01. A&P of GI Tract - Mouth to Small Intestine

Hello everyone, in this class we're going to discuss the anatomy and physiology of the GI tract specifically from the mouth through the small bowel. And our focus is going to be on implications for management of the patient who has a fecal diversion. So here's what we're going to accomplish. We're going to identify the four layers of the bowel. We're going to talk about major structures and functions for each layer. We're going to talk about the major structures of the GI tract specifically with the focus on the small bowel and its role in digestion and absorption. So this just has your learning activities. I'm not going to go through that, you can read it. Okay, so looking at the GI tract from kind of a big picture perspective, you first got the elementary canal which I'm going to try to use my laser pointer here, starts at the mouth and goes all the way to the anus. And of course that's just a long tube that's folded back and forth. My brother-in-law calls this very inelegantly the food and poop shoot because food goes in and poop comes out. But that does capture exactly what happens. You ingest nutrients, they're processed and absorbed and then waste product stool is eliminated. You also have the accessory organs. And accessory organs include anything that contribute to the ingestion, digestion and absorption of nutrients but that are not part of that tube. So salivary glands, teeth, pancreas, liver, all of those are accessory organs. Now the major functions of the GI tract can be divided into the functions of the upper tract and functions of the lower tract. In this class we're going to focus on functions of the upper tract, mouth, esophagus and small bowel and that is ingestion, digestion and absorption of nutrients. In a later class we'll talk about storage and elimination of voice products. Now throughout the GI tract you have four layers of the bowel wall and the histology of the GI tract is pretty consistent all the way through. There are some unique features of the colon that we'll talk about later. First of all you have the cirrhosa and that's the outermost layer and you can see I'm using my pointer to show you that. That's the outermost layer of the bowel wall. It's actually continuous with the mesenteri and a very important consideration when you talk about the cirrhosa layer, there are no mucous secreting glands, no mucous secretion and this layer does not have the ability to keep itself moist. We know this on one level because we all learned in nursing school that if there is evisceration and loops of bowel are exposed that we need to immediately cover those loops of bowel with sterile moist towels to keep that tissue moist and viable. But within the field of ostomy care there are some additional implications. First of all you want to realize that the cirrhosa layer is actually continuous with the mesenteri. When you have patients who have transmural inflammatory processes such as Crohn's disease that can result in severe pain because inflammation of the cirrhosa layer also causes inflammation of the mesenteri which is throughout the abdominal cavity. So a lot of people don't understand that Crohn's disease is acutely painful and that's why. And finally looking specifically at stoma construction we'll go into this in more detail but you see that when you have a stoma they bring the bowel out, they turn it back on itself almost always and that exposes the mucousel layer. The mucousel layer does have mucous accretion glands can keep itself moist but occasionally they do not surgically mature the stoma. They do not turn the stoma back on itself. Typically this is in a situation where there's intense bowel wall edema and they're actually unable to turn the bowel back on itself. Bottom line if you have exposed cirrhosa that cirrhosa will become inflamed and sticky and the bowel will gradually roll back on itself so it will gradually self mature but it takes a lot longer and in the meantime and throughout that process it's normal to have yellow tissue that is obviously non-viable and sluffy. That occurs typically only in stomas that are not surgically matured and how can you tell that when you're evaluating a patient with an ostomy typically you're going to see sutures at the base of the stoma all the way around the stoma at the connection to the skin that tells you the stoma was turned back on itself the bowel was turned back on itself it was surgically matured. If you do not see those sutures if you see a combination of red wet tissue and yellow sluffy tissue go back and read the operative report that stoma may not have been surgically matured. Continuing through the four layers of the bowel wall so the cirrhosa was the outer layer the two middle layers are muscle layers you have actually two muscle layers throughout the bowel wall you have the outer longitudinal muscle and then an inner circular muscle and this highly muscular function of the bowel wall allows for two types of movement first of all it allows for a mixing motion a back and forth that facilitates digestion and absorption and secondly it provides for parasitotic waves where the bowel contracts here relaxes here so contract relax that pushes contents forward another squeeze pushes contents forward now you know that muscle only works if it's innervated and you can see from the picture i hope and from the slide that the bowel wall is richly innervated you have three distinct nerve plexuses you have the sub cirrhosa plexus which is between the cirrhosa and the longitudinal