DIP Episode 443 - The Clutch Acetylcholinesterase Inhibitor Podcast (for Step 1-3)

All right, welcome. My name is Divine. This is episode 443 of the Divine Intervention Podcasts. Into these podcasts, we're going to be talking about acetyl colonnestories inhibitors. We're going to be talking about acetyl colonnestories inhibitors. This is a topic that's pretty high yield. It's tested in many different contexts on exams. Step one, step two, step three. So it's something you want to make sure you understand. So let's start off with a question. What if you get a question about it an 85 year old female? They tell you that for the last six months, her daughter is noticed that she is beginning to forget what her name is. She has to be constantly reminded of things she previously knew well before. She is having trouble coming back from the store on her own. She has had to, you know, the police has had to be called multiple times because she has missed her way back home. And then they tell you that at a mini mental status exam, this person's score was like 20 over 30. Our friends at the USMEL is going to try to put an answer that says mild cognitive impairment, but another answer they're going to put is Alzheimer's. Or they kind of hope that you realize it's Alzheimer's and then they'll see which of the following is the most likely additional finding in the species.

They can put things like this function of the bizzone nucleus of minor which is true in Alzheimer's because you know Alzheimer's we have lost ill calling and that comes because you have this function of the bizzone nucleus of minor. They can just put many different things they can put like poor blood supply in the brain which will be more vascular dementia. They can put a compilation of bidamiloid plaques which will be correct for Alzheimer's. You know the NV Me's love again these things counter-rividives something I talk about a lot in my testing course. But basically this person has Alzheimer's. Long term old person dementia kind of fits the picture. So how do we treat this person that has Alzheimer's? Well you can treat Alzheimer's with an acetylcholine esterase inhibitor because in Alzheimer's as I said the bizzone nucleus of main artist is dysfunctional. So because it's dysfunctional you don't produce adequate amounts of acetylcholine. So you can treat Alzheimer's with an acetylcholine esterase inhibitor that will very rapidly boost your levels of acetylcholine. So that can help with cognition and memory although it doesn't really improve the person's survival it doesn't slow the progression of the disease or anything like that. And by the way another series of drugs I guess you can use for Alzheimer's is a mountain. The mountain is an NMDR receptor antagonist because remember glutamate works on NMDR receptors.

When glutamate over binds to NMDR receptors it can cause over stimulation and that can kill a nerve. That's a phenomenon known as glutamate excited toxicity. So the mountain kind of shuts that down by being an NMDR receptor antagonist but let's focus to the on the acetylcholine esterase inhibitors. Let's focus on them. So I guess the major part, second major part I just want to talk about is how do these things even work? Again acetylcholine esterase inhibitor. If you think about it first things first is understanding what is acetylcholine esterase? Acetylcholine esterase is an enzyme you'll find in many synapses. Its job is literally to break down acetylcholine. It breaks down acetylcholine into acetylcholine that's literally what it does. So the more acetylcholine esterase activity you have in a synapse the less acetylcholine you have because it's being broken down progressively. So if you give an acetylcholine esterase inhibitor it's going to bump up your levels of acetylcholine and that's going to be really great. It's going to be really really helpful. So the thing is one of the major aims I had with making this podcast is to break down acetylcholine esterase inhibitors into four groups. This is not a grouping that is commonly used but think of it as the USMLE grouping of acetylcholine esterase inhibitors.

If you build a framework in your mind like this then you will not mix these things up because even if something is an acetylcholine esterase inhibitor it doesn't necessarily mean that it can treat a particular kind of disease. Like for example it's not every acetylcholine esterase inhibitor that you can use for Alzheimer's. It's not every acetylcholine esterase inhibitor you can use for atropine over those. So it depends on the use. So in your mind for USMLE purposes break down acetylcholine esterase inhibitors into four groups. The first group of the organophosphates we're going to talk about those. Those are like the nerve agents, bioterrorist agents or you see a person that is like a farmer trying to commit suicide. You see this farmer is like leaky from everywhere. He has a lot of diarrhea, a lot of vomiting around the area. That's a cholinergic toxin from organophosphates. Those things are acetylcholine esterase inhibitors. That's group one. Group two we have the Alzheimer's agents. Again as I've said in Alzheimer's acetylcholine is low. So giving an acetylcholine esterase inhibitor is very very very helpful. So that's going to be something like donate pezel galantamine or reverse stigma donate pezel galantamine or reverse stigma. Those are the only acetylcholine esterase inhibitors you should use for Alzheimer's. Pyrateolstigmin is an acetylcholine esterase inhibitor. It does not help. You shouldn't use it for Alzheimer's on your exams.

