Term
| How much acetylcholine is broken down before it even gets to the post synaptic membrane to act on nicotinic receptors? |
|
Definition
| only 50%. B/c the other 50% is broken down by AcHE and diffuses out of the NMJ. |
|
|
Term
| Acetylcholinesterase breaks down AcH into? by process known as ? |
|
Definition
| choline and acetate. Choline is a protein that gets reabsorbed back into the presynaptic terminal. Works by hydrolysis to break down AcH. |
|
|
Term
| for a nicotinic receptor to work and conformational change to allow in Na how many AcH are needed and where do they need to bond to? |
|
Definition
| Need 2 AcH to bond to both alpha sub units. |
|
|
Term
| how many subunits does a nicotinic receptor have? |
|
Definition
| 5 subunits consisting of 2 alpha, 1 beta, 1 delta and either one gamma or 1 epsilon. |
|
|
Term
| In a nicotinic receptor do adults have a gamma or epsilon subunit |
|
Definition
| adults have an epsilon subunit while kids have a gamma. |
|
|
Term
| Immature acetylcholine receptors are normally found when? What's different in their physical makeup? Where are they often expressed most often? Whats their significance? |
|
Definition
| Immature AcHR are made after deneration/immobility from injuries, also found in fetal anatomy, They differ in that they have a gamma subunit instead of a episilon unit. Mostly expressed in the extrajunctional region of the muscle membrane. These receptors depolarize much more easily to sux and AcH. This is significant because the more receptors that are open / longer open means more loss of K. |
|
|
Term
| Whats the significance of Sux and immature AcHR often seen in people with injuries to their spinal cord or from immobility? |
|
Definition
| immature AcHR also known as extra junctional receptors are more sensitive to Sux. So Sux makes them depolarize much more easily which leads to massive hyperkalemia from K loss through the open ion channel. |
|
|
Term
| Our body's have multiple built in safety mechanisms. For instance the presynaptic termian releases such large volumes of AcH to ensure that despite 50% being broken down before the post synapse that enough will get through. So what contingencies does the post-synaptic membrane have to ensure an AP is made? |
|
Definition
| The post synaptic terminal only needs 10% of it nicotinic (AcH) receptors activated to cause an action potential. |
|
|
Term
| Since it only requires 10% of AcH Receptors to be activated for an AP, how does this relate to how its difficult to give muscle relaxants to prevent this? |
|
Definition
| Well since it takes very little # of receptors to be activated AND since an over abundant # of AcH is released from the pre-synaptic terminal we can see the body has multiple back ups to ensure an AP. So when we try and block this process it becomes very challenging. We can block up to 70% of nicotinic receptors on the post-synapse and still see twitches on our TOF. In order to get ride of all twitches then we would need to block 95% of all the AcH receptors. |
|
|
Term
| what is the difference between the two types of AcH receptor inhibitos (Muscle relaxants) |
|
Definition
| There's one that acts on the receptor by non-competitively inhibiting the receptor by attaching to an allosteric site; these are called depolarizing muscle blockers and there is only one drug we use (SUX). The rest of of the drugs that block muscles are called Competitive inhibitors and they work by competing with the NT AcH for the same primary site known as the orthosteric site. |
|
|
Term
| which neruomuscular blocking agent acts by mimicking the AcH and binding to nicotinic alpha sites? |
|
Definition
| competitive inhibitors (non-depolarizing agents) |
|
|
Term
| What is the difference between phase I and Phase II blocks for depolarizing agents? What do they mean in relation to non-depolarizing agents? |
|
Definition
| Phase I and II blocks refer to Sux which is a depolarizing agent. Phase I is a normal block. There are no facilitation after TOF. All four tetany will result in four dampened BUT EQUAL responses. If too much drug is given, or if person has genetic issues or lack of plasma (PLASMA NOT NMJ acetylcholinesterase) Cholinsterase then you may see a phase II block with SUX. If you ever get fading twitches after using your TOF you have a problem. Stop the drug and sit and wait. There will likely be post tetanic facilitation. When giving SUX you should never see fading in the muscle twitches to the TOF. HOWEVER non-polarizing agents will always cause a fade in the muscle twitches to TOF. |
|
|
Term
| what is post tetanic facilitation? |
|
Definition
