02. A&P of GI Tract - Large Intestine and Accessory Organs

Okay, in this class, we're going to talk about anatomy and physiology of the colon and the accessory organs, and again, our focus is primarily going to be relevance to patients undergoing ostomy surgery. We have previously reviewed, and again, we'll identify the four layers of the large intestine and bowel, we'll identify major structures and functions, the anatomic differences in the large intestine and implications for ostomy creation, and we'll briefly talk about accessory organs and their functions as it relates primarily to patients undergoing ostomy surgery. So you have previously heard that the GI tract breaks down into two major components, the elementary canal, which goes from the mouth to the anus, and then the accessory organs that contribute to nutrient digestion and absorption, and which includes salivary glands, but most particularly for this discussion, the liver, gallbladder, and pancreas. We've talked previously about the fact that the small bowel is the organ primarily responsible for digestion and absorption of nutrients. In this class, we're going to talk about the role of the colon and rectum and storage and elimination of voice products. So looking at the colon from a big picture perspective, it's about five feet long. It ranges in diameter from one and a half to two inches, so you'll notice that large bowel stomas are definitely larger than small bowel stomas. There are five anatomic sections. The first that people usually don't think of as a section is the ileocecal valve. And we are going to talk about it specifically because it plays some major roles in protection and function of the large bowel. So the ileocecal valve is located just between the ileum and the seacum, the beginning portion of the large intestine. And it actually plays a very important role. It is a valve. It is a one-way valve. So once contents pass through the ileocecal valve, they cannot go backwards into the small intestine, same thing for bacteria. There's many, many bacteria in the colon and very few bacteria in the small bowel. And one thing an intact ileocecal valve does is it prevents backward movement of bacteria from the colon into the small bowel. So keeps the small bowel in that low bacteria zone. Now for most patients, removal of the ileocecal valve would have limited impact. But for a patient who is borderline short bowel syndrome, preservation of the ileocecal valve would be very important because it actually slows transit between the small bowel and the colon. So it gives you a little bit of extra time for nutrient absorption. And also, the fact that it prevents backward movement of bacteria and that it maintains low bacterial counts in the small bowel, it turns out that low bacterial counts facilitate nutrient digestion and absorption. So typically the ileocecal valve probably not critical to health, but in a patient with short bowel syndrome, yes, a very important structure to maintain. Then you have the cecum. And the cecum is just distal to the appendix and it actually is the section of bowel that is most prone to massive distinction and perforation. Probably partly because it's the area just distal to the ileocecal valve. So you think, okay, if you develop an obstructing tumor in the sigmoid colon, what's going to happen? Well, first the sigmoid will dilate, just proximal to the tumor. Then the descending will dilate, then the transverse will dilate, then the ascending colon will dilate, finally the cecum will dilate, and then there's nowhere for it to go because of the ileocecal valve. So what we find happening, you're going to see this in clinical practice as you have a patient with an obstructing sigmoid tumor. They frequently present with right lower quadrant pain, tenderness, it actually mimics appendicitis. They get in there and they find that their cecum perforation, but the real problem is that obstructing sigmoid tumor. The other thing you should know is that if you do have a patient with an obstructing malignancy and the entire colon is extremely distended, sometimes they have to do an emergency cecostomy just to decompress the colon before they can do anything else. So occasionally you will be caring for a patient with a cecostomy. It might be a tube placed into the cecum. It might be where they bring the cecum to the abdominal wall. Cecostomy is always intended to be a temporary diversion unless the patient is end of life. And we will discuss this more when we talk about colostomy care. So the colon, as we've already referenced, actually has four different sections. You have the ascending colon coming up the right side, transverse coming across the midline above the umbilicus, descending going down the left side, and then finally the sigmoid curving and emptying into the rectum. The rectum itself five to six inches long and of course is intended to be a temporary reservoir for stool. And the anal canal three to four centimeters long, so between one and one and a half inches long, add a critical component of your continent's mechanism. We'll come back to that. So