Gastrointestinal - Gallbladder & Pancreas

Hello, welcome back. Today, we continue our lecture series on the GI system. We're focusing on alterations in digestion. Specifically, we're going to take a look at the pancreas as well as the gallbladder and the biliary tree. So when we split these up for the pancreas, you're going to have to know all about pancreatitis, both acute and chronic pancreatitis, as well as pancreatic cancer. For the biliary system, we're really going to focus on colicistitis, as well as coli-lethiasis. So let's go ahead and get started. When we talk about the pancreas, remember that's the little organ that sits kind of transversely across the upper region of the abdomen. Its major function is in the endocrine system. So we know all about the pancreas related to insulin and glucagon. However, there's some really important digestive factors that are associated with it as well. So that the endocrine functions related to insulin and glucagon, that exocrine is related to digestive enzymes, specifically amylase and lipase, which we will talk about. It also does secrete a little bit of an alkaline buffer solution to help with the overall homeostasis of the system. So what happens with acute pancreatitis is that normally you have amylase and lipase that gets accreted out through the pancreas. Remember, they collected that pancreatic duct that is going to then go deposit those enzymes into the small bowel. It's connected by that duodenum. So if you have inflammation in your pancreas, it is believed to be because instead of those digestive enzymes reaching the duct and then going into the small bowel, they're actually being released into the pancreatic tissue themselves, which is very, very, very toxic. Obviously, they're made to digest substances. So what we get is an auto digestion of the pancreas because those enzymes are being released in the pancreas as opposed to in the small bowel where your food would be. So we get swelling of that area. It can be minor or it can be severe causing life threatening hemorrhaging of that area. So remember, the pancreas sits across in the upper region of the abdomen. If we have digestive juices that are auto digesting that tissue, of course, it's going to break down the membranes and we easily can get blood loss. It can be extreme. We can also get auto digestion of the areas around that. So we think about it can easily transfer up into the lungs as well. We'll talk about that when we talk about complications. So what causes acute pancreatitis? Number one and number one for men in particular is alcoholism, specifically seen after like heavy binging periods or episodes. For women, the number one cause tends to be biliary tract disease. So if we have a gallstone that gets stuck in the biliary tract and blocks, the pancreatic enzymes from being able to enter the small bowel, we get a backflow of them into the pancreas themselves. Of course, trauma can cause it. Car accidents we see a lot where they maybe hit the steering wheel or something. We can cause injury there to the tissue, which can then lead to pancreatitis. Some infections, drugs, you can read through this. But what do we see? Again, that auto digestion of the cells themselves when it is severe can lead all the way to necrosis. And we'll talk about that in a minute too. And the patient actually will feel extensive pain related to this. So pancreatitis is very, very, very painful. We'll talk about some more signs here. So they get left upper quadrant pain and I added to that mid epigastric because you will see, you can't see me in here, but you will see it kind of, some patients say it's just right here in the center, but it can go left, which is, I'm noticing now that video is reversed. So just ignore my visual and think of left upper quadrant pain. We're going to be suspicious for the pancreas. On here, you can also see colon sign. Remember, that's one word. So we just say colon's right around the umbilicus, whereas gray turners, two words, gray turners, I think of flink bruising. Again, this is because that auto digestion can happen in the pancreas, which makes it very leaky, right? Those, all those blood vessels in there can become leaky. And we can very easily bleed into the peritoneal space. It is aggravated by eating. So this is when you're talking about history of a patient. It's pretty easy to identify based off the location of the pain, the description of the pain as well as the pain is increased after eating. And this should make sense because when we eat food, our body naturally understands and it starts releasing digestive enzymes to break the food down. Well, it's not getting to the get to break it down. It's actually being toxic to the pancreas themselves itself. So that's why we have that. It may radiate to the back and this is particularly important when we think about positioning patients. Patients will say that when they lean back in their bed or they're going to sleep because the spine runs along the center of the back and the pancreas sits just in front of that. So when you lean back, the pancreas can actually fall to the spine and cause some pain there. So increase pain while lying supine. The pain is described as severe stabbing and continuous. So as you can imagine with pain that is severe and stabbing brought on by eating, most of your patients are going to come in with some sort of anorexia. They have started to avoid eating because they realized it makes it worse. We can also see flushing cyanosis, maybe some dysnia. Again, the pancreas is right there and then you've got the diaphragm and then you've got the lungs, right? So it's easy. They're very, very closely related. So you can easily have some