muscle innervates the longitudinal muscle you have the my enteric also known as our box plexus this located between the two muscle layers and then you have mice nerves plexus which is located between the circular muscle and the submucosa so rich innervation of those muscle layers now a lot of times you'll hear the terms intrinsic nervous system and extrinsic nervous system the intrinsic nervous system refers to the my enteric plexus and the mice nerves plexus so the nerves located between the muscle layers the nerves between the inner muscle layer and the submucosa the intrinsic nervous system responds to intraluminal stimuli so if the bowel is distended that's going to activate parasitic activity to move things through if you have a lot of irritants in the lumen of the bowel that's going to activate the intrinsic anterior nervous system and increase motility so what would be an intrinsic irritant you think about when you go to a restaurant it's great it's one of those little hole in the wall restaurants probably a lot of the flavor comes from the unique blend of pathogens and the next day you have diarrhea well what's happening there you have increased bacterial loads in irritants within the lumen of the bowel that is activating these nerve receptors basically like let's get this stuff out of here and you have increased motility another structure to be aware of is the interstitial cells of cajol and those cells actually transmit messages from the nerves to the muscle cells so they help to regulate motility so basically this is what happens the nerves and the bowel wall respond to intraluminal irritants and to distinction and then they activate the interstitial cells of cajol which in turn Notify the muscle to increase activity, so it's a loop. You also have an extrinsic nervous system, the extrinsic nervous system responds primarily to stimuli outside the bowel wall itself. So it includes the autonomic nervous system, the autonomic nerves communicate with nerve plexuses in the subsurrosal layer, so I'm going to try to show you where that is. So sympathetic nerves, parasympathetic nerves communicate with and can activate the nerves in the subsurrosal plexus, which also contributes to motility. Sympathetic stimulation tends to slow peristalsis, slow intestinal secretions. We see that a lot in our postoperative patients, we know that Ileus is normal. Well how does that really happen? The stress of surgery, the effects of anesthesia, the effects of opioids, impact on the sympathetic nervous system, which impacts on the subsurrosal plexus, slows everything down. In contrast, what happens when you give a patient reglet, metaclopromide, while we see increased motility, and again, the effects are at the level of the subsurrosal plexus. This will be very important if you're taking care of a patient with a spinal cord injury, because if you have a patient with a spinal cord injury, they lose extrinsic innervation, so they're basically the bowel is cut off from the effects of sympathetic and parasympathetic stimulation. However, the intrinsic nervous system is intact and remains functional, so does the bowel still work? Yes, but at a slower rate. So we've talked about the cirrhosa, we've talked about the muscle layers. The third layer is the submucosal layer, and this is basically a connective tissue layer. You know it contains a nerve plexus, mysinus plexus, also contains large blood vessels, contains the interstitial cells of cajole. Now the fact that you have large blood vessels in the submucosal layer tells you that if you have an intestinal malignancy, once it extends through the mucosal layer into the submucosal layer, it has access to blood vessels, also has access to lymph nodes. Now the mucosal layer is the innermost layer and the layer that we deal with the most in terms of ostomy care. So you see stomas here and you see their bright red and moist and that's because they are showing you an exposed mucosal layer and the mucosal layer is red and wet, is very richly vascularized, so you have lots of blood vessels, that's why it's bright red normally, contains its own mucosal creating cells, so always moist. There are no nerve receptors in this layer, so patients look at a stoma and they're like, "Ooh, that looks so painful, that looks so sore, that looks so weird." And so what you want to say to them is, "Yes, it does look weird, but it's not going to be painful, it's not going to be sore because there are no nerve endings in that layer of the bowel wall." And of course the mucosal layer is absolutely critical to absorption of nutrients, water and electrolytes, and we'll come back to that. So we've talked about what they call the histology of the bowel wall, the layers of the bowel wall, and how they relate to ostomy care. Now we're going to start at the mouth and walk through the GI tract and talk about critical functions of each structure. Now the tongue we're not going to spend any time on, you know how important it is to food manipulation, to swallowing, to taste, to speech, but in terms of ostomy care, not significant. What about the salivary glands? Well there's actually three groups of salivary glands, jointly they produce 1,500 milliliters of saliva daily. That's a lot. We don't realize how much saliva we produce until we have a very sore throat and it kills us to swallow. But that saliva is basically mucos that acts as a lubricant plus an enzyme salivary amylase that begins digestion of starches. And we'll come back to the volume of saliva that is produced because if you have a patient