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64 Cards in this Set
- Front
- Back
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do motor neurons have ganglia involved and if not how do they work
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motor neurons pass through the spinal cord straight to the muscle
NO GANGLIA INVOLVED |
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why can NMB be used during surgery
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they immobilize the patient and allow us to use less anesthesia than we'd need to paralyze the patient using anesthesia alone
NMB HAVE NO ANESTHETIC OR ANALGESIC ACTIONS (you still feel pain but have no muscle responses if you use NMB alone) |
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how do NMB expand the operating field
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allow us to get way down in the body by getting rid of risidual tone
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how do NMB get used in the case of intubators and intensive care ventilators
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they are used b/c you don't want the patient fighting the tube going down their throat so you paralyze those muscles
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what kind of Rc are find at the motor endplate
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nicotinic rc
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what are our Depolarizing NMB
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succinylcholine (THIS IS THE ONLY DEPOLARIZING NMB)
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what are the properties of SCC
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looks like 2 molecules of ACh w/ a bridge
more stable than ACh at the nicotinic Rc so it will bind to it and stay there and continue to stimulate the Rc till it comes off short acting |
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what are the properties of NON DEPOLARIZING COMPETITIVE NMB
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antagonist
competitive but can overcome the competitition by adding more agonist (ACh) bind to two ACh binding sites and prevents ACh from binding but doesn't activate the Rc always has a bridge some are isoquinolines or ammonia steroids |
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what is the order of paralysis when starting a blockade
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eye lids > face > head > limbs > trunk
smaller muscles have more finely motor controlled muscles and are more sensitive and will therefore relax first WHEN THE BLOCKADE WEARS OFF THE REVERSE HAPPENS WHERE LARGE MUSCLES HAVE MORE TONE SOONER |
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what does the membrane do to recover from being depolarized
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excrete potassium through potassium channels
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how does the membrane become depolarized from the binding of ACh/SCC
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once ACh or SCC has binded the Na channel opens and Na comes in and if it is a large enough AP the membrane becomes depolarized
AS LONG AS THE MEMBRANE IS DEPOLARIZED WE CAN'T STIMULATE ANOTHER CONTRACTION |
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what happens in pesticide poisoning with AChE-Inhibitors
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we flood nicotinic Rc throughout the body w/ ACh and we see paralysis because we are activating the Rc so much/so rapidly that it can't repolarize the membrane b/c as soon as one molecule of ACh comes off another one comes on
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what is the #1 reason people die from pesticide poisoning
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paralysis of the respiratory muscles therfore they can't breathe
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what does AChE-I and ACh do to phase 1 of depolarizing blockade
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it reinforces it b/c we're not giving the Rc a chance to recover
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what occurs in Phase 1 depolarizing blockage
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SCC activates the Nicotinic Rc and due to its intrinsic activity it causes a influx of Na that depolarizes the membrane and due to its stability once one SCC comes off another one comes on and we can't repolarize the membrane at this point any further SCC has no inherent activity and will act like a NON DEPOLARIZING COMPETITIVE NMB
this phase looks like you're flooding the system with ACh |
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what is AChE-I role in phase one
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they reinforce phase 1
we already have a depolarized membrane and by using AChE-I we're indirectly giving it more ACh and muscles can't fire b/c membrane is already depolarized SCC itself has no AChE-I action ACh alone will also reinforce phase 1 blockade |
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what occurs in phase 2 depolarizing blockade
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SCC now appears like a non depolarizing competitive nmb
SCC can no longer stimulate the Rc due to it not being able to repolarize the membrane so instead SCC will be sitting at the Rc just preventing ACh from binding |
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how does SCC block Na influx in phase 2
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In phase 2 the membrane is depolarized and has not been given a chance to repolarize and as a result when SCC binds it will just prevent ACh from binding and there won't be any Na influx since our membrane is already depolarized
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when does SCC lose its IA
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in phase 2 once the membrane becomes too depolarized
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what phase of depolarizing blockade is similar to Myasthenia Gravis
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phase 2 since in MG you give the patient AChE-I that they may have too much ACh in the synapse causing their muscles to get weaker
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what is the purpose of the Train of Four
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want to see how much your body responds to electrical stimuli (4 electrical impulses)
THIS IS HOW YOU MONITOR HOW DEEP THE PARALYSIS IS |
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at what point does SCC become a non depolarizing competitive inhibitor
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during phase 2 once it has depolarized the Rc so much that it no longer has intrinsic activity
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when does the Na channel open
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phase 1
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when is muscle fasiculation seen and what is it
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muscle twitching
this is initially seen b/c we're activating the nicotinic Rc and since SCC has Intrinsic activity here when it initially binds twitching occurs until we reach paralysis |
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what is AChE-I role in phase 2 depolarization
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it can be used to reverse the blockade by acting like a competitive agent and competing away SCC and therefore start to wear blockade off by competiting away SCC w/ AChE-I
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what are the side effects of SCC
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cardiac arythmias
stimulates autonomic ganglia (muscarinic Rc in SA node) increase intraocular pressure histamine release |
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what is the cause of hyperkalemia in relation to NMB
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due to K rushing out of the cell in an attempt to repolarize the membrane
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what kind of patients would you see hyperkalemia in
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cardiac patients
burns diuretics |
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what could patients experience due to hyperkalemia
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cardiac arrest
