All right. Hey, everyone. I hope everyone had a good break. So now we're going to move into the part of the course where we're talking about GI tract diseases. And to start off, Dr. Chang is going to talk to us about diseases of the esophagus and the stomach. OK. So the picture that we're all very familiar now, the GI tracts, we'll focus in this talk on the esophagus and the stomach. So GERD is very, very common, estimated to have a prevalence of roughly 30% in the US. And this refers to gastroesophageal reflux disease, basically the reflux of contents that are usually acidic in the stomach coming up into the esophagus, sometimes coming up all the way to the mouth. One of the subsets of GERD or something related would be laryngopharyngeal reflux, or LPR. And that's when acidic contents from the stomach reach all the way up to the upper esophageal sphincter. What sets that apart from GERD would be that that usually results in hoarseness of the voice or chronic cough. So how does GERD develop? We have our lower esophageal sphincter, like we talked about before, which is a sphincter muscle that is located at the bottom of the esophagus and kind of separates the esophagus from the stomach. So it's normally closed when we're not swallowing, when we're not eating. But it does relax. And when it does relax, not necessarily pathologic. There are what are called TLESRs, or transient lower esophageal sphincter relaxations. And again, that's not necessarily considered to be pathologic on its own. You can also relax it when you're burping. So burping, belching isn't necessarily considered to be pathologic. But if the lower esophageal sphincter is too relaxed or doesn't have good tone, and you have excessive acidic reflexant from the stomach, the esophagus, and that can be considered pathologic depending on how much acid is coming up. So some causes of reflux are just normal physiology, such as when you have a transient lower esophageal sphincter relaxation. It can be in response to a food bolus. So the lower esophageal sphincter does reflexively relax when you swallow. But when there's a lot of food in the stomach, again, some of that can come back up and cause some acid reflux. There can be anatomic abnormalities. So we talked about hiatal hernias specifically. So hiatal hernias increase the incidence or the prevalence of acid reflux. Besides a hiatal hernia, other anatomic abnormalities would be a hypotensive lower esophageal sphincter. Or like we'll talk about later on, if your esophagus does not work or you have esophageal dysmotility, then that can be sort of an anatomic abnormality that can be related to reflux. Certain foods can cause acid reflux. So they've illustrated them here. Coffee and chocolate are two common causes of acid reflux. Other foods that can commonly cause acid reflux would be tomato sauces, garlic, fried foods, and alcohol. And then certain medications can contribute to acid reflux as well. The most common symptoms of acid reflux would be heartburn or really feeling like there's acid or burning coming up into the chest. Less commonly can cause dysphagia. Dysphagia is difficulty or issues with swallowing, specifically feeling like food or liquid isn't going down well or it's getting hung up or stuck. Again, it can also cause chronic cough, laryngitis, and it can exacerbate asthma. So in patients who have really poorly controlled asthma and the pulmonologist isn't really sure why, it's so difficult to control. One of the things they want to look at is does the patient have poorly controlled acid reflux. When we think about treating acid reflux, one of the first things that we do is we talk to the patients about lifestyle modifications. So elevating the head of the bed is one of the first things that we do, in addition to counseling the patient to not eat right before bed. Because if you eat right before bed, you have a full stomach, and then you lie down, you don't have gravity as much helping you to keep that food in your stomach. Elevating the head of the bed just sort of uses gravity to help you keep that food down. Weight loss can be helpful, especially if patients have a lot of abdominal fat. If patients don't have a lot of abdominal fat, then losing weight is less likely to help them. And then avoiding exacerbating foods like we talked about. If those don't suffice or patients have a difficult time with those lifestyle modifications, then you can move on to different medications. So proton pump inhibitors are probably the most common and popular class of medications. Those would be medications like brand names would be Prilosec, Nexium, Protonix, Acefix. The other classes of medications that we can use to treat acid reflux would be the histamine 2 receptor antagonists. And those would be medications, drug names would be things like Tagamet or Pepsid. And then the newest class of medications used to treat acid reflux are the PCABS or the potassium channel acid blockers. And the only FDA approved PCAB in the US is Vinoprizan. Finally, if patients have side effects from antacid medications or they don't want to be on them lifelong or especially if they have an anatomic