who has an esophagus to me, where they connect the esophagus to the skin, that will need to be pouched simply because of the volume of saliva produced daily. Teeth, again very important to ingestion of foods but not critical in the world of ostomy care. Oral pharynx is where swallowing is initiated, again, not critical in our world, but definitely critical to patients. Let's talk briefly about the esophagus. It's a 25 centimeter long tube that extends from the oral pharynx to the stomach. It actually is comprised of skeletal muscle approximately. So when you initiate swallowing, you're using that skeletal muscle. But then it transitions to smooth muscle. So you know if you get something stuck halfway between your mouth and your stomach, you can't initiate swallowing mid esophagus. You have to start from the mouth again, take another swallow of water to push something through. The esophagus is bounded by two sphinters. You've got the pharyngoesophageal and the esophagogastric. The pharyngoesophageal opens for swallowing but is closed at other times to prevent reflux from the esophagus into the mouth. And then the esophagogastric also opens during swallowing, close the rest of the time to prevent reflux from the stomach into the esophagus. Now that esophagogastric sphincter, the distal sphincter, is not a true sphincter, is not a muscle. It is a high pressure zone that very effectively maintains closure, but through a different mechanism. The problem is that high pressure zone can fail. There are a number of substances that reduce pressures right at the esophagogastric junction. So hormones can reduce pressures. Why do women have so much acid reflux during pregnancy? Because the hormones produce during pregnancy lower pressures within that zone. Lowers pressures within that zone. Some foods lower pressures within that zone. You do produce mucus throughout the esophagus that helps to protect against both acids and bases and also facilitate swallowing because it's a lubricant. We already mentioned this, but here it is again. So if you have a patient with an esophagostomy, like you see here, that would be a patient who has an esophageal stricter, a patient who requires esophageal resection. And you have the proximal end of the esophagus. And at this point, you cannot reconnect it to the distal end. You can't just close it. You've got to bring that proximal end of the esophagus out to the skin to permit drainage saliva and anything you swallow. And you have to pouch it because of the volume. Next we're going to talk about the peritoneum. So the peritoneum is basically a tough membrane. It supports the bowel, it connects the bowel to the posterior abdominal wall. It also carries blood and nutrients to the bowel. So that tough membrane includes blood vessels and nerve pathways that nourish and innovate the bowel. So it's critical to bowel health and bowel function. All different components of the peritoneum, I think you're probably familiar with most of these terms. The parietal peritoneum is the portion that lines the abdominal cavity. And the visceral peritoneum is the portion that we see. literally wraps around organs, wraps around the loops of bowel. And the mezzantery, which I'm going to try to show you right here, the mezzantery is actually that double loop or double layer of peritoneum that extends between the bowel and the posterior abdominal wall. If you've had the opportunity to watch abdominal surgery, you've seen surges hold up loops of bowel and you've seen that membrane that's supporting the bowel. You've seen the mezzantery. So it's a critical structure. We'll talk more about the mezzantery when we talk about stoma construction later on in this unit. You also have the greater omentum. The greater omentum is a double fold of peritoneum. It hangs down from the stomach. It's filled with that. And what does it do? Not a lot. It just sits there, but it can be used to repair traumatic injuries. It can also be used to create a partition between the abdominal cavity and the pelvic cavity. Next, the stomach. A critical organ. Three different anatomic areas for the stomach. You have the fundus. You have the body and the pylorus. A fundus is at the top. Body is the major portion. The pylorus, of course, empties into the small bowel. Now, in ostomy care, there are only selected situations when we're dealing directly with the stomach, but I did want to quickly review some things that will impact on your ostomy patients and some of your other patients. So first of all, the stomach provides a reservoir with controlled empties. So that allows us to eat at intervals. Because when we eat, then we're full. The stomach is sitting there with all of these nutrients. Those nutrients are gradually passed into the small bowel for processing. And then once the stomach's empty, we're hungry again, and we eat again. Now, if we have to remove the stomach because of malignancy, because of extensive alterations, then the patient loses that reservoir function. And then we have to do constant drip feeds. So your patients with J tubes, those are constant drip feeds because there is no reservoir. The reservoir function has been lost. The stomach is highly muscular. It actually has three muscle layers instead of two. And that provides you with mechanical digestion. The stomach can literally turn contents to help break nutrients down. Also within the stomach, you produce papsinogen, which gets converted to papsin, and papsin begins enzymatic breakdown of proteins. Now, you know that the pH in the stomach is very low