So we're going to do some more lectures. So the difference in this part than the last is now you guys have a general idea of endoscopy and anatomy. And now we'll get into the reason that this field even exists is to deal with the pathophysiology and the diseases. And so we're going to do sort of the same dynamic that we just did going through different parts of the GI tract but from a disease standpoint. So I'm going to once again welcome Dr. Robinson. Okay, so we have looked at this a couple of different times now. So we have our GI tract. We've got our digestive organs of the liver and the gallbladder just underneath there and the pancreas. And then we've got the GI tract, which is the esophagus, stomach, small intestine, and the colon. So we're going to start at the top. And we are, again, doing the GI tract in disease. So we're primarily going to be focusing on diseases. So the first one, which I think is probably near and dear to the hearts of many, is GERD or gastroesophageal reflux disease. Basically the underlying problem is that stomach stuff will come up into the esophagus. Sometimes it comes all the way up into the mouth and that causes a fair amount of symptoms. So the mechanism of disease. So we have the esophagus. I'm just going to go back quickly. So we have the esophagus here, which is going to empty into the stomach. We have our anatomic border here, which is the squamous columnar junction. So you can kind of see the difference in the color of the mucosa delineating the esophageal mucosa from the stomach mucosa. And then what we have is the lower esophageal sphincter, which serves to keep stomach stuff in the stomach and not in the esophagus. And that's also reinforced by the diaphragm, which also kind of helps to keep things closed. So basically what happens is you have your lower esophageal sphincter. This is a closed lower esophageal sphincter. So all of these stomach contents are not able to make their way up into the esophagus. What happens when it relaxes, if you need to belch or if you're passing a food bowl or something like this, is this opens. And then when the lower esophageal sphincter relaxes, you are able to have stomach stuff then go up into the esophagus. So GERD is a, there are a number of things that can cause GERD. Just from a physiologic standpoint, even in the absence of true pathologic disease, everyone will have reflux episodes at some point. So there is a physiologic amount of reflux that will just happen in normal individual, not normal, individuals without GERD or heartburn. Oftentimes there'll be a reflux event in response to a food bowl. Guys, I'm so sorry that I'm useless at this pointer. In response to a food bolus that's passing through the GE junction, anatomic abnormality is the most common one being a hiatal hernia, which is what is the schematic is showing us here. So we have our diaphragm and if we remember our anatomic borders, we have the esophagus up here and then the lower esophageal sphincters all the way up here. So we're like way up in the chest right now, as opposed to being down at the diaphragm where we should be. And then you have some stomach that is up above the diaphragm. So this here is a hiatal hernia. It makes it very, very easy for, because you've lost the diaphragm reinforcing the lower esophageal sphincter. So it makes it super easy for stomach stuff to then just come up into the esophagus. There are certain foods that are certainly common triggers for reflux disease. Pictured here are two of my favorites anyway, chocolate and coffee. Red wine is also high on that list. Tomato-based foods and sauces, onions, garlic, basically anything that tastes good unfortunately falls under that category. There are also certain medications that can incite some reflux symptoms as well. So the most common symptoms that somebody will complain of or the classic esophageal symptoms are heartburn and acid regurgitation. Individuals may also have a, GERD is a very heterogeneous disease in terms of how it presents. So we have our common esophageal symptoms. There are also many symptoms that are less common that one needs to really have a high index of suspicion for GERD for. Difficulty swallowing or things getting stuck with swallowing can potentially be indicative of like very severe esophagitis or a peptic stricture, sorry, which is usually something that we see in the setting of uncontrolled reflux disease. A chronic cough that's not related to like a pulmonary or allergic issue can sometimes be related to ongoing acid reflux, voice changes or laryngitis, asthma, especially if there has been asthma that's not well controlled or is getting worse can sometimes be related to uncontrolled GERD. So in terms of treatment, we have some options. Lifestyle modification is where we usually will start with many diseases. So things like elevating the head of the bed, particularly for our patients who have a lot of nocturnal symptoms. If there's been weight gain recently, weight loss is helpful. Sometimes weight loss is just helpful in general. Avoiding the common trigger foods, if that is a possibility for individuals who either fail lifestyle modification or just aren't really able to make many of those changes. Medication therapy is very helpful in the workhorse of the medical therapy and reflux disease, of course, are the proton pump inhibitors like omeprazole and friends. In the event that surgery is needed, there are a lot of options here. The most common thing that we do is the fund duplication, which involves the wrapping of the gastric fundus around the lower esophageal sphincter, and I just leave it there. But there are also some endoscopic options that are available as well that change frequently, but there are also options that can be used in addition to or instead of a fund duplication. So esophagitis, anything itis is basically like the organ, and itis means inflammation