let's talk about anatomic differences in the bowel wall. There's a big difference between the mucosal layer of the small intestine and the mucosal layer of the colon. We talked about the villi and the mucosal layer of the small intestine. The villi contribute tremendously to nutrient absorption because they tremendously increase absorptive capacity. But when you look at the mucosal layer of the colon, there are no villi. There are no micro villi, so there is no ability to absorb nutrients. If you remember, the villi and the micro villi provide enzymes and the carrier systems that are required to move nutrients from the lumen of the bowel into the bloodstream. If you take away the villi and the micro villi, you take away the enzymes more importantly, you take away the carrier systems. And now there's no potential to pull nutrients into the bloodstream. So you do not get nutrient absorption from the colon. However, you do get reabsorption of water and electrolytes. So the mucosal layer of the colon plays a big role in preventing dehydration, but not in nutrient absorption. Another big difference is the muscle layer in the colon. So throughout the small bowel, the muscle layers form a circumferential sleeve around the small bowel itself. But in the colon, the longitudinal muscle is not circumferential. It breaks down and is concentrated in three muscle bands that are attached to the bowel wall. So instead of being a tight sleeve around the colon, these elastic bands create howstrations or these little outpouches. So when you look at the slide and when you think of diagrams that you see of the small bowel and of the colon, the small bowel is always pictured as pretty much a smooth snake. And the colon is always pictured with all of these little outpouches. These little outstrations. And that's because of the difference in the longitudinal muscle. Now at the rectum, so look at the bottom of your slide. At the rectum, those three bands reform a continuous sheath. They coalesce. So, yes, the rectum is surrounded by a continuous band of muscle but the remaining components of the colon, you have three bands, you have house strations. So, you're probably thinking, okay, and I care about this because, so that's your last bullet point. What is the relevance? Well, I want you again to look at the bottom of your slide. And a loop colostomy is formed when they bring the entire loop of bowel out onto the abdominal wall and they open the anterior wall of the bowel, look what happens. The tinia, those three muscle bands and the natural elasticity that they create causes the posterior bowel wall to pull forward and to form a partition. And then you have a completely separate proximal and distal opening which provides very effective fecal diversion and also gives you access to both the proximal bowel and the distal bowel. So, we're going to mention that now. You will hear that again when we talk about loop colostomy. What are the specific functions of the colon? Well, first of all, you have lots of bacteria in the colon and it's important to protect the bowel wall from bacterial adherence and invasion and from bacterial toxins. So, you have multiple mucus recruiting glands throughout the colon that produce alkaline mucus that actually protects the bowel wall from bacterial adherence and invasion and from the toxins. We've already talked about the fact that the mucosa layer of the colon does absorb water, does absorb electrolytes and helps prevent dehydration. You will find, as we move through this course and in your clinical practice, that patients who have lost the colon, patients who have had a colectomy and who have an aliostomy are very high risk for dehydration because they have lost that function of the colon. So, just remember that we're going to come back to it. The third critical function of the colon is synthesis of symbiotic compounds. Now, what are symbiotic compounds? There are actually protective substances that are produced by the action of bacteria on both soluble and insoluble fiber. It includes signal molecules, it includes all kinds of protective molecules that reduce bacterial adherence, that prevent bacterial invasion into the colon wall and that help protect us against negative factors within the bowel. So, good bacteria and you're going to hear a lot about good bacteria, lactobacillus, bifidobacterium, saccharomyces. So, again, talking a little bit more about symbionics because they're so important to colon health, they're so important to health in general and probably a lot of you are reading more about the microbiome, which refers to what is the mix of bacteria within your colon. If you have a healthy mix of bacteria within your colon, it contributes to overall immune system health, overall body health as well as bowel health. So, three terms you need to know. Prebiotics, probiotics, symbiotics. Probiotics is probably the term you're most familiar with and you know that probiotics refer to the good bacteria in the colon and we've already talked about lactobacillus as one of those bifidobacterium is one, saccharomyces is one as well. What