Post-tetanic facilitation of NMJ transmission refers to the increase in twitch tension after tetanic stimulation during a partial nondepolarising blockade
Caused by increase in mobilisation and synthesis of ACh after tetanic stimulation
Disappears after about 60 seconds of tetanic stimulation |
|
|
Term
| what is the physiology for fade when using the TOF with a patient on a non-depolarizing agent? |
|
Definition
| The non-depolarizing agent also acts on the positive feedback nicotinic AcH receptors on the presynapse. the NDMA inhibits the presynaptic AcH receptors. The AcH receptors on the presynapse normally get activated by AcH and when they do, they increase (Positive feedback) release of AcH which augments transmission to muscles. As a result of blocking these presynaptic AcH Receptors; your overal response fades b/c you dont have the excess release of AcH release on subsequent stimulations of the TOF on the nerve. |
|
|
Term
| if you get 3 twitches then how blocked is your pat % |
|
Definition
|
|
Term
| @ two twitches what % of AcHR blocked? |
|
Definition
|
|
Term
| At 1 twitch what % of AcHR blocked |
|
Definition
|
|
Term
| what is a curare cleft? What does it indicate? |
|
Definition
| On the expiratory plateau phase of the ET CO2 monitoring it indicates that the pt may be spontaneously waking up and pulling air on expiration. |
|
|
Term
| What muscle is responsible for where we test the TOF on the arm? What nerve are we stimulating? |
|
Definition
| We use the TOF on the ulnar nerve. It innervates the adductor pollicis muscle. |
|
|
Term
| If you incompletely reverse someone from a paralytic will you see a change in their tidal volume? |
|
Definition
| NOT ALWAYS..can be deceiving. Patients may have 75% block receptors but still pulling normal tidal volumes. However an incomplete reversal may effect they're inspiratory reserve volume. That's why you should check a NIF. |
|
|
Term
| 'when can recurarization occur with neuromuscular blocking agents? |
|
Definition
| can occur if you give an intermediate blocking agent and then give a reversal that does not last as long. Pt will end up going back into a partial block |
|
|
Term
| What drugs requires plasma cholinesterase to break down and does not respond to giving lots of acetylcholine |
|
Definition
|
|
Term
| If you give a reversal for your muscle block and it does nothing, what are some things you have going through your mind? |
|
Definition
1. Liver problems?
2. Genetics? - lack of acetylcholinesterase
3. Magnesium levels high? = potentiates drug.
4. Is half life of reversal less than the drug? |
|
|
Term
| You're closing a case.. You think you gave enough reversal. What signs or tests should you do to make sure patient is ready to be safely extubated and have most of the drug out of their system? |
|
Definition
1. Make sure on the TOF that they have a nearly as strong muscle response.
2. Check grip strength
3. Can they lift their head and control their airway?
4. Check vital capacity
5. Check NIF.
6. Is there floppiness? |
|
|
Term
| What muscles are poor to respond to muscle blocking agents? Why is this a good built in mechanism? |
|
Definition
| NM blocking agents have a hard time blocking the diaphragm, vocal cords, larynx and abdominal muscles. You needs these for life functions like protecting your airway, breathing and basic torso control. |
|
|
Term
| Do non-depolarizing and depolarizing muscular blocking agents cause malignant hyperthermia |
|
Definition
| ONLY SUX (DEPOLARIZING) Muscular blockers can cause MH |
|
|
Term
| if you get 3 twitches then how blocked is your pat % |
|
Definition
|
|
Term
| @ 1, 2, 3, 4 twiches how many receptors blocked? |
|
Definition
@1 90% receptors blocked
@2 80 % blocked
@3 75% blocked
@ 4 0-75% blocked (Never know!!) |
|
|
Term
| At 1 twitch what % of AcHR blocked |
|
Definition
|
|
Term
| what is a curare cleft? What does it indicate? |
|
Definition
| On the expiratory plateau phase of the ET CO2 monitoring it indicates that the pt may be spontaneously waking up and pulling air on expiration. |
|
|
Term
| What muscle is responsible for where we test the TOF on the arm? What nerve are we stimulating? |
|
Definition
| We use the TOF on the ulnar nerve. It innervates the adductor pollicis muscle. |
|
|
Term
| What are some basic chemical structures of Non-depolarizing muscle blockers...% ionized, cross BBB? Cross Placenta? Protein bound? |
|
Definition
| 100% ionized, highly protein bound, don't cross the BBB and does not cross placenta, |
|
|
Term
| what are the two kinds of Non depolarizing muscle blockers? |
|
Definition
| 1. benzylisoquinolines 2. Aminosteroids |
|
|
Term
| what type of non depolarizing MB are associated with some histamine release? |
|
Definition
|
|
Term
