In this video I'm going to be talking about the autonomic nervous system with a special emphasis on autonomic nervous system pharmacology. That said, although the focus of this video is going to be on all of the different drugs that you need to know regarding the autonomic nervous system, I'm still going to touch on things like the different types of receptors and just general physiology in the autonomic nervous system. to help you establish the background information that's needed to really master the pharmacology. Now let's get into today's video and I want to sort of paint an overview of the autonomic nervous system before we start talking about nitty-gritty details.
The autonomic nervous system is broken down into two components. You've got the sympathetic nervous system and the parasympathetic nervous system. Now classically you might have heard of these as referred to fight or flight.
and rest and digest. So the sympathetic nervous system is what kicks in when your body needs to activate itself in the presence of extreme stress. And the example you can think about is this is the constellation of findings and symptoms that you'll see if you need to decide to fight a bear or to run away from the bear.
And then the parasympathetic nervous system is the complete opposite. And this is the peripheral nervous system that gets activated. when you don't need to activate large groups of muscles and hormones, and instead you're either resting or digesting.
So the classic example is you have a huge meal, and then these are the constellation of symptoms and findings that you'll see as your body is just processing that meal in the viscera. So the way that you should think about this in terms of receptors... is that the sympathetic nervous system works through alpha and beta receptors, whereas the parasympathetic nervous system works through muscarinic and nicotinic receptors.
Now, I'm taking some liberties here when I simplify these two nervous systems down to just two receptors. Again, this is not going to be an all-inclusive list, but this is how you can think about it to form a conceptualization in your brain. Now, one thing that's really important that I must point out before we go any further, is that these two nervous systems, or I should say these two subcomponents of the autonomic nervous system, they work opposite one another. So if the parasympathetic nervous system is activated, it's going to inhibit the sympathetic nervous system. And just likewise, if the sympathetic nervous system is activated, it's going to inhibit the parasympathetic nervous system.
And this just kind of makes sense, right? If you are walking through the woods and all of a sudden a bear... comes charging at you, if your body is going to activate the sympathetic nervous system so that you can either fight the bear or run away from the bear, you don't want your body to be doing things that it would need to do if you were digesting a meal, because that would be a waste of resources, a waste of blood, etc.
So just remember that when one of these systems is activated, the other one is turned off. And that's going to be useful, as you'll see later in this video, to try to figure out what the effects of different drugs are based on the mechanism. Now, before we go any further, what we probably should do is just paint a general overview of the parasympathetic nervous system.
The reason I think this is going to be useful is because the bulk of today's video, in fact, all of the pharmacology in today's video, will be on the parasympathetic side. If you're interested in learning about sympathetic pharmacology, see my other video about the different types of grafts, etc. I have a video on that.
It's not as detailed as this one, but I want the focus of this video. to be on parasympathetic agents because those are by and large the highest yield that come up on USMLE and Comlex. So let's talk briefly about the parasympathetic nervous system. The parasympathetic nervous system functions to control involuntary visceral body organs and it's said to have craniosacral outflow.
Now that's really just a buzzword which means that the parasympathetic nervous system originates at the cranial nerves and has functioning down to the sacral nerves. Now, this is in contrast to the sympathetic nervous system, which is said to have thoracolumbar outflow. So it's really just where those nerve fibers are coming from. What you should really pay attention to, and hence why I put it in red here, is that there are four cranial nerves that have parasympathetic activity.
And within those cranial nerve tracts, there are bilateral nuclei that have very specific parasympathetic function. And I've seen this come up. This is incredibly high yield, especially if you're in your first two years of medical school. When you're learning about cranial nerves, when you're learning about the autonomic nervous system, this will probably be on your exam. So you need to know the cranial nerve and the corresponding parasympathetic nuclei and what it does.
So for example cranial nerve 3 is paired with the eddinger westfall nucleus which controls meiosis and accommodation. Cranial nerve 7 is paired with the superior salivary nucleus which controls salivation specifically in the lacrimal gland. Cranial nerve 9 is paired with the inferior salivary nucleus which controls salivation in the parotid gland and cranial nerve 10 is the dorsal vagal nucleus, which controls secretions in the GI tract and lungs. This is really high yield because other cranial nerves do not have parasympathetic function.