are prebiotics? Well, prebiotics are the fiber, the dietary fiber. The bacteria by themselves don't do you any good. They have to interface with dietary fiber to produce the protective compounds. So, probiotics are the bacteria, prebiotics are the fiber, symbiotics are the protective agents that are produced by the interaction between the bacteria and the fiber. So, you can see there's multiple types, there's short-chain fatty acids, those help nourish the colon cells, the bowel wall cells, antioxidants, we all know the antioxidants help promote physiology, health, vitamins, growth factors, etc. All of these are essential to help, all of these very protective of the colon. We've talked about the functions, I'll review them again. So, these symbiotics taken together help to maintain the mucosal barrier, help to prevent bacterial adherence and invasion, help to prevent bacterial overgrowth and toxin production, and enhances white blood cell functions, so promotes immune function. Now, what about commercial probiotics? We see them everywhere, they're advertised everywhere. If you go into a health food store, you see many options, but even if you go into a grocery store, some of the yogurts you see have live bacteria, live cultures, those are probiotics. So, we have emerging data that suggests that commercially available probiotics can promote bowel health, can protect against antibiotic associated diarrhea, can protect against sea diff, if given at the same time as antibiotics, we have some evidence that externally administered probiotics can shorten the time frame for recovery from a viral diarrhea. We have some evidence that externally administered probiotics may promote health and continent reservoirs. So, still lots of unanswered questions, for example, if I am going to give you probiotics to try to prevent antibiotic associated diarrhea to try to maintain health of a continent reservoir, what's the minimum effective dose? We're not sure. And what's the best combination? Again, we have data that lactobacillus is good, that bifidobacterium is good, that saccharomyces is good, is there one that's better than the others, is a combination better than a single agent, a lot of unanswered questions, but we definitely know that probiotics and symbiotics are critical to bowel health, to overall health, and that externally administered probiotics can help to resolve specific pathologies in the intestinal tract. Okay, what about motility in the colon? Now motility in the small bowel is constant and rapid and everything gets pushed through the small bowel pretty much in two to six hours. Are patterns the same in the colon? No, they're very, very different. One thing that is the same is you still get that mixing motion, that back and forth motion, that promotes water reabsorption and converts stool from liquid to solid. But peristosis in the colon, very different than peristosis in the small bowel. In addition, peristosis is different and the right side of the colon and in the left side of the colon. On the right side of the colon, you have very slow but fairly continuous sweeping motions that very gradually move stool through the right colon into the transverse colon. So up the ascending into the transverse colon. But if you are going to categorize the right side of the colon, you would say it's definitely type B personality, not in any hurry, it's like when it gets there, it gets there. So very gradually pushing stool into the transverse colon. Then on the left side of the colon, peristosis is very infrequent, it's not constant at all. Instead most of the time the left side of the colon is quiet, it's just sitting there. But two to three times a day in most individuals, you'll have a series of what they call propagating contractions, propagating parasitotic ways that can rest. We rapidly sweep stool from the transverse colon into the rectum in less than 10 minutes. Typically this occurs after eating and we've all experienced this. So we've all had days where we wake up late, we look at the clock, we're like oh my god. We run around, we get dressed, we grab a cup of coffee, maybe we grab a bagel, we hop in our car, and even if we had time and the fourth thought to ask our rectum, hey anything I need to know about, anything I should take care of before I hit the road, the rectum will be like nothing going on down here. But 10 minutes later when you're in traffic what happens, you've got that intense urge to go. It's like well how did this happen, where did this come from, from the transverse colon, your activity, eating, and caffeine triggered that series of parasitaltic waves, and what was in your transverse colon is now in your rectum and this far from your underwear. And we'll come back to that and talk about how you keep it in your rectum. Transit time in the colon. Altogether from the ileocecal valve all the way around to the rectum, typically about 24 hours. So a much slower section of the bowel. Now let's talk about factors that control stool elimination, factors that control continents. Because incontinence is one reason for fecal diversion. If