| if a NDMB has vagolytic activity what does that mean? |
|
Definition
| means the activity of the vagus nerve is diminished. |
|
|
Term
| what are the two muscle relaxants that are both metabolized by cholinesterase? Whats the difference between them? |
|
Definition
| Sux and Mivacurium. Sux is a depolarizing agent while mivacurium is a non-depolarizing. Mivacurium is a benzylquinolone just like nimbex and atracurium. Both mivacurium and sux are metabolized by plasma cholinesterase. |
|
|
Term
| which muscle blocker decreases the action of plasma cholinesterase |
|
Definition
|
|
Term
| name two benzylisoquinoliniums |
|
Definition
1. cisatracurium
2. atracurium |
|
|
Term
| What muscle blocker is primarily metabolized by hoffman's elimination? |
|
Definition
|
|
Term
| What non-depolarizing drug is good to use as a replacement to sux? Why? |
|
Definition
| rocuronium. Onset 1-2 minutes like sux but is duration is like pancuronium if you give 3-4 times the dose needed to block 95% of receptors. Otherwise one dose is 20-35 minutes duration. |
|
|
Term
| Why is cisatracurium (Nimbex) a better drug than atracurium? |
|
Definition
| Both are benzylisoquinoliniums. But nimbex is better because as it goes through hoffmans elimination it produces less laundanosine which means less chance for seizures. Its three time smore powerful. Less histamine release. |
|
|
Term
| The only short acting non-depolarizing muscle relaxant? What kind of drug is it? |
|
Definition
| mivacurium - benzylisoquinoline |
|
|
Term
| Name the long acting non-depolarizing muscle relaxant. What class of drug is it? |
|
Definition
| pancuronium - aminosteroid |
|
|
Term
| Why would you do a priming dose for a non-depolarizing muscle blocker |
|
Definition
| to prepare a pt for being muscle relaxed faster since these drugs aren't as fast as SUX. Give about 10% of intubation dose 3 minutes ahead of full dose. That way some of the drug gets into the neuromuscular junction |
|
|
Term
| What kind of drugs increase the blocking action of the neuromuscular blockers? In other words what drugs potentiate your neuromuscular blockers? |
|
Definition
| magnesium, diuretics, lithium, CCB, volatile agents, propanolol, aminoglycosides, acute ETOH |
|
|
Term
| What kind of drugs will decrease the block action of neuro-muscular blocking drugs |
|
Definition
| anticonvulsants and chronic ETOH. |
|
|
Term
| will anticonvulsants increase or decrease a block? |
|
Definition
|
|
Term
| Aminoglycosides will increase or decrease the action of neuromuscular drugs? |
|
Definition
|
|
Term
| Why does lasix increase the effect of NDMB? |
|
Definition
| Lasix inhibits cAMP production, which leads to decrease presynaptic junction release of acetylcholine? |
|
|
Term
| Why does magnesium increase the effect of NDMB and SUX? What kind of patients should you worry about? |
|
Definition
| magnesium increases the effect NDMB by decreaing the release of acetylcholine at the presynaptic terminal. So patients on a mag drip from torsades or in their pregnancy with pregnancy induced HTN would be at risk for toxicity. So if giving SUX you may cause PHASE II. |
|
|
Term
| how do agents such as procaine, ketamine, and anesthetics enchance the effect of neuromuscular blocking agents? |
|
Definition
| they alter the opening/closing characteristics of acetyl choline receptors and they desensitizes alpha receptors to acetylcholine |
|
|
Term
| Explain what desensitization means in regards to drugs effecting the postsynaptic membrane nicotinic receptors in relation to coconmitenant paralytic administration. |
|
Definition
| Desensitization refers to receptors on the post synaptic membrane being less responsive to AcH. As a result they do not open as often and muscle are not innervated. They remain sensitive to blocking drugs and in some cases once a blocker attaches they completely stay closed. In cases an administration of AcH can further desentitive the receptor by causing it to go to the state where it becomes desensitive. So the net effect is less receptors available for depolarizing the muscle membrane. |
|
|
Term
| What four things can cause desensitization of a the post synaptic motor neuron? |
|
Definition
1. high dose of AcH in response to Acetylcholinesterase inhibitor
2. high dose of Sux causing Phase II
3. Poor drug clearance of blockers
4. Any drug that may potentiate the muscle blocker |
|
|
Term
| The biggest concept of desensitization contributing agents such as mag, lasix ect.. is that? |
|
Definition
1. THEY DO NOT BIND TO THE ACTUAL AcH site
2. They only augment the affect of the blocking agent by desensitization |
|
|
Term
| What is a channel block in relation to muscular blocks? |
|
Definition
