Term
| each AcH Vesicle contains how many AcH |
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Definition
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Term
| A quanta of AcH refers to what |
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Definition
| A packet of AcH of which there are 5-10,000 AcH |
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Term
| Acetylcholine is synthesized from what two materials |
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Definition
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Term
| What type of Ca channels are needed to open to release AcH |
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Definition
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Term
| how many acteylcholine receptors at the motor end plate |
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Definition
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Term
| describe the chemical structure of Sux |
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Definition
| Di-ester, bis-quaternary amine |
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Term
| Giving a non-depolarizer prior to sux whille increase or decrease your sux dose requirements |
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Definition
| INCREASE. A non depolarizer prior to sux will desensitize the receptor to future depolarization. So need more sux after |
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Term
| name the three metabolites of sux and which one or ones are active |
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Definition
Metabolites of Sux
1. Succinate
2. Choline
3. Succinylmonocholine - ACTIVE MEtabolite |
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Term
| describe the nicotinic receptor structure |
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Definition
| 5x glycoprotein subunits. Two alpha, one beta, one delta and epislon. |
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Term
| fetal nicotinic receptors have what kind of subunit |
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Definition
| have a gamma glycoprotein sub unit. |
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Term
| pts with denervated areas will have a nicotinic receptor made up of what kind of subunits |
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Definition
| all alpha 7 subunits. VERY SENSITIVE TO AcH |
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Term
| To get a noticeable decrease in twich heigh you have to bblock what percentage of receptors on the motor end plate |
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Definition
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Term
| For a complete block what percentage of nicotinic receptors on the motor end plate need to be blocked |
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Definition
| 92%. So 8% of activated N receptors will not allow enough ions in to cause an AP. |
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Term
| Describe the physiology of non-depolarizing drugs and why we see a fade |
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Definition
| Its related to postiive feedback on the presynapse of the neuromuscular junction. Normally excess AcH will stimulate more AcH release. But when these receptors are blocked then extra AcH will not be released and thereofre all subsequent releases of AcH are decreased overall. So we see fade. |
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Term
| ____ % of a non-depolarizer can be given prior to sux to help with desfasiculations |
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Definition
| 10% of IV intubating dose |
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Term
| When would you see myalgias from sux |
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Definition
| 24-48 hours after injection |
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Term
| What type of surgery north of the chest is a contraindication for sux and why |
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Definition
| NEVER GIVE SUX with an open eye globe injury because sux always increases intraocular pressure. |
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Term
| What is the positive and negative effect of Sux on the GI tract, aspirations ect.. |
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Definition
Negative: It increases intragastric pressure
Positive: Increases lower esophageal tone MORE than intra gastric so it cancels out in favor of blocking stomach contents from coming up and out. |
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Term
| You can expect an increase of ____ in intraocular pressure after administration of sux |
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Definition
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Term
| Is there a link between administering Sux to dystrophy patients and those patients having MH |
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Definition
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Term
| Name five condtions that result in decrease plasma cholinesterases |
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Definition
1. pregnancy
2. liver disease
3. uremia
4. malnutrition
5. burns
6. plasmapheresis
7. oral contraceptives |
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Term
| a normal dibucaine # is? Explain what this means |
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Definition
| refers to how much in % dibucaine (a local anesthetic) can block plasma cholinesterase. A normal person should have cholinesterase that is totally blocked by dibucaine. So dibucaine when administered should block >80% of plasma cholinesterase. IF it blocks only 40-60% then the person has an issue. If it blocks <20% then they have a bigger issue. (homozygeous. ) |
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Term
| You can expect an increase of ____ in intraocular pressure after administration of sux |
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Definition
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Term
| Is there a link between administering Sux to dystrophy patients and those patients having MH |