Even if it has the correct mechanism of action. If you pick it as you answer on a test for Alzheimer's you will get that question wrong. The third group of acetylcholine esterase inhibitors are those that cannot cross the blood brain barrier. Many times these things are called like quaternary acetylcholine esterase inhibitors. So these are going to be things like pyritolstigmin or neolstigmin. These things work more in the periphery. They don't have any brain effects. They don't cross the blood brain barrier. And then the final group is phyzo stigma. So these are acetylcholine esterase inhibitors that can cross the blood brain barrier. Because the thing is when people have the literal effects from atropine they don't just get peripheral effects. They also get some central effects. So if you want to fix an atropine overdose because remember atropine is a muskronic receptor antagonist. So because it has the ability to block muskronic receptors not just in the periphery but also in the central nervous system. If you want to reverse atropine toxicity you need something that can cross the blood brain barrier. Phyzo stigma is a high yield acetylcholine esterase inhibitor to understand because it actually does cross the blood brain barrier. So you can treat both the peripheral effects of atropine poisoning but it can also treat the central effects of the muskronic poisoning that you get with atropine. So again these four categorizations, again number one are the organophores feeds.

And as we also have the nerve gas those things that people used to murder people. And you know farmers used to come into your side. And then number two we also have the Alzheimer's agents. Those are donepes, zeal, gallantamine, or vestigmen. And then number three we have the quaternary acetylcholine esterase inhibitors that cannot cross the blood brain barrier. The classic ones that things like new stigma or pirato stigma. We use pirato stigma for my senior gratis. And then number four we're going to have those that have the ability to cross the blood brain barrier. Things like phyzo stigma. Phyzo stigma is going to be a major, a major model for for this stuff. So again acetylcholine esterase inhibitors, again the inhibitor acetylcholine and they're going to bump up your levels of acetylcholine. The inhibitor, the enzyme that breaks down acetylcholine by doing that you're going to build up your levels of acetylcholine. Now to be honest with you, these things I used for for many purposes. And you do need to know them. Again they kind of present them with different kinds of vignettes on exams. Like for example they can give you a question about a terrorist attack where many people died within like an hour or so of being exposed to an agent like at a train station or whatever. And then they tell you that many of these people had right in Oria, they had a lot of diarrhea, they were sweating profusely, they have had profound breathing cardio.

And you see that you want to think about organophosphate poisoning. You want to think about nerve gas right there. There are many, the stuff kills people pretty pretty quickly right. And again how those it work are some of them are like irreversible inhibitors believe it or not. Obacetylcholine esterase is going to bump up your levels of acetylcholine and that's going to cause problems. That's going to cause problems. That's going to cause problems. And this look can dive very quickly. Again why do we have breathing cardio? Well your parsy and pathetic system slows conduction down your EV node. So you're going to have pretty cardio. Your parsy and pathetic system rest and digest you're going to have a lot of diarrhea. You're going to have a lot of vomiting. You're going to have a lot of ryanoreal. The person is going to be sweating. Remember acetylcholine stimulates your sweat glands. Stimulates your sweat glands. So you're going to sweat a ton right. And you're going to have like just increased secretions from that high level of acetylcholine. Remember acetylcholine raises your secretions. I'm going to talk about some of different contexts in a bit. But it does cause you to secret a lot of stuff. So all these people are going to have problems and then they're busy. You're going to suffer, keep and die. You know many things are going to shut down. Which is obviously not a good right. So we're going to fall sweet poison. That's that's the story there.