of. So esophagitis is inflammation of the esophagus, and so the main symptoms that one will see with esophagitis, usually there'll be a history of longstanding reflux disease, and then these individuals will either have difficulty with swallowing, so they will tell you that things are getting stuck when they swallow, or there'll be a lot of pain with swallowing. Common causes of esophagitis are reflux disease. There are certain infections that can cause this presentation as well. Some medications, particularly sometimes iron tablets can do it, or medications for osteoporosis are common offenders as well. A history of radiation to the chest can cause a radiation type of injury or radiation esophagitis. Injection, caustic ingestion will cause esophagitis and cause strictures later down the road, or eosinophilic esophagitis, which is an allergic type condition whereby there are eosinophils, which are certain type of cells, which will infiltrate the esophageal mucosa. So this is how it looks endoscopically. I don't know how well you guys can see this, but basically up here, actually it doesn't really look that normal either, but basically the whitish stuff is the normal looking esophageal mucosa, and then you can kind of see all of this pink stuff here, which is inflammation, and then there's some inflammation here, and you can actually see that this is actually starting to get a little bit narrow. So this is the esophagitis that's causing a little bit of stricturing. So there are, for reflux esophagitis anyway, we have a classification or the Los Angeles classification that we will use that just kind of provides a standard for us to kind of speak to each other to let us know how severe somebody's inflammation might be. So there are four grades to the LA classification. Grade A is the least severe, and so what we're looking at are these mucosal breaks that are shorter than five millimeters. So again, we have kind of normal looking esophageal mucosa, which is kind of white. We see this pink stuff, which means there's inflammation, and there's a little break there, and it's pretty short, and it's kind of the only one, so it's really not that bad. Looking at grade B basically means that we have more breaks, and they're a little bit longer than five millimeters. So we've got these, again, the white stuff is mostly normal-ish, but then there's all of this pink stuff here, which shows that there's inflammation, and you've got these linear breaks that are probably more than five millimeters in length. This is actually pretty severe looking grade B esophagitis, to be honest. I'm the worst, I'm sorry. Grade C means that you have mucosal breaks, not necessarily linear, but they're taking up quite a bit of the circumference of the esophagus. So you've got these breaks that are between the tops of at least two mucosal folds, usually taking up less than 75% of the diameter of the esophagus, so that's grade C. And then grade D is pretty severe esophagitis, where these mucosal breaks are taking up more than 75% of the surface. Barrett's esophagus. So Barrett's esophagus is a condition that we get very worked up about. It is, by definition, a precancerous condition. What is happening physiologically is there's replacement of the normal lining of the esophagus with the lining of the small intestine. So I'm going to say that again. There's replacement of the normal lining of the esophagus with the lining of the small intestine, not the stomach. And so basically that's happening in response to just kind of chronic acid exposure in the esophagus. So the stomach is super well suited to deal with acidic conditions. The esophagus does not enjoy acid at all. So if there is a whole lot of acid that's kind of coming up into the esophagus, that will often present with the symptoms of GERD that we will often see patients for. And then the lining of the esophagus, you'll either develop an esophagitis-type picture, or sometimes in addition to that, what will happen is the cells, like on a cellular level, the esophageal cells will kind of transform to be better suited to deal with an acidic environment. And so that change is called metaplegia. And the esophageal cells are starting, when you look at them under the microscope, they're starting to look more like intestinal cells than they are esophageal cells. So by definition, every time a cell is kind of changing its characteristics, we call that metaplegia or sometimes dysplasia if it's really severe. And that is a precancerous condition, which indicates that individuals with Barrett's esophagus are actually at increased risk of developing esophageal cancer. The scary thing about Barrett's is sometimes people, oftentimes we'll screen in patients who have a longstanding history of reflux disease, but there's not really any symptoms that will let you know that someone's then developed Barrett's. So we have to have a pretty high suspicion of screening the right patients so that we can find it and then survey it appropriately. So this is just looking at the progression of Barrett's esophagus. So right here we have our normal Z line, which you've seen a couple of times already, which is, again, the transition zone from the esophageal to the gastric mucosa. And that looks very uniform the entire way around. So contrast that to here, this does not look uniform at all. We see that that line gets kind of squiggly. It kind of comes up here. There's this little area here where there's some pink that's coming up that's not really supposed to be there. There are these little kind of scattered islands there. All of those are changes that are suggestive of Barrett's esophagus. So this individual, if they were getting a screening upper endoscopy, all of this would get biopsied. And what you can see down here is that these are normal-looking squamous cells. And then these cells are changing how they look to kind of look more