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141 Cards in this Set
- Front
- Back
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when do you use NMBs
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surgical procedures and ICU paralysis
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when do you use spasmolytics
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reduce spasticity in a variety of neuro cond'ns
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MOA of NMBs
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competitive blockade of Ach at presynaptic and postsynaptic receptors
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with NMBs how does the presynaptic blockade work? Postsynaptic?
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presynaptic blocks receptors and dec. amount of ACH generated; postsynaptic occupy ACH receptors and block them
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what is the clinical usefulness of NMBs
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achieve adequate muscle relaxation for Sx w/o depressant effects of deep anesthesia
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what is NM blockade most often used for
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intraoperative management of pts
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what are the 2 types of NMBs and which is most common
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non depolarizing and polarizing; non-dep is the most common
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MOA of non-depolarizing NMBs
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block ACH, prevent access of the transmitter to its receptor and prevent depol.
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what is the only depol. NMB used
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succinylcholine
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MOA of depol. NMBs
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block transmission by excess of depol. Agonist.
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all NMBs bear a resemblance to …?
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Ach
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all NMBs are _____ soluble in lipid which ____ entry into the CNS
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poorly
prevents |
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all NMBs are _____ polar and active/inactive when given PO
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highly
inactive |
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t/f NMBs are only useful if given by injxn
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T
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sux is metabolized by....
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plasma cholinesterase
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sux has ___ onset and ____ durations
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rapid
short |
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sux produces paralysis very ____ and wears off ___ making it useful for ....
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rapidly
rapidly intubation |
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t/f sux will have a short duration and rapid onset in a pt w/ low plasma cholinesterase
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F
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the most common use for sux is...
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intubation
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DOA of sux is ____. Why?
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5-10 mins. max
b/c not much gets to motor end plate |
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what is the MOA of sux
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phase I block (depolarizing - like ACh)
phase II block (desensitizing - memb. can't be be depolarized by ACh) |
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MOA of nondepol. agents
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bind to same receptors but don't depolarize the end plate (duh!)
1. block Ach from receptor then block receptor channel 2. block presynaptic Na channels, preventing ACh from moving from synth. sites to release sites |
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rout of elimination of non-depol NMBs is correlated w/..,
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DOA
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non-depol NMBs excreted by kidney have ___ half lives and ___ DOAs. by the liver?
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kidney = long half life and DOA
liver = short half life and DOA |
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steroidal muscle relaxants are metabolized in the ___ to their ___ products
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liver
3-hydroxy, 17-hydroxy and 3,17-dihydroxy products |
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__-hydroxy metabolites are usually 40-80% as potent as the parent drug
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3
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what are the 2 groups of nondepol. NMBs
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isoquinolone derivatives
steroids |
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name the isoquinoline derived NMBs
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tubocurarine
atracurium mivacurium cisatracurium metocurine doxacurium |
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name the steroidal NMBs
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pancuronium
vecuronium rocuronium |
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what is the short acting NMB
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mivacurium
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what are the intermediate acting nondepol. NMBs
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atracurium
cisatracurium rocuronium tubocurarine vecuronium |
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what are the long acting non depol. NMBs
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doxacurium
metocurine pancuronium |
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MOA of nondepol NMBs
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produce a surmountable (competitive) blockade
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nondepol drugs are characterized by ___ initial dist. followed by ____ elimination
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rapid
slow |
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t/f nondepols. cross membranes well and have a wide volume of dist.
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F!
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what was the first steroidal muscle relaxant
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pancuronium
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onset and DOA of pancuronium
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onset in 2-3 min.
long |
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ADRs of pancuronium
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-CV effects (inc. HR and BP)
-inc. secretions (prob. for intubated pt) -bronchospasm |
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what happens when you combo sux and pancuronium
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intense blockade
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t/f you don't need to adjust pancuronium for hepatic/renal failure
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F
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vecuronium and rocuronium are ___ acting drugs and more/less commonly used than pan-?
they are more dependent on ______ for metab/excretion |
intermediate
more biliary excretion/hepatic metab. |
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the DOA of vecuronium depends on ___ and is ____ than pancuronium
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dosage and age of pt
shorter |
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recovery time of vecuronium inc. w/ ____
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number and size of doses
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how are ADRs of vecuronium different than pan-
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-minimal CV effects
-less/no histamine release than other NMBs -no bronchospasm |
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concurrent steroid use ____ effect of vancuronium
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prolongs
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which nondepolarizing muscle relaxant has the most rapid onset time
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rocuronium
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t/f the DOA or rocuronium inc. if you give more than 1 dose
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T
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Peak and DOA of rocuronium
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peak in 60-90 sec.