And remember we're going to try to go to fall sweet poison with first with atropine. Atropine is a most grainy receptor antagonist. But then secondly you're going to trip with with pre-lidoxine. So number one is atropine. Atropine will very rapidly reverse the effects. But the thing is organophosphate poisoning is is salvageable. Let me put it this way. Solveageable if you act quick. Because the thing is ultimately organophosphates at least many of them are irreversible as they're called in history as inhibitors. Once the but the thing is for a season for a short period of time they are reversible. They don't bind and be irreversible immediately. No, it actually does stick some time. So the thing is there's almost like this window of opportunity during that reversible phase where you can rescue those people. So that's where pre-lidoxine comes in. Pre-lidoxine prevents you from going from that reversible phase of acetylcholinesteris inhibition with organophosphates to the it prevents you from going from that reversible phase to that irreversible phase. So you can resurrect acetylcholinesteris in that way. Just something you kind of want to keep at the back of your mind on the exams. And then what if they give you a question about a patient and they tell you that this patient has a rock hard poop here. Well, and he develops suddenly he per se has a lot of eye pain. Well, I'll really be thinking about you then go closer to glaucoma.

Again, one of the ways we can treat that stuff is we can actually use acetylcholinesteris inhibitors. Because again by using an acetylcholinesteris inhibitor that's going to bump up your levels of acetylcholine and that can cause populary constriction. When you have populary constriction that's going to increase the outflow of EKS humor and that's going to very quickly lower your entrachyl pressure. Although remember, you can also keep pylocarpin. Pylocarpin is a most chronic receptor agonist that can help you with those purposes. So notice these acetylcholinesteris inhibitors that kind of indirect cholinergic agents. They're indirect cholinergic agents. They indirect cholinergic agents. Okay, what if they give you a question about a lady, she's like 51 years old and you know she tells you that for the past few weeks she's been having trouble swallowing and that in the evening she has in the evening she has trouble reading and that her eyes get tired and she just has to go to sleep very quickly. Well, this lady has my stenogravis. I remember my stenogravis. The pathophases you literally have autoantibodies that are formed against the nicotinic acetylcholine receptor. You form autoantibodies against the nicotinic acetylcholine receptor. So one of the ways we can treat my stenogravis is we can use acetylcholinesteris inhibitors like pyridolstigmin. Pyridolstigmin is very good at concentrating at the neuromuscular junction.

So you can get a red of my stenogravis with pyridolstigmin. It's going to raise your levels of acetylcholine and it's going to help those people's symptoms. And then what if they give you a question about a patient that you know this patient got anesthesia, this patient was into beta and now this person has to be working up for my anesthesia. Well think about it. An anesthesia does not just involve mocking people out with an with opioids or fentanyl or purple follow whatever. You know these people to into beta person you need to weaken their muscles. So you're going to do that with these neuromuscular blocking agents. Many times they're non-depolarizing neuromuscular blocking agents. So things like rocoronium, vecoronium and things like that. So rocoronium vecoronium. Well since they're neuromuscular blocking agents that means they have things that pretty much binds to and inactivate the acetylcholine receptor, the nicotinic acetylcholine receptor. Well if you want people to wake up from this problem you know if you want to reverse your neuromuscular blocking then you have to use an acetylcholine esterase inhibitor. Something like neo-stigmin. You can use that is going to inhibit acetylcholine esterase. It's going to raise your levels of acetylcholine. And by raising your levels of acetylcholine it's going to outcompete those non-depolarizing neuromuscular blocking agents. And that can ring the personnel of neuromuscular blockade.

So that's another use of acetylcholine esterase inhibitors. Again as I've said you can use these things to fit Alzheimer's specifically. Donepesil galantamine and reverse-stigmin. There's no one known as tachrin but it's not really available in the US. So you're very likely you're going to see that on your US MLE exam. Again those are the only ones that are approved. You'll remember it as drg. Donepesil reverse-stigmin galantamine. You know drg like doso reganglian. Donepesil reverse-stigmin and galantamine. Again these things are centrally active. So they're very helpful in this in people that have Alzheimer's. And then also don't forget that acetylcholine esterase inhibitors you can use them for people that have like they have like overflowing continents right where they are. The trussromosols just do not sense that the bladder is full. They don't sense that the bladder is full and then you know the bladder just keeps building they have these very high pulls voider as it wants. So they don't pee in a timely fashion but you know obviously the bladder has a great capacity just doesn't have a limited capacity. So after a while these people are going to literally pee on themselves. So you don't want that right. So you can meet those the trussromosols do their jobs. You can meet those the trussromosols do their jobs by giving an acelcholusher inhibitor like neostigmin. It's going to raise the levels of acetylcholine and that's going to cause these people to pee.