respiratory issues related both to the pain as well as to the damage if those pancreatic enzymes move into the lungs. We can have issue, too. Taca cardia, we might see some jaundice. That is because the inflammation of the pancreas can affect that biliary tree which can then block the biliarumins ability to get into the small bowel just like we learned with all of our liver stuff. Crackles. So if you have crackles with a patient with pancreatitis, you have to be thinking that those pancreatic enzymes that are being leaked into the pancreas can easily cross into the lungs. When we have digestive enzymes that get into the lungs, what do you think it's going to do there? The same thing. It can digest that lung perincoma. So when we see crackles or we hear crackles related to this, we have to be assuming that we have lung injury now and this is going to put them at risk for, let's see, let's think back to week one or two, exam one at least. We can have destruction of the actual alveoli space and so that was related to arns, acute respiratory distress syndrome. So when we see crackles related to pancreatitis, we're really worried about arns and there's your colons and great turners sign again. So what do we see diagnostically? We're going to take lab values and we're going to see elevated levels of amylase and lipase. Those are the two digestive enzymes. Amylase is really good for breaking down carbs, lipase for fat and we're going to see increased levels in the blood. Why? Well, because I told you it's not being released through the pancreas and then making it into the small intestine where it's supposed to go to break down the food, it's getting stuck in the organ which will eventually lead to the blood, right? So we've got high levels of amylase and lipase in our labs. We see a low calcium with this oftentimes. Now, pancreatitis is one of those things we see it. We know what it is. However, we don't quite understand all the mechanisms. Like we see it after binge drinking episodes but we're not sure how that's related to it. The current thought is that when you drink high levels of alcohol, your body makes more digestive enzymes, releases more digestive enzymes and that might be part of the problem. Same thing with the low calcium. They see it happen, we know it happens, but the direct mechanism for how it happens we still haven't proven yet. But when we say things like low calcium or hypocalcemia, it's important for you as a clinician to think about how would I know if my patient may be showing signs of this. So remember, low calcium, we see lots of tetanate, sorry, tetanate. So let's say you put a blood pressure cuff on them and they start to show the trusose sign, right? That would be one. Or if they're seeming a little twitchy and you do the chowstech, that might be signs of low calcium. So what can we do to diagnose these? We can do an abdominal ultrasound that can look for inflammation or enlarged pancreas. We can do an x-ray or the gold standard really is a cat scan because that's going to be able to show us acute pancreatitis as well as striations from chronic or old pancreatitis, which we'll get into in a minute. The other thing we can do, and I should note that an ultrasound and x-ray and a cat scan are all non-indasive. When we talk about an ERCP, endoscopic retrograde, Kalangio-pinkriad-tography is a long word. To say that we're doing an endoscope, we're doing a scope going down retrograde, meaning we, once we hit this sphincter of ody, we are reverse entering. So remember, the biliary trees are one-way system. It all goes from the pancreas, from the liver, all the way to the small intestine. One directional. We are going in the opposite direction. So we are going upstream from that. So that's the retrograde part, Kalangio-pinkriad-tography. This means that we're going to inject dye and look at the imaging. So an ERCP is great for identifying strictures, gallstones, whatever is going on. However, it's very important to know that because we are shooting dye in a reversed formation of how the flow comes, we're increasing the pressure, which just by itself puts them at risk for pancreatitis. So just know that. These patients already have pancreatitis. They would just need to know the risks associated. When we talk a little bit later about gallstones, those patients typically hopefully do not have pancreatitis, so they would need to know that that is a potential complication. And you, as a clinician, would need to know to look for signs and symptoms of pancreatitis if they didn't have it pre-perceitor, because it is one of the risks. You can also do an MRCP, which is just, if you can take a typical MRI, except it's specifically of the pancreas and organs in that region. So again, this would be non-invasive as well. The only invasive procedure here is your ERCP. And speaking of ERCP, since it's kind of interesting, it's considered an advanced procedure, I have a really good video here. If you want to click on this and look at it later, I highly suggest you do. It does a great job of explaining the relationship of kind of all the neighboring organs as well as expectations of what it can and cannot do. So I encourage you to take the time to look at that on your own. When I told you with pancreatitis, we do see signs of hypocalcemia in some patients. So we're looking for tetany, the tropestex sign, and then the trusos. And remember trusos isn't like how we would think of a tremor. If you put the cuff on your patient, they automatically do that. So when we look at collaborative care, I already told you they're going to have pretty severe pain. So relieving pain is going to be a pretty big focus for us. Iving morphine has been shown to be