondepolarizing neuromuscular blockers
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what is vecuronium?
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a nondepolarizing neuromuscular blockers
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what is rocuronium?
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a nondepolarizing neuromuscular blockers
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what is pancuronium?
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a nondepolarizing neuromuscular blockers
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what is tubocurarine?
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a nondepolarizing neuromuscular blockers
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what is mivacurium?
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a nondepolarizing neuromuscular blockers
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what is the structure of antracurium?
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isoquinolone based
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how long is the duration of action of antracurium?
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medium
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how is antracurium metabolized?
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hoffman degeneration
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what are 3 adverse effects of antracurium?
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hypotension
histamine release broken down into laudanosine which is a toxic metabolite that can cross the BBB and cause seizures with long term use |
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what will cause more laudanosine built up?
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kidney failure
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what is the structure of cistracurium?
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isoquinolone based
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how long is the duration of action of cistracurium?
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long
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how is cistracurium metabolized?
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hoffman degeneration
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what are 3 good things about cistracurium?
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much less hypotension, histamine release, and formation of laudanosine
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what is the structure of vecuronium?
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amino steroid based
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how long is the duration of action of vecuronium?
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medium
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how is vecuronium metabolized?
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liver metabolism and clearance
renal elimination |
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what are 3 adverse effects of vecuronium?
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generally fewer
may cause prolonged paralysis may promote muscarinic block moderate block of cardiac muscarinic receptors |
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what is the structure of rocuronium?
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amino steroid based
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how is rocuronium metabolized?
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liver metabolism and clearance
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what is an adverse effect of rocuronium?
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may promote muscarinic block
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what is the structure of pancuronium?
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amino steroid based
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how long is the duration of action of pancuronium?
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very long
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how is pancuronium metabolized?
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liver metabolism and clearance
renal elimination |
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what are 2 adverse effects of pancuronium?
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slight tachycardia
no hypotension |
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what is the structure of tubocurarine?
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isoquinoline based
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how long is the duration of action of tubocurarine?
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very long
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how does tubocurarine work?
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it blocks autonomic ganglia (opposite of succinyl choline)
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what are 3 adverse effects of tubocurarine?
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most likely to cause histamine release
hypotension due to block and release of histamine bronchoconstriction due to histamine |
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what is the structure of mivacurium?
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isoquinolone based
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how long is the duration of action of mivacurium?
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short
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how is mivacurium metabolized?
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hydrolyzed by plasma cholinesterase
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what is important about mivacurium?
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no longer manufactured
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what is phase I of the MOA of depolarizing blockers?
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acts as an agonist at nicotinic receptors and initially depolarizes the muscle membrane, relaxes calcium, and causes fasiculationsand then flaccid paralysis
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what will worsen phase I of depolarizing blockers?
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an ACE inhibitor
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what is phase II of the MOA of depolarizing blockers?
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upon continued exposure to succinylcholine, the membrane is repolarized but resistant to further activation
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what 2 receptors will depolarizing blockers also block?
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autonomic ganglia
cardiac muscle receptors |
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what is succinyl choline?
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a depolarizing blocker
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how is succinyl choline metabolized?
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by pseudocholinesterase (not acetylcholinesterase)
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how can the duration of action of succinyl choline be prolonged?
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in patients with generic variants of pseudocholinesterase or hepatic damage
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what are 4 adverse effects of succinyl choline?
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post-op muscle pain due to fasciculations
hyperkalemia decreased HR and increased IOP at high doses hyperthermia |
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what causes malignant hyperthermia?
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massive calcium release from the SR of skeletal muscle
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how do you treat hyperthermia?
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dantrolene
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what is the goal of spasmolytic agnets?
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reduce excessive skeletal muscle tone caused by neurologic or muscle end plate disease without reducing strength
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what are chronic diseases of the CNS associated with?
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abnormally high reflex activity, specifically the neuronal pathway that control skeletal muscles, resulting in painful spasms
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what is carisoprodol?
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an acute spasmolytic agent
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what is cyclobenzaprine?
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an acute spasmolytic agent
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what is metaxalone?
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an acute spasmolytic agent
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what is methocarbamol?
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an acute spasmolytic agent
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what are 2 adverse effects of carisoprodol?
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drowsiness (increased by alcohol)
CNS effects much more prominent in the elderly |
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what is the possible MOA with cyclobenaprine?
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believed to act at the brain stem, possible interference with polysynaptic reflexes that maintain skeletal muscle tone
may act as a TCA |
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how is cyclobenaprine administered?
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orally
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what are 3 adverse effects of cyclobenzaprine?
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marked sedation
antimuscarinic action confusion/hallucinations (increased with co-administration of other drugs) |
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what is cylobenzaprine not effective for?
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chronic muscle spasm
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what is metaxalone used for?
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indicated in the relief or discomfort associated with acute, painful musculoskeletal conditions
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what does metaxalone not have?
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a direct effect on skeletal muscle (most therapeutic effect comes from actions on the CNS)
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what are 3 adverse effects of metaxalone?
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drowsiness
dizziness irritability |
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what is methocarbamol used for? (2)
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used in the treatment of muscle spasms associated with acute painful musculoskeletal conditions
supportive therapy in tetanus |
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what are 4 adverse effects of methocarbamol?
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drowsiness
dizziness hypotension syncope |
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who is methocarbamol contraindicated in?
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renal impairment
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how do chronic spasmolytic agents work?
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act in the spinal cord to reduce tonic output of primary spinal motor neurons
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how are chronic spasmolytic agents usually administered?
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orally
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what may refractory cases of chronic spasm require?
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intrathecal administration of baclofen
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what is diazepam?
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a chronic spasmolytic agent
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what is baclofen?
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a chronic spasmolytic agent
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what is dantrolene?
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a chronic spasmolytic agent
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what is tizanidine?
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a chronic spasmolytic agent
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what is the botulinum toxin?
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a chronic spasmolytic agent
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what is gabapentin?
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a chronic spasmolytic agent
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how does diazepam work?
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facilitates GABA-mediated inhibition
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what is an adverse effect of diazepam?
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sedation
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how does baclofen work? (3)
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acts as a GABA agonist and opens K channels causing hyperpolarization
closes Ca channels decreased the release of excitatory neurotransmitters, especially substance P |
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what is an adverse effect of baclofen?
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sedation (less than diazepam)
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how does dantrolene work?
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acts in the skeletal muscle cell to block ryanodine receptors to reduce the release of calcium from the SR
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what are 2 adverse effects of dantrolene?
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significant muscle weakness
less sedation than bactofen or diazepam |
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how does tizanidine work?
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significant alpha-2 agonist activity that reinforces both pre- and postsynaptic inhibtion at the spinal cord
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what is tizanidine closely related to?
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clonidine
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what are 2 adverse effects of tizanidine?
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drowsiness
hypotension |
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how does the botulinum toxin work?
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prevents synaptic fusion and release of Ach
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what can the botulinum toxin be used for? (2)
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can be injected into selected muscles to reduce pain
can be used in the management of cerebral palsy |
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how does gabapentin work?
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analog of GABA designed to cross the BBB but has no direct GABA-mimetic effects (thought to either interfere with its breakdown or enhance its release)
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what is gabapentin used for?
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manage spasms in a patient with MS
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