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eso, um, Must've welcome. Thank you so much to everyone for joining on for this visit, but revision Sachin hosted by engineering. Um, very, very, very grateful for them to be hosting this by exciting times on. And I'm very much looking for tens. I, like, say, massive. Thank you to, um, Cheryl to be and I he's going to do a short presentation of start and on. Then it should be discussion revision techniques to prevention tips and all very useful for particularly for also universe A shins. Who you have exams come up in the next few weeks. Um, and then after that, I'll be hunted over to drawn for quick injection on some high schools before we got started with the aggravation session. Who said find engines? Um, once again, most of funky. And this is a brilliant opportunity for a soul. Were really grateful a woman's massive thank you to Joan for his efforts and organizing this event. And so how just 100 over night to Charlotte from the B m A for a quick presentation. Thank you very much. Do you mind if I just take control with sharing my screen? Please? Oh, Oh, yeah. Yep. Fantastic. Thank you. Excellent. There we go. Hopefully you can I see my slides. I'm just gonna put that on percent or mood. Fantastic. There we go. So, hello, everyone. Get afternoon. Thank you very much for the opportunity to speak with feel older and a virtual manner. Um, welcome to see where if you're Mike is on me, we can hear you at the moment. Oh, can you give me know? Okay. Um, just imagine, Why can hear Cheryl. Okay. Excellent. We can hear. Oh, great stuff. I conceal the champ. Come in. Three soldiers kick off again. Thank you very much. It is quite difficult in the virtual room, but we will get their role on the in person and face of ius events. So we'll just start from the beginning. So hello again. Get afternoon, everyone. And thank you very much for the opportunity to speak albeit and a rectal manner. Welcome to the short presentation. So, over the next 5 to 10 minutes, I planned out line. Hard to be, um, a support. She started medical school on towards your future met medical career. So hopefully you'll get a better understanding of who The BMA or on any sign post in of resource is to benefit. You're a vision exam Technics. So my name is Cheryl, but lay thank you very much for the introduction. My rule is a member engagement coordinator at the, um a Northern Ireland's on it Quickly, like, just like the highlight of the presentation slides will be shared after this event on, of course, the events being recorded. So don't worry about frantically taken newts, um, in regards to have what's being shared. So the BMA is a trading in on professional association, um, organization for doctors and medical students joining the BMA allow it to become part of a large community of over 160,000 members. So, as a first year medical student you're being my membership is completely free on. In fact, over 80% off you fresher cohort is utilizing many off the resource Is 10 hunts their medical studies so high Does it be, um, a support you? As a medical student, we offer study on life support. Eso you take out the link on the screen on the B m. A website has a wealth of information and includes blood posts, free access to the BMA Library to live from recorded webinars, which would benefit your medical career. We also represent your sales as the medical students, so we have the and I M F C, which is the Northern Art um Medical Student Committee on it represents all medical students across Northern Ireland's So considers and acts on moderate affecting. Knows that study medicine on the keep priorities include supporting surgeon straight the pandemic. I think I have made Campion or racial Harris harassment shorter. Whiting participation should have financed the new medical school in north and island to medical workforce planning. Consequently, if an issue does arrive in your arise in your medical school, please share your concern for Easter and I m A C reps with a new year. If you don't know they are Jennifer Jury, Michelle Hannah or Richard Packs. Um, we also help Teo affects your medical journey by offering learning on professional development. So this includes, um, of ice in your medical See they tree and a few skills when I be our best to your career. Accessing the special exploring explore it'll if you haven't already from survival tips and high today, but fresher at medical scope on. We also provide STT a vice, the hosting localized profession, offense or revision factory switch. You'll get an insight on later on this presentation. So we just like to say to watch this bs. More information will be sure to your inbox if you are student member on. If not, be sure to just check in in your communication preference is to make sure you get information from the local office. So Akeem Ember membership benefit on a revision toe is to be in my library so that be in my library is home just thighs and stuff online. Resource is which you can access whenever you need to. Do you have access to over 22 million journals, articles, research services? Ebx he journals anywhere at any time. The library team is a great support system on that supported so many students right from freshers right through to their finals. So I would ultimately just use them as your starch engine. If you're confused or you need about a guidance. So you need about a help of a checker area. Just recheck to the team. They're fantastic. I'd also like to just do a set of clinical key is one of her new slightly benefits. You may have heard of it before, but just to emphasize is a powerful medical search engine. Support both doctors. I'm medical students with the latest evidence and a variety of four months, and it's extremely easy to use. There's also like a belt and presentation maker that helps you to like export images and you slide, show or create sort of citations, which is great, especially if you found adding a project or group. You can also improve your procedure conferences with step, step by step values, which may be hungry whenever you're up by on placement. So clinical key is going to help you cut through the information you need and a very quick and fast four months on. You can ultimate sure and collaborate anything that you're working on, and it could be access. Um, so your desktop or on your tablet or mobile is what's accessible anywhere, and it's always at your fingertips. I'd also just like the highlight BMJ on on examination. Some of you may be a worthless that form, so if you may not, I would just like to say it's a great resource which can help you to ensure that your exam righty. So as it says on screen, that provides members with access to the highest quality questions written by clinical experts so you can track your progress. Identify like your weakness is under strength and see how I like the yard a passing exam So the up allows you to revise on your commits between lectures or whenever sexual schedule. Really, so you can access mock tests dissimilar at what your ex experience on exam. They give you the best chance to pass your exams. Hopefully, that first time, right? Not only that, we also offer BMJ. Learning it's free is part of your membership prescription on here, and you get access to thousands of category learning marshals, so they're useful courses for your exams as yours medical students right up to complete in your portfolio. Whenever you begin your friend a shin years as a doctor so you can build on your knowledge, utilized the interactive website. There's audio, and there's video modules to help you learn in a simulated environment. Um, there's a great way to kind of keep up to date with practicing or changing developments in one of the world's largest trusted on online CPD providers for doctors and medical students. And it's also great cause you can print Undine load certificates as you go, and it can help with your proof of learning. So here is also a great resource. I know today's topic is just in regards to the liver, so you can click on the link there and see what modules are available. So you could maybe check that I later home, as I should have some free time. So I appreciate that many first year students on the kind dying ticks. I'm success. They come second fast, and they're always approaching. So they help break up your vision, or maybe to learn or check your revision techniques. Just follow the like on screen so you can perhaps like a pro with our ultimate study guides from the ultimate um, exam checklist. Teo Top 10 steps too hard a GI and Oscar success whenever that occurs or happens to come. Assessment time. Um, that's what the guys will look up just a mixture of your rights action off the website that would go Alaska, not least. I just also wanted to highlight um, this pre record of Doctor Martin Morgan. Doctor Morgan is inattentive care Doctor Author on BMJ on examination expert So he is sure his top tip exams for success, which is protective the relevant for students today, as they feel, is the shift towards online learning on the rise and concerns, or what the last sort of face to face time might mean for summer exams. So Doctor Morgan's key takeaways include the importance of hard to use your time efficiently. Hey, also, guys, and hard to motivate yourself with the 80 20 rule on hard to follow the coat hanger. Real dio ensure you understand the concept on before diving into the finals details. So there's the link. As you can see, just here it's already been embedded are those they actually have you tried, like just up here? It's around 20 to 22 minutes. Um, I wouldn't I wasn't gonna fly out for today for you because I could be like an exam revision technique itself. There we go. So lastly, um, just on this sort of slide, these a revision steps which, assured by your colleagues and your peers um, Jennifer Ruland on Michelle has had the pleasure of meeting the and I am a see third year reps, um, in a virtual manner. So we thought it be useful to share their experiences with you'll because they've been in your shoes. At one stage, Askew began and commence your medical journal. So they've implied a list compiled. A list of resource is to consider what, starting your revision. So it's good to kind of use different platforms to get difference. Um, hum techniques accepted to see what works best for you. So last but not least just like to say thank you very much and just includes, and I greatly appreciate your attention today. That was a quick Wessel stopped er, and I know there was a lot of information on length that you do need to follow up with. So hopefully you against some useful if I stand sign Post in resource is if you do you have any questions or queries. You can retract me at any stage. I'll just pop my information in the chart or so successful, I would just like the highlight that old this information is off readily available to be in my members. So if you're not a member, you can scan the QR code or follow myself directly, and we can definitely help you important you in the right direction. I'm very conscious of time. I'd be happy to take questions, but like I said, I can pop my email address into the chop. Or we can follow up with those and do course, Thank you again for watching last night. And I hope you have fantastic afternoon. And it's definitely going to be very, very interesting. Thank you again. Thank you so much, Cheryl, for the presentation and highlighting the great resources that they may have not for first in terms of our revision, come up to exams a swell. Just keep an eye on our instagram vegetable. Definitely sharps of those resources. I'm definitely showed the link to that. And that video as well for the intense this that you highlight it and on apologies. That's well, Cheryl for me, really interrupting in the middle. It seems like it was only my audio was problematic. So I really apologize about that. And thank you so much again, I'll just no Honda over to John just to introduce the next part of the presentation. Thank you. Very much. Um, I suppose I would just like Aqua Mother as well. Thanks, Cheryl. And then I really think at a ninja nerd on his team for providing us with a section today. Um, it is a phenomenal amount of work. Husband in behind scenes for this, um, just in basic in terms of basic housekeeping. Could be pleased Keeper are makes on mute. Um, if you have any questions, you can pop them into the chart function. Er on. I will. I will monitor them through it. I know. I know. As act, um, honesty know our king for this to be interactive, but they've allowed to get through s so we will we will work with them by email in the child function and keep keep things fluent. Um, suppose you're sort of on a note from the school. Um, from the gp society. We we We are a new, um, graduate Andrew Madison course. Uh, the amount of information coming