because you produce hydrochloric acid. You need hydrochloric acid for two reasons. First of all, it's tremendously protective of you because we ingest all kinds of things every day. We ingest a lot of pathogens. We don't think about it. We probably don't want to think about it, but yes, we ingest a lot of pathogens. However, everything we take in goes through an acid bath. So that extremely acidic pH, typically 1 to 3 kills almost all bacteria. So it protects you from infection. The other thing that that very low pH does is it converts papsinogen to papsin, and papsin is the active enzyme for protein digestion. So that low pH, very important. But also very threatening to the stomach itself. How do you keep that very acid fluid from damaging the lining of the stomach? Well, you have mucus-ocrean glands, so they maintain a mucus blanket that literally protects the gastric wall. Also, you have very tight junctions between the cells and the gastric wall, so it's very hard for anything like hydrochloric acid to penetrate those junctions. It's like this is a brick wall you can't get through. You also have prostaglandins that provide protection. Now we know that insides can cause gastric distress, can cause ulceration, and one reason that insides are so damaging to the gastric tissue is that they have an anti-prostaglandin effect. So prostaglandins are there to protect. If you take insides, you're inactivating the prostaglandins which allows the very acidic fluid to backwash and to damage the gastric wall, so three things that protect prostaglandins, tight junctions, and the mucus blanket. You also secrete intrinsic factor in the stomach, so why do we need intrinsic factor? Intrinsic factor is critical to B12 absorption. B12 by itself cannot penetrate, cannot get into the bloodstream, but once it's connected to intrinsic factor, it can. So intrinsic factor is the key, literally the key. It unlocks the door to allow absorption of B12. B12 of course is critical to multiple functions throughout the body, so is intrinsic factor. The stomach provides limited absorption, primarily carbohydrates, alcohol, some drugs, and very controlled emptying. So you have this reservoir is emptying into the duodenum, the duodenum controls the rate at which the stomach empties. So liquids empty faster than solids. That makes sense. Solids have to undergo some initial breakdown. Fats empty slowly, proteins empty slowly, carbohydrates empty quickly. Everybody who's ever been on a diet knows this, so if you eat something that's basically carbohydrate-based and no time you're hungry again, if you eat something that's protein-based, if you eat something that's fat-based or a combination of fat and protein, because it empties much more slowly, you do not get hungry nearly as quickly. And notice that the transit time from the stomach into the duodenum ranges from 30 minutes to five hours. So you've been on both ends of that spectrum. Now let's talk about the small bowel. A lot of our patients have small bowel stomas, so you want to be very familiar with normal function of the small bowel. So how big is the small bowel? What's the lumen? How big is the stoma going to be? Well it's about one to one and a half inches. The duodenum is typically one and a half inches in diameter. The euleum is typically one inch. It's about 22 feet long. We have a lot of redundancy in the small bowel. Also you should know that links vary based on whether they're giving you link from a cadaver, which is usually about 22 feet, but the bowel's very relaxed in a cadaver. If they're giving you living link that's more like 15, 16 feet. So you want to keep yours at 15 to 16 feet for as long as you can. Okay, three major sections. The duodenum, jajunum, ilium, all have slightly different functions. We're going to talk about each of them. There are some differences in the histology of the bowel wall when you compare the small bowel to the colon. So you've got those four layers, cirrhosa, muscle layer, submucosa, and mucosa. But look at the bottom of the slide. So the mucosa layer is very different in the small bowel because you have all of these villi. And the villi are basically mucosal projections that tremendously increase the absorptive surface of the small bowel and promote absorption of nutrients. In addition, each villus, each projection is covered with microvillai, additional small projections, and those microvillai contain enzymes and little carrier substances that finalize the digestive process and facilitate absorption. Those little carrier substances are like little fairy boats that attach to nutrients, carry them into the bloodstream, release them, and go back for more. The microvilli and the li are sometimes known as the brush border critical to nutrient, digestion, and absorption. A couple of things you need to know about the villa. First, they can hypertrophy to some extent following major bowel resection. So if you have six feet of small bowel removed, the villa and the remaining small bowel tend to elongate to help compensate for loss of that section of bowel. So the ability of the villa to hide hypertrophy is a protective function. On the negative side, if a patient is in PO for any length of time, more than five to seven days, the villa tend to hypertrophy. So normal function, the villa are swinging around, they have a muscle fiber in each villa, looking for nutrients competing with each other, grabbing nutrients, taking them into the bloodstream, releasing them very active layer of the small bowel. But if you make me MPO after a while, these