the best medication for this specific type of pain. Also possibly not as good, but anti spasmodics might help just a little bit. We do like to position the patient sitting up, if possible, but also on their side. So we do see relief with that sideline position. If the patient can handle it, tucking their knees to their chest also helps relieve some of that pain. So rationales behind all of these, we want the patient sitting up for their breathing because that might be affected. The mayor may not be. You're just going to have to go off patient case scenarios, sidelining, relieves pressure, and the knees to chest also helps. So we just kind of get them in whatever position is appropriate for them to try and help relieve some of that pain. The other thing that's very possible because of the auto digestion of the organ and then the seepage of fluids, if you will, is it's very likely this patient could go into hypovalemic shock. So we're going to be watching their vital signs pretty closely, particularly their blood pressure to ensure that they have adequate fluid on board. And if needed, we might give some albumin or fluid replacements. Another type of shock this patient could be at risk for if we have diffuse damage to that area is they could go into septic shock because if we have cells in the pancreas that are actually becoming necrotic, we can get an abscess or an infection that can spread very easily to the rest of the system. We're going to try to reduce those pancreatic secretions. So remember I told you the patient is usually going to feel more pain after they eat. So whenever we get a patient and we usually drop an NG tube first thing and we're going to pull everything out of their stomach, which should decrease their pain. No food, no relative enzymes, no pain. That's the thought. Treat fluid and electrolyte imbalances and keep in mind, we're really focused on hypocalcemia, prevent infection and then remove the cause. So possibly surgery or an ERCP or whatever needs to be done if it's an obstruction or constriction that is causing it. So the major complications for acute pancreatitis, one is a pseudocyst. And so this is kind of like a like cyst and I think of this on the pseudopart is because luckily it's not as terrible as an abscess. So what happens is you have inflammation in the pancreas and the pancreas like other kind of GI organs has a capsule around it. So when you have the inflammation, you've got all that fluid, all those cells and then it starts to heal and go back to its normal size. You can sometimes get these little pockets or like blebs of fluid. So a pseudocyst is benign. It just has fluid, leftover fluid, maybe some debris left in a little pocket on the outside of the pancreas. Now this can be painful to some patients depending on where it is if it's bumping against something else. If it's on the anterior surface of the pancreas, maybe a very experienced clinician could actually feel it, but really we're not going to do anything to treat it because over time those pseudosis tend to just dissolve and get absorbed by the body. And it would cause more harm to try and go in and intervene on that. However, if that area is infected, we would call that an abscess. So if we have a necrotic tissue in there, bacteria in there, something that's really causing an issue or concern, that would be a pancreatic abscess. And that's actually this picture down here that I don't think you can see because my head's underneath it, but don't worry. Just know that an abscess is a completely different situation that we would go in and try to drain or aspirate an abscess because we don't want it to rupture and then cause a bigger problem later on. So pseudocyst, pretty benign, we watch it over time. We'll do serial cat scans to make sure that it's resolving over a few months or whatever. Whereas an abscess is a true infection, the risk of that rupturing, we can't take. So we go in and we surgically drain it. Also, again, respiratory involvement, arDS would be a very big concern related to pancreatitis. So again, if those digestive enzymes, possibly that necrotic tissue, whatever it is, crosses the diaphragm and goes into the lungs, it's going to start to eat away at the alveoli, which will lead into arDS. So anytime you hear crackles on a patient where they don't have something else, they're not fluid overloaded, they're not in heart failure, anything like that, you would be concerned related to the pancreas that we're looking at arDS here. And again, hypocalcemia, just make sure to know it's a risk factor and how to check for it. So when we're talking about caring for these patients, we're going to try to either avoid or catch very early any sort of severe complications. So we're going to be watching their vitals signs very closely. These patients are managed in the ICU because of their high risk of complications. So we're watching vitals signs particularly the blood pressure for signs of hemorrhage or shock. We're looking at fluid and electrolyte imbalances. Now I've talked a lot about hypocalcemia, which you absolutely have to know. But there could be other things related to their nausea and vomiting, potential for diarrhea, GI upset. So just know that we'll be watching their electrolyte pretty regularly. Monitoring for lung function, looking at SPO2 very frequently as well as listening to the adventitious sounds of the lungs, remember they are very high risk for arns, which could lead to respiratory failure. They also, just because of the pain in the location, might not really be breathing very deeply. So we could easily have ABG variances here with this as well. Decrease pain. So again, that patient positioning as well as