| the neurmuscular non-depolarizing drugs can block the ion channel and this can be increased when giving too much acetylcholinesterase inhibitors. |
|
|
Term
| If you give a acetylcholinesterase inhibitor along with a neuromuscular blocker what happens? Are both non-depolarizing and depolarizing neurmuscular blockers affected? |
|
Definition
| If you inhibit acetylcholinesterase then you will have more AcH in the synapse. This will compete with non-depolarization muscular blocks such as nimbex or vecorunium. So you will hopefully decrease the block. An example of an acetylcholinesterase inhibitor is neostigmine. IF given with a depolarizing agent such as Sux you actually risk causing a phase II block. Extra AcH risks desensitizes the receptors to AcH which means they wont cause contraction. IT also means you increase risk of a channel block. Also acetylcholinesterase inhibitors also decrease the amount of plasma cholinesterase so now your SUX lasts longer. |
|
|
Term
| which drug is excreted unchanged in the urine? |
|
Definition
|
|
Term
| The aminosteroid drugs are metabolized where? excreted where? examples of aminosteroids? |
|
Definition
| deacetalyted in the liver and are excreted unchanged in bile. Panc and Vec are metabolized in liver. Roc is not metabolized it is just excreted. |
|
|
Term
| This neuromuscular blocker is known to cause the hr to go up...IN this physiology remember the drug is some how acting on the PNS. |
|
Definition
| pancorunium. Its most vagolytic out of the drugs. |
|
|
Term
| You give Sux and then the person begins to twitch..whats that called...why?> |
|
Definition
| Sux is a depolarizing drug and when it initially binds at an allosteric site it causes a conformational change in the muscle acetylcholine receptor and the muscle initially depolarizes. |
|
|
Term
| You may have prolonged paralysis from giving Sux b/c |
|
Definition
| Pts may have genetic issues and lack enough plasma cholineserase |
|
|
Term
| What can non-depolarizing agents do to our drive to breath? |
|
Definition
| They can suppress the signal from the carotid body to the CNS since they connection uses nicotinic AcH receptors. If they are suppressed then we have a decrease in response to hypoxia. |
|
|
Term
| What neuromuscular blocking agents trigger release of histamine? |
|
Definition
| sux and benzylisoquinolines ( nimbex and atricurium) |
|
|
Term
| who's at more risk for histamine release from muscle blockers? |
|
Definition
| women > than men. SUX can CAUSE THE WORSE ANAPHYLAXIS. |
|
|
Term
| Histamine release from administration of a muscle blocker may cause anaphylaxis. Either way what is the immune response involved..what Ig... |
|
Definition
| IgE causses antigen-antibody reaction. Then the complement system is activated IgG and IgM. |
|
|
Term
| For induction what is the dose for a paralytic |
|
Definition
|
|
Term
| Which types of non-depolarizing agents have a larger VOD? |
|
Definition
| steroidals b/c they can more easily access other areas of the body due to their lipid structure. |
|
|
Term
| Does increase or decrease VOD cause increase potency? Why? |
|
Definition
| decrease VOD. VOD = volume of distribution. There's more of a drug in the blood which means less where it actually works. Ask yourself what kind of drugs like being in blood? Well they must like water, be somewhat lipidphobic. decrease VOD means the drug wants to get where it needs to and avoids being every where. |
|
|
Term
| if pt SNS is increased like increase CO ect.. then what happens with effect of the neuromuscular blocking agent |
|
Definition
| induction is not as fast. Drug gets diluted everywhere. Duration is longer. |
|
|
Term
| Why do obese people need more sux? |
|
Definition
| because they have more plasma cholinesterase which breaks down SUX |
|
|
Term
| since nimbex is primarily eliminated via hoffman's reaction what factors effect this reaction |
|
Definition
1. temp: .So low temp = more potent drug 2. pH : so acidosis means more potent drug
Think of the surgery pt coming out of the OR..what is the triad of death? Hypovolumia, hypothermia, acidosis. All three of these kill patients and also potentiate the effects of paralytics which use hoffman for elimination (mivacuronium, nimbex and atracuronium) |
|
|
Term
| What is accommodation in relation to NM block |
|
Definition
| the muscles which are blocked from further AcH transmission can still respond to outside electrical stimulation from our TOF because we have only inhibited the motor end plate. Past that we can still activate outside perijunctional zone. B/c in perijunctional zone are inactivated sodium channels. So beyond that is able to depolarize to our TOF. |
|
|
Term