glandular, like intestinal cells. So this is just Barrett's, just standard Barrett's without dysplasia, so just the metaplastic change. When things start to become dysplastic, then we have low-grade dysplasia or high-grade dysplasia, which are two very concerning findings, which usually mean that someone needs to get their Barrett's treated. And those are kind of the first steps on the way to esophageal cancer. So you can see that with the low-grade dysplasia to high-grade dysplasia, things are starting to look progressively more disorganized on a cellular level until you get to kind of malignancy. This is our progression from normal to Barrett's to esophageal cancer on these last two schematics. So treatment for Barrett's, typically when we start treating individuals for Barrett's, there's been a finding of dysplasia. So either the low-grade dysplasia, which I guess is maybe controversial, but definitely high-grade dysplasia. And one of the things that we'll do is radiofrequency ablation, which involves actually ablating and kind of burning the cells that are problematic. So we have a device here that gets put through the scope, and you're kind of burning the cells that are involved in the entire circumference of the Barrett's. That's what that looks like at the end. If there is a focal lesion, that can usually be removed by endoscopic mucosal resection. So that involves injection of saline underneath this lesion to kind of, same with the polypectomies like we talked about before actually, to lift your lesion away from the mucosa of the esophagus. And then you're able to kind of remove that area that had those concerning dysplastic findings. So moving on from GERD and Barrett's, we're going to talk about esophageal motility disorders, which are basically, I mean, the esophagus has one job. It really is to move a food bolus from the mouth into the stomach. So if that is not working, if somebody has symptoms of esophageal dysfunction, then we start to get a little bit concerned that there may be some sort of motility issue where the esophagus is not doing that one job of moving a food bolus from the mouth via peristalsis into the stomach properly. So common symptoms that make us think that there could be a motility issue are, again, difficulty swallowing. So things are sticking somewhere in the chest because a food bolus is not getting all the way into the stomach or it's not getting there smoothly. Pain with swallowing, chest pain, heartburn is actually also common. The tests that we will often do, there are several tests that we'll do, but one of the tests that we will do to the gold standard, I guess, to assess an esophageal motility disorder is an esophageal manometry. So we have a manometry catheter here, which is this thin catheter. And there are these little sensors, there are these pressure sensors that exist along the catheter. And so that catheter gets inserted into the nose. It's very uncomfortable, but once it's there, after a few minutes, people do okay. That gets inserted in through the nose, goes down the back of the throat, and then it goes down at the esophagus and sits in the stomach. And because there are those pressure sensors along the catheter, we can see kind of what's happening from a pressure standpoint at different points at the esophagus and at the lower esophageal sphincter. This is how it looks when it's getting placed in a patient that is sitting up. And then over here, you can kind of see, this is kind of how things look representatively on the software that is attached to the catheter. So the major motility disorders that we will see are achalasia, nutcracker esophagus, which used to be called jackhammer esophagus. You can have esophageal spasm, or systemic sclerosis, which has a very classic esophageal dysfunction pattern, and that's something that we see often in patients with scleroderma, which is a connective tissue disease. So achalasia, from the Greek word of does not relax, there are two things that need to be necessary in order to meet criteria for achalasia. So somebody has to have symptoms, but then what we're looking for are the loss of peristalsis, so that the muscular contractions that are supposed to happen to move a food bolus from the mouth to the stomach. And then the other issue is that you need to have some sort of functional obstruction. So at the GE junction, the lower esophageal sphincter, as we talked about before, should relax to allow a food bolus to go from the stomach or from the esophagus into the stomach. That does not happen in achalasia. So the lower esophageal sphincter in achalasia is very tight and doesn't relax. So you have this non-relaxing lower esophageal sphincter and the esophageal body is not peristalsing the way that it should be. And both of those things need to be present in order for someone's motility disorder to be characterized as achalasia. So a couple of different options for treatment. Botox used to be the only thing that we had. It is an option that's still available. There are some better options available, but there are some patients who are very good candidates for Botox, especially if we don't diagnose their achalasia until late stage and they're no longer candidates for more invasive therapy. So basically what we're gonna do is, remember, we have that lower esophageal sphincter that's not relaxing. Botox will relax muscle so we can inject Botox into the lower esophageal sphincter. I think, should I just stop using the pointer? I'm not very good at this, I'm sorry. So you have your injection needle. So this is our scope. We have our scleral needle that's gonna come out. So there's the catheter and then the five millimeters of the scleral needle that comes out after that. We're at the lower esophageal sphincter, which is where the esophagus and the stomach meet. And we are going to inject Botox into the lower esophageal sphincter such that that area