And they're also not, you know, they're not associated with these nuclei in their tracks. So you need to know, again, just to summarize here, you need to know the cranial nerve, the nucleus that it's paired with, and what the function of that nucleus slash cranial nerve tract does, which is shown in blue on this slide. The major neurotransmitter of the parasympathetic nervous system is acetylcholine and that's really really important to understand if you're going to keep all of the pharmacology straight here and we'll touch more on that in just a bit.
But what we need to do now is talk about all the different types of parasympathetic receptors. Now the parasympathetic nervous system, if you go back to the slide a couple slides ago, I told you that it functions through muscarinic receptors and nicotinic receptors. And the way that you'll see this written out in review textbooks or question banks or even on your exam is with the capital letter M or the capital letter N.
For the purposes of today's video, we're only going to talk about muscarinic receptors because the nicotinic receptors are really not that high yield. They're just not. The muscarinic receptors, they very much are.
So we're going to talk about all these different subtypes of muscarinic receptors, which I will denote with the capital letter M. And these are the receptors. that acetylcholine is binding to or that the drug is binding to and either being an agonist or an antagonist.
So again before we get to the pharmacology you need to understand receptors. So let's just kind of make a chart here. I don't love charts but you'll see some charts in today's video because it'll help your brain keep all of this information neat and tidy. So the first receptors that we should talk about are M1, M4, and M5 muscarinic receptors.
These are all located in the CNS, the central nervous system. And really, they control cognition. So when you give somebody a drug that is an agonist at any one of these three receptors, it has pro-cognitive effects. So it helps them learn.
It helps them pay attention. It helps them speak. It helps them do spatial tasks, verbal tasks, etc. And then consequently, if you give somebody a drug, which is an antagonist at M1, M4 or M5, this has the opposite effect. So it's anti-cognitive, which means if you give somebody an anti-muscarinic drug, meaning you're blocking a muscarinic receptor, specifically M1, M4, or M5, it makes it harder for them to learn and do cognitive tasks.
The next receptor that we need to talk about is the M2 receptor, and this is located in the heart. If you... Give somebody a drug which is an agonist at the M2 receptor, it causes bradycardia.
And if you give somebody a drug which is an antagonist at the M2 receptor, it causes, well, the opposite, tachycardia. And it also causes increased AV nodal conduction. The next receptor we need to talk about is the M3 receptor.
And there's actually five different locations where this M3 receptor is found, as you can see in the cells that I bolded there for you. So every other site that I'm going to talk about now, these are all M3 receptors. So they'll all fall in that line and below. The first M3 receptor that we're going to talk about is found in the urinary tract.
And if you give somebody a drug, which is an agonist at the M3 receptor, it will cause bladder contraction, which will cause urination because the bladder has to squeeze and contract and push that urine out. And then consequently, if you give somebody a drug, which is an antagonist, at the M3 receptor, it will cause bladder relaxation, which will be the opposite of urination. So it'll cause urinary retention.
Now this should make a little bit of sense to you because if you've studied any of your cholinergic versus anticholinergic medications, you might be familiar with the fact that if you give somebody an anticholinergic drug, it causes urinary retention. And the reason is on a microscopic level, because you're antagonizing M3 receptors found. in the urinary tract.
The next location that we'll talk about for M3 receptors is the GI tract. When you give somebody a drug which acts as an agonist at the M3 receptor in the GI tract, it causes peristalsis. So this causes bowel movements, diarrhea if you give too much. But if you give a drug that's an antagonist at the M3 receptor in the GI tract, it causes the opposite effect.
It decreases peristalsis. So giving somebody too much of an anti-muscarinic agent that's antagonizing the M3 receptor in the GI tract causes things like constipation. So just try to keep all of this information straight in your head.
And I hope you're building a framework to understand cholinergic versus anticholinergic as we go. The next location of M3 receptors are the exocrine glands. When you give somebody a drug which acts as an agonist, at the M3 receptors in the exocrine glands, it causes an increased level of secretions coming from that gland. And then if you give somebody a drug, which is an antagonist at the M3 receptors in the exocrine glands, it causes the opposite effect.
It decreases secretions. So this is why when you give somebody an anticholinergic, also known as anti-muscarinic drug, that blocks the M3 receptor in the exocrine gland, you- cause the side effect of dry mouth. The next location that we'll talk about for the M3 receptors is in the eye.
If you give somebody a drug which is an agonist at the M3 receptor in the eye, it causes meiosis. If you give somebody a drug that's an antagonist at the M3 receptor in the eye, it causes the opposite. It causes medriasis.