you have intractable, uncorrectable fecal incontinence, you'd be much better off with a colostomy. So let's talk about the factors that contribute to fecal continents and that can go wrong. So the first thing we already talked about, normal parasitaltic activity. So if everything's working correctly, you're going to have saw-form stool that's delivered to the rectum maybe once or twice a day, maybe every other day. The second thing that's critical is sensory awareness. If you have stool in your rectum, you need to know about it so that you can contract this fincter and prevent an accident. And we have a very well tuned sensory system that allows us to immediately recognize rectal distinction and also allows us to differentiate between liquid-solid and gas. So first of all, within the rectal walls, you have stretch receptors. And as soon as the rectum distance, those stretch receptors are activated and you get a message to the brain, major delivery, stool in the rectum. And that alerts you, contracture's fincter. So sensory awareness is very high level and a patient with intact sensory fibers, intact spinal cord pathways and normal cognition. In addition, if you think about it, first you get this message that you've got to go. And then in just a few seconds, you get follow-up information that says, "Yep, it's the real thing or you better hurry as liquid or it's only gas. Who's there and do you care?" Where does that come from? That comes from special cells that line the anal canal just distal to the rectum. And those cells have nothing to do in life but sample rectal contents and give you a readout, give you feedback. And they're actually very important to continents. Now one thing that's very different for our ostomy patients is they have no sensory awareness that they're about to have output. They cannot differentiate liquid gas solid. So that's a question patients ask me all the time. So I know will I have any control? No. What's going to happen is you're going to get normal motility, normal peristosis. It's going to move stool along the colon when it gets to the stoma is going to come out. So you will not know and you will not have control. That is a huge change for patients. The third thing that impacts on continents is your sphincter mechanisms. And we actually have two sphincters. We have the internal anal sphincter which is a condensation of the circular muscle, the smooth muscle from the rectum and it encircles the anal canal. It's circumferential sheath of smooth muscle. Now the internal sphincter is not under your voluntary control. The external sphincter is, the anus is, the internal sphincter is not. It is smooth muscle is primarily slow twitch fibers that maintain constant tone within that muscle encircling the anal canal is controlled by the autonomic nervous system, the ontaric nervous system and the internal sphincter is normally closed. It stays closed. That's its function. Keep the door shut. Keep rectal contents in the rectum. The internal sphincter acts like others fincters throughout the GI tract. It stays closed until there is distention of the proximal bowel. So the internal sphincter is closed until the rectum distends and then the internal sphincter opens. So you notice that you get transient relaxation when you have five to twenty milliliters in the rectum. So what does that do? It opens briefly. That allows rectal contents to come in contact with those special cells. That's what gives you that additional information. And then normally it closes right back to maintain contents. Once you've got 60 milliliters or more in the rectum, the internal sphincter pretty much stays open because the rectum is distended enough that it's signaling the internal sphincter we need to evacuate the rectum. The overall function of the internal sphincter, contents at rest. If you get irreversible damage to the internal sphincter, you're going to have a major impact on fecal contents. What about the external sphincter? The external sphincter, look at your last bullet point. That's what provides you continents during periods of rectal distension. This is a striated muscle, a voluntary muscle. So it actually is located outside the internal sphincter. It surrounds the internal sphincter. It's continuous with the whole pelvic floor muscle sling. It's mechanically contracted, so partially contracted at rest. But when you voluntarily contract, you double the anal canal pressure and you hold still within the rectum. So sensory awareness prompts fincter contractions, fincter contraction maintains continents. It closes the anal canal. Now there's a couple of other things that contribute to continents as well. One is the anal rectal angle. So when you contract this fincter muscles, it closes the anal canal. But the other thing it does is it maintains this very acute angle between the rectum and the anal canal. You can see that in the slide on bottom. So when the anal sphincter is contracted, the pelvic floor is contracted. See how that sling pulls at the anal rectal junction and creates that 90 degree angle that makes it very difficult for stool to