| What is E95 for paralytics? Is that the dose for clinical dose? |
|
Definition
| E95. is the dose necessary for 95% block in 50% of patients. |
|
|
Term
| What does it mean when you give a "defasiculating dose" ..what is the physiology involved here? |
|
Definition
| It means you're giving 1/10 dose of a NDMB like roc several minutes prior to giving Sux to offset the uncomfortable feeling of fasiculations associated with Sux. By giving a NDMB you are inhibiting nicotinic receptors. That means less receptors available for Sux. Sux needs nicotinic receptors in order to work. NDMB inhibit those receptors. So you need to give larger doses of Sux to get the same effect to account for the decrease in receptor numbers from the non-depolarizing agent. |
|
|
Term
| what is the physiology of how SUX works? |
|
Definition
| Sux is two acetylcholine molecules combined by an ester link. It competitively binds to the alpha sites on nicotinic receptors of the postsynaptic muscle fiber membrane. Unlike acetylcholine,sux only needs to bind to one site to illicit a depolarization. Also unlike AcH, Sux stays bounded to the receptor for much longer keeping it in a longer state of depolarization. As a result the voltage gated sodium channels remain open much longer in their inactivation state (The gates that need a repolarization to occur for them to close) this keeps the membrane depolarized. |
|
|
Term
| decrease the number of nicotinic receptors on the motor end plate and what does that do to sux |
|
Definition
| Sux will not work as well!!! It needs / Wants receptors. |
|
|
Term
| what is the role / physiology of the extrajunctional receptors on motor fibers and Sux |
|
Definition
| Extra junctional receptors exist on all muscle fibers. All that means is that they are receptors in other places than the neuromuscular junction. (spread out). Keep in mind the only way to cause akinesthesia is by acting on the neuromuscular junction receptors. So these extra EXTRA junctional receptors are more of a nuissance and not helpful. People who don't use their muscles a lot like spinal cord pts or mysathenia gravis have lots of extra junct receptors. They too get activated by AcH or by Sux. More activation means more channels open and more K loss!!! But they do NO contribute to paralysis. |
|
|
Term
| by giving 1/10 of roc to pre treat for fasiculations what will you have to do with your sux dose? |
|
Definition
| double it. B/c ndmb just decreased the # of available receptors for Sux to act on. |
|
|
Term
| what are four contraindications for sux |
|
Definition
1. spinal cord damage
2. anaphylaxis to sux
3. muscle dystrophies
4. extensive burns
5. MH hx |
|
|
Term
| a majority of Sux's side effects are caused by fasiculations..why? Explain the physiology |
|
Definition
| Fasiculations associated with Sux is a result of sux acting on presynaptic AcH receptors. Although the fasiculations are short they are enough to cause damage to the muscle and release of myoglobin, CK. The muscle fasiculations in themselvs requires increase O2 needs. The byproduct of all this energy consumption is CO2. High levels of CO2 cause cerebral artery vasodilation and increase ICP, that then causes release of catecholamines to counter dilation and vagal mimetic stimulation. So then you get tachy and HTN. |
|
|
Term
| defasiculating also known as |
|
Definition
|
|
Term
| What is the ideal dose for precurarization |
|
Definition
| Give 10% of normal roc E95. NOT THE INTUBATING DOSE!! Give 3 minutes prior to pushing sux. IT helps offset discomforts and SE of fasiculations and myalgias. |
|
|
Term
| What is the duration to 25% receovery of Sux |
|
Definition
|
|
Term
| Sux can cause brady but often it is in only what population? |
|
Definition
|
|
Term
| what is the normal time it takes after giving sux for diagphram to come back? Why is this important clinically? relate to preoxygenation |
|
Definition
| it take 5 min after sux is given until diag is back working. This is very important because in a unable to ventilate / unable intubate we know that the drug will wear off and hopefully the patient will start breathing on their own. Also by adquately pre-oxygenating a patient we know that they have highly o2 rich resevoir of air (2L in their expiratory reserve volume) where oxygenation can occur at 250mL/min for up 5 min efficently). |
|
|
Term
| how much K is increased in the body as a result of giving Sux? |
|
Definition
|
|
Term
| YOu should be wary to give Sux to any patient with a condition that UP OR DOWN?? Regulates extra junctional receptors? |
|
Definition
| UP Regulates extrajunct receptors. AVOID SUX. Up = more Extra junct receptors. More of these means more channels to loose K. These receptors dont contribute towards paralysis. So risk cardiac arrest. |