And these receptors, these M3 receptors in the eye, this is the reason that certain muscarinic or anti-muscarinic drugs are used in glaucoma. The final location of M3 receptors that we'll talk about is in the airway. If you give somebody a drug which is an agonist at the M3 receptor in the airway, it causes bronchoconstriction.
And then the opposite, if you give somebody a drug which is an antagonist at the M3 receptor in the airway, it causes bronchodilation. Now let's pause for a second. because I just threw a ton of information at you and I don't want to overwhelm you.
Let's try to keep things straight here. If you look at the agonist actions here, you look at that whole column of agonist actions, what you should notice is that muscarinic agonists equals cholinergic effects because you're using acetylcholine, which equals anti-sympathetic effects. So think about this. When you give somebody an agonist, you're turning on a receptor. When you turn on a muscarinic receptor, you're allowing acetylcholine to do its natural job at all of these different muscarinic receptors.
And the clinical effects, procognition, bradycardia, bladder contraction so that you urinate, increased peristalsis so that you have a bowel movement, increased secretions so that you salivate, meiosis, that the eye narrows, and bronchoconstriction, it's a little harder to breathe. All of these effects are anti-sympathetic effects. So go back to my classic example.
If you're walking through the woods and a bear jumps out at you from behind a tree and you don't want to turn on the muscarinic aka cholinergic system because doing so is anti-sympathetic. And think about this. If you're about to fight or run from a bear, which is stuff that you would do through the sympathetic nervous system, do you really want your body peeing, pooping, salivating? narrowing your pupils so you can't see and pay attention to the bear, bronchoconstricting your lungs so that you can't breathe as you're about to start this fight for your life, right?
Think about it. You just don't want these effects. So to summarize, when you give somebody a drug, which is a muscarinic agonist, you're giving them a cholinergic drug and the clinical effects are anti-sympathetic. I hope that that makes sense to you. Let's talk about the opposite.
Look at the antagonist column here. All of these antagonist effects, these are muscarinic antagonists. If you give somebody a drug that blocks these receptors, it's a muscarinic antagonist, aka anticholinergic, and clinically anticholinergic or anti-muscarinic, you could say anti-parasympathetic, that is sympathetic. Okay, so let's look at all these effects. Anticognitive, tachycardia, the bladder relaxes so you won't urinate, you'll hold the urine.
Peristalsis turns down so you will not have a bowel movement. You'll keep the poop in your GI tract. Your secretions go down.
Your pupils will dilate and you'll bronchodilate. Now let's think about our classic example. A bear jumps out at you from behind a tree and you basically turn off the parasympathetic nervous system. And that's functionally identical to giving somebody a muscarinic antagonist because an antagonist would block. the parasympathetic nervous system.
i.e. it would be anticholinergic. So if that bear jumps out at you, you get tachycardia because your heart rate goes up. You're going to have to have an increased cardiac output to either fight the bear or run away.
Your bladder will relax, meaning you won't urinate because why would you want to urinate when you're about to fight for your life? Peristalsis will go down so you won't poop, which makes perfect sense to me. If I'm about to fight a grizzly bear, I definitely don't want to be having diarrhea. Secretions will go down. Your pupil will dilate, which makes perfect sense because you need to see what's happening in front of you and react accordingly.
And your airway will bronchodilate because you're going to need to be able to breathe more efficiently as you try to put this bear in its place. So the reason I'm simplifying this is to just point out that whether you're agonizing muscarinic receptors or blocking muscarinic receptors, the clinical constellation of findings can be said to be either anti-sympathetic or sympathetic. And if you make that framework in your brain, it's a lot easier to understand these receptors and the effects that all of these different drugs have.
Now let's go back and start talking about actual pharmacology now. When you give somebody a medication that acts on the parasympathetic nervous system, it's going to have one of two effects. That is to say that medications can either be parasympathomimetic, meaning it mimics the parasympathetic nervous system, or it can have the opposite of that.
It can be anti-parasympathomimetic, meaning it is an anti-cholinergic agent. So the right side of this chart, these are your cholinomimetics, meaning it mimics the natural function of acetylcholine when acetylcholine would bind to and agonize all of those muscarinic receptors we just talked about. And then on the other side, on the left side, these are anti-cholinergics or anti-cholinomimetics, meaning that when you give these medications...