And then it's going to stimulate those the trussromosols are going to pee. Right. Obviously if you also have like a bowel upstairs like a you know your your gotis hypomotal after surgery you know because anesthesia really shots that a presence of GI tract. So you know all these opioids kind of drains your GI tract to a halt means you can't stupid it. But one way you can kind of fix that problem is you can literally give something like neon steaming. You know steaming is like acetylcholine nestries inhibitor is going to raise your levels of acetylcholine and by doing that that can actually that can actually help with your GI motility that can actually help with your GI motility okay that can actually help with your with your GI motility that can actually help with your with your GI motility. Again you know you can also use these acetylcholine nestries inhibitors to treat like atropinovredox remember atropino as I said earlier on is an acetylcholine receptor antagonist. So you know you're going to get an anticholinergic toxic drum. So you're going to be dry you're going to have ultra mental status delirium you're going to be tacky cardic cannobal stents you're going to just be really really dry. So you can treat that atropinovredox with phyzo steaming. Again you can know you really shouldn't be using any of the kind of acetylcholine nestries inhibitor to treat atropinovredox because the thing is atropinovredox is the blood brain barrier so that's brain effects.

So if you want something to reverse atropinovredox you want something that doesn't just work only in the periphery but can also work in the brain you can actually cross the blood brain barrier and inhibit acetylcholine nestries in the brain so you can raise your levels of acetylcholine to outcompete that atropinovredox that's why you need phyzo steaming phyzo steaming is used to fix an atropinovredox you fix an atropinovredox with phyzo steaming. And I guess I'll just you know because I know people in medicine are coffee lovers I'll just throw this in. And I've noticed that people that take coffee if you notice that especially people that take like heavily caffeinated coffee every notice the minions will tend to have diarrhea. You know there's some people you just notice that man this person just pooping a lot they're like she I take this coffee keeps me awake but man I always like poop a lot after I take this coffee. Well call me surprised.

The thing is caffeine believe it or not is a non-competitive is a non-competitive inhibitor of acetylcholine nestries right caffeine literally inhibits acetylcholine nestries well if you inhibit acetylcholine nestries acetylcholine levels are going to go up well guess what's going to happen you're going to poop a lot because you're going to be like in a hyperperperacid pathetic state like in it's just one of these you know where things that you know people wonder like why do I always poop with all this coffee well that's the reason you know so taking the caffeinated coffee mean not being on wise idea although I kind of feel like when you take the caffeinated coffee it's like what's the point of taking coffee at all you're kind of losing people take coffee for the for the caffeine obviously right people people take coffee for the caffeine and they remember one of the tests you can use to diagnose my senior gravies is the edrop is the tensilent test right edroponium. Edroponium is the drug that we use for that test well how in the world does edroponium work?

Edroponium is actually an acetylcholine nestries inhibitor when it acts for a very short time literally the duration of action is like like 10 minutes it doesn't work for very long at all doesn't work for very long at all so that's why you cannot use it to like treat my steener gravies if not the person who have to take it almost like every every 10 minutes kind of ridiculous but basically you'll notice that man a person that has my steener gravies their neuromuscular transmission is going to improve with the administration of adrofolium and why is that because again it's a sedalcholine nestries inhibitor it's going to bump up your levels of acetylcholine and that's going to help with neuromuscular transmission right you can use it as a diagnostic test in my steener gravies although remember you can also use this ice test for my steener gravies because acetylcholine nestries you don't just inhibited by drugs acetylcholine nestries is also a temperature sensitive enzyme okay temperature sensitive when the environment around acetylcholine nestries is cold it really doesn't work very well so the thing is if you slap ice on a muscle group that is weak and a person has my steener gravies by slapping ice on it you lower the temperature locally that's going to inhibit the activity of acetylcholine nestries so you're going to have decreased breakdown of acetylcholine so acetylcholine levels are going to go up and that's actually going to improve temporarily those people's neuromuscular symptoms obviously as you start warming up warming up warming up those people again as you remove the ice the symptoms are going to literally come right back okay so that's the kind of the pathophase behind that test again I really hope you're getting you're getting a lot of benefit from this podcast because again many of these things are pathophysiological things that you'd actually have to un