can now relax and a food bolus can pass in these patients. And this is what it looks like in cross-sectional view. We're gonna do circumferential injections of usually about 25 millimeters. It's usually, I think, 100 units. We do 25 units into each of those four areas right at the SCJ. Another option, basically all of the things that we do for achalasia are gonna involve disruption of the lower esophageal sphincter. So we're either gonna try and disrupt it by using medication to relax it, or we're gonna try and disrupt it mechanically. So pneumatic dilation involves a dilator that actually gets passed beyond the lower esophageal sphincter. It's not the standard dilator that we would use for an esophageal stricture or something like this. It's actually much bigger and is placed under fluoroscopy and things like this. So you have a wire that is gonna get placed into the, or a guide wire, that's gonna get placed into the stomach. And then you have this very large balloon that's gonna get placed over that guide wire. And that large balloon is gonna sit at the lower esophageal sphincter, which again is very tight because this person has an outflow obstruction. And then you're gonna blow up that balloon and it's gonna tear those muscle fibers to kind of open things up a little bit. Still used pretty often, but there are some things that have kind of become more effective than pneumatic dilation as well. But one thing here that you can see at the end of your dilation. At the end of your dilation, you can see that the lower esophageal sphincter is now open. From a surgical standpoint, doing a certain type of myotomy, so cutting the muscular layer of the lower esophageal sphincter is still a fairly common thing that we do. It's surgery. It can be done laparoscopically. Sometimes it's done open. It kind of depends on the patient and the surgeon. But basically what you have is an incision here and then you can kind of expose the esophageal mucosa. And then there's a cut of the muscle and sometimes there's also an associated partial wrap because those patients will probably have very bad reflux after we've kind of disrupted that lower esophageal sphincter. And then this is probably where what's done most often, at least at centers that have the volume. So it's still a myotomy, so it's cutting of the muscle, but it's done endoscopically. So it's called POEM, which stands for peroral endoscopic myotomy. What we have is, I'm gonna go back one. We have our scope up here. And then there's an incision that, so this here is like the esophageal lumen. And then we're going to have an incision that goes into the submucosal space here. And then you create a tunnel through the submucosal space that gets you from the esophageal mucosa, submucosa. And then here is your muscular layer, which is what we're gonna cut. And then you start your myotomy incision. And then that's a POEM in three easy steps. So moving on from the esophagus, we're in our stomach now. So one of the most common disease processes that we see in the stomach is peptic ulcer disease. So basically by definition, an ulcer is a mucosal break in the GI tract. So common areas that we will see ulcers are the stomach and in the duodenum. And so here are some schematics of a stomach ulcer. And then here's our pylorus. Here's the duodenal bulb. And then there's a duodenal ulcer. You can kind of just see that there are these little, sometimes they can be very large, but in this schematic, these are these little breaks that we can see endoscopically. So the two major causes of ulcers are a stomach infection called helicobacter pylori, or H. pylori. That's what this looks like underneath the microscope. Very, very common. The second most common are NSAIDs. There are other things that can cause peptic ulcer disease, but they are further down the list. So number one and number two, H. pylori and NSAIDs. So the symptoms of a gastric ulcer, unfortunately, are kind of nonspecific. So somebody may have abdominal pain, a patient that presents with GI bleeding, they're either vomiting blood or they're passing black stools, which is suggestive of a bleed that's coming from the upper portion of the GI tract. And a patient who unfortunately has an ulcer that's become very large, they may not be able to tolerate any food or liquid, and they present primarily with nausea or vomiting, or in very severe cases, which thankfully we see less of now in the PPI era, there's been an ulcer and it's gotten very large and it's actually perforated or created a hole, those patients come in very sick. So from a diagnostic standpoint, we're gonna do an upper endoscopy, and we are going to look for things that look like this. So here is normal mucosa back here, and then here we see this kind of break in the mucosal layer and this ulcerate, this is the bed of the ulcer, this white area, and then it's surrounded by these very heaped up edges of inflamed mucosa. So treatment, again, two most common things, H. pylori, or H. pylori is probably one of the most common reasons that someone may have ulcer disease, so treating the H. pylori, withdrawal of offending agents, so again, NSAIDs come up a lot, and then use of proton pump inhibitors, so omeprazole, pentoprazole, what have you, to heal that ulcer lesion. So upper GI bleeding, also something that we see often in diseases of the GI tract. So by definition, an upper GI bleed is something that is bleeding somewhere between the mouth, and it involves the stomach, the esophagus, the stomach, the duodenum. Anywhere in the upper GI tract before the anatomic area that we call the ligament of trites, which is kind of around the third or fourth portion of the duodenum. So anything proximal to that or above that classifies or fits under the category of upper GI bleeding. So blood in the GI tract can present a couple of different ways. I guess there are really only two exits, but somebody