abnormality, then there are different more invasive ways to treat acid reflux such as a Nissen funnel application which is a full 360 wrap of the fundus of the stomach around the lower esophageal sphincter. There's also now a TIF. So it's a transoral incisionless funnel application that can be done endoscopically. OK. So acid reflux can cause esophagitis. And esophagitis is a broad term which just refers to inflammation of the esophagus. Some symptoms of esophagitis can be odynophagia which describes pain on swallowing. But more commonly, the symptoms are just the symptoms of heartburn, reflux, GERD, can occasionally cause dysphagia as well. Esophagitis, again, can be caused by GERD, it can be caused by infection. When we think of infections causing esophagitis, we think of viral infections such as CMV or cytomegalovirus or EBV Epstein-Barr. Candida, which is a fungus, can also cause esophagitis. Certain medications can cause esophagitis, radiation especially to the chest. Some patients unfortunately will ingest caustic substances usually in the setting of a suicide attempt. But if patients are taking things like bleach or cleaners, a bronzy esophagus, it can cause a pretty severe esophagitis. And then eosinophilic esophagitis, which is an eosinic infiltrator of the esophagus that typically presents with dysphagia. So again, food getting stuck, typically seen in younger white males and oftentimes can present as a food impaction. So food getting stuck in the esophagus that has to be removed endoscopically. When we think of esophagitis, especially reflux esophagitis, there's the LA classification, which just describes the severity of that esophagitis. So it's A, B, C, and D. A describes mucosal breaks that are less than or equal to 5 millimeters in length. Grade B is mucosal breaks that are larger than 5 millimeters in length. Grade C describes mucosal breaks that extend between the tops of two or more mucosal folds. And grade D esophagitis describes esophagitis that is 75% of the circumference of the esophagus. So actually, when we think about GERD and how we diagnose GERD, if patients have LA grade B or more severe, then that is something that we can use to diagnose GERD. Other ways of diagnosing GERD, just kind of moving back a little bit, would be looking at how much acid is coming up from the stomach into the esophagus. So we do that by assessing pH. And that can be done using a wireless capsule or a nasal probe. And we look at a high acid exposure time. Barrett's esophagus is when there is excessive acid reflux from the stomach into the esophagus. And the esophagus gets damaged over time. And what Barrett's reflux is, it's a replacement of the normal lining of the esophagus with what appears to be lining of the small intestine. So we looked at before when we looked at normal physiology of the esophagus, the esophageal mucosa should be a stratified squamous. So when we looked at the cells underneath the microscope, they looked like those flatter types of cells. With Barrett's esophagus, if we were to biopsy the Barrett's, what it would look like underneath the microscope are more cuboidal type cells. So it looks more like small intestine or stomach. And this is really the esophagus' way of defending itself. And so if it looks more like the stomach or the small intestine, those cells are more designed to have mucus and have protective mechanisms against this acid. Unfortunately, it's also a precancerous condition. So we know that those patients who have Barrett's esophagus are at increased risk of developing esophageal adenocarcinoma. Oftentimes these patients have no symptoms, so they don't necessarily have really severe GERD. Again, it's sort of the esophagus' way of protecting itself, and unfortunately, it also means that they're at increased risk for cancer. So like we saw before, this is a normal-looking Z-line where you see a pretty distinct demarcation between here is stomach and here is esophagus. And this is the top of the gastric fold, so here's your lower esophageal sphincter. This is Barrett's esophagus, what we describe as a salmon-colored mucosa. So here you can see that normal esophageal mucosa. And then this is actually still esophagus, even though it kind of looks like stomach. So the G-junction would be probably somewhere over here, and then from here all the way up there, it's all Barrett's esophagus. Over time, Barrett's esophagus can become sort of more and more dysplastic, meaning that the cells look more and more disorganized. And if you have dysplasia, that's really a high risk for progression to esophageal adenocarcinoma, and the reason why we want to survey Barrett's so frequently is because we want to try to stop the progression to esophageal cancer. So if you see things like this or nodularity in the Barrett's, that's when you really want to engage your interventional gastroenterologist to try to ablate that tissue. And then here, it's a little bit too late. Here you already see the progression to cancer. So how do we treat Barrett's esophagus? One of the ways is to treat it with radiofrequency ablation, and this sort of just burns the tissue. You don't need to