|
|
Term
| why do kids need more Sux to get the same effect |
|
Definition
| Kids have more extra junc receptors. So lots of the drug gets bonded to the wrong receptors. Sux needs to get to the junctional receptors to illict paralysis. |
|
|
Term
| elimination of NDMB such as roc and vec is done via what process? |
|
Definition
|
|
Term
| Name out of these drugs which are most potent in order... then which one drug out of these four will have the fastest onset and why? Atracurium, Nimbex, Roc, Vec |
|
Definition
| In order from strongest to weakest. Nimbex-->Atracurium-->Vec--> Roc. The fastest onset for these drugs is Roc. Since roc is lease potent you need to give lots more quanities of the drug to illicit same effect. The result is higher concentrations in the blood. Concentration gradients decide how fast a drug starts working on receptors and crosses into NMJ. So higher gradient then faster effect! |
|
|
Term
| Whats the main benefit of atracurium and whats a draw back |
|
Definition
| Benefit is you can give it and it does not matter about disease state of patient. Down side is you can't give larger control dose and get a faster onset like you can with roc. Also any higher than normal dose will cause increase histamine release. |
|
|
Term
| what are the advantages and disadvantages of pancuronium |
|
Definition
Advantages: no histamine release, counteracts bradycardia if need be like from opioids
Disadvantages: long acting, increase SNS BP and HR so bad for heart patients, more difficult to reverse |
|
|
Term
| What are the advantages and disadvantages of Vec |
|
Definition
| advantages: no histamine, no cardio effects Disadvantages: active metabolites, metabolized in liver. primary excretion in biliary. |
|
|
Term
| What are the advantages and disadvantages of Roc? |
|
Definition
Advantages; no histamine, no cardio effects, no active metabolites, duration is similar to vec, Fast onset 1.5-3 min
Disadvantages: more incidences of allergic reactions. |
|
|
Term
| What is myotonia. if you have myotonia and give sux what happens? |
|
Definition
Myotonia refers to the condition in which muscles are slow to relax after contracting. It occurs in a
number of diseases such as myotonic dystrophy, myotonia congenita and paramyotonia congenita...so giving sux causes a depolarization and fasiculation except in these patients THEY STAY CONTRACTED!!!!! |
|
|
Term
| sustained head lift by patient will indicate what regarding their % muscle blockade? |
|
Definition
|
|
Term
| mechanism for recovery form sux is from? |
|
Definition
| diffusion of Sux out of the NMJ. Once out of the junciton it can be hydrolyzed by pseudocholinesterase. REMEMBER NON DEPOLARIZING AGENTS GET OUT OF THE S"YNAPSE BY REDISTRIBUTION. SUX IS BY DIFFUSION AND GRADIENTS. SO IF LESS PLASMA CHOLIN then less breakdown of sux in plasma. So if no break down of sux in plasma then how do you create that change in gradient to get sux out of junction!! Hence why toxicity!! |
|
|
Term
| What organ makes pseudocholinesterase? Why is it important to know this? |
|
Definition
| the liver makes cholinestersase so if pt has liver problems they may have low levels of pseudocholinesterase and therefore have prolonng muscle blockade after SUX or mivacuronium. |
|
|
Term
| What is dibucaine number? How is it used? What is a normal dibucaine #? What is a bad #? How will this influence your clinical decisions in drug choice for muscle blocks? |
|
Definition
| Dibucaine test will tell us how well the plasma cholinesterase is functioning. We need plasma cholinesterase to break down sux and mivacuronium. Dibucaine inhibits normal plasma cholinesterase. So if we can inhibit 80% of enzyme then the patient is normal. If we only inhibit 20% of plasma cholinesterase then we have to worry the patient has abnormal plasma cholinesterase and it will prolong our muscle blocks for hours. |
|
|
Term
| bradycardia as a result of giving sux is a result of stimulation of??? |
|
Definition
| muscarinic receptors are stimulated by sux (remember its two AcH molecules combined). The stimulation of muscarinic receptors on the SA node result in brady. (Vagal response) |
|
|
Term
| All triggers for Malignant Hyperthermia include? |
|
Definition
| Halogenated inhalation agents and Sux. |
|
|
Term
| Why would you not give Pancuronium for precurarization of sux |
|
Definition
| Panc was found to inhbit plasma cholinesterase. So although it may help with diminishing the fasiculations of sux, it prolongs sux. So its not a good choice. |
|
|
Term
| Name contraindications of Sux |
|
Definition
1. denervation, burns, immobilization and severe sepesis after 2 days.