towards us on a daily basis is is really intense on it. It really helps the Harvard number of resources at our fingertips to try and break things down on non least more show than I'm engine art at. He really has helped me along the way. And I know from talking to some of my colleagues, um, that that that he has help them understand from things as well. So I think your passions act whenever you're teaching is really evident. We're really excited. Toc what's in store today? We know the liver is an absolute monster of a topic on board. Sorry we did today that we they put ah, sort of a survey to see which it's not actually one that people wanted to cover in the liver chemistry. So thank you for doing that for us. I'm We were really excited. I'm looking forward to tell what's in store here. So we'll hold you over to Zack and his team there, I think Rob your controlling things there. Are you? Yeah. He got everything all set up for me. I'm I'm pretty technological stuff, so, yeah, we're also up here, and I wanted to just take the time really quick to say, you know, thank you guys for inviting me to do this. You know, it's an honor. I'm extremely excited. And I hope I'm able to, you know, uh, you know, provide the best possible, you know, lecture here that I can, uh, my mouth isn't working all of a sudden, I apologize. Here we go. But, yeah, I'm very thankful. Hopefully, I'm able to meet the standards of everybody. The liver is a pretty big topic, and we also are not used to doing like, uh, these physiology, lectures and a power point type of fashion. So, you know, one of the things that me Robin kristen sat down and thought about is hey, you know, what could we do that would make this? I don't know, similar to what we do on the white board, um, for our YouTube videos. And so we we decided, Hey, we'll do something a little bit different, and I hope that you guys like it. I really hope. I hope you guys do. So we'll see what you guys think at the end of this, but yeah, I'm excited. I'm excited to go ahead and talk about this. Really, Guys, if you guys are ready to roll, let's, uh let's get right into it. All right. So we're gonna talk a little bit about the liver, my friends, and, uh, this is exciting. All right, let's go ahead. Let's see here. So the first thing that we have to know we talked about the liver. There's a lot of things to go over, right? This is meant to be an overview, but obviously we have to have the basic kind of gross anatomy down for you guys. So first thing is obviously knowing where the liver is located. That's a simple thing, right? For the most part, patients, it's going to be located in that right upper quadrant just beneath the diaphragm. And, ah, one of the interesting things about the liver is that it's actually like the largest, like Oregon and particularly like one of the largest glands in the entire body. It's actually one of my one of my top favorite organs. I think it's just a really cool organ itself. But there's many different lobes of the liver, right? So we have particularly four different lobes. So we have the right lobe, the left lobe, and then there's two other, like tiny little ones that don't get enough respect. We have no respect, so that's your quadratus lobe, and you're caught a lobe. So those are tiny little lobes that usually you can see under the undersurface of the liver, So there's actually like these little kind of like ligaments that we have all around. The liver is usually one of those ligaments. You have what's called the round ligament or the ligamentum Terry's and usually that kind of like little ligamentum Terry's. It is usually the and these patients the quadrant load will be located to the left of that, and then you have another one, which is called You're Caught a Low. But that's another tiny little guy, and that's usually located on the left of the ligament of the nose. Um, but we have these different lobes of the liver. The whole thing that I wanted to show you guys is really when we talk about the liver here, I think this is the one I'm gonna start with. We talk about the liver here. We have a couple different things that we have to talk about, and the first thing is like the blood supply. That's really kind of the big thing. We talked about the liver, so there's a bunch of different supplies to the liver. The first one we should talk about is the arterial supply. So coming off of that big fat artery that you have within your abdomen, your abdominal aorta, there's a particular vessel here called the Ciliac Trunk. So here's your abdominal aorta. The abdominal aorta is going to give off this branch called the Celiac Trunk. And then there's different branches that come off the celiac trunk, right? So you have, like your left gastric artery. You would also have your splenic artery, and then you have this big soccer here called the Common A pad a card, the common a pad. A card will also branch into a couple of different things, but the main one that we need to know that feeds into the liver is called the a panic artery proper. So the paddock artery proper is going to be the main primary artery that will feed into the liver. That's going to be the primary arterial supply, and the big thing that you need to know for that a pad a card reprocess A is that it's a supplying oxygen rich blood to the liver. Okay, so whenever somebody goes into maybe some type of significant shock, maybe they have some significant hypertension from cardio cardiogenic shock or septic shock. There's a significant reduction in this arterial blood flow to the liver, and over time that can lead to, ah, significant oxygen deprivation of those liver cells. And they can start to, unfortunately die and lead to something called a shock liver. That's kind of like a clinical relevance there. So sometimes when people go into shock and you measure their LFTs, sometimes they may have these bumps in there. LFTs. There's a ST and lt because of a reduction in the arterial supply not to deliver. All right, so that's one of the big, big supplies. The other one that actually supplies. It's more significant volumes of blood to the liver is actually called the portal venous system. So that's this big, big blue sucker right here that's called your portal vein. Your paddock portal vein. Now the paddock portal vein. What's interesting about this one is it has a lot of different tributaries that you see kind of feeding into it. One is, it's actually coming from the pancreas. I guess my question is, is this this this blood that's coming from the pancreas? I have a question for you guys. What would it be the significance of having blood coming from the pancreas. There might be a very specific hormone that's actually released by the pancreas that are liver needs to metabolize a very specific molecule. What kind of hormone to be coming from the pancreas that are liver would generously want to utilize? Yeah, so James said insulin. A lot of guys, they're saying insulin. That's a pretty cool thing. So when we think about that, I just think that makes perfect sense Is having this blood coming from the pain Greece is gonna be donating insulin? And one of the reasons why that's important is think about where the rest of the blood supply is coming from. So you have what's called your superior mesenteric veins in your inferior mesenteric veins. Right? So the super mesenteric veins are particularly taking blood from parts of your small intestine and then generally from the proximal part of like your large intestine. And then you have your information and tear it bands, which are taking blood from like your transversing. You're descending corner parts of that area, so that's gonna be containing nutrients, things like glucose. And if you have high amounts of glucose that are going to the liver. You're gonna want to be able to have insulin that maybe could be readily available to help with that process, to shuttle the actual glucose into those cells and accelerate it. And also, it's going to get, you know, insulin gonna get distributed into the circulation. Your general circulation go to many different organs as well. That will help to push that glucose into the cells, so I think that's a pretty cool thing. So the main tributaries for the portal vein is we have the pancreatic veins. We have the superior mesenteric veins. Your information, Teravainen's and again, that's taking the blood of thinking, particularly blood from the intestines. So this is going to contain nutrients. Glucose fatty acids. This will take also some amino acids. Uh, and again there's a lot of different molecules. They're going to be coming from the intestine, lots of nutrients. Unfortunately, there's also a bacteria that are in her intestines, and sometimes a little bit of bacteria can actually leak into the intestines, leak through the intestinal walls and into the actual circulation. So sometimes you can get small amount of pathogens that can actually get entered into the circulation as well, and so there's a lot of different things that are moving through there. Also, you're taking any kind of medications when you ingest any kind of medication, for example, you're ingesting some type of medication for your BP, and it has to get taken in through the esophagus into the stomach, get broken down in the stomach, moved to your intestines. And some of that actual drug means to get absorbed across the actual intestinal one into the blood. So you get the point here. Lots of things are moving via the superior in fear. Mesenteric veins the gastric pains. They don't get no respect as well. But they also have, ah, significant function that they help with the absorption of things that are more fat soluble, substance is and even aspirin, So these things can also get moved. So alcohol, aspirin, Lipitor soluble substance is convertibles orbed across the G. I t, particularly the stomach into the gastric greens, but when you have your superior mesenteric means your information, Terek veins, your gastric veins, your splenic veins and your pancreatic veins. When they all come together, they form like this big, large structure here called the a panic Portal vein and that will enter into the liver. And again it'll distribute into the smaller venues that will go to these others, like that's called the structural and functional unit of the liver. That's these tiny, little like, hexagon shaped structures here. This is actually called your portal Triad. And so, generally, these will also go to your portal. Try it again. My mouse is not working. I apologize for some reason here, it's not working. Let me There you go. Don't know why I was doing that politics. But again, that's the big thing that I want you guys to think about here is that we have lots of arterial blood that's getting delivered via the, um, uh, paddock artery proper. And then again, your portal vein is taking blood from your GI I t particularly the intestines, stomach spleen in the pancreas. Oh, another thing for the spleen. Uh, the spleen is also very interesting, right? Because, uh, it's it's obviously refer to sometimes like the red blood cell graveyard. So a lot of red blood cells could get broken down in the spleen, and there's a very important component which are in our red blood cells that we actually utilize our liver utilizes to make a very specific substance. We'll talk about later. Do you guys know what that that actual molecule is? That gets broken down, particularly it's red blood cells to get broken down in the spleen. And then there's a molecule that gets released from the actual hemoglobin and get taken up into delivering, utilized to make something called bile. He has no what that actual molecule is or that pigment is. And you guys are so darn good. Uh, have Billy Rubin. So Billy Rubin. So that's again, another interesting thing there. So what I think is significant here clinically is that a lot of patients that I see in the sometimes nice you they Unfortunately, they consume lots of alcohol. They maybe have some viral infections. They have some destructive process of their liver that over time leads to extensive fibrosis and that fibrosis can also extend into these portal veins, and it can reduce the amount of blood that's being able to get pushed through these portal veins. We can jack up their actual pressure of their portal circulation, and when that pressure gets jacked up blood is not going to be able to easily flow to the actual liver because again pressure like, you know, things like to move from areas of high pressure, too low pressure. So if this pressure in the portal vein is getting high, it's going to start causing blood to back up into these different venous circuits. And so this can obviously lead to many different manifestations. One of the worrisome signs that you don't want to have to see. And it's a little bit of a pocket factor. If you see this in the