get from the rectum into the anal canal. When defecation is desired, then you relax the pelvic floor, relax this fincter that straightens the angle and allows stool to pass from the rectum into the anal canal. Now the last thing that contributes to continents is normal rectal capacity and compliance. So you think, okay, I've got this parasitic wave, it's pushed stool from the transverse colon to the rectum. Really it's goal is to push stool all the way out. But you have sensory awareness that alerted you. You contracted the anal sphincter that closed the anal canal, maintained that 90 degree angle. And also, when that parasitic wave hits that closed anal canal, it subsides. Just like when a wave crashes onto a beach, it subsides. When that parasitic wave subsides, rectal walls normally relax and the rectum provide. temporary storage. But there are times when the rectum cannot provide temporary storage. First of all, if it's very high volume stool is going to override the rectum's capacity to stretch and store. But also you're going to take care of a lot of patients who have inflammatory bowel disease, ulcerative colitis, Crohn's disease where the rectum is extremely inflamed. And when the rectum's very inflamed, even small amounts of stool act as a major irritant that causes spasticity, causes persistent and ongoing contractions of the rectal muscle so that the rectum never relaxes to provide storage. So what you hear from patients with ulcerative colitis and Crohn's disease, I know when I have to go. I can tighten up, I can hold on to it for maybe a minute, maybe two. But then that urgency just overrides everything. And if I don't make it to the bathroom fast enough, I'm going to have an accident. A subject of intense concern to anyone with an osteomy is gas production because they have no control over when gas comes out. And everyone with an osteomy has major concerns about things that would be embarrassing to them. And we live in a society where you just don't go around and fart whenever there's rules. So they're going to ask you what about gas? Am I going to know when I have gas? Am I going to be able to stop the gas? What can I do? So to answer those questions, you have to know about factors that increase gas production. And you have to be able to provide real live recommendations to your patients. So the first source of intestinal gases swallowed air. So if I drink coke or any kind of carbonated beverage, I'm swallowing air. If I drink through a straw, I'm swallowing air. If I chew gum, I'm swallowing air. Now typically air is fairly rapidly absorbed. So it's usually swallowed air is usually not an issue for a patient with a colostomy. But it might be an issue for a patient with an Iliostomy. Metabolic processes do produce gas, but not enough to be clinically significant. The major factor and definitely the important factor for a patient with a colostomy is bacterial action on dietary fiber, specifically on complex carbohydrates that are not broken down by enzymes. So you know foods that are gas producing. You know beans or gas producing. You know broccoli is gas producing. You know cabbage is gas producing. And most people know which foods cause them a lot of gas. How much gas is produced daily? Well, you can see there's tremendous variability. It's impacted by genetics. It's impacted by dietary intake. It's impacted by malabsorption syndromes. And varies from 400 milliliters to 3,000 milliliters a day. Now if I ever have an osteomy, I want to be on the 400 milliliters a day end of the spectrum because then gas would be much less of an issue than if I produce 3,000 milliliters a day. Here's what patients need to know. The lag time between ingestion of a gas producing food and actual flatulence, actual gas production is usually four to six hours. For a patient with an iliostomy, it would typically be three to four hours for a patient with a colostomy more like six. So that means if I'm going out to dinner with friends, I need to be careful with what I eat at lunch because what I eat at lunch is going to produce gas that's going to be eliminated about dinner time. And again, we'll come back to this and talk more about it. Now, we're going to spend our last few minutes talking very briefly about accessory organs. So accessory organs, as we've said, contribute a lot to nutrient digestion and some to absorption. They're not nearly as important for most of our patients. So that's why we're going to go through this pretty quickly. So you all know the livers located in the right of a quadrant. You know, you have two major lobes, multiple hepatic lobules, which is just liver cells that surround these sinusoid that are lined with fagicitic cells. And then you have these little bowel capillaries that are located between the liver cells and they drain into the hepatic ducts, which eventually empties into the ampula of water through the common bowel duct. You know the liver is critical to life. You all take care of patients within stage liver disease and you know how many problems they have. So you know the liver plays a major role in metabolic processes