morphine, which is the number one drug to help with the pain for these types of disorders. For chronic pancreatitis, we have moved from the inflammatory process to now the fibronic process. Because again, any organ in the body, constant inflammation leads to scarring and fibrosis. So here, we have actual strictures and calcifications of the tissue, where anytime we have that, we're going to have organs that are no longer functioning the way that they should. Common causes of this, again, for obstructive, it's going to be gallstone. So any sort of stone or possibly a cancer that has formed that is not allowing the flow of the gastric juices, so the amylase and the lipase, it's a gastric. I meant digestive juices to go from the pancreas to the small intestine. So blockage in that flow can cause this. For non-abstructive, again, it's alcohol use. So typically what we see is that we see people that have acute pancreatic issues where maybe that is then resolved. However, six months, three months, two years from then, they have another acute exacerbation. So when we have those multiple times over and over again. So either a patient that's getting multiple stones, we resolve it, but they get them again. So a body that just likes to produce gallstones. Or we have a patient who will maybe stop drinking or goes kind of on vendors and has multiple episodes of acute pancreatitis, that will eventually get us to chronic pancreatitis. For chronic, a lot of the symptoms are the same, so we continue to have the left upper quadrant pain, except instead of this feeling like a sharp stabbing sort of pain, it turns into a having kind of gnawing cramping like pain. It may be constant or it may be diminished. We do see weight loss because over time they have learned that the pain gets worse when we eat. Now we're seeing a trend of actual weight loss, not just not wanting to eat, but we're seeing weight loss. Constipation, we might see some mild jaundice with dark urine. Here we're usually seeing foul smelling fatty stool. So remember, it's your digestive enzymes, it's your lipase in particular, I think it's released in the pancreas, goes to the small bowel and breaks down so your body can absorb that fat for nutrition. When your pancreatic enzymes are not reaching the small intestine, any fat that you eat will immediately go up to your stool, so we know this from previous lectures, we call that Stay Adorea, so that's that really fatty kind of floaty, shiny stool that they might see. So anytime we have a patient with chronic pancreatitis, we get worried that they're probably having some issues related to that. And there's medications, once we do get into chronic pancreatitis, we're going to give them pancreatic enzymes to make up for the fact that they no longer are getting this enzymes to the gut. Diabetes malitis, so of course as you can imagine if we have diffuse destruction of the pancreas, we most likely are going to have issues with insulin release and all of that wonderful stuff. Very common for people with chronic pancreatitis to end up with type 2 diabetes. We're still going to focus on pain management, again morphine number one, we might get some fentanyl patches for some longer lasting pain management. We do the pancreatic enzyme replacements, crayon is the most common one that I can think of. And just remembering back to when we talked about with kids with cystic fibrosis, you have to take the enzymes with your food or it won't do anything. So with meals, with foods, with snacks so that they both enter the gut and the small intestine at the same time. They usually contain amylislypase and tripsin, although you might see a few different things on the market. For nutrition, we like high protein, moderate carbs and low fats. We have seen that with pancreatitis and this might be counterintuitive to what you're thinking related to the pancreas and insulin. But just know that fat in particular, the release of lypease, tends to be the most toxic for the pancreas. So we want as low as possible fats, medium carbs and high protein. We do want them to avoid caffeine and spices because at this point, they might have issues with diarrhea. And we do not want anything that's going to increase that GI motility. So we usually talk to avoid caffeine and really heavy, thick spices. Control of diabetes, of course, at this point, they might be on insulin to regulate their blood sugars. And if, sort of, a last-case scenario, we might recommend that they do some surgery techniques, which I think I have on the next slide for you. Here we go. So we might recommend a ruin wine where they actually are going to take out part or disconnect part of the GI system. So here, you can see what we're actually doing is we're dissecting the biliary tree. And we're connecting the top portion directly to the small bowel. So we are bypassing all of this. So by the time we get to chronic pancreatitis, you have to imagine that this whole pancreas is thick, swollen, or very atrophied. Either way, we're putting pressure on the ducts that run through it. So if we're causing blockages here, we might just go ahead and bypass it by connecting these two things here, and then we would take the stomach and put it lower down on that small intestine. So we're really just bypassing this whole part of the pancreas where we likely have issues and we're not allowing good flow through that area. When we talk about pancreatic cancer, I don't know if you guys know anyone who's ever had it, but it's a very difficult diagnosis to receive because of the high mortality rates. It's a fourth leading cause of cancer-related deaths, most likely because of how quickly the patient sort of declines, very, very poor