They would block the muscarinic receptors that we talked about on the last slide and have the opposite effects. So we need to talk about all of the different drugs that are either anticholinergic or cholinergic. So let's start on the left side of this chart because it's a little bit easier to start on that side. So let's get the easy stuff out of the way.
Your anticholinergic agents that you need to memorize for medical school exams, graduate school exams, USMLE, and COMLEX are shown here. Atropine, scopolamine, benchtropine, trihexfenadol, oxybutynin, dicyclamine, glycopyrrolate, and ipratropium or teotropium. Now, the way to think about this is that all of these drugs are anticholinergic.
All of these drugs block muscarinic receptors, a.k.a. all of these drugs block either M1, M2, M3, M4, M5. Now, let's talk about them individually, and I'll do that. on a chart.
So we've got all these drugs. We're going to talk about two things. They're use clinically and my mnemonic if you need help memorizing something about these drugs. So let's start with atropine. Atropine is used in the treatment of cholinergic poisoning.
It's also used in unstable bradycardia. So I'm sure if you've done any ACLS, you remember in the algorithm that in unstable bradycardia, you're actually giving people atropine. And now that you understand how the M2 receptor in the heart works, this should make perfect sense to you because when you antagonize the M2 receptor in the heart, you cause tachycardia. So you're treating unstable bradycardia.
Now because atropine is a highly anticholinergic medication, if somebody has cholinergic poisoning, meaning they overdosed on a cholinergic agent, well you give them an anticholinergic agent because you're just going to reverse those clinical effects. My mnemonic for remembering this is that atropine treats the atrocious effects of organophosphate poisoning. Atro reminds me of atropine.
Atropine, atrocious. And organophosphates, those are the substances that are highly cholinergic. So on test day, if you have a question, somebody does like yard work or they even maybe overdose on an actual medication, and they...
show a constellation of symptoms that are all cholinergic. So they're like having diarrhea, et cetera. Um, you.
would give them atropine because you're going to treat the cholinergic poisoning. Now let's talk about scopolamine. Scopolamine is used to treat motion sickness. And if you live on a coastal town or you've ever gone to the beach, you have a boat maybe because you're a baller and you've got your $5 million yacht, you'll notice that a lot of the stores around those areas, they all sell scopolamine. Scopolamine is taken by people that get seasickness.
It treats motion sickness. It can treat some of the vertigo symptoms that people with vertigo experience. The way that I memorize this is scopukamine instead of scopolamine because it treats the motion sickness that would make you puke.
Benztropine and trihexfenadol, I'll tell you at the same time, can both treat extrapyramidal side effects. More so benztropine than trihexfenadol. Trihexfenadol really has more uses in Parkinson's disease.
But both of these, because they... are able to cross the blood-brain barrier and get into the central nervous system. They can act on the receptors in the central nervous system and because they're anticholinergic they treat extrapyramidal side effects.
I don't have a good mnemonic to memorize these so if you have one please put it in the comments section of this video. Oxybutynin classically is used to treat overactive bladder. It's pretty easy to memorize my mnemonic is you just look at the O and the B in oxybutynin that stands for overactive bladder.
OB, overactive bladder, oxybutynin, OB, pretty easy to remember. Dicyclamine is used for a couple different reasons, but mostly in irritable bowel syndrome. And the way that I memorize that is diarrhea that's cyclical. So DI and diarrhea for di and then cyclical for cyclamine. So dicyclamine, diarrhea, cyclical.
People with irritable bowel syndrome tend to have cyclical diarrhea and this treats that. So think about it. When you give somebody an anti-cholinergic drug or an anti-muscarinic drug, you're blocking the M3 receptors in the GI tract that usually, if agonized, would cause increased peristalsis. So by doing that, you treat irritable bowel syndrome in the sense that you slow down peristalsis and treat the diarrhea. Glycopyrrolate has a couple different uses.
The two main ones that you should know are it treats salaria and it treats It's used in surgery to control heart rate. Don't have a great mnemonic, so drop it in the comments if you got one. And then epitropium and the related teotropium are used in COPD slash asthma because when you give somebody an anticholinergic agent, you're causing bronchodilation, which is obviously extremely useful in these diseases. Again, not a great mnemonic there. So if you have one, please put yours in the comment of this video.