treat Barrett's unless there is some dysplasia. So if there's no dysplasia and there's just Barrett's esophagus, then we just survey it, and we survey it based on, in terms of the frequency that we survey, based on the length. Or if there are any progressions to dysplasia, if there is dysplasia, then we want to treat it, and oftentimes it's treated with radiofrequency ablation, and this kind of just burns the tissue. Another way to treat it, especially if there's any nodularity or any suspicious areas, would be with endoscopic mucosal resection. Moving on to other diseases of the esophagus, the esophagus, again, is just a hollow lumen that connects the mouth and the stomach, but its role is to move things down. So when we think about motility disorders of the esophagus, those are disorders in how things are moving from the mouth to the stomach. The most common symptom of an esophageal motility disorder is dysphagia. So patients don't say, I have dysphagia. I ask them questions like, does food get stuck? Do you feel like things are moving down slowly? Dysphagia specifically refers to pain with swallowing. That's not a common symptom of a motility disorder. But chest pain and heartburn, which are very, very similar to the symptoms of GERD, can be symptoms of esophageal motility disorders as well. So going back to this slide, chest pain and heartburn can be symptoms of a motility disorder, but they can also be very vague symptoms. So we're going to talk about a motility disorder called achalasia. And usually, there's about a four-year lag to the diagnosis of achalasia, because when patients say they have chest pain or heartburn, probably 999 times out of 1,000, it's going to be GERD. And so these patients end up cycling through all the different antacids before they finally get diagnosed. So how do we actually diagnose esophageal motility disorders? There's a few different ways, but the gold standard and the best way is with esophageal manometry. So this is a metal catheter that is inserted into the nose, down the oropharynx, into the esophagus with the bottom part of the catheter is in the top part of the stomach. So it's inserted while the patients are awake. We don't give any kind of sedation, because the patients need to be swallowing for the study. We do place some lidocaine on a Q-tip and have that sitting in theirs. How she's inserting is not how you want to insert. You actually want to go back. So it's more like a perpendicular insertion. If you go up, you actually can go into the brain. So you don't want to insert up. You want to insert back. I tell my fellows, you're aiming sort of towards the lower earlobe. So achalasia we'll talk about in more detail. That's sort of one of the more well-known motility disorders. Nutcracker, so some of these nomenclatures were from the Chicago classification, the third version. Now we're on the fourth version. So the Chicago classification is what we use to diagnose and name motility disorders. So nutcracker esophagus is now something called jackhammer esophagus, and we'll talk about in more detail what that means. Diffused esophageal spasm is now distal esophageal spasm. Systemic sclerosis is not a motility disorder in and of itself. So patients who have systemic sclerosis, scleroderma, often have a combination of an aparastaltic esophagus with a hypotensive lower esophageal sphincter. So that combination we see, we often call that a scleroderma esophagus. During manometry, when we see that too, we'll also always sort of mention that. Consider working the patient up for a skin or connective tissue disorder if they don't already are known to have one. So achalasia comes from the Greek term meaning does not relax. So a hallmark of achalasia is that the lower esophageal sphincter, which should reflexively relax as soon as you swallow, that is gone. And so not only does the lower esophageal sphincter not relax, there's a loss of peristalsis. So those are the two hallmarks of achalasia. So what happens when your lower esophageal sphincter doesn't relax? What will happen with achalasia is that the esophagus gets bigger and bigger and more and more dilated. And so once that happens, patients can have what is called a sigmoid esophagus. That's really sort of end stage achalasia. But what sigmoid esophagus means is that the esophagus becomes so big and so dilated that it actually becomes tortuous in the chest and can look like colon. So that's really end stage achalasia. Prior to that, though, it usually just becomes bigger and more dilated. This imaging is what's called esophagram, usually used with barium. So we call it a barium esophagram. What you see is classically a birdspeak appearance. So you see a dilated esophageal lumen. And then it kind of really tapers down so that the barium just sort of trickles out of the esophagus into the stomach. Sometimes patients will complain of sort of chest pain after eating, things sitting in the chest, regurgitation. So it sounds a lot like reflux. But I'll ask them, you know, what does the refluxant taste like? Does it taste very acidic? If it doesn't taste very acidic, then it may be achalasia. They'll also