derstand okay the things you do have to understand you know I again I also kind of talked about glaucoma earlier you know I was throwing a drug called echofiopheat and you don't find any many resources anymore but every now and then it has this nasty habit of showing up on exams equal phyopheat is literally spelled as ECH O THI O Ph-A-T-E equal phyopheat sounds an awful lot like organophosphate right so it kind of works that way at least pretty is a pretty good acetylconnestory is inhibitor so the bumblepill levels of acetylculin has a pretty long duration of action pretty amazing drug but you can use it to treat glaucoma I mean it's actually a very good eye drop okay it's actually a very very good eye drop actually pretty pretty good eye drop okay so as we wrap up I'm gonna go ahead and maybe talk about some contraindications to these acetylconnestory inhibitors like what are some situations where you should not give those and again if you're interested I do offer before I continue I do offer review sessions I do offer a review courses for step one I have one actually ticking please next month and for step two and step three I actually have one ticking please right now and then I also have a bio statistics review course it's a four hour course I have an MBME testing strategy classes for step one to step three so two and a half hour course and then I have a social sciences ethics you know quality improvement professionalism communications healthcare systems review this that one is for five hours again if you're interested in any of these classes just shoot me an email through the website again the thing is many of my classes don't have they're not lecture beast they are problem beast so it's gonna be a lot of scenarios because that's literally what your exam is gonna be and you know me I love explaining pathophys especially when it matters so you're not just gonna be

getting facts thrown at you you're actually gonna understand the understand concepts that you can understand content so again if you're interested in any of these classes just shoot me an email again many people have taken these classes and they found you to be extremely helpful I mean like some that attended the social sciences class and the bio stats class email me recently and say that you know what I don't think I go to single bio stats or single ethics question or healthcare systems or qi question on my exam again these these courses are pretty comprehensive they're pretty thorough again obviously no course can cover everything but they cover a lot of the high old things you're gonna see when you're exempt okay but if you interested in any of them I have podcasts out there announcement podcasts on these you can also just shoot me an email through the website and I can give you some more information okay so what are some contraindications to these things because the thing is our friends at the mbms they're they're very wise right again they know that we live in an onkey generation so what do they try to do these days they just try to find like ingenious ways to test the same concept so remember I said that oh you can use an acetylchol in history and you better like new steaming for like overflowing continents I also said you can use it for like a bowel obstruction but you got to be careful you can there's a particular kind of obstruction you cannot use it for so see for example if a person has a bowel obstruction because there's actually like something anatomical or whatever blocking that g i truck please do not use an acetylchol in history is inhibitor and again I'm gonna shout out this disclaimer again none of this that I've seen any of my podcasts is medical advice it's just more for again exam prep purposes so you might leave me very with this please don't use

any of these things to make medical decisions that's not smart consult with a physician or you know whatever okay so the if a person has a bowel obstruction from an anatomical problem you know let's say they have like adhesions in the bowel or whatever please please please do not give an acetylchol in history is inhibitor because think about it I said that oh if you if your zone for no pio is and you have constipation yeah an acetylchol in history is inhibitor will help but if you have like a high grade obstruction from like something actually including your g i truck you don't want your g i truck to be contracting in those circumstances you you want to keep pushing food pushing food through pushing food through when there is an actual obstruction that can actually cause the person's bowel to rupture that can cause bowel rupture so you don't want to do that also if you have urinary tension because you have like again an actual obstruction an anatomical problem let's say for example you have like a like your your urethra is dysfunctional so it's up like it's physically obstructed with something with fibrosis or whatever given an acetylchol in history inhibitor is not smart because again if you keep giving that you're going to keep stimulating those the trussure muscles stimulating those the trussure muscles stimulating those the trussure muscles the thing that's going to happen is your bladder can literally rupture so again you don't want that when people have these high grade obstructions I'd be very careful about giving acetylchol in history inhibitors and also you want to be really careful about acetylchol in history inhibitors you know in a person that has COPD cause people that have COPD or people that have like really bad asthma their herways are not great to start right because think about it one of the ways we treat COPD or asthma is to use drugs like eapratro