ice, you is. You have someone that actually has what's called, uh, softgel varicies so that pressure so high that it backs up into these esophageal veins causes them to dilate again. They rupture law. You know, massive amounts of blood can actually be examination, that process, and you can develop. You know, it's something called esophageal various things that can cause I'm gonna go in a hemorrhagic shock. So again, that's another big thing to think about. Also, if it backs up again into the around, the areas of the liver around the areas of the GIP can cause massive amounts of ascites It also can cause these things called anal varicies and again, in worst case scenarios that come back up and recanalization thing called the ligamentum Terry's and cause something called a cap it Medusa, which could be these visible evidence off enlarged and cords vessels on the actual superficial part of the skin on the abdomen. So again, these air just kind of really important clinical, accused to kind of make sense. We understand our anatomy, but we can apply some clinical correlations to it as well. So I kind of gives us the big thing that I want you guys to think about with livers again. Too big blood supplies here. Arterial supply, Big one, a pad, a card reprocess supplying oxygen particularly. And then the portal vein is it's taking blood from your intestines, your stomach, your pancreas, your spleen, pancreas. To give you some insulin, the spleen will give you some Billy Rubin and your G I t will give you all of your nutrients. Unfortunately, some small amounts of pathogens and drugs and things that were absorbing from you know, things that maybe we're taking for whatever reason, whatever condition you have that you're taking any medications for and all of these things are getting taken to the GI I thi I'm sorry to the liver, and the liver will actually sift through all of that in a very beautiful way. And again, big things to take away clinically is that whenever there's a significant reduction in the arterial supply and something like shock, it can cause significant manifestations of necrosis of those tissue cells, such a shock liver. And if there is a reduction in the actual portal, flow into the liver because of things like fibrosis or very significant inflammation and fibrosis of the liver than that can actually cause back flow into these venous circuits, which in present, things like pop attic portal, hypertension, which is clinically manifested as ah softgel varicies anal varicies cap it Medusa as well A societies Okay, all right. And this is actually cool. What I was hoping toe also kind of manifest with these is that on our website we have, like, these keys and so what you guys could do if you guys are watching any future videos as you could print these often follow along with us in the video. So I thought that was pretty cool. If you guys are going to still need some more time on the liver, go and watch one of our videos print one of these bad boys off and follow along during the process. I think it will enhance your learning, but same thing. Okay, so let's actually go back now, So we have a little bit out of order, So here we go. Now that we take that liver right, we have the actual understanding of the blood flow into the liver. We have the arterial supply, We have the venous supply. We know what happens when the arterial supplies jacked up. We know what happens when the venous supplies jacked up. If we actually take and really zoom in on these actual supplies in the liver again, there's that structural and functioning. You know, the liver, which is called the liver lobules. Right. We're going to zoom in and talk about little bit more about that microscopic anatomy in just a second. But there's something that we have to understand on the bottom surface of the liver. So usually on the bottom surface of the liver, there is this little hole where a couple different structures will enter into the liver and exit out of the liver so you'll have a hepatic artery that'll be entering in. You'll have the portal vein that'll be entering in. You'll have the common a patent doc that's coming out. You'll have the lymphatics that are coming out, and then you'll have your actual ah Paddick plexus, which contains sympathetic and parasympathetic fiber's going into the liver as well. There's a little hole where the structures tend to go through. Do you guys know what that structure is called? It may be different and, Ah, different areas, but we call it the Porta Pakis. I don't know if you guys ever heard of that's called the portal hepatic, so it's a little kind of like whole, usually on the bottom surface of the liver. And that's where a lot of structures are kind of moving in, and particularly out off the liver. And so again, if we were to kind of imagine it here, imagine there's a hole in the bottom surface of the liver, and again there's a bunch of different structures here. You have your hepatic plexus. You have your paddock artery proper. You have your portal vein you have your lymphatics, and then you have also your biliary duct and again the ones that are entering or you're a pattern reprocess portal vein and then the a panic plexus. And the things that are exiting is the bile duct in the lymphatics. That's a pretty cool thing to think about their the other thing. I think that's kind of interesting. Here is we have when you take a look like at the liver, it's it's kind of it's pretty cool when you think about it. There is these different delivers, technically in intraperitoneal organ, so it's covered by like a visceral kind of layer. And there's different ligaments that we'll talk about that are involved in like like the fowls, a form ligament. And there's also something called the Lesser Omentum. But there's a little like five embraced tissue that also surrounds deliver, and it's called Glisson's capsule. And one of the benefits to understanding this is that Glisson's capsule isn't actually innervated by your hepatic plexus, which is your parasympathetic in sympathetic plexus. This is end of innovative by the intercostal nerves, and so one of the interesting things about is that if somebody has some swelling of their liver like a pattern megaly. Or they have some type of inflammation of their liver, like in hepatitis. This can actually agitate or irritate that Glisson's capsule, which can then actually cause the intercostal nerves to be aggravated and sends signals that are, well, localized. And so that sometimes when patients have very specific paddock processes that are going on, it's a well localized type of pain. It's usually that right upper quadrant and again, that ability to, well, localized that pain comes from that beautiful a Glisson's capsule. Another thing I think is cool is again. We have a bunch of ligaments, right? We have, like your fowls a form ligament. The primary function of the valves form ligament is to kind of separate the two lobes, your liver right, the right lobe of the left lobe that also kind of anchors the the liver into into the anterior abdominal wall. The other one. That's another really important one. Is this one here on the bottom? And it's actually a particular type of omentum. Okay, so it's called the Lesser Omentum. There's two parts to the lesser omentum. Okay, one is the there's actually called ligaments one is. It connects the liver to, particularly the lesser curvature of the stomach. And that's called the A pad. Oh, gosh, strict ligament. And then there's another one, which is kind of a ligament that connects deliver down to the duodenum. Okay, And so there's these two ligaments, and that's called the a patio duodenum ligament. What's really interesting is that you see all these things that we were talking about pretty much know the big ones is your portal vein, your paddock artery proper and your biliary duct. These are the three main ones, and if you forget these other one, that's okay. But these air three ones, I want you to remember a pad, a card, a proper portal vein, biliary duct. They run through that thing called the Lesser a Mental, which is made up of the two ligaments again, the, uh gastro Paddick ligament or the a paddle duodenal ligament. What's important is that sometimes when you're doing particular surgeries and let's say for whatever reason, there's a decent amount of bleeding that's occurring sometimes what we will do in their surgeries if we think all man were mucking around in this area near the lesser a mental where those two ligaments are. We'll take a clamp and clamp down on that area to reduce any kind of significant examination from those areas. And that's kind of an interesting thing. So sometimes we use this is a landmark and guiding where these actual vessels will be. So whenever you're in surgery and they're saying, Oh, okay, well, what do you think's actually running in these areas here? Of the lesser omentum, there's some various critical structures, and again, that is the A pad, A card and proper, the portal vein and that biliary duct. Okay, so now that we got that done, let's take and actually zoom really deeply into this liver lobule, where the a pad a card reprocess for the portal vein. The biliary duct are pretty much kind of dropping things off or picking things up. And if we do that, this is that big boy right there. That's your liver lobule. And it looks like this, you know, beautiful, like hexagon shaped right in the center of it is your central vein. Okay, so the central vein is basically going to be picking up any blood that is coming from these particular areas here. So there's a very specific name to these three structures when they're at, like the edge or the corner of these hexagons. You guys know what it's called when it's made up of the little bile duct, a little vein. You'll and a little arterial near like the edge. What are these things called here? Have the portal Triad all right, and again, you can see it down here. That's our portal Triad. Not technically, if you really, really think about it. There's also lymphatics, and those are also picking up any kind of waste products. And so, technically in some textbooks will consider this a portal tetrad. But you can't really see these on the microscope. Lymphatic vessels are so tiny. Is there so blind ended that we literally impossible to be able to see these on and actual microscopic slide. So generally we call these a portal triad. In reality, there is a tiny little vessel there, the erratically that would be there. You just can't see very well on microscope, and that's called the portal tracks. What nonetheless, we have this central vein and then, if you look here, these like maroon colors here that are kind of moving from the portal triad towards the central Maine. These are called your sinusoids. Okay, so your sinusoids is a fancy name for saying like the Sinus total. Kapler's okay, They're Sinus sort of capitalism. A couple different organs. Uh, can you guys tell me at least, like three particular organs where Sinus little capital areas are prevalent and primarily gonna be found? It's a cool thing to think about it. So got spleen? Yeah. Yeah, kidney. So the big ones would be particularly, we would want bone marrow. There we go. So yeah, so it be the spleen, the bone marrow and the liver, those your three primary ones. And the reason why that's important to think about those is that Sinus or capital is one of their big functions is that they trap red blood cells. And so when they trap red blood cells, they can take those red blood cells and it gets stuck. And these little like cleft, like these, intersil or clefts are finished rations, pores, and then you usually have some type of macrophage in those areas that will actually go and actually digest up that hemoglobin or the red blood cell and release the different contents of it that you is utilized. So in the spleen, it's the red blood cell graveyard, so that's an obvious one. We want those macrophage is there. We want those Sinus sort of Kapler's to catch all those old defective red blood cells that their time is over. We want this deliver to do that because the liver needs that Billy Rubin and we also wanted to happen in the bone marrow because the bone marrow will actually use a lot of those different components to make more red blood cells. What needs the Billy Rubin? It needs some of the other amino acids and Iran and different things like that to review synthesize more red blood cells. That's why they should be located in those areas. But we have these sinusoids, and what the sinusoids do is they're picking up blood. So and when we have direction of flow, here's your arterial dart. Iria will drop off some of it's oxygenated blood, and it'll move towards the central vein, and they see all these like little black cells. All of these air you're have pad A sites that's pretty much making up like a