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31 Cards in this Set
- Front
- Back
name the main ingredient that was used in curare blow dart poison; it is the prototype neuromuscular blocking drug.
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tubocurarine
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what neurotransmitter is responsible for eliciting a muscle contraction on striated muscle?
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Ach
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what type of receptors are in the somatic nervous system (on muscle)?
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nictoinic ACh receptors
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an influx of what causes the depolarization and releases the vesicles full of ACh?
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Ca2+
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there are two types of nicotinic ACh receptors (neural nicotinic and muscular nicotinic), what makes them different from eachother?
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subunit composition, affinity for drugs, use different ligands (but must be cations);
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describe the shape of almost all agonist and antagonist to the nicotinic Ach receptor.
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quaternary ammounium compounds
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how many subunits make up the nicotinic receptor?
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five (usually the types of subunits are mixed - alpha, beta, etc.)
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in muscle there are four types of subunits with alpha repeated twice; which subunits do Ach bind to?
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Ach binds to each alpha subunits (in nerve there may only be alpha, or a mix of alpha and beta)
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explain how the nicotinic receptors work.
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at rest the gate is closed; when ACh attaches to its alpha subunits, the gate opens and allows ions to pass
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there are two major subdivisions of neuromuscular blocking agents, nondepolarizing and depolaring blocking agents. what is the difference in their MOA?
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NONDEPOLARIZING (tubocurarine, pancuronium, atracurium, vecuronium): competitively block ACh from binding; (antagonists at the nico. receptor; all or none: dose response curves are very steep) and DEPOLARIZING: drug directly binds and opens Na+ channels causing depolarization followed by flaccid paralysis; it also desensitizes the receptor to ACh (SUCCINYLCHOLINE is the only depolarizing agent)
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are all muscles equally effected?
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no. the muscles of the eye and face are affected first and respiratory are affected last. thus muscles of respiration have the greatest "receptor reserve"
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released ACh acts retrogradely on presynaptic neuronal nicotinic receptors. can these presynaptic receptors be blocked?
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yes; (also, know that the amount of Ach that is released in the nerve terminal is finite and each subsequent release of ACh is not in the same amount)
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list some adverse effects of tubocurarine (nondepolarizing agent).
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blocks ganglia and lose control of BP; affects muscarinic receptors - lose parasympathetic control and get tachycardia; releases histamine (hypotension, bronchoconstriction, anaphylaxis); long duration of action (over 30 min) this is too long to use for short procedures such as RSI (rapid sequence intubation)
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when choosing a muscle relaxant, what do you think of?
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1)Class of muscle relaxant; 2)onset time; 3)duration of action; 4)pharmacokinetic profile; 5)cardio effects; 6)need for reversal
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what is the shortest acting muscle relaxant?
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succinylcholine
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list the physio-chemical properties that make up a good muscle relaxer.
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highly ionized at physiologic pH; positively charged (since the cholinergic receptor is neg); resemble ACh and are quaternary ammounium compounds; they are highly WATER SOLUBLE/relatively HYDROPHILIC (easily excreted in urine, don't cross BBB, placenta, small Vd, and not actively metabolized in the liver since the cyP-450 system requires lipophilic substrates)
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describe the shape and size of nondepolarizing agents.
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heavy, bulky, rigid molecules that block but don't activate cholinergic receptors
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name an alkaloid curare drug that releases histamine.
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benzylisoquinolines
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name a drug that promotes a muscarinic block.
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aminosteroids (muscarinic receptors are located on the post-synaptic cleft in the parasympathetic ANS) -
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name an aminosteroid nondepolarizing blocking agent that has an onset of 3-5 minutes and 12 min recovery of twitch.
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vecuronium
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name an aminosteriod nondepolarizing blocking agent that has a very short (60-70sec) onset but a duration of action of 28 minutes.
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rocuronium (min. CV side-effects)
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name two short-acting nondepolarizing blocking agents that degrade spontaneously or are metabolized by plasma cholinesterase.
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ATRACURIUM (release histamine and good for renal failure pts) and MIVACURIUM (eliminated by plasma cholinesterase)....side note: depolarizing succinyl. is also eliminated by plasma Cholinesterase
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describe pancuronium.
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bis-quaternary aminosteriod; slow onset, long acting, little BP effects, vagolytic, renal clearance
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cis-atracurium is a stereoisomer of atracurium; it is eliminated by ___________ and its major differences from atracuirum are what?
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eliminated by Hoffman degradation; it doesn't release histamine therefore it doesn't have the CV effects of hypotension like atracurium
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the duration of action of NDMR in pediatrics is generally _______________; and ______________ in elderly, renal failure and hepatic failure.
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shorter in peds and longer in elderly, renal and hepatic failure (exception - atracurium and cis-atracurium is the same in elderly, renal and liver failure)
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the only depolarizing agent, succinylcholine differs from ACh how?
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it can't be broken down by SYNAPTIC acetylcholinesterase (only by plasma AChE)
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what will you see on initial depolarization with depolarizing succinylcholine?
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fasciculations and twitches
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there are two phases in depolarizing agent succ; phase I is the binding of succ and opening the Na+ channels and getting depolarizations - fasciculations followed by flaccid paralysis; explain phase II.
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Phase II: eventually the membrane will partially repolarize. however, the membrane is desensitized to Ach and further action potentials are prevented.
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there is a deficiency that may cause a prolonged blockade of succinylcholine. name it.
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pseudocholinesterase deficiency (dibucaine is a local anesthetic that inhibits normal pseudocholinesterase)
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explain malignant hyperthermia and name a drug used to treat it.
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uncontrolled Ca++ release from the sarc. reticulum leads to muscle contracture and a rise in body temperature; succinylcholine (esp. with halothane has been known to do this). dantrolene will block the release of Ca++
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name some anticholinesterases. what does this mean?
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an anticholinesterase is a way to reverse the blockade (it inhibits the cholinesterase enzyme from breaking down ACh and thus increases the action of ACh); edrophonium and neostigmine
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