little villa, they get tired and feel kind of stupid swinging around looking for something that's not coming, so they sit down. And then after a while, they lay down. They're still looking, checking, anything coming, anything coming. And when we start to feed the patient again, the villa responds, they gradually get back up. But here's what happens in the meantime. When the villa atrophy, you have flattened the absorptive surface. And so when you start to feed that patient again, instead of nutrients being absorbed, they just shoot through the GI tract. And it's very common for patients who are initiated on tube feedings to have a lot of diarrhea initially. Sometimes the instinctive responses, we need to start the tube feedings, the patient's not tolerating this. But actually that's the worst thing we can do, because the only way to get the villa standing tall and functioning again is to continue to feed the patient. So instead of discontinuing the feeds, we want to provide them at a slower rate. If we're not worried about CDIF or impaction, we can give anti-motility agents just to slow everything down. So you want to know about villa, they're very important. Now the absorptive capacity of the small bowel is highlighted by the fact that 80% of nutrients are absorbed in the first 100 centimeters of the small bowel. So the first 40 inches, you're gonna take care of a lot of patients who have short bowel syndrome because of multiple bowel resections. And our facility, we frequently find noted on the surgical report how many centimeters of functional small bowel remain. And in general, 100 centimeters is considered to be the minimal amount for a patient to live off of TPN. So if you have 100 centimeters or more of healthy functional small bowel, have a pretty good chance of living off TPN. We can probably gradually wing you off TPN. But as that number comes down, if you're under 100 centimeters of functional bowel, you may very well be TPN dependent for the rest of your life. Another thing to be aware of is fluid secretion and the small bowel. You actually make 3000 milliliters of fluid a day. There are cells throughout the, or glands throughout the small bowel known as the crypts of lubricant. That's to create this fluid. This fluid mixes with the food you eat, mixes with the nutrients to support absorption because it's easier for a fluidized nutrient to be absorbed than a solid. And finally, notice that the small bowel has low bacterial counts because most bacteria get killed in the stomach. And then transit through the small bowel is pretty rapid. So there's not a lot of time for bacterial replication. And as a result, you have relatively low bacterial counts in the small bowel. Why does that matter? Well, notice that patients who are scheduled for colon resection frequently undergo a bowel prep to clean out the bowel to reduce bacterial loads. Patient schedule for small bowel resection typically do not require a bowel prep because bacterial counts are so much lower. And also, you'll frequently notice that if you're caring for patients with Iliostomies and caring for patients with colostomies, in general output from a colostomy has more odor and those patients have more issues with gas, again, because of higher bacterial loads. So now we're gonna talk about the three specific sections of the small bowel. We're not gonna spend a lot of time on the duodenum. We very rarely have a patient with a duodenostomy. But the duodenum is a little seashape segment that connects the stomach to the remaining components of the small bowel. It's about 10 to 12 inches long. It contains the ampula of water. And that's the point at which the pancreatic and common bowel ducts dump into the small bowel. That's where they connect right there at the ampula of water. Now that's significant because if you have a patient with cancer or the head of the pancreas, they frequently develop obstruction right in here. And so they present with bowel obstruction, nausea, vomiting, distinching, because the pancreas, the head of the pancreas, is full of tumor and compressing the duodenum. Remember that gastric contents are highly acidic and they're dumping into the small bowel at the level of the duodenum. So one thing the duodenum has that no other section of small bowel has is runoglyans. And their cell function is to produce mucus that helps to neutralize the acidic time from the stomach. So what does the duodenum do? First of all, it neutralizes the time before it sends it on to the jujumin. Where do ulcers occur? Where do gastric ulcers occur? And the stomach and in the duodenum, because those are the two organs exposed to highly acidic gastric contents. The digestive process is continued in the duodenum. Primarily, it's through stimulating the pancreas to release pancreatic fluid that's enzyme rich. So the duodenum produces pancreas Simon, causes the pancreas to contract. If the contents are high in fat, it also produces colostochinin that causes the gallbladder to contract. So basically, the duodenum is the receiving port. So it gets this acidic time from the stomach. It neutralizes it so that it's safe from a pH perspective. It sends for pancreatic fluid to continue the digestive process. It analyzes the contents. And if there's high fat content, it also sends for bile to help break down the fat and continue digestion. And finally, the duodenum is the best place for absorption of iron, calcium, magnesium. And it's a great place for absorption of carbohydrates. So carbohydrates can actually be absorbed a little bit