pium well how do you think eapratropium works eapratropium is a most chronic receptor antagonist so it's basically like an anti-cholinergic agent it makes absolutely no sense to say oh gee let's let's give this person an acetylchol in history inhibitor if you give them those acetylchol in history inhibitors you're literally going to bump up their levels of acetylcholine and then you're going to close their airway and then they're you're going to die so you don't want to do that you don't want to do that that's not a good thing to do and then also remember acetylchol in history inhibitors they're not going to be good for certain arrhythmias like for example if a person has a heart block you're going to work in that heart block by giving an acetylchol in history inhibitor well why is that because again if you give an acetylchol in history inhibitor you're going to raise your levels of acetylcholine you're literally going to slow down conduction through the EV node you're literally going to slow down conduction through the EV node and that's not going to be a good thing because these people they already at baseline have a slow conduction through the EV node so do you think it'll be a particularly smart idea to give them something that will slow the EV node down even more that's not a really good it's not a great mix I will tell you that is is it's not a great mix you'll really really slow down the heart rate you can take them into into assisted and again that's that's not a that's not a good not a good alto so do you gain something you want to keep in mind on on exams right you want to keep in mind on exams or like say for example a person has WPW W like a killer question on the exam president has wolf Parkinson white you don't want to give an acetylchol in history inhibitor because the thing is especially less than they have like a fib with WPW right the thing is if a p

erson has if it would with WPW or person has WPW in general you want that a red near to stain the atrium you don't want it to go to the ventricle because that can precipitate V fib so in general one of the ways you do that is you try to encourage flow through the you you you try to encourage flow through the oh sorry sorry sorry sorry sorry sorry sorry yeah yeah yeah you you try to encourage flow through the AV node because when people have WPW they have this bundle of Kent that is transmitting signals is taking away signals from the atrium to the ventricles instead of letting go through the AV node instead of letting go through the AV node because you want things to go through the AV node because those signals that are going through the bundle of Kent in WPW is not it's not really good those signals going through the bundle of Kent is not particularly good when those things go through the bundle of Kent you know let's say you have if it would WPW that if it can just zip real quick to the ventricles and precipitate V fib and then that's a big problem if it is bad but V fib is worse when the presence V fib the essentially dead they essentially dead so you want to try to prevent that so you want to try to encourage flow through the AV node so if you give an acetylchronicization inhibitor to these people that will really grind things to a halt in the AV node they'll literally grind things to a halt in the AV node because again you're going to have an increase in acetylcholine so that's proper acid but that's going to slow conduction down the AV node that's going to encourage more flow because if the signals from your HMC that man this AV node is pretty slow it's a pretty it's like a slow traffic road let me take the fast traffic or let me take the bundle of Kent right so you're pretty much worsening your Rhythmia in those people so again acetylcholine series inhibitors t

hey're not good ideas in people that have certain arrhythmias again like hard block for presence WPW if it would WPW not a good idea right or if people have like peptic ulcer disease or they're taking in sets man you're going to raise the risk of GI bleed by giving an acetylcholine industries inhibitor because remember your parasympathetic system encourages gastric acid production it literally encourages gastric acid production so if a person is taking something that can mess up gastric acid production or the person already has like peptic ulcer disease then giving an acetylcholine issues inhibitor is going to make them make more gastric acid right so let me sorry let me not say messes with gastric acid production but anything that kind of makes your belly develop ulcers like NSAI Ds right or again let's say you have peptic ulcer disease already throwing an acetylcholine series inhibitor on top of that that's like throwing a light on on gasoline that's going to worsen things right this will going to make a lot make a lot of acetylcholine it's going to really stimulate the production of gastric acid by those parietal cells H Cl and those will are going to develop ulcers right so if a person has like a GI and acetylcholine series inhibitor is not smart because again they're going to produce more gastric acid going to cause more risk and worsen those GI bleeds so again I know you'd be like wow these things are not testable I wish you all the best on your exam all these things I've described in this podcast they're super super high yield to know so again I think I'm going to go ahead and pause here again as I do at the interview podcast I do offer one or one tutoring for all the USMLE exams step one to step three complex one to three I just don't tutor OMM I don't tutor that so on for that I was talking I was seeing women I didn't mean women I mean OMM I guess I can see wit