can vomit blood, and they can vomit frank blood that looks very bloody, and so that is what we call hematemesis. If there's blood that's maybe been sitting around for a while and then comes out that looks maybe a little bit darker, kind of we call it coffee ground emesis. So if someone's having this black vomit or very dark brown vomit, then we're worried that maybe there's something that either bled and maybe stopped or is bleeding slowly, but it's still something that kind of is, not kind of, is definitely an indication for an upper endoscopy, although maybe a little bit less urgently than somebody who's having frank hematemesis. From the other end, we're looking for blood in the stool. Usually very bright red, bright red blood in the stool in somebody who you're concerned is having a GI bleed is usually either a lower GI bleed or a very, very brisk upper GI bleed, so those individuals can come in looking very, very ill. Or because we talked about the anatomic location being above the ligament of trite, so esophagus, stomach, first part, or the small intestine, or the first part of the small intestine anyway, sometimes if something up there is bleeding and it's making its way through the GI tract, it'll start, like it'll look like blood up in the stomach or in the duodenum, and as it makes its way through the GI tract, it kind of gets a little digested, which is gross, but by the time it comes out through the rectum, it looks very black, so we call that melanoma. So those black stools, they're a very tarry, sticky consistency. That is not normal. That needs to be investigated. So causes of GI bleeds. Esophageal varices are in the top left. Those are basically these distended blood vessels that we'll often see in patients with liver disease with some decompensation. There are a couple of other areas or times when you'll also see esophageal varices, but far and away, it's something that we see quite a bit in our hepatology population. Erosions and ulcers. So erosions are kind of like baby ulcers, where there's still kind of a little bit of a break, but it's not quite as large or deep as a standard ulcer. Gastropathy. This we see often in our liver patients as well, where there's just a lot of inflammation. You can see this looks very beefy and red, which is not how any of the stomachs that we've looked at earlier today looked. Here is a duodenal ulcer. So we have the, actually, I think it's gonna be a little gastric, but so here is normal-looking stomach here, and then you see this lesion up here that's kind of punched out. This is actually a cratered ulcer that probably either bled recently or will bleed soon. In the esophagus, if somebody has had a lot of nausea and vomiting, they can develop a tear at the GE junction, and that's called a Mallory-Weiss tear, and so that is something that we can see right here. There's this tear, and there's some bleeding there. That patient will usually present with hematemesis. GAVE, often seen in patients with connective tissue disease. We can actually also see it in patients with liver disease. Always in the antrum of the stomach, and are these, it's a vascular lesion, basically, but it has this kind of striped appearance. It almost looks like a watermelon, so we sometimes will call it watermelon stomach. Gastric varices, similar pathology, oftentimes, not always, to esophageal varices, but very common in our hepatology population, and angiodysplasia are basically these abnormal-looking blood vessels, which can bleed quite a bit, actually. So management, first thing that you wanna do is make sure that your patient is being adequately resuscitated, so we are going to get IVs. They're usually gonna be very large IVs. We're usually gonna place more than one of them, and our critically ill patients, they may get a central line, and then we're gonna be pumping a lot of fluid. Depending on how someone's hemoglobin is looking, they may even get blood transfusions, so that's definitely step one in managing our GI bleeders. And then proton pump inhibitors, because a lot of these, the pathology that we just looked at, particularly with ulcers and things like this, respond very well to proton pump inhibitors, particularly through the IV. Sometimes in very sick patients, we may need to administer a continuous infusion of the proton pump inhibitors, and then if there's someone that we're managing as an outpatient, like let's say we've done an upper endoscopy because they were having abdominal pain and we see an ulcer, and there's no bleeding or anything like this, usually just an oral over-the-counter agent is fine, although usually we will use prescription strength. From an endoscopic standpoint, we have a couple of different options for therapy. So here's our injection needle again. You can actually inject epinephrine into an ulcer or some other lesions that might be actively bleeding, and the epinephrine works to basically induce hemostasis or cessation of the bleeding. We can use thermal therapy, we can put our clips on, or with the varices, we can use band ligation. And so there's our needle. Here is a lesion that's been clipped up and is no longer bleeding. This is the bipolar probe, which can be used on an ulcer that has maybe a visible vessel that's kind of poking out at you. And then this here is a, you can kind of see this right here looks kind of juicy. So this is the column of a varice, or a variceal column. And here is the very end of that varice that then gets that rubber band placed around it. Gastric outlet obstruction is basically a mechanical obstruction that prevents emptying of the stomach into the small intestine. So from an ulcer standpoint, you can have, oftentimes it'll occur at the, like right at the pylorus, and things in the stomach are not really able to pass, so that patient presents with inability to tolerate food and nausea and vomiting and usually abdominal pain. So