in the mouth, a lot in the stomach, and again in the duodenum. What about the jujumin? Even though I can cover everything about the jujumin and just a few points, it is the workhorse, the powerhouse of the small bowel. It's about nine feet long, one to one and a half inches in diameter, throughout the jujuminum, you have extremely prominent villi. Not prominent is, and very well known, but prominent is an anatomically prominent tall. Because the major function of the jujuminum is absorption. That's where most nutrients get absorbed. The vast majority of your proteins, your carbohydrates, your fats, your vitamins all absorbed in the jejunum. Think about this. When we need to bypass the stomach, where do we place feeding tubes? Not in the LM. We place them in the jejunum. Unfortunately, the jejunum is typically spared from a lot of disease processes that result in bowel resections. So, jejunum critical to normal nutrient absorption. Well, what about the LM? The LM is actually the longest portion of the small bowel, 12 feet long. It's usually about an inch in diameter. It's also very well equipped to provide absorption, but it's pretty much stuck in an understudy role most of the time. So, you think about anybody who's in an understudy role. They have to show up to work every day. They have to be ready to go on stage. They have to learn the lines, be ready to act. What about the LM? It has to show up to work every day. It has to be ready to absorb. But most of the time, it's just sitting there, hanging out in the break room, waiting for work. It might say to the jejunum, "Hey, you know, I could handle some of that. I could do some of that absorption." Jejunum is like, "No, I've got it." But if the jejunum is removed for any reason, then the LM is fully equipped to step up, take over, and provide digestion and absorption of nutrients. Now, one thing unique to the LM is the last 100 centimeters, also known as the terminal ilium. That is the only place in the bowel where intrinsic factor B12 complex can be absorbed at the very last point. Can't be absorbed in the jejunum at all. That's very important to us in caring for ostomy patients because many disease processes that result in an ostomy do involve the terminal ilium. It's important for us to look at the operative report and determine once section of bowel was removed. How much of the terminal ilium was removed? If it says that they took out 60 centimeters of terminal ilium, now I have a marked reduction in my capacity to absorb vitamin B12 intrinsic factor complex. I have to really watch for signs of B12 deficiency. Important to know that typically we store B12 in the liver and we store enough to last us for one to three years, which is both good and bad. Good in that it gives us that cushion. But think about what happens. People have surgery, they go back, they get followed up by their surgeon for a period of time. But within six months typically the patients discharge from care. Surgeons like you're doing great, you know surgical complications, no issues. Call me if you have any problems. When do symptoms B12 deficiency typically surface? Not for at least a year, maybe two. So it's really important for us to educate patients who have undergone resection of the terminal ilium to notify their physicians to have their B12 levels checked at routine intervals and to begin replacement when they develop any symptoms or when their B12 levels start to drop. Just a couple of last things about the small bowel. The small bowel actually has two different types of motility. Segmentation is what we call back and forth. So contract here, relax here, then contract here, relax here, back and forth. That causes mixing the intestinal contents. That mixing motion helps to promote digestion and absorption. And also you have peristaltis where peristalsis where one section contracts, oops, I'm sorry, see if I can go back. Where one section contracts, the next session relaxes, then this section contracts, the next section relaxes and it moves contents throughout the small bowel. Motility in the small bowel is constant and pretty rapid. So notice usual transit time in the small bowel, 15 feet, but only two to six hours to get all the way through the small bowel. It moves things right along and that's why you have minimal time for bacterial replication. You have phenomenal, absorptive capacity in the small bowel. So let's just back up and do a little bit of math. If you add up the 1500 milliliters of saliva, the 2500 milliliters of gastric juice, the 3000 milliliters of small bowel fluid, throw in 500 of bile, 700 of pancreatic fluid, altogether the intestinal tract produces seven to nine liters a day. And then typically we take in two to three liters orally. So all together you're looking at 10 to 12 liters. So wonder we don't slosh when we walk, but most of that fluid gets rapidly reabsorbed in the small bowel. Typically only about one liter, two liters max, pass into the colon. That has major implications. What if we have a patient with a small bowel fistula and they're losing small bowel contents constantly? What if we have a patient with a high output iliostomy and they're losing two to three liters of fluid a day? Then they're losing a lot of sodium. They're losing a lot of potassium. They're losing a lot of bicarb and we have to work really hard to maintain fluid electrolyte and acid base balance. So in summary, we have covered the upper GI tract. What are the critical functions of the upper GI tract, ingestion, digestion, and absorption of nutrients? Thank you.