oftentimes say that when they lay down at night, they spit up a lot because saliva accumulates in the esophagus. And when we scope these patients, we go in and we see usually a fluid-filled esophagus and a lot of bubbles of saliva. So this sort of leads to a functional obstruction of the esophagus. There's three different subtypes of achalasia. But again, all of them have the loss of peristalsis and the failure of the lower esophageal sphincter to relax. Some of the ways that we treat achalasia noninvasively are by injecting Botox. And so what we're trying to do, Botox basically paralyzes the muscle. And using the endoscope and the needle, you basically perform an intramuscular injection. So you're not trying to create, like Dr. Goh showed, you're not trying to create this big bleb. You're actually trying to jam the needle into the muscle. And so if you see a big bleb, you know that you're actually not deep enough. And we usually do this in four quadrants. For achalasia at the lower esophageal sphincter, I usually do about 100 units. And I like to look at the lower esophageal sphincter sort of like a clock dial. So I do 12, 3, 6, and 9. It can be quite effective. So I've had patients be able to go from eating only liquids to eating a hamburger later that day. But I do usually counsel patients because I'm injecting volume into an area that's tight. I'm more conservative and I say try to stick with a clear diet the day of the procedure because symptoms may potentially worsen before they improve. I do Botox a lot. I love Botox. The biggest issue with Botox, though, is that it doesn't last forever. A lot of patients will have return of the symptoms within six months. Some patients can go a year. But just like when it's used for wrinkles in the face, you have to have repeated injections. And if you're repeatedly injecting the area with Botox because you have to do it with a needle, it can potentially cause scarring and make something like a pull-on procedure a little bit more difficult down the line. You can also dilate the lower esophageal sphincter. And to dilate the lower esophageal sphincter, you need something called a pneumatic dilation or a pneumatic balloon. There's different types of balloons that we use in different areas of the GI tract to dilate certain things such as strictures from scar tissue. But because this is a muscle that you're trying to dilate, those balloons that you use through the scope usually are not stiff enough to tear the muscle. So oftentimes, the balloon is introduced with a guide wire under fluoroscopy. You visualize that you're at the lower esophageal sphincter. You blow up the balloon. Then you bring the balloon down, and you look at that area you want to see blood because what you're trying to do is rip muscle. If you don't see any blood or any damage, then you probably haven't done enough. I don't do a whole lot of pneumatic dilation, and we don't do a whole lot of pneumatic dilation at our center anymore because there are just better ways to treat achalasia now. And any time we do a pneumatic dilation, there's about a 5% risk of perforation. And oftentimes, these need to be done multiple times. So if you're having a 5% risk each time, you're doing it three, four times, and we usually just go to safer therapies. Some of these, I guess, safer therapies, depending on how you define safe, would be something like a surgical myotomy. So there's pros and cons, of course, to a pneumatic dilation versus a surgical myotomy. A pneumatic dilation, assuming that there's no perforation, which is the vast majority of the time is done endoscopically. Patients go home later that day. With a surgical myotomy, this is a surgery. It has to be done by a surgeon. Oftentimes it's done laparoscopically. And what they're doing is they're going in to the abdominal cavity, and they're making an incision in that muscle at the lower esophageal sphincter. Sometimes when this is done surgically for achalasia, they'll combine this heller myotomy with a partial fundoplication. So like we talked about for GERD, one of the treatments for GERD is a Nissen fundoplication. It's a full 360 wrap. You cannot do a Nissen fundoplication in a patient with achalasia because they don't have forward peristalsis of the esophagus. So that's where you'll see terminology such as a door or a toupee fundoplication. Those are just partial fundoplications. When you are doing a myotomy, you are taking away the patient's natural barrier to reflux. So oftentimes we'll do a partial fundoplication so that there's still some kind of barrier that the patient has because, again, with achalasia, there's no forward peristalsis. So if you cut the lower esophageal sphincter and acid comes up and you're not upright, then there's nothing to push that acid back down. The POAM, or the peroral endoscopic myotomy, this is in contrast to the laparoscopic myotomy. And what's nice about this is you do it through a natural orifice, so it's done through the mouth. And this is done by interventional gastroenterologists in what's termed the third space. You make an incision sort of higher up than the lower esophageal sphincter, and you