Okay, guys, I'm back for round two, esophagus and stomach. I still can't hear, and I'm still in the fog, so that hasn't changed at all, sadly. Anyhow, okay. Okay, so again, we're back to these questions. So esophageal disorders can result in A, maldigestion, B, difficulty swallowing, C, chest pain, D, both B and C. Put your answers in. Lock them. Wait, zero percent. Well, that was, no one saw the answer, put your answers in. Oh, good, you guys are, you guys are so smart. Okay, and then the second question is stomach disorders often lead to A, maldigestion, B, abdominal pain, or C, jaundice. And I would just, for Aria, I feel like maldigestion, technically, like in its true, true, true meaning is probably not the best, but maldigestion oftentimes, like we know that maldigestion means there's a difficulty in digesting your food, but oftentimes it's used interchangeably with malabsorption, which I think is kind of the use here, but I think personally, C, right, because you guys are listening, like digestion starts in the mouth, like it could be in the esophagus or the stomach, but really the answer is abdominal pain, and I think the reason why it's confusing is because I think we're using maldigestion as malabsorption. I could be wrong, I'm not super smart, so I could be wrong, but that's, that's my thought. Okay, so back to our schematic that we all should now have ingrained in our, in our hearts. What I think is so important to know, why we keep like referencing this, especially for this particular part of the course where we talk about like a, you know, disease state, is that, you know, it's really important to see the relationship between the different GI organs with each other, with other non-GI organs, and just kind of where they are as far as like thinking about their implications of the location when we talk about perceived pain and symptoms associated with each diseased organ. Okay, so what better way to start off our talk of GI and the disease state than with GERD, gastroesophageal reflux disease, also called GERD, is one of the most common disease states that we see as GI docs, but it really has a huge, like, burden to primary care physicians, otolaryngologists, pulmonologists, dentists, so it's a pretty common problem that can be seen across disciplines, and it's notable for its really high prevalence in a variety of clinical presentations. It's really an under-recognized morbidity in the community, and has a lot of substantial economic consequences, so it's estimated that like 20% of adults may have GERD at some point in their life, and it's defined as reflux of stomach contents, be that food or acid, into the esophagus and maybe even all the way up into the mouth, leading to erosive esophagitis or non-erosive reflux disease. So in normal digestion, the lower esophageal sphincter, as we've talked about a lot, opens to allow food to enter into the stomach, and then after the food goes into the stomach, it's supposed to close to prevent that reflux of the stomach contents back up into the esophagus, and in GERD, you have a weak lower esophageal sphincter that kind of relaxes inappropriately, and it allows that reflux of the stomach contents back into the esophagus. So what causes GERD? So it's important to remember, actually, that some degree of reflux is physiologic and expected and normal. Physiologic reflux episodes typically occur postprandially. They're really short-lived. They're asymptomatic. They don't usually occur at night, so you're not usually getting someone that's coming in with nocturnal physiologic reflux, and they're called transient lower esophageal sphincter relaxations, and they last like 10 seconds, so they're very 10 to 30 seconds. They're very, very transient, and they're seen in normal patients, but there are anatomic abnormalities that can also lead to GERD. Somewhat controversial in the GERD community is the importance of the crew of the diaphragm and how much that pinch really helps to prevent GERD, but it is thought that that pinch does help the LES work into keeping the LES tight enough to prevent that reflux. Dietary and lifestyle changes definitely contribute to GERD as well. Different foods and beverages, including our favorites, like all the best, like chocolates and caffeine and fatty foods and spicy foods, alcoholic beverages, carbonation, all the good stuff can lead to GERD trigger reflux. It does this by either changing gastric emptying, increasing gastric distention, causing pressure and causing the inappropriate LES relaxation, and then, of course, medications, lots of medications can also lead to this inappropriate LES relaxation. And really common things, like anticholinergics, like oxybutynin, tricyclic antidepressants that a lot of people are on, amitriptyline, which is a common GI medication, actually, that we use, calcium channel blockers, nitrates that a lot of older patients are on for their hearts, opioids, progesterone, benzodiazepines, the list is endless. Obesity can also lead to GERD and also leading to that inappropriate LES relaxation. And then, sadly, GERD just increases with age. I can tell you I'm getting GERD and I don't feel like I'm that old, it's really sad. Okay, so we're all probably familiar with the common symptoms of GERD, so that heart pain, that burning sensation in our substernal chest, that can really be pretty significant and can really mimic chest pain. Sometimes it's really hard to differentiate true chest pain from GERD because it can be so dramatic. Regurgitation, a lot of people will kind of talk about tasting acid in their mouth or kind of feeling like they're having that acid contents all the way up into their mouth or hypopharynx. And some less common, but common for