chunk of your parenchyma. So this is what making up most of your liver parenchyma like 80% of it. And it's right here. And then what happens is as the blood from the van you all and the arterial are moving through here. These the Paterson. It's art tasting that blood in taking the different things that they need from it. So they're taking the drugs that you consume so we can metabolize it. It's taking the glucose so can metabolize it, taking in the different types of, um, you know, acid so it can metabolize it, taking the alcohol that you're getting from your points and metabolizing it right. It's utilizing all those things metabolizing and then based upon when it's done, it will say, Oh, I did everything I needed to let me spit it back out into the Sinus sides and this concludes my central veins. The whole point behind that is that whenever these central veins you have like, let's imagine, here there's millions of these liver lobules. That means that there's like millions of these central veins. When all these central veins come to gather, they form like a ton of interlocutor veins and these interlocutor veins will form these things called hepatic veins. And you know what? The A patent veins empty into this big old vein in the abdomen? The information I gave a right. So the whole point here is that the blood is going through the small little sailor areas. Getting the small venous channels that have been sifted through the liver is appropriately said, Hey, everything that I've actually sifted through is appropriate to go into your general circulation. I gave it to go ahead. I gave it the stamp, and now it can actually go into the inferior vena Kaveh, go to your heart, eventually, go to the left side of the heart and then get pumped out to the rest of your body. So that's the benefit of the liver functioning really? Well, if it doesn't, a lot of things could be missed. And unfortunately, it pushed into your circulation undesirably. So that's a big thing to think about. Okay, so we think about all of these things. What I really want you guys to also do is realize that there's something else that is not just only present. Besides the sinusoids, the portal Triad the A pad asides. There's these little green channels, and the usually they're located between the blocks or the chunks of these of Paterson. It's and those are called your biliary canalicular. I and those are responsible for picking up the bile. So you're Apatosaurus and not just good at metabolizing different things in synthesizing particular things in sifting through things. But they're also good at synthesizing things like bile because bio is extremely important to the metabolism of fat substances when your GI i t. So it also pushes some biliary substances behind it, and then these moved towards your biliary duct. So when you look at flow these air flowing in words, sorts of central vein and then in this way the biliary is flowing towards the biliary duct. If we really wanted to zoom in on this, imagine I take like this chunk right here and I assume in on I looking at all this big boy right here. Okay, so here's my central vein. Okay, which would be this part right here. And then here's my Sinus sort of capital zoomed in on Here's my pad A sites. Okay. And then here's the biliary canalicular. I between them. And then here's where that actual part of the portal triad would be, which is where you have the arterial, your van, you'll and again your biliary duct and we look at it, we can actually see why this is super important. So again, the paddock arterial is dropping off oxygen to these cells. So that's one thing. Obviously, if you have some type of shocking process, these cells don't get what they need. They undergo necrosis, and they spill out different molecules into the blood stream, like a S T and a little molecules. Right? The portal vein. You'll is bringing nutrients so those nutrients can get taken up into the liver cells and we'll have another slide. We'll look at see what they do to all these nutrients, which is pretty cool. But it's going to utilize these things and make all these different processes cellular processes they they have with inside of these cells. So we'll zoom into the cells a little bit later and see what they're doing with these nutrients. The other thing that's coming through these area that I told you is bacteria. Unfortunately, bacteria is gonna be naturally small amounts of Bacteremia is present in our body. That doesn't mean that everybody is has bacteremia and their septic. You can have small amounts of bacteria within the bloodstream, but usually it's in a lower amount, and you can thank these beautiful cells in our liver called the cup for cells. And what the cup for cells do is any of that blood that's coming from the portal vein that contains some type of pathogenic molecules. Such a bacteria or maybe little toxins like endotoxin is from Gram negative bacteria like light bill polysaccharide or certain types of parasites. These cup for cells when they encountered there like You ain't going nowhere, baby, I got you, and it's going to go ahead and phagocytosis the different types of substances. The bacteria, the different parasites may be fun guy, and when it phagocytosis it, it obviously Kenbrell those molecules down with lysosome. And if it needs to cup for cells are macrophage is they're indigent presenting cells so they can present the piece of that antigen of the bacteria. The parasites to your different T cells. Activate your T cell response cause T cells to come to the area antibodies to come into the area and clean up whatever that half a cardiogenic molecule is. And if you guys were taking your step one, you also need to know this dang pathway here. This is kind of a little additional pathway that life of polysaccharide. They love to bind on to these things called your toe like receptors. And these told like receptor type four and the CD 14 protein. Whenever the life of polysaccharide is bind, it just causes the macrophage is to get super ticked off sometimes and again. These, like, probably saccharide in your nastygram negative bacteria. And when they get ticked off, they released a lot of these different chemicals. But the big ones that I would say is the most important one is these top 32 minute product factor alpha interleukin one interleukin six. These can really kind of get out into your bloodstream, causing tense vasodilation. They can cause increased capillary permeability and they can lead to symptoms like shock. And so that is one of the big things to think about as well. They can also precipitate fevers, right, because these can activate your hypothalamus. So if you guys go back into your ah, a little bit of the immunology component here. I remember that. That's one of the other things that can happen here. Unfortunately, whenever the pathogens, particularly the label polysaccharide, get encountered within our liver. But again, we've covered the nutrients. We covered the oxygen. We've covered some of the pathogenic molecules that can get into this area of the GI I t. The other thing that we said concomitant, um, the GI I t. Is particular drugs, so I didn't have that mention here. But we'll also see what do these have pad asides do with the drugs? How did they metabolize? Those will take a look at that a little bit later as well. The other thing, I said that there's also hormones coming from different areas. Such a, the pancreas again, we don't need. We already have an idea of what that's going to do. But something else is really important here. And that's coming with that bile. So, you know, red blood cells, we said, right, they have to go to the spleen. They have to go to the bone marrow or they go to the liver and they get stock up in those areas well, in red blood cells. It's an old, decrepit red blood cell. It's, you know it's walking around with its walker. At this point in time, it's at that 100 120 day range. It gets caught up in these little inner sailor clefts and the Sinus Woods Cup for cells. Break those bad boys down. So then the cup for several phagocytose that red blood cell. When it does, it utilizes enzymes to break down. Globin, which is the protein component, give you some amino acids. But the other part is it breaks down the hemophilia globin and guess what? He eventually gets broken down into Billy Rubin and that Billy Rubin can get taken up into our liver cells. And, you know, what do we say? It was the big thing about Billy Reuben. It's one of the components off bile, and so these actual pad A sites will take that Billy Rubin and make by a lot of it. It's That's one of the cool things that think about it again. We talked about Bio. We'll have another little slide. That focus is is on the bile synthesis, but you see, there's three main components. If you forget all the things about bile. You at least need to remember three components of it. One is phospholipids. This is the big one, though, which is bio salts and then Billy Rubin when she gives it that pigmentation component. So these have pad asides when they make that bile or something that's again really cool here. It makes the diagram look good. This is the biliary. Can I let you lie? But in true reality, this is not what the biliary cannot like. It looks like it's actually this little space between the A patent sites when they're just opposed. They have, like a little tight junctions and adherence junctions, which are sticking them together. But there's these little like cavities that are between these juxtapose cells. That's actually the biliary canalicular I when we truly think about it. This just makes the diagram look prettier, though, But when we have this process, when these of Paterson, it's airbrushing down to different components to put into the bile, such as making bowel salts, phospholipids, Billy Rubin, water electrolytes, all these different things, they're secreted. Get into these biliary canalicular I and these biliary canalicular. You're taking this towards the biliary ducts. Sometimes I don't know if it's worth the sweets, but I thought I'd mention it. Here is that when you're talking about membranes, sometimes this is mentioned. Um, especially if it comes up with in some psychology. Aspect of a question is when you think technically, when you usually think about membranes, you think about the basil lateral membrane being the one that's usually towards the base near like a connective tissue membrane. Right? And you would think that would be on this side. And then apical membrane, you would think, would be the part that's coming into contact like the interstitial fluid and things like that. However it's flipped, and the reason why is when you look at it, there's a lot of connective tissue that gets deposited on this top part where, like the Microvillus area is, and so whatever they have this connective tissue bed that actually is the area where you have what's called your basal lateral membrane. So that's gonna be the area that's closest to the sinusoids and then the back part where the biliary canalicular I would theoretically be. That is actually the apical membrane, and so sometimes that's described in certain tax books another big thing. Sometimes it may come up is that we just like to call this little space between the capillary Z and the cells, the interstitial fluid. I don't know who this guy is, but he decided to make our little life a little bit harder. And he had called that interstitial space the space of Disi. All that is is just the space that actually is where particular cells exist. I don't know if they're truly worth remembering, but they're there. And these cells that sit with in your space of deceit are called your stellate cells. What's the true thing that you should know about them? One is they store vitamin A. But the other thing is when Stella cells are injured from, let's say, alcohol. Ah, virus, some type of pathogenic molecule that's causing continuous insult to the actual liver. These Stelly cells respond to that injury and they convert into these ugly little cells here called the Myo Fiber Blast. And these mild fibroblast like to increase the collagen deposition around these areas and imagine having college and just deposited all around these vessels. It's gonna cause extensive fibrosis and squeeze down on these vessels If I squeeze down on the sinusoids and make them super fibrotic, it's gonna increase the pressure in those Sinus soy's. And that's gonna cause the back pressure in the portal vein to skyrocket and precipitate portal hypertension so you can see how they could sometimes be worth remembering just because they're the problematic portion and tissue injury to the liver and precipitating that, um, hepatic portal, hypertension and liver fibrosis. The next thing I want to talk about real quickly is that this is sometimes also refer to This is really