create a submucosal tunnel. And then you basically cut through the lower esophageal sphincter muscle. Pros and cons for the POEM procedure versus a laparoscopic halomyotomy would be that there is a shorter recovery time, because this is not actual surgery. You're going through the mouth. You're not going through a natural orifice. Sometimes they go home the same day. Sometimes they stay in the hospital overnight. Probably the biggest benefit of doing POEM, and this is probably more detailed than you need to know, but there are three subtypes of achalasia. The third is called a spastic achalasia. And on manometry, we can tell an interventionalist basically how high up that spastic segment goes. You can achieve a longer myotomy with a POEM than you can with a laparoscopic halomyotomy. So when we think about how we treat achalasia, when we compare pneumatic dilation versus POEM versus a halomyotomy, so the more robust treatments, for the two subtypes of achalasia, their type 1 and type 2, the outcomes are really similar for all three. Basically the only type of achalasia that POEM is better for is type 3, the spastic achalasia. The biggest drawback of the POEM procedure versus something like a halomyotomy would be that because this is all done endoscopically, it's usually not combined with any kind of a fundoplication. So there may be a higher risk of acid reflux in patients who are receiving a POEM procedure. And what that means is that there's a higher likelihood that patients will need an antacid after the procedure. OK, so moving on to the stomach, one of the most common pathologies of the stomach is peptic ulcer disease. And this can occur in the stomach or the duodenum. And what an ulcer is, it's a mucosal break. It can occur really anywhere in the GI tract. But for when we think of peptic ulcer disease specifically, we're referring to the stomach and the duodenum. The two probably most common causes of peptic ulcers are helicobacter pylori. And you can see in this stain, it's these little brown things that we see over here. That's all the H. pylori. NSAIDs such as ibuprofen, Aleve, can also cause peptic ulcers. And if you have H. pylori and you take NSAIDs, that increases your risk for peptic ulcer disease even further. Some of the most common symptoms of peptic ulcer disease would be sort of dyspepsia, so pain, discomfort in the stomach after eating. GI bleed would be if the ulcer is large and kind of erodes into a blood vessel. That can present as hematemesis, which is the term that we use for vomiting blood. Or melanoma, which is when patients have black, tarry, sticky stools. It can cause, in some instances, gastric outlet obstruction. So if the ulcer especially is involving the pyloric area, that can make it harder for things to exit out the stomach. And usually that causes nausea, vomiting, sort of oral intolerance. And then in sort of more extreme cases, it can actually perforate the stomach or the duodenum, which usually causes a very severe acute abdominal pain. So there's multiple ways actually to diagnose peptic ulcer disease. ERs are pretty aggressive sometimes with imaging people. So sometimes you can see it on imaging, especially if there is a contrast study where the patients take an oral contrast. But most commonly, ulcers are diagnosed using an upper endoscopy. So this is what an ulcer looks like. This is the ulcer right here. And this is a break in the mucosa over here. So how do we treat peptic ulcers? First we want to see if H. pylori is present. And if it is present, then we want to treat it. H. pylori has evolved with us over many years. And so it's very common to have antibiotic-resistant H. pylori. So we always recommend that if you see H. pylori, you treat it, and you always confirm eradication afterwards. And so if patients don't eradicate the H. pylori after the initial antibiotic regimen, then there's second, third, and fourth line treatment strategies, different antibiotics. You can also treat peptic ulcer disease with proton pump inhibitors. Again, proton pump inhibitors inhibit that proton pump that is making gastric acid. And so by suppressing gastric acid secretion, you have a less acidic gastric environment and a more conducive environment to healing. Sucraphate or caraphate is a protective agent for the lining of the stomach. We oftentimes use that in patients who have especially larger, more higher-risk ulcers. When we think of upper GI bleeding, which can be from peptic ulcer disease or various other etiologies, what we mean is that this is bleeding from the GI tract that is located proximal to the ligament of trites. And I don't think the ligament of trites is here, but it's basically where the duodenum and the jejunum are meeting. How do we know that someone has a GI bleed? Well, they could be vomiting blood, which is referred to as hematemesis. If they vomit what looks like coffee grounds, that is also a sign that they may be bleeding in the esophagus or the stomach. In the stool, if they have bright red blood perectum, it actually can be coming from the upper GI tract if it's bleeding briskly enough. Most commonly, if patients are hemodynamically