DOA is ~30 min. |
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t/f rocuronium does not inc. in renal dysfxn
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F, it does
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t/f atracurium has no cumulative effect w/ repeat doses and does not accumulate in renal failure
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T
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t/f atracurium's stereoisomers are also approved for use
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T
cisatracurium |
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atracurium induces hist. release in ___% of pts
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20
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t/f atracurium is good for a renal failure pt
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t
no cumulative effect blockade is not prolonged in renal failure |
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how is atracurium inactivated
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spontaneous hofmann breakdown
-plasma cholinesterase -not renal/hepatic |
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what is a product of atracurium breakdown
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laudanosine
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what is laudanosine and what does it do
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toxic metabolite of atracurium
no NMB effect crosses BBB may cause seizures long half life |
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what drug needs to be given w/ laudanosine and why
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benzodiazepines
prevent seizures |
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differences b/w atracurium and cisatra-
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less laudanosine
less histamine |
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DOA and ADRs of doxacurium
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long acting
free of dose-related CV effects |
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what nondepol. agent has the shortest DOA. is this good or bad
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mivacurium
good, once it's turned off it's gone |
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metabolism and ADR of mivacurium
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cleared in plasma
induces hist. release -expensive |
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3 ways to assess NM blockade
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-diaphragm strength
-other muscle strenght (head lift) -nerve stimulator |
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t/f perpheral nerve stimulation can hasten pt recovery
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FFFF!!!!
it's an assessment tool only |
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what is the most commonly used pattern for testing for effect of muscle relaxants during Sx
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'train of four' transdermal stimulation
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t/f peripheral nerve stimulation can be painful if pt is not sedated
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T
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what NMBs have little or no CV effects
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vecuronium
roc- doxacurium cisatracurium |
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which NMBs produce hypotension. how do you treat it
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tubocurarine
metocurine mivacurium atra- *pre-medicate with anti-hist. |
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CV effects of pancuronium
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moderate inc. in HR and CO
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CV effects of sux
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bradycardia in kids/infants
tachycardia in adults (prevented w/ thiopental) |
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what effects are only seen w/ sux
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hyperkalemia
inc. intraocular pressure intragastric pressure muscle pain |
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DDIs of nondepol. NMBs
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-anesthetics
-ABX -other NMBs -local anesthetics & antiarrhythmics -corticosteroids -metoclopramide -OCT -tacrine |
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how does aging affect NMB response
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inc. DOA -->need to dec. dose
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how does myasthenia gravis affect NMB response
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blockade is amplified
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how does dec. liver fxn affect NMB response
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you have to dec. dose
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t/f electrolyte disturbances affect NMB response
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T
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severely burned pts and upper motor neuron probs are often _____ to non-depol. agents
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resistant
receptors develop far from NMJ inc. dose to compensate |
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what drug class reverses nondepol agents
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cholinesterase inhibitors
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what are neo/physostigmine and what do they do?
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cholinesterase inhibitors
reverse nondepol. agents |
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MOA of neo/physostigmine
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inc. availability of ACh by inhibiting ACHesterase at motor end plate and inc. ACh release from motor nerve terminal
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MOA of edrophonium
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inhibits just ACh-e
(neo/physo inhibit ACh-e and inc. ACh release) |
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skel. muscle relaxants are also known as...
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spasmolytics
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define spasm
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sudden, violent, involuntary contraction of a mucle or group of muscles
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define spasticity
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state of inc. tone of a muscle
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muscle weakness accompanies spasm or spasticity
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spasticity
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most central acting SMRs are indicated for....
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relief of acute painful musculoskeletal conditions of local origin
some are for spasticity |
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antispastcity agents
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baclofen
tizanidine dantrolene diazepam |
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antispasmodic agents
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benzodiazepine
cyclobenzapine carisoprodol metaxalone chlorzoxazone methocarbamol tizanidine orphenadrine |
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t/f all SMRs are sedatives
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T
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SMRs have additive CNS depression w/...
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booze
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t/f most SMRs are not superior to analgesics/anti-inflamm
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T
but they make the pt rest |
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t/f the MOA of SMRs is not totally known
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T
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MOA of baclofen
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-GABA-mimetic agent (GABA-B receptor)
-presynaptic inhibitory fxn, reducing excitatory transmitters -dec. pain from spasticity by inhibiting release of substance P |
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valium works at ____ receptors
baclofen works at... |
GABA-A
GABA -B (B for baclofen) |
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indications for baclofen
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spinal spasticity
multiple sclerosis spasticity |
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t/f baclofen is as effective as diazepam
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t
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routes available for baclofen
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PO (harder to cross BBB)
intrathecal (more central acting) |
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t/f baclofen readily crosses the BBB
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F
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intrathecal baclofen is good for....