prognosis. They're silent tumors, meaning we usually don't have signs until they're very advanced. And the majority of patients die within five to 12 months after their diagnosis. So very, very quick turnaround here. Causes are really unknown. We do see a adenocarcinoma of the pancreas, however, we can't really trace it back to a specific link yet. However, we do see risk factors, which is chronic pancreatitis, as you guys know, constant inflammation, fibrosis scarring leads to cellular disruption, more at risk for mutations, and things of that nature. Increased age puts them at risk if they already have diabetes as well as smoking. Clinical manifestations might be dull aching abdominal pain. We do see anorexia, sorry, with rapid weight loss, nausea, and some jaundice. Again, with these, it's a very quick rapid decline. For diagnostics, we can do lots of different imaging techniques. Trans-abdominal ultrasound is exactly what it sounds like, ultrasound of the abdomen. And EUS is an internal ultrasound that's put on the end of an endoscopy, CT MRI. You guys are familiar with, again, an MRCP. is an MRI but it's specifically around that pancreatic region. So again it is non-invasive but it's very specific to that area. We can do the ERCP which again is that scopes that goes down and retrograde goes through those biliary ducts. We can do a fine needle aspiration so that would be if we do see a mass or a fluid sac or anything that we're seeing on imaging. We can go in through ultrasound biopsy and extract some of that fluid to see what's going on there as well as a typical PET scan that we think of as being common for cancer. Some collaborative care really is related to removing the body, removing the cancer from the body. So most of our cancerous lesions on the pancreas are found in the pancreatic head. So the most common procedure we do is a Whipple procedure where we take out the head of the pancreas and then we attach the stomach to the pancreas and then the small intestine. And again my picture here is. So now when we talk about the biliary tract or sometimes it's called the biliary tree because you have all of these little finger-like projections that start in the liver and they come down to a final trunk. You also have some biliary tracks that go through the pancreas that would be right here but you can see both the hepatic and the pancreatic duct come together to form the common bile duct which is where it then gets deposited into the small intestine. So the whole point of this is to concentrate and store the bile, secretes the bile into the small intestines. It also will carry waste products from the liver to the small intestines as well as bile salts that can break down that fat. So when we have. So when we have disorders that can affect that biliary tree or block the biliary tree, you can see how easily it will affect other things in the system. Some disorders that can affect that are coli-lithiasis. So coli-lithiasis is the formation of gall stones. Now it's not uncommon for people to form gallstones and small gallstones that stay in the gallbladder are really no problem at all. Lots of people have them. It's when we get too many or when the gallstones travel out of the gallbladder and get stuck in that biliary tree or the biliary ducts that we can cause obstruction of the flow and that really is what's causing problems. The other thing we'll talk about is coli-cystitis which is inflammation of the gallbladder. Now I will say this inflammation is typically correlated to an infection as well but coli-cystitis is the inflammatory process of it. It's usually started by gallstones that sit in there if we have multiple multiple gallstones. Like this picture you can see these are actual gallstones from a real gallbladder. If you're a little aggressive you can think it looks a little like some of these look like caramel to me but when you see it in real time in a real patient it's not very appetizing at all to say the least. At coli-cystitis we can have acute or chronic inflammation again usually related to gallstones. So again coli-cystitis inflammation which leads to edema and distension of the gallbladder. We can have bile or pus associated with it and because of the inflammation we can cause occlusion of that bile duct. If we cause any sort of occlusion to the duct we know that we're gonna have some inflammation and some backflow of that bile that can go into other places. So when we talk about occlusion of the bile duct like I said with the liver lecture the bile has billy rubin in it. Remember so if the billy rubin isn't able to get to the small intestines it's going to back up into the circulatory system into the blood. So we see high levels of billy rubin as well as tea colored urine and then because it's not getting to the small bowel we will have clay or light colored stools. What we can do for this if the patient has a lot of pain which we like to call biliary colic, almost like a colic-y baby. A biliary colic is when they have pain in the right upper quadrant related to gall bladder issues. We can control that with NSAIDs or morphine. We can also use anticholinergic or antisposmotic agents that might help a little bit. We want to be sure to control the risk of infection so we might give them antibiotics either appropriately or prophylactically. We're going to maintain fluid and electrolyte balancing as well as trait nausea and vomiting. So typically with somebody with gall stone or gall bladder pain we are going to decompress the abdomen with an NG tube and we also expect that they come in with usually some previous history of nausea and vomiting. Percipitation of bile salts, calcium and cholesterol can occur. So when we think