h Maxine kind of sounds like women but I don't I do tutor men and women okay just FYI but I don't tutor to OMM OMM OMM I don't I don't tutor to that and then I also have review courses again for step one step two step three preclinical medical exams 30-a-shelf exams and then I also have an MBME test-taking strategies class a biostatistics class and a five-hour social sciences and ethics review in that class I cover ethics social sciences quality improvement healthcare systems communications and things of that sort and then finally I have this podcast on the major apps Apple Podcasts Google Podcasts and Spotify I also have a You Tube channel Divine Intervention USMLE podcast and videos that's where I post the videos that I make and some all your versions of this podcast I post them on You Tube and then finally have a website called Divine Intervention Life Lessons.com that's where I post the life lessons that I make many people they they're like man Divine I really love the life lessons you put at the end of some of your podcasts so I actually started a new website Divine Intervention Life Lessons.com there is actually an Apple podcast associated with it is called the Divine Intervention Life Lessons Podcast and this podcast right now we have I think about 160 episodes most of them are like 10 to 20 minutes long I post to every week for the most part and you know using a biblical perspective it addresses a problem that many people face so again it's something that I think you'd find to be helpful you can really speak to you and can really give you some guidance on you know testy situations you may kind of be dealing with now the the final thing I want to say I guess I want to give a quick life lesson here is just play the long game many people try to play the play the short game in life but it doesn't really help it's better to be patient take the long path but surely su

rely get to your destination and say let me drive through let me fast track and then don't make it or you have to go back and go back on that long road that you you avoided in the first place so I'll just encourage you play the long game just be methodical on your path to success don't be the kind of person that's skip steps right again you've heard me say this before but short cuts will literally call you short so stop skipping steps just follow the path I feel like we leave it in the world these days where many people just want to skip steps they want to get there very quickly you don't want to follow the path that every reasonable person is following don't be that kind of person follow that path like for example there's no there's no quick and dirty with a study for the USM at least you got to put in the work over a sustained period of time and then you'll get a good result that is just the truth so play the long game stop stop skipping steps and all be well with you well I'll see you in episode 444 it's gonna sound good 44 I'll see you then have a wonderful first of your week and God bless you bye for now

Acetylcholinesterase (A ChE), which breaks down acetylcholine (A Ch).

Donepezil, Rivastigmine, and Galantamine.

Organophosphates/Nerve Agents.

Physostigmine.

It will stimulate peristalsis, potentially worsening the obstruction and causing bowel rupture.

They increase A Ch levels at the neuromuscular junction (NMJ), helping to overcome autoantibody blockade of nicotinic receptors.

Pyridostigmine.

COPD/Asthma (worsens bronchospasm), Heart Block, and WPW syndrome (slows AV node conduction).

Atropine (for muscarinic effects) followed by Pralidoxime (2-PAM) to reactivate A ChE.

Reduced intraocular pressure (IOP) via miosis, which increases the outflow of aqueous humor.

It inhibits the enzyme and causes increased A Ch levels, leading to hyperperistalsis and diarrhea.

The Tensilon test; it has a very short duration of action (minutes).

Pyridostigmine.

COPD/Asthma (worsens bronchospasm), Heart Block, and WPW syndrome (slows AV node conduction).

Atropine (for muscarinic effects) followed by Pralidoxime (2-PAM) to reactivate A ChE.

Reduced intraocular pressure (IOP) via miosis, which increases the outflow of aqueous humor.

It inhibits the enzyme and causes increased A Ch levels, leading to hyperperistalsis and diarrhea.

The Tensilon test; it has a very short duration of action (minutes).