But this is just an overview of the very high yield anticholinergic, also known as anti-parasympathomimetic agents that all are acting as antagonists at the various muscarinic receptors that we've talked about. So in terms of creating a concept in your brain, a framework in your brain, look at this chart. In the parasympathetic subsection of the autonomic nervous system, these are drugs which block the natural function of acetylcholine. So they're known as anti-muscarinic, anti-cholinergic, anti-parasympathomimetic. And because they are blocking the parasympathetic nervous system functionally or clinically, the findings in the body are the same things you'll see if you turned on the sympathetic nervous system.
So I hope that that makes sense. Now let's jump and talk about the right side of this chart. So what happens when you give somebody a parasympathomimetic drug?
also known as a cholinergic or cholinomimetic agent. So these drugs will agonize the M receptors, and by doing so, will cause the effects that you would see if you allowed acetylcholine to naturally agonize different receptors. Now there's actually two subtypes of groups that can carry out this effect.
We've got, first I'll talk about the direct muscarinic agonists. So what these drugs basically do, is just as the name implies, they directly agonize different muscarinic receptors. So you've got a muscarinic receptor shown in black.
You've got these drugs, which are acting as the ligand shown in blue. And literally, the drug will sit in the receptor, bind to the receptor, and carry out the clinical effect. The other option is you've got indirect muscarinic agonists. And these are a little bit more complex.
And because of that, unfortunately for you, on USMLE... comlex and medical school exams these tend to get tested more often so let me just take kind of an extra minute or two here to talk about what's going on so to do that let's look at a neuromuscular junction or any synapse for that matter in the synapse you've got little acetylcholine floating around as depicted by the little pink neurotransmitters on this slide and let's kind of take a snapshot of that black box and zoom in a hundred times to look at what's happening microscopically So what's happening microscopically here is normally you've got acetylcholine, which would kind of go around, it would do its thing, and it would bind to that postsynaptic muscarinic receptor. Now, the body doesn't want acetylcholine binding to the postsynaptic muscarinic receptors for too long, right? Because if that were the case, then you would have way too many clinical effects of acetylcholine agonizing receptors, and you'd have things like diarrhea, blah, blah, blah, all the stuff we talked about. So what does the body normally do?
Well, there's an enzyme called acetylcholine asterase. And what that enzyme does is it comes and it approaches acetylcholine. It attacks the acetylcholine. and breaks down the acetylcholine.
And now there's no more acetylcholine in the synapse available to carry out its clinical effect. The way that these indirect agonists work is that they actually interfere in this process. So let's say that you have acetylcholine esterase, which would like to approach the acetylcholine neurotransmitter and break it down. But you give somebody a medication, which is an indirect muscarinic agonist.
The reason that they're called indirect muscarinic agonists is because they actually block acetylcholine esterase. So by doing so, they indirectly increase the amount of acetylcholine available in the synapse and therefore acetylcholine can bind to the postsynaptic muscarinic receptor and carry out its clinical effect. So the way that you should keep this in your brain is that you've got direct muscarinic agonists and you've also got indirect muscarinic agonists.
And specifically, the mechanism of all of the indirect muscarinic agonists is that they are acetylcholine esterase inhibitors. So they inhibit the thing that normally breaks down acetylcholine, thereby increasing, effectively increasing acetylcholine, which allows those drugs to carry out parasympathomimetic effects. So these are the two options on this side of the chart. Let's start by talking. about the four main drugs you need to know that are direct muscarinic agonists.
They include bethanacol, carbacol, methacoline, and pilocarpine. Now, let me try to simplify this for you. Look at the name of all of these agents. And with the exception, of course, of pilocarpine, they all have col in the name. And that's because these are direct col-inergic agonists.
So if you get caught up on test day and you can't remember what the exact mechanism is, if it has col... In the name, it's a direct cholinergic agonist. Let's talk about these medications briefly in a chart.
So we've got bethanacol, carbacol, methacoline, and pilocarpine. You need to know the use, and I'll give you a mnemonic if I have one. So for bethanacol, it's used in urinary retention. Carbacol is used to decrease intraocular pressure in glaucoma because it causes meiosis.
Methacoline is used in the bronchial. challenge tests, sometimes referred to as the methacholine challenge test to help diagnose asthma. P-locarpine is used in the treatment of Sjogren's syndrome.
It's used in the treatment of dry eyes because it causes lacrimation. And it's used in the diagnostic test to diagnose cystic fibrosis because it makes you sweat, right? It increases secretions and that's useful to help diagnose cystic fibrosis in the sweat test. Now, I have two mnemonics for you. for bethanacol and for pilocarpine.