stable, meaning they're not tachycardic, their blood pressure is normal, bright red blood perectum is usually coming from the colon. But if someone is really tachycardic, low blood pressure, then hematokesia, so bright red blood from the bottom, can actually be from the upper GI tract. More commonly, though, upper GI tract bleeding will present as melanoma, which is classically the black, tarry-colored stools. So there's a lot of different causes of upper GI bleeding. Esophageal varices are what is pictured here. And these right here are the varices. So these are really large blood vessels in the esophagus that occur in the setting of portal hypertension, typically decompensated cirrhosis. So cirrhosis is end-stage scarring of the liver. These are erosions here. So erosions can ooze, ulcers can bleed. Gastropathy is here. Gastropathy can be from various etiologies. But one of the more common causes of gastropathy is portal hypertensive gastropathy, so also a sequela of portal hypertension and cirrhosis. You can have ulcers in the duodenum, although I think this picture is actually in the stomach because this looks like pylorus to me. But you can have ulcers in the duodenum, especially really large ulcers in the duodenum are oftentimes supplied by the gastroduodenal arteries, so really have a propensity to bleed quite a bit. Mallory-Weiss tears, I think right here is a Mallory-Weiss tear. This is classically a tear in the mucosa of the esophagus that occurs with a lot of retching. So patients often describe that they were throwing up, whether it be because of food poisoning or something else. They were throwing up a lot, a lot, a lot. And then eventually, they started throwing up some blood. And when we think of that, when we hear that, we oftentimes think, you know, are they throwing up blood after throwing up not blood for quite a bit because of a Mallory-Weiss tear, or they have given themselves severe esophagitis? GAVE was kind of discussed before. This is a picture of it. This is the pylorus, and this area is the antrum. Some people sort of nickname watermelon stomach because you can kind of see these markings sort of look like the markings of a watermelon. You can also have varices in the stomach. So oftentimes, in the fundus or the cardia that we see better on retroflexed views, treated a little bit differently than esophageal varices. And then angio-lactasias, angio-dysplasias, or aberrant blood vessels that can also bleed. And then there's also dullifoils, like that was mentioned before. The first step in management of a GI bleed is resuscitation. So this needs to occur really before we can scope them because when we scope patients, we sedate them. We give them medications that can further decrease their blood pressure. And so resuscitation would be with typically crystalloid fluids, like normal saline. If they need blood, then we give blood as well. We talked a little bit about the medications that can be used for peptic ulcer disease. And we use those same medications for GI bleeding, so proton pump inhibitors typically. And if the bleed is severe, we typically just do intravenous. In terms of how we treat GI bleeds endoscopically, we can inject epinephrine around the ulcer, which is a vasoconstrictor. We don't use that as monotherapy, so we always use that in combination with another modality. And those other modalities can be, like was discussed previously, thermal therapy. This looks like a gold probe right here. We can deploy hemoclips, such as here, or we can put some rubber bands. And so rubber band therapy or band ligation can be used for esophageal varices, can also be used for GAVE. Peptic outlet obstruction refers to a mechanical obstruction of the outlet of the stomach, typically at the pylorus. And this can be from benign causes, such as peptic ulcer disease or sometimes pancreatitis. Unfortunately, usually when I see it, it's malignant and usually from a gastric cancer or a pancreatic cancer. The symptoms would be, as expected, nausea, vomiting, early satiety, distention, weight loss, and abdominal pain. And this is what it looks like on imaging. So this is a huge gastric bubble, or I think that's what I'm looking at here. On CT, it's a little bit more obvious. This is how big the stomach is. And the reason why the stomach is so big is because of the outlet obstruction. So if things can't empty out of the stomach, it gets really, really huge. And endoscopically, it can look something like this, or more typically, it looks like a pinhole. And sometimes it can be difficult to traverse with the scope. So the first thing we do when we see a gastric outlet obstruction is we place a nasogastric tube. And the purpose of the nasogastric tube is to just try to decompress the stomach as best we can. Patients often get pretty instantaneous relief with that. And that's a tube that just goes from the nose down the esophagus into the stomach. In terms of how we actually treat it, though, besides decompressing the stomach, one of the things that we can do is place a stent across that area of obstruction. And this is typically done by one of the interventional gastroenterologists. It