when you're getting more into the, you know, intense physiology, but I don't think it's super super critical. I think it makes sense whenever you thinking about Shaq conditions. When we talk about the liver, we talked a lot about the flow of blood in the flow of bile. There's ways that we can describe it a little bit further, so sometimes when you actually take a look at these liver lobules, we can look at blood flow in three particular ways, or or we can look at flow. It's just a flow in three particular ways. We can look at blood flow, we can look at biliary flow, and then we can look at oxygenation throughout the actual hepatic, the lobules of the liver. So let's say that we have the classic way that we look at a flow through the liver. There's the classic liver lobule. That's what we've been talking about this whole time. The a panic. Ah, reprocess the arterial there and the van you. It drops off blood at the edge of these sinusoids, and the blood will move always in the direction of the central vein. That's the classic liver lobule. Okay, there's another way that we can describe these liver lobules, which is called the portal Lobule. That's when you're actually focusing on, particularly the biliary flow with respect to the portal Triad. And so what you do is you take like three of Paterson, it's you find their central veins and you connect them together to make a triangle, and then you draw a line in this towards the center off those areas, and that usually always ends you on some type of portal triad where the biliary canalicular I or biliary ducts will be picking up the biliary flow. So with classic liver lobular talks about the blood flow towards the central vein with the portal. Lobular talks about the biliary float towards the portal Triad. And then the last way that we can describe the liver lobby was called in a sentence. Lobule. This is actually the one I think is important to remember and the reason why it's it's clinical. You have these different zones, so we Here's your portal. Imagine, Here's your portal Triad, right, this area him. Let's think about blood flow. If you have your paddock artery proper, that's giving blood, and it's moving through the Sinus or it's and it's going towards the central vein. The farther it gets away from the portal tried, and the closer I get to the central vein, the less oxygen is gonna be present. Okay, and so that's why we use own them. In these three zones, we have Zone one, which is the most oxygenated portion of blood that's being delivered to the, uh, pad aside zone to intermediate amount of oxygen. And when you get to zone three, that's the least amount of auctions being delivered to the pad A sites. If someone goes into shock and they have less oxygenated blood being delivered via arterials. Which of these zones is gonna be most affected? Undergo necrosis undergo some type of destructive process. It would be which one Zone three. And so that's a very interesting thing to think about. And the other concept here is that think about other processes that require higher amounts of locked in. This is why the liver is actually kind of cool. It has this head originated. E where compartmentalizes It's different functions into different hepatocyte zones. So zone one, you would have what you would have areas of metabolism that needs lots of oxygen. That's your any kind of electron transport chain activity. Any types of like synthetic pathways are gonna need 100. Ah, Cajun. And then for your zone three. Those are going to be the areas that don't really depend upon oxygen very much. You're glycolipid pathway, right? Different types of like fatty acid pathways as well and and xeno biotic metabolism. Drug metabolism don't depend on too much oxygen. And so that's a cool thing that we think about with the liver. I I think that's a pretty interesting thing. So we got our anatomy down. We got our microscopic anatomy down. We through some clinical correlations in there. Well, we have to kind of dig into a little bit more. That we didn't talk about is he's a pad a sites. We know how they're getting blood. We know how they're secreted in things. We know the significance of all of that. We have to start talking about a little bit more now is what does it do with all of these things that it's getting all the nutrients that it's receiving? And we talked a little about the pathogens, what it's doing with the pathogens. We already knocked that out. But what is it doing with the oxygen and the nutrients that it's receiving? And there's, Ah, boatload of things that it's doing right? We could spend most of the today talking about this, but what I really want you guys to understand here is a couple just overarching themes. So when the liver is receiving nutrients, it conducing Zwick those nutrients at different times off the day, depending on if you are eating or if you're not eating. So the liver has the ability to respond to different hormones and then that lights of fire under the liver to either increase its metabolism of certain things or decreases metabolism of certain things. So when you're in something called the Fed stage, that means that you are eating. If you're eating, your glucose levels in your blood are going to go up. If that goes up, which hormone should be the primary one? Insulin right? And so if that is the case, if insulin is just going up and up and up, it should be telling the liver to perform processes that insulin does. So my question to you is, what are the things that insulin tries to drive for carbohydrate metabolism first, what would be the big thing that I would want to do with the actual glucose if insulin is the one that's in charge? So if insulin is the one that in charge, he's usually a synthesizer, so that should give you a hint What would have want to do with the glucose? If it's a synthesizer, that's definitely one. It can definitely use that excess amounts of glucose and shifted into making glycerol and making fats. Glycogen is the big one. Yes, so Glyco Genesis would be a huge one. Yep, Glycogenesis and also one other one would be oxidate in the glucose. So it also loves to be able to drive the glycolax pathway and use that glucose for making some ATP. So it helps with the glucose oxidation as well, to it's minor minor degree. So it helps with glucose oxidation. But the big thing is synthesizing things from glucose so it can use the glucose and shunted into making fats definitely. But the first thing I would do before it makes fats is shunted into making glycogen. And so, if you look here, glucose comes into the cell when it gets into the cell influence, gonna push it right into glycogen. But it can also, as you guys so astutely saw, push it into making dihydroxyacetone phosphate into glycerol. If there's lots of fatty acids present, it'll combine and make your triglyceride. So you guys are super students. All that Okay, Second thing, what would it do to the actual fat metabolism again? It's a synthesizer. So if you're consuming and, uh, last that question first, what would it be doing to the fats? And I have another question for all of that? Well, you guys think you'll be doing with the fats, so we know it's synthesizing glucose into glycogen. It would be trying to make what else kind of already set a little bit with the glycerol. It would be doing like Genesis. Yes. So, Lipo Genesis So good. So I want to try. I don't know if I said this prior, but if I did, I want to Ah, revise That. Is that technically, the nutrients that air coming to the liver directly through the portal system is your glucose, your proteins, those air, the big ones and even some other things as well. But really the lipids, right. So your cholesterol, your triglyceride, your fat soluble vitamins. Those aren't technically going through Europe. Attic portal circulation. Okay, those air going via your lymphatic circulation, okay. And when they go for your lymphatic circulation, your triggers, quick cholesterol, your triglyceride, your different types of fossil lipids. What happens is you have all these fats and and fat soluble vitamins. These things called bio salts which we're gonna talk about later. That deliver also generally makes squeezes and clamps down onto those makes them smaller into these things called me cells, which makes it easy to absorb across the giant T when they get into the Paterson. It's patency. It's. Take that cholesterol the fact and the cholesterol triglyceride phospholipids and puts a little protein core around it. And these little lipoproteins get pushed out into your lymphatic circulation. Go three lymphatics and eventually get into the bloodstream. What are those tiny little molecules that carry triglyceride? Cholesterol phospholipids be a little fat, It's and then get pushed into the blood. You guys know and you guys were good. Chylomicron is Yeah. So that's these little bad boys. These chylomicron so technically, to revise what I said the a panic portal circulation. It technically does not carry fats. It actually indirectly will take that V a little emphatic circulation, then into the systemic blood. Then from the systemic blood, you'll actually take the actual fast. They're so chylomicron is they're carrying all these fatty substance is they're gonna go vehicle emphatic system from the one fattest to get into the blood. They'll get taken to the liver and they get taken up by the liver and the liver will say, Give me those triglycerides. Give me that cholesterol. Give me the fossil. If it's, I'm gonna use these bad boys and what I'm gonna do is I'm going to actually make try. I'm gonna consume the triglyceride and keep them as stories triglyceride. Or it's gonna take that cholesterol and synthesize it into a couple of different things. When I take the cholesterol, I can actually utilize, we'll talk about this. We take that cholesterol that we get from the chylomicron and make bile acids like colic acid, the oxyco like acid, which is important bile. It can also store it as things things called cholesterol Esther's. Or it can take that cholesterol and put these different types of things on them, called aprile proteins. So there's different types of April proteins, and the different April proteins tells you what type of lipoprotein it is. But we have these different types. We have VLDL LDL's HDL's ideals. All of those things are made by your liver, and the liver actually utilizes the cholesterol from those chylomicron is to make these beautiful VLDL, which are triglyceride, rich and cholesterol low. The ideals, which is kind of an intermediate between those two LDL cholesterol rich and triglyceride low and the HDL, which is actually primarily designed to pick up tons of cholesterol and triglyceride, is from the periphery and bring it back to the liver. So that's kind of the beautiful thing about deliveries, that it's helping with synthesis of lipids, particularly synthesizing triglyceride and synthesizing cholesterol. But you realizing that cholesterol, particularly to make bile acids, store it or make lipoproteins. And that's a cool thing that's also happening in the liver, you know. And the last thing is protein metabolism, uh, insulin. Again. We already got the point here. It likes to send the size right, so Glycogenesis lipo Genesis cholesterol synthesis. But there's also going to be protein synthesis, and that's super important because, as you'll see here, I obviously two rows down. The liver is a protein factory baby, so it needs to have a heavy amount of protein sentences that's going on. And so those are the three things that are happening during the Fed state lipid synthesis glucose synthesis in the glycogen protein synthesis, cholesterol synthesis and also making some steroid hormones Well, particularly on the serotonin level proteins, I apologize label protein such as VLDL, LDL, IDL and HDL. Okay, that's that during the feds stage, whenever you're in the fastings, a draining so and you're not eating your glucose levels theoretically should be low. When glucose is gone, you should release glucagon. Okay, so when glucose is gone, you should release things like glucagon. And then also, in addition to that, you should release some other things. You know, when you're in a fight or flight situation, if you're in a fight or flight situation and you have to, like, run away from, like, eight or something, you need as much glucose that your muscles compositely consume to make it much ATP for those muscles to continue to keep generating energy to run away. So during that active fighter flight situation, things like epinephrine, norepinephrine can get released, and their whole design is to try to be able to increase the glucose levels in the blood. Glucagon is whenever your glucose is gone, I want to get more blood in the glucose, more glucose into the blood. And then there's other things. I'm not too worried. If you remember