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controlling severe spasticity and pain not responsive to other meds
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ADRs of baclofen
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dizziness/vertigo
muscle weakness/hypotonia reduce seizure control in epilepsy impair motor coordination/ability to drive |
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baclofen dose should be dec in...
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elderly and MS pts
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how do you minimize ADRs w/ baclofen
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gradual dose adjustment
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MOA of botulinum toxin
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blocks pre-synaptic release of ACh from nerve terminal
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local IM botulinum toxin A treats...
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strabismus
blepharospasm off label use for spasticity |
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t/f botulinum toxin is just for wrinkles
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F
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for what is carisoprodol most useful
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pain due to acute musculoskeletal conditions
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carisoprodol is not effective for...
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chronic conditions
inferior analgesic |
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carisoprodol ADRs
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drowsiness
inc. HR flushing CNS depression trembling hiccups angioedema |
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what forms is carisoprodol available in
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alone
Soma compound (caris. + ASA/codeine) |
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t/f chlorzoxazone has been shown to be more effective than placebo
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T
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t/f chlorzoxazone is for short term use only, and is inferior to other active agents
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T
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t/f diazepam is more effective than chlorzo
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F
chlor. has less ADRs too |
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ADRs of chlorzoxazone
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-most common - same as carisoprodol
-hepatocellular toxicity!! can be fatal, monitor |
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t/f you will die if you don't take your chlorzo. w/ food or milk
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F
you won't die but you should just do it |
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MOA of clonidine
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central acting alpha agonist which dec. sympathetic effects
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t/f clonidine is useful as monotherapy
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f, rarely used alone
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ADRs of clonidine
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bradycardia
hypotension dry mouth, constipation, dizziness |
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t/f cycloben is only useful for short term therapy
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F
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ADRs of cycloben
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drowsiness
lightheadedness dizziness xerostomia facial edema polyuria/problems urinating blurry vision muscle weakness |
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half-life of cyclo ben
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1-3 days (long)
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indication of cycloben
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-better than diazpem for acute musculoskel. pain/trauma
-significant improvement in 1-2 weeks for spasm, local pain and ROM -long-term intractable pain aggravated by spasm |
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indication of dantrolene
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spasticity
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MOA of dantrolene
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direct effect on skel. muscle by interfering w/ excitation-contraction coupling in fiber
-cardiac and smooth muscle depressed only a little |
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ADRs of dantrolene
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dose-dependent muscle weakness
-inc. LFTs in some |
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MOA of dantrolene in malignant hyperthermia
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interfere w/ Ca release from sarcoplasmic reticulum -->prevents inc. in mycoplasmic Ca --->deactivates acute catabolism in skel. muscle cell
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t/f dantrolene for malignant hyperthermia is only useful if given IV
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T
oral bioavailability is only 30% |
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malignant hyperthermia is usually seen in ...
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general anesthesia
NMBs |
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indication and MOA of diazepam
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antispastic for muscle spasms due to sundry causes
works on GABA-A receptors |
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ADRs of diazepam
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very sedating
fatigue ataxia inc. NM blockade amnesia (28 active metabolites) |
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t/f diazepam is the gold standard drug for it's class
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T
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t/f the beneficial effects of metaxalone are from sedative effects, not relaxation.
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T
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ADRs of metaxalone
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very sedating
dry mouth urinary retention exacerbate seizures |
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t/f metaxalone is useful for long-term therapy
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F
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MOA of methocarbamol
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NOT direct skel. muscle relaxant, probably sedative properties
-doesn't alter neuron conduction, NM conduction or muscle excitability |
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ADRs of methocarbamol
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nystagmus
nasal congestion facial flushing bradycardia lightheadedness/dizziness |
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methocarbamol is used as an adjunct med in...
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tetanus
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MOA of orphenadrine
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anticholinergic
antihistaminic local anesthetic effects slight CNS stimulation *no direct SMR activity |
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DDIs of orphenadrine
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propoxyphene (additive CNS fx)
*alcohol (she read this from her notes) |
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MOA of tizanidine
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-Antispastic
-centrally acting alpha agonist - inhibit release of excitatory AAs |
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t/f tizanidine is better tolerated than baclofen or diazepam
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T
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t/f tizanidine is NOT sedating
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T
*from special Ks notes |
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DDI of tizanidine
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Cipro
fluvoxamine OCT *all read from her notes |