they can be benign. So up here we have just an ulcer that's causing an outlet obstruction in the pylorus. The pylorus we've looked at before looks a lot bigger than this, but things are so scarred and ulcerated here that it's really kind of now a small hole that is probably very difficult for any solid food to get down. Liquids are probably okay. Somebody with bad pancreatitis may present with a gastric outlet obstruction type picture as well. And then along those same lines, someone with pancreatic cancer may present with gastric outlet obstruction or gastric cancer. So if this ulcer is actually a malignant ulcer, it will probably look a little bit more like this and can also cause an obstructive picture. And I think we talked about some of these. Early satiety basically just means getting full very quickly. So someone who is traditionally able to eat a normal-sized meal, now they're telling you they can only have a couple of bites before they feel like they really can't finish, finish their meal anymore. Weight loss, definitely unintentional weight loss is something that kind of gets us a little suspicious about something happening in the GI tract or elsewhere in the body as well. So gastric outlet obstruction, we will sometimes see it if somebody, usually imaging is the way that we will find it or find something that makes us suspicious that there is some sort of obstructive pattern. So on an X-ray, here's the spine. So this person's looking at us. And so this is the left side of the body. This is the right side of the body. Here's the spine. Here is where the stomach would be. And the gastric bubble is usually, like you can see it on an X-ray, but it's not really that large. But here what you can see is that there is this clear air fluid level. So air on an X-ray shows up black, and then fluid shows up a little bit gray. There's this very clear air fluid level, and this looks really distended. So the stomach is kind of full. There's this kind of meniscus here. So things aren't really emptying the stomach. So that is a very suspicious looking X-ray. Maybe the same person then gets a CT scan, which confirms that the stomach is massive. This is the liver here up on the right side. And the stomach is usually a left-sided organ. So this is crossing the midline. So this is taking up all sorts of space. The liver is all squished here at the top, where it's not usually, because the stomach has taken up all of the space that is available. So this is a super distended stomach that is not emptying at all. So this person clearly has some sort of obstructive picture that we then need to go figure out why. Endoscopically, we've seen this picture before. This is how this looks. This is the pylorus, which, again, is very scarred and narrow. Not a whole lot is going to be able to get through there. So somebody that's this obstructed needs to get decompression. So we do place an NG, or a nasal gastric tube, another tube that goes in through the nose, another tube that is not very comfortable, but it does serve a very important purpose. Goes in through the nose, down the esophagus, sits in the stomach. This part here, there's a little blue thing here. It gets connected to a suction canister. And then we're able to decompress the obstruction from above. Usually what we'll do if somebody has one of those CT scans that look that concerning is we'll place an NG tube. We'll decompress them for a day or so. And then we'll go in with a scope to see if we can't figure out what's wrong when most of that stuff has been kind of sucked out. Other things that we can do for individuals who have an obstruction, especially if it's a malignant obstruction, we can place a stent across the area that is obstructed. That works best in the pylorus. And so this individual here has an obstruction probably from a malignancy right here. And so what you're able to do is place the stent across that area. And then things are then able to kind of restore continuity between the stomach and the small intestine. That's done fluoroscopically or with the assistance of fluoroscopy. And so this is how it looks under x-ray right after it's placed or as it's being placed. And this is how it looks endoscopically. For obstructions that are not amenable to stenting, surgery is an option where we're then going to bypass the area that's obstructed. So here we've got the top part of the stomach or the fundus. Here is the pylorus. And that's where obstruction is. What we're going to do is all of this area is going to get cut away. And we're going to have things are going to be reattached from the stomach to the small intestine or duodenum. So we go from here. We lose this area that's shaded in. And then this area here, which is healthy, and this area here, which is healthy, get reattached. And that is called the Bilroth 2 gastrojejunostomy. So the gastro is the stomach or gastric. And then the jejunum here, that's where the attachment is. So we have the gastrojejunostomy. Did I skip a slide by accident? No, OK. Gastroparesis sometimes presents with an obstructive type picture. But there's actually no obstruction in gastroparesis. So gastroparesis just means there is delayed emptying of the stomach into the duodenum in the absence of mechanical obstruction. And the absence of the mechanical obstruction is probably the most important part of this definition. The most common cause of gastroparesis is diabetes, especially diabetes that has been longstanding and poorly controlled. Some individuals may develop gastroparesis after surgery, particularly if there's a surgery that involved the vagus nerve. Sometimes if there's been a GI infection, patients can develop a gastroparesis type of picture after the infection. Or sometimes, unfortunately, we just don't know. And so the medical term for we just don't know is idiopathic. Symptoms of gastroparesis are very similar to the symptoms that somebody