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why do people who wake up from SCC paralysis feel sore and what can you use to reduce soreness
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muscle fasiculation in phase 1 resulting in the build up of lactic acid
non depolarizing NMB can be used as an adjunct to reduce soreness |
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what is the benzylisoquinoline prototype
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D-tubocurarine (dTC)
competitive non depolarizing no intrinsice activity side effects: histamine release, bronchoconstriction, salivation, hypotension, ganglionic effects (less than SCC) |
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when is the wave of paralysis seen
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seen for depolarizing and non depolarizing blockade
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why is Mivacurium shorter acting than dTC
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due to its functional groups
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what is the only exception that Mivacurium has
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shorter duration than dTC
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what are the modifications of dTC
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mivacurium
Atracurium Cisatracurium |
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what are the type, chemical class, and metabolism, duration of SCC
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type: depolarizing
chemical class : none metabolism : plasma cholinesterace duration : short |
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what are the type, chemical class, and metabolism, duration of mivacurium
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type: non depolarizing
chemical class : isoquinoline metabolism : plasma cholinesterace duration : short |
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what are the type, chemical class, and metabolism, duration of atracurium
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type: non depolarizing
chemical class : isoquinoline metabolism : plasma esterases, hoffman reaction duration : intermediate |
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what are the type, chemical class, and metabolism, duration of cisatracurium
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type: non depolarizing
chemical class: isoquinoline metabolism : plasma esterases, hoffman reaction duration: intermediate |
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what are the type, chemical class, and metabolism, duration of rocuronium
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type: no depolarizing
chemical class : steroid metabolism: hepatic duration: intermediate |
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what are the type, chemical class, and metabolism, duration of vecuronium
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type: non depolarizing
chemical class: steroid metabolism: hepatic duration: intermediate |
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what are the type, chemical class, and metabolism, duration of pancuronium
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type: non depolarizing
chemical class: steroid metabolism: renal (little hepatic) duration: long |
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what are the steroids (ammonia steroids) [non depolarizing]
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pancuronium
rocuronium vecuronium |
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which NMB have histamine release
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all of them except cisatracurium
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why does cisatracurium not have histamine release
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it is a purified isomer form of atracurium and histamine release has been minimized by removing the inactive isomer
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what are the properties of pancuronium
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has 2 positive charges which make it soluble so soluble that it is mostly renal
has vagal activity and will increase HR by inhibiting the vagal nerve |
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what are the guidlines for NMB use
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duration of procedure should match duration of blockade
look at patients kidney fxn, liver fxn, do they have asthma, glaucoma what kind of metabolism side effects: ganglionic activation, histamine release |
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what are the types of metabolism NMB can undergo
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hoffman reaction
hepatic renal plasma cholisterase |
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what is a hoffman reaction
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doesn't require the kindey or the liver atracurium and cisatracurium can undergo this
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what drugs would be good for people w/ liver/kindey failure
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atracurium
cisatracurium mivacurium SCC |
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what happens with plasma cholinesterase
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some NMB (SCC, mivacurium, atracurium, cisatracurium) can be broken down in the plasma
good choice for people w/ renal/hepatic excretion problems |
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where are fasciculations seen
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depolarizing phase 1 only
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where are tetanic fade seen
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non depolarizing
depolarizing phase 2 |
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what is AChE-I role in Non depolarizing, depolarizing phase 1, and depolarizing phase 2
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non depolarizing ANTAGONISM
depolarizing phase 1 POTENTIATION depolarizing phase 2 ANTAGONISM |
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what are depolarzing blockers role in Non depolarizing, depolarizing phase 1, and depolarizing phase 2
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non depolarizing ANTAGONISM
depolarizing phase 1 POTENTIATION depolarizing phase 2 N/A |
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what are non depolarizing blockers role in Non depolarizing, depolarizing phase 1, and depolarizing phase 2
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non depolarizing POTENTIATION
depolarizing phase 1 ANTAGONISM depolarizing phase 2 POTENTIATION |
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what is the ADME of NMB
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contain 1-3 ammonium groups
ionized at physiological pH very soluble in aqueous solutions poorly lipid soluble poorly absorbed some steroids have hepatic metabolism |
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what do NMB have interactions with
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Antibiotics
Local Anesthetics AChE-I chlorpromazine |
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what interaction occurs between antibiotics and NMB
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aminoglycosides reduce the release of ACh by competing for Ca
Lincomycin, clindamycin block open channels (block nicotinic Rc channels) |
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what interaction occurs between local anesthetics and NMB
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local anesthetics reduce ACh release and open channel blockade (potentiate the effects of NMB)
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what interaction occurs between AChE-I and NMB
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AChE-I interfere w/ NMB but we give them as needed
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what interaction occurs between chlorpromazine and NMB
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chlorpromazine potentiates non depolarizing
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what are examples of AChE-I
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neostigmine
edrophonium |
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what do AChE-I antagonize
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non depolarzing blockers and depolarizing phase 2
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