kind of depends on what the etiology of the obstruction is from. And then this is just an x-ray image showing the stent placement across the pylorus. And this is what it would look like endoscopically. You can also have surgery for a gastric outlet obstruction. Again, really depending on what the etiology is, you typically wouldn't do this for malignant obstruction unless it was really, really early stage, which unfortunately, that's not typically what we see. A biliruot surgery is classically surgery that is done for peptic ulcers. So peptic ulcers that are medically refractory are complicated by a perforation or cause of obstruction. And so this is kind of similar to a Roux-en-Y in some ways in that you're basically bypassing the obstruction and connecting the jejunum up to a smaller sort of gastric pouch. Before we knew that H. pylori was a common cause of peptic ulcer disease, these surgeries were performed quite frequently. And a lot of patients would have issues with these limbs and sort of limb syndrome. But nowadays, with the knowledge that H. pylori causes peptic ulcers and better medications to treat peptic ulcer disease, these sort of surgeries are not very common anymore. Gastroparesis refers to delayed emptying of the stomach in the absence of a mechanical obstruction. So it's commonly associated with diabetes. It can happen also as a complication of surgery, especially foregut surgery. And usually, the reason why it comes after surgery is because of damage to the vagal nerve. It can be post-infectious. Typically, that is a little bit more transient, gets better with time, or it could be idiopathic. Symptoms of gastroparesis would be nausea, vomiting, early satiety, pain, bloating. Sometimes can present with weight loss, but not all the time. The reason why gastroparesis doesn't always present with weight loss is patients learn to adjust their diet to things that can pass more readily. And those are not always low calorie. So how do we diagnose gastroparesis? The gold standard is with a gastric emptying study. And this is a nuclear medicine study. So patients take a meal, which is normally eggs that are mixed with a tracer, with some toast, sometimes some juice, has to be a very standard carbohydrate, protein, fat composition. And they're looking at, over a period of time, how much of that food is exiting a stomach. And our sort of gold standard for the diagnosis of gastroparesis is at the four-hour mark, is there more than 10% of the meal remaining in the stomach. Nowadays too, besides the gastric emptying study that is done by nuclear medicine, there's also a home gastric emptying breath test. It's still used with egg, but the egg is combined with spirulina that is mixed with a carbon tracer. And patients eat that. It turns into green eggs, actually, green eggs and saltine crackers. They blow into test tubes. And that also gives us a graph so that we can assess gastric emptying. So how do we treat gastroparesis? Before we move to medications, we counsel patients on a gastroparesis diet, which would be small, frequent meals. Foods that empty out of the stomach slower would be foods that are higher in protein, fat, and more fibrous foods. So things like a lot of roughage will be harder on patients who have gastroparesis. If that's not enough, then we talk to patients about prokinetics. And what prokinetics are medications that increase or stimulate peristaltic activity of the stomach. Erythromycin is an old antibiotic that is a pretty good prokinetic that affects the stomach and the small intestine. It works on the motillin receptors. Metoclopramide is also a medication that increases gastric contractions. Metoclopramide is available in a pill form as well as a newer sort of nasal spray. There are a couple prokinetics that we use for gastroparesis that are not FDA approved for gastroparesis, but that are pretty potent promotility agents or prokinetics, and that would be procalipride, as well as pruritostigmine. You can also treat the symptoms. So anti-medics are basically anti-nausea medications. So medications like ondansetron, compazine, scopolamine. And finally, there's something called a gastric pacemaker. And this is very similar to a cardiac pacemaker. It has to be surgically implanted as well as surgically removed if it doesn't work. But you have leads that are implanted actually into the stomach. When it was first developed, it was thought that it worked just like a gastric pacemaker or like a cardiac pacemaker. And by stimulating the contractions of the stomach, you would increase gastric emptying, and then patients would feel better. We actually know now that even though you can adjust the amplitude and the frequency of the stimulation, the gastric pacemaker actually improves symptoms because of modulating the vagal nerve. So that's kind of interesting. It is FDA approved for gastroparesis under what's called compassionate use. So when patients have not responded to other therapies, then oftentimes you can place a gastric pacemaker. I think the biggest hurdles to it are that it doesn't work for everybody, and it has to be surgically placed. And if it doesn't