growth hormone and thyroid hormone cortisol is another one. It's another one, but it's not in the cute stress response. It's the long term stress response. So in patients that are having that long term stress response, cortisol will also jack up and again. It's designed to be able to increase your glucose levels as much as possible. But again, the whole thing here is that the glucose levels in the blood are low. They're going to drive. All of these particular process is particularly glucagon cortisol, epinephrine, norepinephrine to shoot up. And the whole goal here is to get those glucose levels in the blood higher because they're low. And I don't like that. Okay, so how does it do that? Well, what particularly glucagon epinephrine, norepinephrine, cortisol will do is they're kind of trying to break down everything that insulin built up, so they're trying to oppose it. So instead of glycogenesis, it's gonna be glycogenolysis. Instead of taking the glucose and oxidizing it to make ATP, it's gonna take other molecules and make glucose non carbohydrate molecules like amino acids, glycerol, lactic acid. And technically, there's another one called odd change Fatty acids. We can use all those bad boys and make glucose. What is that process? Fall. We haven't talked about that yet. We're making new glucose molecules from non carbohydrate sources. What is that called? Too good. All right. So gluconeogenesis. Yes. So we're breaking down glycogen. We're making new glucose because the whole problem is the glucose low in the blood. I got to get the glucose up. The other thing here, when you're just chucking through these amino acids like a wood chipper to make more group close, you're generating a lot of these molecules here called glutamate. Okay, this process here, where you take like a mean Lasses like glutamate and utilize it to make glucose is called transaminations. And what happens is that glutamate has to go through a process called oxidative damage a shin. So it wants to take that glutamate and get a pneumonia molecule off. And so when it pops out ammonia molecule, we don't want that thing high in the blood, because if that thing is high in the blood, it's going to start causing toxic effects. And one of the most toxic effects is it can lead to encephalopathy, right. It can make people very confused, and it can change a lot of the activity within the brain and even increase the risk of seizures. So I can really alter patients mental status, and so we want to try to do is not let that thing be high, and so we send it through a molecule in the liver up. I don't jacked up senator Molecule that we sent to a pathway in the liver called the urea cycle, and that actually converts the ammonia into urea and that urea is actually less toxic and can be excreted into the urine. That's that's a nice benefit there. So again we got glycogenolysis. We have luego neogenesis. We have the urea cycle as a byproduct from a lot of this gluco neogenesis occurring. The other thing is that we want to again oppose everything in some was doing so I was trying to build up fast. We want to break down fats. So, like pollicis when you break down lots of lipids, particularly fatty acids, that you got to break down on 16 carbon fatty acid into two little carbons like a seal coat way. Every time you do that, you cause the cervical. A level was to just jack up and his prostate go from fatty acids with sickle beta oxidation. When this happens so intensely, the seal colase or getting consumed and the Krebs cycle to make ATP, they start shunting into making other molecules called key tone bodies. And this is called ketogenesis. And these are the things that you can see, particularly in patients where maybe they're actually having an insulin deficiency, right? So if they're in an insulin deficient state, they actually can't break down. I mean, they can't build up fats that can't utilize glucose. And so what happens is they start actually metabolizing tons of their fat molecules because they don't have glucose to utilize. And then that starts precipitating these high high keys, own body production and picking conditions like diabetic ketoacidosis. Or if you're like starving yourself from carbohydrates and on eating any carbohydrates, then your body has to find a fuel somewhere else. And so it also breaks down triglyceride, and that will also again increase the acetylcholine a production, and push that in to keep some bodies. And so you could get was called starvation ketoacidosis. But that's the whole point is that during the Fed state, the liver bills things up, and during the fasting state, it's going to break things down pretty cool. The last thing Well, the next thing is with the proteins. I really think this is probably more important clinically relevant things to think about here. It's cool to think about this stuff, but what's really, really interesting is this stuff here because this is what we see a lot of the time in patients that we actually care about. So, you know, the liver makes a protein called albumin, and so a few minutes actually helps to maintain the the osmotic pressure within our blood vessels. And so in patients who have liver failure, they don't produce albumin. Can they hold on to that fluid in the actual blood vessel? No. And so if they can't hold onto the fluid within the blood vessels, what starts actually happening to the fluid? Where does it start accumulating? What kind of clinical manifestation would that present that yes, definitely can lead to ascites. It can lead to things like a Dema. Yeah, so it's gonna That's one of the problem Attic issues in these patients is that they start third, spacing a lot of fluid into their interstitial spaces. Maybe that's their peritoneal cavity. Maybe that's their lungs. Maybe that's their legs. And so that's the problem. Attic issue here. The other thing is it makes than's of other proteins and do so many things. And so, you know, your make these things called globulins. Okay, so there's ceruloplasmin that transports copper transferring with transport. Iran Haptoglobin was chance to actually binds hemoglobin. All of these different things. When these proteins are actually not produced, are they able to transport? I'm buying the proteins that they're supposed to carry throughout the bloodstream. Okay, No. And so maybe you're making adequate amount of thyroid hormone and you're not actually having the amount of thyroxine binding globulin. It's present to transport that diet hormone. That's that's a big thing. This is another one able teens. It makes all these different April proteins that actually are important to bind on to this cholesterol and lipids molecules to transport them around that transport things like VLDL LDL, HDL. So on so forth. Here's what I think it's super important. Don't forget this one. It also synthesizes factor to 79 10 protein C and protein s okay. And all of these air vitamin K dependent. There is a drug that we can give that actually inhibits the synthesis of these proteins. You guys know what that drug is called? Yeah. Warfarin. And so warfarin. inhibit the synthesis of these proteins. I get, like, a million buttons. Okay, so it inhibits the synthesis of these proteins. If you can't make these proteins, are you going to be able to induce a clot? So in this case, you're not gonna have these proteins that are generally wanting to stimulate clot formation. So what happens is with warfarin, it prevents clot formation. But there's also the risk that it could potentially cause bleeding. And that's something that we need to think about. Also, if your liver is failing, if you're in full blown liver failure and your liver isn't actually functioning well, can you make these proteins? No. And so your factor to factor seven factor nine factor 10 c and s all go down. There's an important reason to know this because we also have a blood test that we can order to see the function of these proteins. You guys know what the blood test is that can actually test the activity of these proteins? It's the same one we use for warfarin. I and our Yes, we can use the prothrombin time and particularly we utilize that prothrombin time toe extrapolated there I and R. They're international normalized ratio, and you guys are so good. That's a big thing to think about there. I think that's a big one is they may comes of proteins. Albumin is a big one. Caught in proteins is a huge one. The other one is again. They also help with making something called plasminogen, with helps to be able to make break up clots as well. Okay, because when we make plasminogen, we have particular molecules like, you know, plasma, which helps to digest up the fiber, which is important. We also have a molecule called anti thrombin three. And again, this is also kind of acting as a natural kind of anti coagulant because it's going to inhibit factors. Two factors. 10, which also inhibits the clot activity so it tries to maintain a nice balance between. But I really think it's more important to remember that in liver failure your clotting protein production goes down. That's the big one. It could make a bunch of hormones, I think the two that I think are worthy of remembering here thrombopoietin because if your liver actually fails and you don't produce drama queen, you can't make platelets. What's that condition called when you have low levels of platelets within the bloodstream. Thrombocytopenia. Yeah, so it's a It's a cause of someone having thrombocytopenia and then angiotensinogen that actually helps to convert. Well, you utilize Renan, made by your kidneys that activates angiotensinogen into angiotensin one, goes to the lungs and then gets converted the angiotensin two. So I think that's also a big one to remember as well. Because if your liver fails, you potentially alter the activity of angiotensin two production. And then the last things here is it makes your complement protein, which are important and urinate immune response. But even more significant than that, it makes these things called acute phase reactant proteins, which is clinically relevant. So whenever somebody has some generalized inflammation, interleukin one interleukin 62 and a chronic I factor Alpha are being released, they tell the liver, Hey, inflammation's going on, buddy. We should probably alert the actual body. And so it causes the liver to release different types of molecules that tell us that there is some systemic inflammation going on, and some of those are like C reactive peptide. We can also do another one called the ES are the Erythrocin sedimentation rate. We can check molecules like Ferritin's and all of these other molecules, but this seems to be the big one that sometimes we have a high regard for such a CRP, and es are so you get. The whole point is that it uses the, um, you know, acid is getting from the GI tract to make tons of proteins and the big ones. I think that's important that you know it's worth the squeeze remembers albumin, your clotting proteins, some hormones and then some of your actually cute phase reactive proteins. And then it also is utilizing tons of different nutrients in the metabolic pathways when you're eating when you're not eating. And the last thing to think about here is that it stores all of those fat soluble vitamins that are coming from your chylomicron know. You're kind of my crowns only carry triglyceride. It doesn't only carry cholesterol, but things like vitamin A, vitamin e, vitamin D, vitamin K, all of those air fat soluble vitamins that get absorbed with chylomicron and those have to go to the liver to be stored because we use them for particular reasons. So obviously vitamin A. We can use that for the skin. We can use that for the rods, the rhodopsin protein, and we can actually have it be stored in the stellate cells. Vitamin E has a lot of anti oxidant functions, but here's the one I think is interesting. Vitamin K. If you're not actually storing that vitamin K, the vitamin K is needed to make factor to 79 10 c and s. So if someone has a vitamin K deficiency, they're not actually taking vitamin K. Maybe they have some type of Ah, sometimes a recent reason for this is like a malabsorptive syndrome, where they're not actually absorbing things across the G. I. T. Or another interesting one is, you know your bacteria make vitamin K, and so if someone has actually on antibiotics in a very heavy regimen, and they're on the antibiotics and they knock out a ton of their bacteria within the G I T. That reduces their vitamin K. And if you reduce their vitamin K, you reduce the production of these proteins, and so sometimes you can see in patients with malabsorption syndromes where they're not absorbing vitamin K or they were on a heavy antibiotic regimen, and they start like bleeding from their gums or having nose bleeds, maybe go thinking about like a vitamin K