will have with an actual gastric outlet obstruction. So nausea, vomiting, early satiety, unintentional weight loss, a lot of bloating, those are kind of the main things that somebody will come in with. And the way that we diagnose gastroparesis, usually we'll do an endoscopy to make sure there's not a gastric outlet obstruction. And once that is normal, the next step is to do a nuclear medicine study called a gastric emptying study, which usually involves a patient eating some sort of meal. Usually it's eggs. Maybe it's oatmeal. And it's radio tagged. And so they kind of eat this radioactive breakfast meal. And then we take subsequent x-rays, like usually every hour until four hours, to see how much food stays in the stomach at each point. And so this is how that looks under the nuclear medicine on the scintograms. And so we've got time 0, time 30, time 90, time 120. And this is normal over here. We can kind of see that the amount that's left in the stomach is less and less and less. We see that this radioactive breakfast meal is leaving the stomach and is into the intestines. And here in our patient with an abnormal gastric emptying study, I mean, everything looks pretty much the same at 0. And then at 30, not a whole lot's left the stomach in either health or in this diseased state. But then things start to look a little bit different at 90. There's still not much. The stomach is still pretty full at 90 minutes. And then the kicker is that two hours after the meal, the stomach is actually still quite full, whereas over here in your normal control, the stomach is at least, there's probably not a lot there. Maybe that's like 30% full. And most of this meal has kind of made its way into the small intestine, where over here, the small intestine barely has any food in there at all. So treatment for gastroparesis. These patients really can't tolerate the standard three normal-sized meals a day. So we usually recommend like five or six very small meals. From a medication standpoint, prokinetics that kind of help the stomach to propel food along are very helpful. Red gland or metclopramide is the most common one that we use. Erythromycin is an antibiotic that has promotility features. That's often commonly used as well. And those actually, unfortunately, are the two options in this country that are available. I guess procalipride is a constipation medication that also has an indication for gastroparesis. But those are really kind of the three. There are really not very many agents that are particularly useful for gastroparesis, which is something that's frustrating for both patients and providers alike. Because these patients are so nauseous, generous use of antiemetics is certainly paramount. And then in some very severe cases, inserting a gastric pacemaker, which is a device that basically works the same as a cardiac pacemaker, to work with the gastric electric currents to kind of promote food moving out of the stomach is an option. So we're going to look at some subepithelial masses, which are basically bulges or masses in the GI tract. They can either be within a layer of the GI tract or intramural, or they're coming from somewhere outside, like a neighboring organ, and pressing into the GI tract. There are a lot of things that can do this. There are some benign causes. So here is a pancreatic rest, which we see often. This is like a congenital. This happens in embryologic development, basically. This is a totally benign lesion that you don't need to do anything with. This is a muscular layer that is kind of poking into the GI tract. A lipoma is basically a collection of fat cells that can be really anywhere in the body, but we see them in the GI tract, in the stomach, and the colon pretty often. There are also some malignant things that can do that. So this is a gastrointestinal stromal tumor, which is kind of, you can tell that this isn't a mucosal lesion, which we've been looking at before, but it's coming from somewhere underneath the mucosa. Or there is a carcinoid tumor, which is what this little guy is here. So endoscopic ultrasound, any of these lesions are much better evaluated with endoscopic ultrasound. Because if we try and biopsy things, our biopsy, remember those little biopsy forceps that we had? Those can get you very good mucosal samples, but all of these things are underneath the mucosa. So we need to look a little bit deeper. Chances are, if you try and biopsy it, there's not going to be a whole lot that we're able to actually see underneath the microscope. With standard biopsy forceps. So endoscopic ultrasound is the most accurate way that we can evaluate these lesions that look like they're coming from somewhere else. And you can usually identify which layer of the GI tract they're coming from, the echogenicity, the size. And then you can actually use a needle through the echo endoscope to aspirate a lesion that looks like it might need to be aspirated. And that also is another way that we may be able to diagnose something that is benign versus something that is not. That's it. Questions? I have a question. I'm just curious. So when you use some of these to see, you might not know until you start scoping. Yes. Are you always prepared to do a procedure? Or do you ever have to? How would you prepare the patient? What could be happening? Or do you have to take the scope out and then have the patient come back? That is a good question. It depends on our index of suspicion for what we're looking for. For example, actually a good example would be a subepithelial lesion. Let's say we're doing an upper endoscopy because someone had maybe a CT scan that showed that there was something in the stomach that we aren't sure what it is. So we do a standard upper endoscopy. Things look OK. We're bringing the scope back. And then we notice, oh, wait, this is here. Or maybe this patient showed up with a GI bleep. But