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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.
what neurotransmitter is responsible for eliciting a muscle contraction on striated muscle?
what type of receptors are in the somatic nervous system (on muscle)?
nictoinic ACh receptors
an influx of what causes the depolarization and releases the vesicles full of ACh?
there are two types of nicotinic ACh receptors (neural nicotinic and muscular nicotinic), what makes them different from eachother?
subunit composition, affinity for drugs, use different ligands (but must be cations);
describe the shape of almost all agonist and antagonist to the nicotinic Ach receptor.
quaternary ammounium compounds
how many subunits make up the nicotinic receptor?
five (usually the types of subunits are mixed - alpha, beta, etc.)
in muscle there are four types of subunits with alpha repeated twice; which subunits do Ach bind to?
Ach binds to each alpha subunits (in nerve there may only be alpha, or a mix of alpha and beta)
explain how the nicotinic receptors work.
at rest the gate is closed; when ACh attaches to its alpha subunits, the gate opens and allows ions to pass
there are two major subdivisions of neuromuscular blocking agents, nondepolarizing and depolaring blocking agents. what is the difference in their MOA?
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)
are all muscles equally effected?
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"
released ACh acts retrogradely on presynaptic neuronal nicotinic receptors. can these presynaptic receptors be blocked?
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)
list some adverse effects of tubocurarine (nondepolarizing agent).
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)
when choosing a muscle relaxant, what do you think of?
1)Class of muscle relaxant; 2)onset time; 3)duration of action; 4)pharmacokinetic profile; 5)cardio effects; 6)need for reversal
what is the shortest acting muscle relaxant?
list the physio-chemical properties that make up a good muscle relaxer.
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)
describe the shape and size of nondepolarizing agents.
heavy, bulky, rigid molecules that block but don't activate cholinergic receptors
name an alkaloid curare drug that releases histamine.
name a drug that promotes a muscarinic block.
aminosteroids (muscarinic receptors are located on the post-synaptic cleft in the parasympathetic ANS) -
name an aminosteroid nondepolarizing blocking agent that has an onset of 3-5 minutes and 12 min recovery of twitch.
name an aminosteriod nondepolarizing blocking agent that has a very short (60-70sec) onset but a duration of action of 28 minutes.
rocuronium (min. CV side-effects)
name two short-acting nondepolarizing blocking agents that degrade spontaneously or are metabolized by plasma cholinesterase.
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
describe pancuronium.
bis-quaternary aminosteriod; slow onset, long acting, little BP effects, vagolytic, renal clearance
cis-atracurium is a stereoisomer of atracurium; it is eliminated by ___________ and its major differences from atracuirum are what?
eliminated by Hoffman degradation; it doesn't release histamine therefore it doesn't have the CV effects of hypotension like atracurium
the duration of action of NDMR in pediatrics is generally _______________; and ______________ in elderly, renal failure and hepatic failure.
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)
the only depolarizing agent, succinylcholine differs from ACh how?
it can't be broken down by SYNAPTIC acetylcholinesterase (only by plasma AChE)
what will you see on initial depolarization with depolarizing succinylcholine?
fasciculations and twitches
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.
Phase II: eventually the membrane will partially repolarize. however, the membrane is desensitized to Ach and further action potentials are prevented.
there is a deficiency that may cause a prolonged blockade of succinylcholine. name it.
pseudocholinesterase deficiency (dibucaine is a local anesthetic that inhibits normal pseudocholinesterase)
explain malignant hyperthermia and name a drug used to treat it.
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++
name some anticholinesterases. what does this mean?
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