For bethanacol, the way that you can remember this is that Beth pisses me off. Beth for bethanacol and pisses me off because it's used in urinary retention. Okay, because since it is a cholinergic or a muscarinic drug, it agonizes the M3 receptors in the urinary tract, which helps bladder contraction, which helps cause urination.
For pilocarpine... you want to say that all the gross stuff happens on the pillow, right? So this is kind of a gross mnemonic here, but you've got sweat, tears, blood, like there's all these different substances that you can wake up in the morning and see on your pillow.
I know you, don't lie guys, I know you're all drooling on your pillow all night and crying yourself to sleep because of how awesome my videos are. It just makes you so happy that you cry. But anyway, you wake up in the morning and you see all of that gross stuff on your pillow. P-Low for P-Low Carpene. And all the gross stuff is salivation, lacrimation, and sweat, which is the use for P-Low Carpene because you are agonizing the M3 receptors in all of your different exocrine glands.
Again, unfortunately, I don't have a good mnemonic for carbacol or methacholine. So if you have one, please help all of my... subscribers by putting that in the comment of this video. But back to our chart, we've now talked about the direct muscarinic agonists, and let's conclude this video by talking about the indirect muscarinic agonists. So again, these are drugs that are acetylcholine esterase inhibitors, meaning they inhibit the enzyme that normally breaks down acetylcholine, which makes more acetylcholine available, which means more parasympathetic effect, more muscarinic effect, more cholinomimetic effect.
So what drugs are they? Neostigmine, pyridostigmine, physostigmine, rivastigmine, donepezil, galantamine, and edrofonium. Now, this isn't the case for all of these medications, but just like there was Cole in the name of the direct muscarinic agonist, these all have, most of these have STI in the name, which is there to remind you that these are acetylcholine S-T race inhibitors, okay?
I kind of... fudged with the word a little bit, but the STI tells you that it's an acetylcholine esterase inhibitor, right? The STI is esterase inhibitor.
So these are acetylcholine esterase inhibitors. Now let's talk about the four really high yield ones that you need to know for test day. I'm not going to go through all seven of these because they're not all that high yield, but four of them definitely are.
Now those four are mesostigmine, which is used in atropine overdose. It's also used in belladonna alkaloid poisoning, which is known as deadly nightshade. So I feel like this was in some Shakespeare play. You know, someone eats deadly nightshade and then, well, too bad they didn't have physo stigmine back then. But that's what it's used for.
So just like atropine was used to treat cholinergic overdose or cholinergic poisoning, physo stigmine is used to treat atropine overdose or anticholinergic poisoning. And also belladonna alkaloid that... I think deadly nightshade is a plant, I'm not sure, but back in the day when people used to eat that or poison people with it, if they had physostigmine around, they could have treated it. Now, the way that you can remember this is that physostigmine helps treat the physical symptoms of atropine overdose, and phys reminds me physostigmine. The next one that you need to know is pyridostigmine.
This is used to treat myasthenia gravis, and the way that you can remember this is that this drug gets rid... of myasthenia gravis for pyridostigmine you should also know about edrophonium edrophonium is used in the diagnosis of myasthenia gravis um no good mnemonic here so if you have one drop it in the comments section and then lastly donepazil this is used in the treatment of alzheimer's disease and the way that i remember this is that his memory is done done for done epazil um because this is a acetylcholine esterase inhibitor, when you increase the amount of acetylcholine, you're allowing more acetylcholine to agonize those M1, M4, M5 receptors in the central nervous system that creates pro-cognitive effects, which helps the cognitive decline in Alzheimer's. But this is your summary chart.
This is what you should take away as far as knowing the pharmacology and the parasympathetic subsection of the autonomic nervous system. This video was a lot of information and I recognize that and I understand that you might have to watch this a couple times before you're really comfortable with it. But what I will leave you with if I can just tell you how to approach this material is not necessarily to memorize the individual agents, but start by really understanding the physiology, the different types of M1, M2, M3, M4, M5 receptors and what happens when you stimulate or inhibit each of those receptors.
And as you build this framework and you understand the opposing actions between the parasympathetic and the sympathetic nervous system, this will start to make a lot better sense. So if you want to dominate this on test day, this is a topic where understanding is much more important than memorization. So please do that.
Do not just memorize this. You need to understand this pharmacology. I hope that this video was useful to you. This was a long one. A lot of information.
Let me know in the comment section what you'd like to see next. Best of luck.