about the development of gall stones we typically think of super saturation of these materials. So if you can relate it to kind of like forming a clot in the blood system it's very similar. So if we have lots of particles or lots of substances in the bile and then the bile sits for a very long time. It doesn't have movement. We're more likely to form stones. Again they can either stay in the gall bladder which is usually asymptomatic, non-problematic whatever term you want to use there. Lots of people have gall stones that stay in the gall bladder and that's okay. They never have issues. But when we have them that migrate out into the actual duct, then that's what puts us at risk for causing an obstruction. And again here's that term biliary colic where we start to feel the pain associated with it. So for the colila thysus remember that's the gall stone portion of this and also remember that these two things oftentimes happen together. We form gall stones which then eventually leads to the inflammation. So for collaborative measures we might give them bile acids to help dissolve the stones. That would be ideal. That would be pretty non-invasive. We can give them medications that may help to dissolve the stones and then we don't have to do anything. A step up from that would be like lithotripsy. It's at the bottom but it's kind of the next non-invasive thing where we can give them, send them shockwaves through their body to try and break up that stone and hope that they will pass it on their own. We can do an ERCP for stone removal which is linked to the video on the ERCP page but remember it's the scope that goes in. The catheter will then go in through the biliary duct. You can inflate a balloon and then sweep that duct and pull out all the stones that are in there. I have seen an ERCP. The most we ever pulled was 12 stones. I know there's many more than that but we pulled 12 stones on our biggest one. It was very very satisfying to see them come out of the little sphincter. And then our most invasive would be a colicisectomy where we're gonna actually go in and take out the gall bladder. This is one of the most common procedures done in the United States so you will absolutely take care of someone at some point that's how to colicisectomy. The question is how long ago did they have it? But the most common way we used to do an open colicisectomy where they had a big incision, now we do laparoscopic. The thing to remember about laparoscopic surgeries is that they're gonna make puncture wounds in and around the abdomen usually at the umbilicus and then some on each side. And they put their utensils in there to be able to perform the surgery but we also inflate the belly with CO2 so that it blows everything up so we can get good visualization. So laparoscopic colicisectomy are preferred over open because they have less complications if you can imagine cutting through all the muscle and all of that getting to the internal organs, moving them around, cutting, clipping all of that. Your body senses that and has a very strong reaction to open surgeries Whereas if we can do minimally invasive, so only go through a couple. little peep holes and touch as few things as possible. Your body typically responds a little bit better to that. The one thing to think about though is that because of the CO2 that gets injected into that abdominal cavity, they can have some pretty severe post-op pain related to the CO2 retention and not so much the actual surgery themselves. So go ahead and take on your own time. Watch this video and think about it in terms of if you were caring for this patient, how would you prep them for surgery and what are some educational points you would think about post-op for these patients. So with the lapper scopic, they can remove bandages and shower just one day post-op. So oftentimes these patients come to us and they just have little tiny stary strips or bandages on their puncture injection sites. We do want to be very aware of signs and symptoms of infection though. We would expect their white blood cells to go up a little bit post-op related to inflammation, but anything more than just a baby fever or a tiny little jump in white blood cells, we might be worried about infection. Again, the management of the pain from the CO2 pockets, sometimes that CO2 can crawl up under the diaphragm and cause referred shoulder pain for these patients. Oftentimes getting them up and moving will help move those gases so that the body can rid themselves of it. The other thing that can help sometimes is laying them in a sim's position, which is where you kind of lay almost on your belly with one knee up. You can Google that picture if you want it, but that can be effective in relieving the pain and help moving that CO2 for some patients, but getting them up and moving will absolutely help them. They can gradually resume normal activities, much less recovery time than a full open colicisectomy, which they have to be out for at least a week. This is a couple of days. However, we do recommend that that low fat diet is most appropriate for the first few weeks as we're getting used to the body system and their ability to kind of work with what they're left. Because remember, we're taking the gallbladder out, so we're moving that whole storage unit for bile, and remember, bile is used to break down fat. So we really want everything to just kind of have a slow initiation back into the world. So we really want low fat diets for the first few weeks at least. Okay, and so for our case study, I'm going to go ahead and hold off. We will do this in class. As always, reach out to your faculty members if you have any questions or concerns and happy studying.