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Definition
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Term
| Name five condtions that result in decrease plasma cholinesterases |
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Definition
1. pregnancy
2. liver disease
3. uremia
4. malnutrition
5. burns
6. plasmapheresis
7. oral contraceptives |
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Term
| a normal dibucaine # is? Explain what this means |
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Definition
| refers to how much in % dibucaine (a local anesthetic) can block plasma cholinesterase. A normal person should have cholinesterase that is totally blocked by dibucaine. So dibucaine when administered should block >80% of plasma cholinesterase. IF it blocks only 40-60% then the person has an issue. If it blocks <20% then they have a bigger issue. (homozygeous. ) |
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Term
| following Sux administration, what sign, often seen in pediatrics, is indciative that patient may have a 10-20% risk factor for MH |
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Definition
| Masseter muscle spasm despite all other muscles being paralyzed. |
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Term
| describe post-tetanic facilitation and its use in the OR |
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Definition
| The physiology of post tetanic fade is as follows: A tetanus burst causes a large release of acetylcholine. The AcH flushes out the nicotinic receptors of NDMB drugs. Then wait 5 seconds (for the flushing out to take full effect) and then do a TOF. This post tetanic TOF should be stronger than if you HAD NOT done the tetanus. |
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Term
| anti-convulsant therapy such as __ and ___ can do what to your neuromuscular block? WHY |
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Definition
Anti-convulsant therapy such as:
1. carbazepine
2. dilantin
Can create resistance to NDMB (roc, vec and pancuronium) If therapy is long term due to increase extra junctional receptors. Since body tries to accommodate for decrease Na. |
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Term
| Acute adminstration of dilantin will do what to neuromuscular blockade |
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Definition
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Term
| Reglan does what to neuromusuclar blockade? |
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Definition
| inhibits plasma cholinesterase so it PROLONGS BLOCKADE IF SUX IS GIVEN. |
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Term
| describe post-tetanic facilitation and its use in the OR |
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Definition
| The physiology of post tetanic fade is as follows: A tetanus burst causes a large release of acetylcholine. The AcH flushes out the nicotinic receptors of NDMB drugs. Then wait 5 seconds (for the flushing out to take full effect) and then do a TOF. This post tetanic TOF should be stronger than if you HAD NOT done the tetanus. |
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Term
| Anticonvulsant therapy such as __ and ___ can do what to your blockade |
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Definition
| cabamazepine and/or dilantin can create resistance to getting a good block if the therapy is chronic. |
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Term
| Acute administration of what anti-convuslant can intensify a block |
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Definition
| Acute administration of dilantin will increase your block |
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Term
| What drug used for GI motility inhibits plasma chlinesterase and therefore may prolong Sux |
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Definition
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Term
| What class of ABX, and name some drugs under them, which can depress the neuromuscular function |
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Definition
| Aminoglycosides (neomycin and streptomycin athe most) |
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Term
| what autoimmune disease targets post-synaptic receptors on neuromuscular junction |
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Definition
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Term
A patient with Myasthenia gravis will respond how to
1. Sux
2. NDMB |
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Definition
Myasthenia gravis pts have immune systems that attack the nicotinic receptors.
1. Sux - resistant response., Bc sux works by activating the receptor. But these receptors are screwed up.
2. NDMB: work by competively binding to receptor. So if there are less viable receptors than a NDMB will increase the sensitivy of the receptor to NDMB. |
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Term
| If a patient has a thymooma than you suspect they have what disease |
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Definition
| Thymoma is a tumor originating from the epithelial cells of the thymus. Thymoma is an uncommon tumor, best known for its association with the neuromuscular disorder myasthenia gravis;[ |
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Term
| duchenne type muscular dystrophy is genetically described as? |
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Definition
| X linked, hereditary disease |
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Term
| another name for duchenne type muscular dystrophy |
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Definition
| pseudohypertrophic muscular dystrophy |
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Term
| two major complications of giving sux to a patient with duchennes are |
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Definition
1. Severe hyperkalemia
2. Rhabdo |
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Term
Pts with plegias will respond how to administration of
1. sux
2. NDMB |
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Definition
If its 1 week - 6 months after injury they will:
1. Sux: sensitive!
2. NDMB: SENSITIVE!
This is due to the flacidness stage. After which they enter spastic phase. |
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Term
| patients with burns and Sux what happens |
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Definition
| Lots of extra junctional receptors on burn patinets so sux will cause profound hyperkalemia. NDMB will be resistated. |
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Term
| A patient with liver disease will need more or less NMB? Why |
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Definition
| Need MORE. B/c NMB are very ionic and love fluid. But in liver pts the ECF is increased as it finds its ways all over hte body like ascites ect due to decrease protein. So need more drug in body to fill out this larger tank/reservoir. |
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Term
Lower motor neuron diseases and
1. sux
2. NDMB |
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Definition
1. Sux: sensitivty
2. NDMB: Resistance |
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Term
| describe the chemistry of atracurium and cisatracurium |
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Definition
| both are biquaternary ammonium benzylisoquinoline compounds of intermediate duration |
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Term
| Name the two ways atracurium and nimbex are broken down |
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Definition
1. hofmann elimination
2. Ester hydrolysis |
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Term
| Hofman elminiation is dependent on what two things |
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Definition
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Term
| at a dose of ___ atracurium causes histamine release |
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Definition
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Term
| name a toxic product of atracuium and nimbex..what does it do potentially |
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Definition
| laudanosine may cause seizures |
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Term
| Which nondepolarizer has a active metaoblite. What is it called |
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Definition
| PAncuronium has a active metabolite called 3-OH. This has 1/2 the neuromuscular blocking activity of the pancuronium |
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Term
| name side effects of pancuronium |
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Definition
| increase HR, increase BP and increase C |
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Term
| rocuroium is in what chemical class |
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Definition
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Term
| elimination half life of rocuronium |
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Definition
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Term
| How is the drug eliminated |
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Definition
| almost entirely in the urine, bile or feces. So not metabolized. Major clearance is liver |
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Term
| at a dose of ___ atracurium causes histamine release |
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Definition
|
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Term
| name a toxic product of atrcurium and nimbex. What does it do ptoentially |
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Definition
| laudanosine may cause seizures |
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Term
| which nondep has a active metabolite whats its name |
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Definition
| panocuronium and vecorunium Active metabolite is 3-OH which has 1/2 the blocking power as pancuronium |
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Term
| name the side effects of pancuronium |
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Definition
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Term
| ROC is what type of chemical |
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Definition
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Term
|
Definition
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Term
|
Definition
| MAJORITY IS ELMINATED VIA LIVER. ALMOST NONE IS METABOLIZED> So what is elminiated is the drug itself unchanged. |
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Term
| what concept/physiology decides duration of action for drugs like roc or vec |
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Definition
| REDISTRIBUTION! Not elmination. |
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Term
| name the muscle in the airway that holds open airway |
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Definition
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Term
| the TOF is used to sitmulate what muscle on the hand |
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Definition
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Term
| Tetanus occurs when you use a frequence greater than ___ on the stimulator |
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Definition
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Term
| if you only get 1/4 on TOF then you know ____ % of receptors are blocked by your NDMB |
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Definition
| 80-90% blocked with a TOF 1/4 |
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Term
| If you get no twitches on TOF then you know what % of receptors are blocked |
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Definition
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Term
| A TOF of 3/4 or 4/4 can have a block involving what % of receptors |
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Definition
| 75-80 % of receptors blocked |
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Term
| After a 5 second tetanus of 50 Hx you wait 5 seconds and then do a TOF. What are some of the possiblilities of the TOF and what do they indicate |
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Definition
| TOF, Post tetanic stimulus, will indicate how long a person will t ake to come back to illiciting normal twitches without tetanus. So the more post-tet #s then the more likely they'll be back sooner. |
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Term
| You know after giving a tetanus and then checking post-tet TOF that if you only get 1 twitch that you have how long until normal twitch returns |
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Definition
| 15-20 minutes (if intermediate drug given). |
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Term
| what can a patient do that correlates very well with a TOF ratio of > 0.86 |
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Definition
| pt clamping jawas shut or biting down on tubs or bite block |
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Term
| the breakdown of AcH of acetylcholinesterase is what type of reaction |
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Definition
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Term
| what is the structure of physostigmine that allows it to cross the BBB |
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Definition
| it is a tertiary amine unlike the others which are quantenary amines. So it can cross the BBB. |
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Term
| neostigmine binds to what site of the acetylcholinesterase |
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Definition
| binds to the esteratic site |
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Term
| what drug is broken down by acetylcholinestersase by binding to its anionic site |
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Definition
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|
Term
| principle route of excretion for Achase blockers is |
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Definition
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|
Term
| peak action of edrophonium is? While peak action of neostigmine |
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Definition
1. edrophonium: 1-2 minutes
2. neostigmine: 7-11 minutes |
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Term
| physiologically why does edrophonium peak onset so much faster |
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Definition
| b/c it binds to the anionic site on acetylcholinesterases to inhbiit while neostimine has to covalently bond to the esteric siste which is much longer to do. |
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