work, then it also has to be surgically removed. Finally, other treatments for gastroparesis, if these don't work, would be surgery. So a pyloroplasty would be done laparoscopically or robotically. And that's actually sort of splaying open the pylorus and making it larger. There's the GPOAM, which is a peroral endoscopic myotomy of the stomach. So making a tunnel in the antrum and cutting through the pylorus muscle. And then especially if patients are very overweight or obese, then even gastric bypass surgery can help with gastroparesis. So sometimes when we're scoping patients, we see subepithelial masses. And these are masses or bulges that we see. They can be intramural, meaning that, just like in the picture here, they're rising from the layers of the GI tract, or they can be extramural. So sometimes when we're scoping, we see what looks like extrinsic compression from something outside of the lumen of the GI tract. There's a lot of benign masses that we see, such as leiomyomas, pancreatic rusts, or lipomas, which are just fat collections. So those typically are really soft and pillowy. Sometimes there's a little bit of a yellowish hue that we see. Or they can be malignant, such as a GIST, which is a GI stromal tumor or a carcinoid tumor. And so oftentimes, looking at these things, we can tell what they are, such as with a pancreatic rust or a lipoma. But other times, such as with a GIST or a carcinoid, we need a biopsy and work those lesions up further. Endoscopic ultrasound is really the best test to evaluate these subepithelial lesions, because they can tell you from which layer of the GI tract or which layer of the mucosa or some mucosa or muscularis is the lesion originating from, what it looks like in terms of echogenicity, how big it is. And then during the EUS, you can do a fine needle aspiration and sample whatever it is you're seeing. Any questions? You mentioned the muscle fungification. Mm-hmm. What exactly happens during that? Yeah. So if you think about the anatomy of the stomach, and the stomach is sort of that J shape, like I talked about in the first lecture, the fundus is that top part of the stomach that accommodates with meals. So the surgeon basically takes that fundus, and they wrap it around the lower esophageal sphincter. And so it's usually a 360 wrap. You can see it, actually, on endoscopy best during a retroflexion. But since I don't perform ischium fungification, because I'm not a surgeon, I think that's as much as I can describe it. So can you fully heal gastroparesis, or is it just about treatment of it? Yeah. So I think it really depends on what the etiology is. So you can actually have transient gastroparesis just from hyperglycemia. So if your blood sugars are high enough, then it actually slows stomach emptying. So if your gastroparesis is from hyperglycemia or poorly controlled diabetes, and you really control those blood sugars, then some patients don't have gastroparesis anymore. If it is from a viral or post-infectious etiology, again, that should improve with time. If it is from vagal nerve injury after surgery, nerves are a little bit more difficult to heal. So when there is post-surgical vagal nerve injury, then we look at, OK, what are the sequela? Is the patient having slow gastric emptying? Sometimes it's from a pylorus spasm. And so we'll look at the pylorus more closely. We'll look at the stiffness of that area. I would inject Botox if that area were stiff. And if the patients respond really well to Botox, then pursue more pyloric-specific interventions such as a G-POM or a myotomy or a pyloroplasty of that area. A lot of times with idiopathic gastroparesis, if we're not able to identify why they had the gastroparesis or something that's reversible, then it's something that we treat with agents that help to empty the stomach or the symptoms. And are you seeing higher rates of it with the increased usage of the weight loss drugs? Sure. So we know that those medications sort of slow stomach emptying. I'm not sure. And I don't know. Maybe when we do the panel, if my colleagues want to chime in, my practice is so specific that it's second opinion. And so, I mean, my wait time used to be like 13 months for a new patient. So usually, a community gastroenterologist will know what a patient's symptoms are at baseline. And then they start one of these medications. And then if patients say, OK, it was only after I started one of these medications that I started having early satiety, nausea, vomiting, then they would just stop those medications. So I usually don't see much of it in my practice, just because it's something that's usually picked up by the person who's prescribing the medication. Where I think those medications become really relevant in our field is, how do we safely scope patients on those medications? So what is the best time frame to them stopping those medications so that when we go in, there's less of a risk of aspiration because there's retained food in the stomach?

Gastroesophageal Reflux Disease

Laryngopharyngeal Reflux

Esophagitis

Barrett's esophagus

achalasia

peptic ulcer disease

Gastroparesis

esophageal motility disorders