again, we're using a standard upper endoscope, which will only let us. This is the best that that view is going to get. So the best I can do with this lesion is maybe I can grab some biopsies, which may or may not be helpful. But you identify this as something that's not originating from the mucosal layer. And so you know that that person then needs to get an endoscopic ultrasound. So I mean, I don't do endoscopic ultrasounds. What I will do is call one of my colleagues. I think you're going to meet both of them, actually, later today. And then they will get on their schedule, usually within the next day or so, maybe a week, to get an endoscopic ultrasound to further evaluate that lesion, depending on the urgency of the situation. So that's just one example. For bleeders, yes, we're usually pretty able, or at least in our endoscopy lab, there are enough tools there where we can probably handle most bleeding that are just kind of there all of the time. Same with a foreign body. We have a foreign body kit that's in all of our endoscopy suites that we're able to use as needed. Did I answer your question? Sort of. I don't know anyone's name. You can just go ahead. When you're doing a colon and you get the scope outside of the esophagus, how do you sew that back up after the procedure? What do you do to cleanse that for a bridge that you made? That is a great question. So you're not actually leaving the esophagus. You're not going through the muscular layer. You're just kind of cutting the muscular layer. I don't think that they, I don't, I mean, I send a lot of my patients for POMs. I don't actually do the procedure myself. But I don't think that they, it's not a technical perforation because you're not going through the muscular layer. So there's not anything that needs to be closed. Because if you close it, then you're going to have the same issue you had before. So it's going up and down, having to go through the esophagus? Exactly. Yeah. The tunnel, the tunnel bridge that's coming in. OK, just like in the diagram, it kind of looked like there was a big hole. But it was, I know it was just like a 2D picture. So I was just curious if that was something that you did. Yeah, I think that you could try that. There's space. So in between, in between layers. OK, I got you. Thank you. What's the toughest bleed? Like, if you can't find the bleeding, what do you do? And what's the hardest bleed to find? Hardest bleed to find? There's actually an entire term to describe GI bleeding that we cannot find a source for. And it's overt, meaning that we can see that somebody is bleeding. They're needing blood. They're passing melanin. They're having just blood coming out of their rectum or they're vomiting. So we can see that there's blood loss. And we've done an endoscopy, an upper endoscopy. We've done a colonoscopy. And we can't identify with those particular procedures what the bleeding is. And so we actually call that obscure, overt GI bleeding. Now, the terminology is changing a little bit. Those usually end up being small bowel bleeds. And so we didn't talk about this here, but we will sometimes do a capsule endoscopy to see if we can find the area. It's usually in the small bowel, usually like an AVM or something like that. So those are the most frustrating to deal with. The most, what was the other part of your question? What's the hardest to treat? The hardest to find, it was one of the questions on the exam. Oh, probably a small bowel bleed. I don't know what the question was. I don't remember that exact question either. All right. And I'll tell you how I'd answer, theoretically. GI bleeding can be identified with routine upper and lower endoscopy. However, about 10% of the time, a bleeding source is not identified. Which of the following is the most likely origin of obscure GI bleeding? I put pancreatic biliary system, which I thought you probably couldn't see. So that would be the most hardest to find. Any other choices? Esophagus, stomach, small intestine, large intestine, and pancreatic biliary system. I agree with you that pancreatic biliary system bleeds are maybe a little bit harder to identify than some of the other standard things that we've talked about here. But I think that what they might be getting at, potentially, maybe with that question, is a small bowel bleed. Based on the treatment, it's a lot more common. Yes, sir. It doesn't say anything about small intestine. Yes, yes, yes, yes. Sorry. I was noticing that during your treatment options for bleeds, you didn't mention hemostatic powders or sprays. I did not mention hemostatic powders or sprays. That is correct. And when we update these slides, we will add that. Is that something you use, or? Yeah. It's not first line in at least, I mean, I guess from a guideline standpoint, it's not first line yet. But things like NexPowder, HemoSpray are nice adjuncts if, for example, something is not able to be controlled endoscopically with the tools that we have now. So with epinephrine, with clips, if a lesion just is in a weird spot, or it's too big to clip, or something like this. Or if somebody has had an attempt at a hemostatic clip, and we think we've done an OK job, and that patient's still bleeding, then using a HemoSpray, NexPowder, or one of those hemostatic sprays are a very nice adjunct. Why would you not use that as a first line? The US guidelines for management of GI bleeding do not have it as the first line yet. And there are some trials where they're starting to look at the hemostatic sprays as being first line options. I think there's actually a global trial, which has some US centers and a lot of centers in Europe where they're looking at that. But it's just not standard of care everywhere yet. It's also not available everywhere yet. OK. Dr. Glenn.

endoscopy

anatomy

pathophysiology

gastrointestinal tract

GERD

esophagitis

diagnostic procedures

treatment options