and patients who have advanced liver disease have all kinds of metabolic issues. You know that the liver synthesizes blood proteins and produces bile and produces clotting factors. You've seen patients with liver disease and they have all these acymodic lesions. They bleed very readily. It's very hard to control bleeding. So you're already aware of that. The liver plays a major role in storing vitamins and minerals. So we just talked about its role in storing B12 and the fact that it stores enough B12 typically to last is for one to three years. And finally the liver is absolutely critical to detoxification. Blood from the colon flows through the liver for elimination of toxins and bacteria before it's allowed back into the systemic bloodstream. So the liver plays many critical roles. But the role that we're going to focus on right now is production of bile because bile is critical to break down a fat. And you know that the liver produces bile but it stores it typically in the gallbladder unless of course the gallbladder has been removed. But assuming the gallbladder is in place you know it's located underneath the liver that it stores the bile, concentrates the bile and then delivers the bile to the duodenum in response to colocystochine. What about the pancreas? I'm imagining many of you have already taken care of patients with pancreatic disease, with chronic pancreatitis, with necrotizing pancreatitis. Those patients have major issues with facial reformation and with non-healing wounds and frequently end up in our caseload. So the pancreas located, left and up required, and extends to the midline. The pancreas produces multiple enzymes that contribute to nutrient digestion, amylase, tripsin and lipase. So a major enzyme for each major type of nutrient. Also produces of course insulin and glucagon so has both endocrine and exocrine functions. Now we're focused right now on exocrine functions. We're going to talk about the fact that the pancreas produces enzyme-rich fluid. Typically that enzyme-rich fluid initially the enzymes are in an inactive form, particularly the tripsin, which contributes to protein digestion and absorption. And typically that tripsin is not activated until it reaches the duodenum and is ready to go to work. That's important because you don't want activated tripsin flowing through pancreatic ducts and damaging the pancreatic tissue. But sometimes our patients have an obstructing lesion. They have an obstructing stone that causes activation of the tripsin within the pancreas and causes major damage to the pancreas. When we're dealing with the patient with a pancreatic fistula we always assume that that pancreatic fluid that that tripsin is active because it's so damaging through the tissue and to the skin we never want to take a chance. So bottom line if you have a patient with a pancreatic fistula you're going to pouch it. And then the last thing the blood supply to to the colon. So there's two main blood vessels involved in maintenance of colon viability. You have the superior mesenteric artery, which actually supplies the small bowel and the right half of the colon. And then you have the inferior mesenteric artery that supplies the left half of the colon, and the proximal portion of the rectum. What about venous drainage? Venous drainage is very important when we're dealing with a patient with a malignancy because we know that the cancer cells may invade the veins that are draining the tumor bed. And then we have to think where is that blood going because it explains patterns of metastasis. So most colonic blood, most GI blood, drains into the portal vein, which empties into the liver, passes through the liver for detoxification. Then goes into the hepatic vein, which empties into the general venous circulation. So frequently, when we have a patient with a GI malignancy, when we have a patient with a colon tumor, we are doing liver studies and liver scans because we know that the blood from the tumor bed goes right into the liver. And that would be a primary point for metastasis. Now, the rectum is unique and interesting because veins from the proximal rectum follow that same pathway. The blood drains into the portal system, goes through the liver, and metastatic disease would typically involve the liver. But veins from the distal rectum emptied directly into the systemic system. And so metastatic disease could involve the brain, the lungs, bone. So I'm going to summarize the classes for upper GI tract, anatomy and physiology, and for this class. The upper GI tract, which starts at the mouth and goes through the small bowel, is responsible for ingestion, digestion, and absorption of nutrients. Your accessory organs do contribute to digestion and absorption of nutrients. The lower GI tract, which comprises the colon, the rectum, and the anal canal, is responsible for absorption of water and electrolytes, converting liquid stool to solid stool for producing symbiotic compounds, maintaining a healthy microbiome that contributes to host health, and for storing and providing controlled elimination of stool. Thank you.