deficiency that's going on here because they're not producing those clotting proteins. And then the other thing, which is really cool, is our liver is also utilized in the vitamin D. I did it again vitamin D process. So it also is utilized because, you know, when our, uh, skin the photons hit the skin, it causes the precipitation of the molecule called 70 hydroxyl estriol. That's a molecule that's actually made from our skin. Our liver takes that molecule and adds, uh, hydroxyl group on to it when it as the hydroxy group on to it. It's still not activated enough so has to go to the kidneys and then in the kidneys, they release an enzyme that activates vitamin D and so vitamin D will store this. I'm a liberal store, vitamin D, and whenever we need it, it can actually release it sent to the kidney, and the kidney can actually activate it and utilize it to absorb calcium across our gi i t. So again, there's a lot of cool things there and then two micro nutrients that it's involved in is I run and copper and these air clinically relevant, my friends. So you know, the the liver. It's constantly holding onto iron, particularly in the form of like, uh, Hemosiderosis or Ferritin's. And what happens is in patients who have what's called chemo chromatosis. They don't make a very particular protein called helps it In and helps it in whenever it's reduced, you lose the complete ability to a regulate your iron absorption across the G I T. And so what happens is iron is just excessively absorbed across the G I T. When you don't have that helps it in protein and so iron gets deposited into the liver. And the problem with that is that iron could be somewhat toxic. It can actually trigger free radical formation, and when it caused these free radicals, they start damaging different areas of binding on two different proteins binding on two D and A and inhibiting the functions of those proteins and the nasty thing that can happen With hemochromatosis. You can get all of this iron deposition in different organs of the body, such as the liver such as the pancreas such as the heart, and you can get these devastating effects of hemochromatosis. And then the last one here is It also stores copper, but it also again when it stores this copper. The interesting thing here is that there's a particular gene that whenever it's there's a mutation within this genes called ATP seven be. Don't memorize that, uh, What happens is that this ability of the liver to excrete copper is inhibited. You can't get rid of copper and the copper that dang copper just starts building up. And when the copper builds up, it all that congenital free radicals and those condemn itch deliver. When that damages the liver again, that's gonna be one of the problem education's. You see things like hepatitis and the copper also deposits into your eyes and causes something called Kaiser Fleischer rings, which you can see on the exam. It deposits in the brain, and then these people start doing things like this. They have this thing called Korea, so they look like they have Huntington's disease, but it's a similar kind of thing, and so that's when the big things, I think are worthy of remembering for the metabolism of the liver. Okay, so the next thing is, I don't want to go to Ham. The in this part of the world, particularly the South. Oh, wow. I didn't know. I guess that is, that makes sense. Yeah. The genetics in that area, huh? Those HIV genes. Oh, man. So what I would say is another thing to remember here for the liver is those drugs that it metabolizes. So we talked about the nutrients and how it stores things and synthesizes a lot of different things. The other thing is, what does it do it? The drugs? I don't want you to get two bar down into this because I don't think it's really that intense that you need to know all of these things here. What I think is cool is that the liver has these enzymes, and they're called the cytochrome P 4 50 enzymes on. So these enzymes are responsible for metabolizing pretty much most of the drugs that we actually take it on a daily basis. The one that I think is actually really important. You might actually see on different exams or rotations. Is your c y p. Three a four. This is the one that actually a tablet is is most of the drugs that we consume in a daily basis, like 50% of them. And the whole point I don't know if you guys know this, but cytochrome is the super family of proteins, and then we use this. This one here, like the number right after, is the family. This is the sub family, and this is actually the gene that's involved here. What I really think is important about the liver is let's say that you met you to observe, you know, you consume some type of drug. Okay, The whole point is that most of the drugs that we actually consume or usually lipid soluble in some kind of form there hydrophobic. They're not really good polar molecules. And so what are liver has to do is metabolized that to make it more polar. The whole point is that we need that polar molecule to be distributed in our blood plasma, two different organs that it needs to work on. We needed to be polar to actually deposit into the the to the actual feces. We needed to be polar to pee it out. And so the liver will utilize the cytochrome p 4 50 enzymes to take something like a drug that is very non polar and make it super polar. Okay. And the whole point is by doing that, if we have it very polar, it could get put into the plasma to be distributed into the bile, to be pooped out or in the urine to be peed out. Now what I think is also ah, kind of really cool here is that we utilize all these different enzymes, right? The cytochrome p 4 50 enzymes that some other ones as well. There's a couple different phases. The phase whenever you're actually liver is metabolizing a drug in the act by the cytochrome p 4 50 system. This is called the phase one whenever it's being metabolized by these additional enzymes. Okay, it's called phase two, not the cytochrome p 4 50. These other enzymes is called your your face, too. And then, when it's excreted into the plasma, excreted into the bile, excreted into the urine, this is called the phase three off the actual transformation process. You call this bio transformation of drugs. What's actually clinically relevant here is that whenever you're taking particular medications. Some drugs can inhibit this side, a crampy for 50 system. And if that happens, let's say that you're taking a drug. For example, let's say that you're taking a drug like ah, like warfarin. Okay, And let's say that when you take this drug, you take warfarin. Warfarin is designed to be able to try to make your blood a little bit thinner. Let's say you take another drug at the same time for another perception issue and what that other drug does, is it? It accelerates the actual activity. Let's say that stimulates this this molecule, it stimulates your cytochrome P 4 50 system. If it stimulates that, what it's going to do is it's going to take warfarin and metabolize it more quickly and more efficiently. And it caused the warfarin levels in the blood to be a little bit more therapeutic in general. And so if you take a medication that's actually stimulating that cytochrome p 4 50 system, it might metabolize it a little bit more quickly and cause the warfarin levels to be a little bit elevated. Whereas if you take another drug and that drug actually inhibits decided crampy for 50 system. Now it's not metabolizing that warfarin as readily, and maybe the warfarin levels are a little bit sub therapeutic. And so sometimes this is something to think about in patients who are taking these medications. This is what their liver is actually doing. It's metabolizing these drugs, but the big ones that I really think are worth remembering is that cytochrome p 4 50 system. The other thing that's important with our liver is alcohol metabolism. So if you're just downing pints after pints and you have lots of alcohol that's being taken up via the the paddock portal circulation getting taken to the liver, what's the problem with that? Well, the alcohol is metabolized via three pathways, right? One is it goes through. Your cytochrome P 4 50 system gets converted into a seat out by the other. One is it reacts with this molecule called anti diuretic up note. Just in. It's the alcohol Dehydrogenate is. It's It sounds like a T H i antidiuretic hormone, but it's not. This is alcohol dehydrogenase, and then the other one is is metabolized by proxy Jones, and there's an enzyme called Catalyst. So these are the three ways that it can happen. Irish people don't drink alcohol. Okay, whatever you say. But you have all of this. Um, you have all of this alcohol that's going through their side of crampy for 50 system or is getting out metabolized by the alcohol. Dehydrogenate swore by catalysts when these all get metabolized via these three pathways, that makes this molecule called a seat aldehyde. Now that may be like Okay, what's the significance of that? I see the out of height is a bear of a problem. Whenever you have lots of alcohol and you're getting metabolized via this pathway making tons of a seat aldehyde a seat aldehyde unfortunately will bind with proteins that are in our cell and make these things called a CT aldehyde add ducks and then the going expose themselves on the actual membrane of the liver cells activating immune system cells to say, Hey, something's present here. We need to jack up the inflammatory response. And what happens is this unfortunately causes damage and and destruction of the hepatocyte. And the other thing is that when a seat out high binds to these proteins and ourselves, they stopped functioning. So if you have a protein that's involved in an enzymatic pathways that's critical to the cell. You lose that critical pathway, and that's also a disastrous type of effect. Here is where it could be also bad in this pathway as you go from Cal, call to a seat aldehyde. Whenever your cytochrome P 4 50 system are going through this metabolic pathway to break out called down into a Seat, I'll hide. They make a lot of reactive auction species, and the problem with these reactive auction species does they like to just be pains in the butt and donate a lot of their actual, like little electrons on two proteins and different dina molecules. And, um, Avam. Do you get damage of these DNA molecules? Damage of these proteins and they stopped functioning. And if they're critical, two different cell function again, you lose particular cell function liver. Here's another problematic issue. Whenever you have lots of alcohol metabolism, you generate Aton of this molecule NADH, because a lot of this pathway, they're requiring any positive to be converted into any pH. Here's where it's very interesting. You guys may have heard what's called a patio steatosis so high amounts of NADH you have to take that bad boy to the Krebs cycle. It gives you drop those electrons off, too. It makes tons of ATP. The problem with this high ATP is that it shuts down the Krebs cycle. So now all this is see, like a way that you're generating from other sources. And because of see, the aldehyde eventually can get broken down in the acetate acid take and just get converted right into a surgical way. If you're just tanking this alcohol, you're shutting this pathway into lots of acidic away. You're also shunting this pathway to tons of what else NADH is. Tons of NEDA just makes tons of ATP. Ah, lot of ATP inhibits this Krebs cycle. Now. Acetylcholine can't go into the Krebs cycle. Where is it going to go? It's going to get shunted right into making tons of fatty acids. Tons of fat get actually accumulates in the liver and you end up with a pad ST a ptosis or this fatty liver type of the fact, and that's one of the devastating effects here. And so the liver is you know, it's nice and the way it tries to metabolize alcohol. But Unfortunately, if there's too much of it, it can lead to a seat. I'll died at ducts. It can lead to reactive auction species. It increase your any DHA, which actually can precipitate Ah fatty liver type of syndrome. And these a seat aldehyde adducts lead to loss of function. So I think it's one of the big things that the liver is also great at metabolizing drugs. Be of what that system is called the cytochrome p 4 50 system, and it's also great, um, metabolizing alcohol via these three pathways. But the devastating effect of it is all these things that we just talked about. I don't know if you guys would ever be asked this, but sometimes whenever patients are actually for whatever reason, I don't know why they would. But if they ever consumed things like methanol or isopropyl alcohol, we can actually utilized drugs toe actually counter act the different pathways here. Um, So, um, the alcohol dehydrogenate is actually conjugate. Worked on by another particular molecule