2. allergy to sux
3. MH hx
4. homozygous for atypical plasma cholinesterase
5. Hyperkalemia
6. Eye wound. |
|
|
Term
| If you decide to pre treat for fasiculations associated with sux what should you do to your sux dose? |
|
Definition
| increase sux dose by 25-75% since the NDMB will decrease the # of available receptors for sux to work on. Therefore you need to increase the # of Sux molecules to ensure they can act on enough receptors to illicit the safe intubation outcome you desire. |
|
|
Term
| How does Vd effect the potency of the muscle blockers? |
|
Definition
| increase Vd means less drug. b/c more volume that drug has to dilute into. So a patient with fluid retention will have an increase Vd |
|
|
Term
| Which muscle blockers have active metabolites? |
|
Definition
|
|
Term
| The characteristics of a non-depolarizing neuromuscular blockade differ from those of a depolarizing neuromuscular blockade except that both exhibit |
|
Definition
| decreased response to single twitch stimulus |
|
|
Term
| In planning your anesthetic for the day, you (the student CRNA) decide you want to use pancuronium because it is so cheap (and will make you appear cost-conscious). However, your patient presents with ____ and ____ so you choose another neuromuscular blocking agent, knowing that the patient’s condition contraindicates the use of pancuronium. |
|
Definition
| chronic renal insufficency and tachycardia |
|
|
Term
| . Pancuronium is not administered as a(n) infusion because it exhibits ____ with repeated doses |
|
Definition
|
|
Term
| Atracurium should be used very cautiously, if at all, with ____ because it exhibits histamine release. Other agents that exhibit histamine release include ____ |
|
Definition
| use carefully with asthmatics, other drugs that illicit histamine release are mivacurorium, nimbex and sux |
|
|
Term
Pharmacologic and physiologic variables that enhance non-depolarizing neuromuscular blockade include all of the following EXCEPT:
a. volatile anesthetic agents
b. hypothermia
c. magnesium
d. burn injury |
|
Definition
|
|
Term
| Edrophonium inhibits acetycholinesterase by forming ____, whereas neostigmine and pyridostigmine inhibit acetylcholintesterase by forming ____. |
|
Definition
| an electrostatic attachment to the anionic site on acetycholinesterase; a carbamyl-ester complex at the esteratic site on acetylcholinesterase |
|
|
Term
Of the three commonly used reversal agents, ____ exhibits the fastest onset while ____ exhibits the longest duration.
a. edrophonium; neostigmine
b. neostigmine; pyridostigmine
c. physostigmine; edrophonium
d. edrophonium; pyridostigmine |
|
Definition
| edrophonium; pyridostigmine |
|
|
Term
Of the three commonly used antimuscarinics, ____ exhibits the most sedation effect, ____ exhibits the most antisialogogue effect, and ____ exhibits the most increased heart rate effect.
a. glycopyrrolate; scopolamine; atropine
b. scopolamine; glycopyyrolate; glycopyyrolate
c. scopolamine; scopolamine; atropine
d. atropine; atropine; scopolamine |
|
Definition
| c. scopolamine; scopolamine; atropine |
|
|