is someone who consumed lots of methanol. We can give them a drug called for Meprazol. Don't know if you guys have ever heard of that from that is also action work, too, particularly work on this alcohol dehydrogenase enzyme, and the whole point of it is to try to be able to kind of inhibit this continuous process from occurring. Um, And then there's another one where we can actually utilize other drugs that actually work against the aceta aldehyde an acidy. There's another drug that we give to patients who are trying to stop drinking. It's called Drysol free, Um, and what Disulfiram does it actually helps to work in this part of the pathway. And it tries to precipitate, like, kind of a nausea type of effect, that kind of help patients not want to discourage them from continuously drinking. And so there's different drugs that we can utilize these alcohol pathways as well, which is pretty cool, all right. I also don't think we need to go through all of these as well. I think one of the big things to because this art, it just gives me like anxiety. One of the big things I think about is with the liver and this bio synthetic pathway that it's actually involved in deliver. The big thing I want you to remember is that it utilizes three particular molecules like we talked about to make bile, bile acids and war those bile acids coming from That's really all I want you guys to think about here. Chylomicron is which are dropping off cholesterol that cholesterol through this massive like anxiety producing pathway produces a ton of different types of bio salts. And if you really wanted to go ahead and remember them, the main ones, that's Chino deoxycholic acid and colic acid and all these other ones. But all I really want, you know, is that these are all your bio salts. The whole point of these biosolis is that they help they get pushed into your GI. I t particularly into the small intestine, right, So the's get put pushed into your gall bladder to your biliary ducts. When your biliary ducts get emptied into the small intestine, it'll have these biosolids to bind on two different fat molecules different cholesterol molecules, triglyceride to help with their absorption. Okay, the other thing is the Billy Reuben that is another important one, and we already know that that comes from the Hemed opponent of hemoglobin. And the whole significance of this bad boy is that when Billy Rubin is actually released from your. Whether it be from these macrophage is these Billy Ruben molecules they combined with albumin, and this is called unconscious, gated Billy Rubin. When it gets to the liver, the liver puts on a see this cute little enzyme. It's called a glucagon. Oh, transferring it puts a molecule on to Billy Rubin and convert it into conjugated Billy Rubin. And that conjugated billion just makes it more polar and pushes that into the GI I t. Eventually. And that also is important to be able to, um, again help with the whole bile of the fat absorbed of process. What I think is actually clinically relevant for you guys to think about is that sometimes whenever we're trying to determine if a patient has just like they're jaundiced, they have that yellowish orange is type of appearance, and we're trying to figure out Is it because there's something going on with the liver, or is it something else that's going on? Generally, if the Billy Reuben that is unconscious gated is really, really, really high, it hasn't gone to the liver yet, so the liver hasn't done anything with this. Billy Rubin just yet to conjugated. And so in patients where there's lots of homologous cysts, your red blood cells are just popping open and releasing all of this. Billy Reuben. It's not conjugated yet and patients with him Humalog sick cause of John Does this uncontradicted Billy Rubin will be extremely high, and this conjugated bilirubin will be normal toe like lower age in a patient who has a panic injury. Their liver has been destroyed, damage injured. They aren't able to add that glucarate I'll molecule onto the Billy Rubin. And so this conjugated Billy Rubin will be what it will be. In this case of the liver's damaged. It will have, at least in some part, if the liver's been damaged. It'll have some of these molecules that are adding on the Billy Rubin, adding on the glucagon a molecule and a Billy Rubin, and so some of them will be elevated. But you may have an increase in both the unconscious, gated and conjugated Billy Rubin and patients with liver injury. And then the last one is if you have some more like a biliary duct blockage, like their biliary duct, is blocked. The liver is actually worked completely to congregate all of those Billy Ruben molecules. But what happens is the biliary system kind of starts back flowing, and some of that starts leaking back into the bloodstream. So in patients who have, like, a biliary duct obstruction like a postobstructive John, this will have very high conjugated Billy Rubin levels and very minimally elevated uncontradicted bilirubin levels. And so that's kind of like a little clinical tidbit on these. Well, really, what I want you guys to take away from all of this is that the liver synthesizes bile and the three main components is by Elasis, which remained from cholesterol. Billy Ruben, which is made from the he moved hemoglobin and fossil lipids were actually coming from the triglyceride your triglyceride to get broken down into fatty acids. We use some of those fatty acids and compiegne on a dove, a bunch of different like molecules on to them. And these are your fossil lipids. But these are the three main components of bile that you have to remember. Okay, I know that was a lot of stuff. I hope I didn't overwhelming anybody. Um, one of the things that I kind of wanted to quickly show you before we kind of like, you know, finish up. And if there's any questions is I wanted to give you guys a little like thing here to look at it since you guys are in your step one right now, we've made a lot of Step one videos and we've made a lot of notes and illustrations that I really think would be helpful to you guys if you guys ever want to look at, um, this is actually kind of augmentation of what we just talked about today. So we have all of these notes which go into a lot more detail, explain things into more thorough detail and give you also these little cool diagrams on the side to help. Better explain that, especially what we talked about today. We talked a lot about, like the liver metabolism the protein sent. This is all that storage. Was that one big slide, and we have all of this. If you guys want to go through them, we have the one on our liver histology with some a lot of additional notes that you guys can go ahead and check out and again digging into like the anatomy of the liver as well. Uh, and so all of those things are there. So yeah, I I really think that this is ah ah, cool thing that if you guys want some extra help, go ahead and check some of these out there. Pretty awesome that we have there. But I think that, for the most part, covers a lot of us things for, like, the anatomy and physiology of the liver. We manage gone overboard on some things, but, uh, I hope it was helpful. I hope it kind of made sense. And if there's any questions whatsoever on anything, let me know or anything that you guys want to talk about. Let's let's let's do that. Now If that's if that's okay with you guys, that was fantastic. And I think I speak on behalf of the class are in san that It was It was me. Isn't to go through that, um, on the C that you have up there as well. For for those supports that you guys have on your website that you're very kindly giving us that this current, um when we use that that cold all star 40. So that's that's really important to know that as well. But phenomenal, phenomenal lecture there. Is that going to conceive the comments coming through? There are People are so grateful. Um, just in terms of questions, Does anybody have any questions are exactly Wanna jump in there yourself? Oh, I just wanted, you know, I want to say thank you guys so much. I I, uh I was kind of nervous because this is not, like, the typical kind of lectures that I do. So I wanted to make sure I do justice and give you guys the best possible kind of lecture here on this. But I was very thankful. I'm I'm glad that you guys like that. I really hope that it helped you for, you know, you guys upcoming exam and stuff. And, you know, I I'm so happy if there's any kind of questions. Do you guys had it all about, um, you know, particularly Maybe it's not even about this lecture. Maybe it's about something else. Like, you know, other videos that you guys would be interested in that's producing. Maybe it's like, Hey, what? You have any questions about future particular areas of the field that you want to go into, um, any questions about how it a better study? Whatever it may be, Feel free to ask me anything that you guys have. Also. 11 of the million questions come through exact on. I know you guys are busy, and you have to get on a swell, but one of the main questions that have come through is liver function tests. I'm not sure if you have anything briefly or not that we can we can Can you take away? But I think that's went on a lot of people's minds Is hydro interpret those tests? What do they mean? Um, like, in terms of our own actors, they're very clear about a supposed hum, um, from you as well on the passion that you can't have when you're talking about these things that would help us for others. So anything on liver function tests, failure function was all right. All right. Yeah, I would have probably I guess I could have added those into this lecture, but yeah, that would have been a great thing to do. Yeah, so I think that would be an awesome video to do it. We did do a small little video on like types of jaundice. I think it was a little bit overboard on some of the underlying like physiology and path of his butt. There is a little tidbit in there about LFTs, but I think that'd be a great idea to do something like that in the future. So we'll have to put that into our, ah, our bank of a lot of videos that we got to get on the process of making. I think a lefty's would be a great one. Perfect exact just before you go and just by way of thanks from from us, we did get you at a T shirt. I'm not sure if you can see that there. So we got a T shirt. It's You can see the ninja nerve there and are are also, you know, varsity logo. But more important, portly on the back. It does say I, Linda and engine are number one. Ah, so so we're we're Viagra. If on there's a very special place for for you in the McGee campus here, if you ever do come the Visit Ireland, so we'll be glad. And there was also a hot as Well, uh, so we'll get that all. Yeah. Got to get I got to get that. Ah, Rahman. My common Ireland man. I got to get there now. Uh, we'll have to have, ah, chat with our lectures. Add to see if we can get you in the one of the halls, if you ever do. Yeah, that'd be cool. That was so sweet. Thank you guys so much that that was, honestly, super kind. And, uh, yeah, I I enjoyed this. I did. And I'm very thankful that I was able to be a part of this today. And I'm glad that people, you know, enjoyed it. And, uh, yeah, this is awesome. This is super awesome. Grij or grow, I rat Zack. Thanks. The Robin Crescent as well. They work so well with us and trying to get this up and running and on massive thanks to you again. So hopefully we'll see. We'll see some more video shoot. Absolutely. Yeah. Thank you so much, man. Thank you. Thank you for, uh, you know, planning this whole thing. Thank you so much for kind of going back and forth with me. It was worth it, you know? Really, really great on all Start 40. All the way, guys, I know I would have to be standing up. So who 100%? All right, guys? Well, we But we close it off there, then I think everyone's just really, really thankful. Well, we'll take we'll we'll be talking. What? We hopefully talking and see him or very soon. So much of an engineer Attainment was absolutely brilliant. Tons. All the comments were just coming through that everyone is so grateful without so thank you so much again. Muscle recognition to John in the hard work is but endorphin assists. We all really appreciate it. And again, thanks a million. Oh, no, thank you. Guys. This is so cool. Thank you guys so much. I I really appreciate this. Absolutely. I wish you guys all the best of luck. I hope that, you know, maybe we can do this again and we like Kathryn said we could go. I'll take it, get together and get a point for sure. Yeah, but that this was awesome. I was super thankful for this. It was a great experience, and hopefully we can do it again sometimes. So thank you guys for everything. Thanks, sec. Thanks for all thanks for us today. That's all right. You guys always all of that time