GI, I suppose, GI doctors' symptoms of GERD would include things like dysphagia, that difficulty swallowing, feeling like things aren't actually going down into the stomach appropriately. You can get a sore throat, you can get painful swallowing, which is called odoniphagia. You can get kind of like a hoarseness or change in your voice related to this. You can actually get dental caries. Sometimes dentists are the first to diagnose this. Asthma, laryngitis, all of those can also be actual symptoms, manifestations of chronic GERD. So, if you're found to have, so if you have GERD, how do we treat it? So, treatment of GERD is generally based on how frequent you're having it, how severe your symptoms are. For patients with mild to intermittent symptoms, your doctor may just recommend lifestyle and dietary changes, which can be very effective. So this includes weight loss for patients that are overweight, elevation of the head of bed. We usually recommend doing that with like cinder blocks underneath the frame of the bed. Sometimes you can buy like a pillow wedge specifically designed for this. I don't recommend pillows. Usually, you know, as the night goes through, you just like end up falling. I like to tell my patients if they want to use like sofa pillows, sometimes those are a lot harder. But anyhow, elevating the head of bed and, you know, avoid eating two to four hours before going to bed allows movement of the stomach contents into the duodenum appropriately. Standing upright after you eat for like 30 minutes to an hour just by pure gravity, try to help that food go down. We kind of recommend that sometimes. And then avoidance of triggers can be really helpful as well. A variety of medications are used to treat GERD as well. These range from antacids like Tums, which don't really, you know, promote healing or really protect against further peptic, but they protect against further peptic injury by neutralizing stomach acid. The histamine 2 receptor block antagonists, they work by blocking the histamine receptors. And then, of course, like the PPI medications are really the most potent inhibitors of gastric acid secretion. And they irreversibly bind to those proton pumps that release the acid. PPIs are most effective when taking at least 30 minutes prior to a meal so they have time to bind those pumps. And they're actually most effective of taking daily rather than on a, quote, as needed basis. And if you take them in the morning, you're really getting those parietal cells which have probably a buildup of the most acid at that time. Of note, many patients are prescribed PPI medications and sucrophrates. Sucrophrates kind of coats the GI system. And in order to really use that effectively, you really have to time that appropriately. So a lot of times, you know, when physicians are prescribing medications, we're not the best at always kind of going over the other medications that you're taking and how best to time them. There can be a lot of interactions. So PPI and thyroid medications, for example, are a really big offender. But in any case, so with PPIs and carafate, you want to take the PPI first, wait half an hour or so, then take the carafate, and then let that carafate or the sucrophate, sorry, coat the stomach, allow it to coat before you eat. But there's a lot of discussion in the community as far as whether or not you should even be on both of those at the same time. But that's neither here nor there. And then in patients with refractory GERD, meaning that they continue to have symptoms, they continue to have problems related to the GERD, despite optimal medical management with lifestyle medications and everything else, they are oftentimes referred to surgery, which could be an operation, to really help them control their GERD. And it's usually a laparoscopic procedure. Nissen fundamentation is the most common. And they kind of wrap that cardia around the distal six centimeters of the esophagus to really try to help that gastric contents from going back up. And why do we care about GERD and reflux so much besides the fact that it causes so many symptoms and problems for our patients? It's really because it can lead to this bare esophagus that we had kind of heard a little bit from Bill earlier. As you know, the esophagus was not created to be exposed to a lot of acid. And repeated episodes of exposure can really lead the esophagus to be smart and say, hey, I don't like this acid. I'm going to change my mucosis. I can kind of tolerate this acid exposure. And the lining of the esophagus actually changes to more mimic the lining of the small intestine. You guys all got that question right. Excuse me. So Bayer's condition is really considered the condition where that normal squamous epithelium of the esophagus is replaced by the intestinal metaplasia and goblet cells that is normally seen in the small intestine. And the reason why we worry about it is because it's considered a precancerous condition in which it can develop into adenocarcinoma of the esophagus. Bayer's esophagus in and of itself is asymptomatic. So you might have symptoms from the reflux. But once that reflux changes into Bayer's esophagus, you may become usually are completely asymptomatic and don't know that that transformation of the mucosa has happened. Other risk factors for Bayer's esophagus besides GERD would include things like central obesity, family history, males over the age of 50, which is not old, and then history of smoking. So currently, the diagnosis of Bayer's is really made endoscopically and histologically. We can use specialized imaging such as narrowband imaging and chromoendoscopy to help diagnose this. And the findings can be really subtle. It kind of always gives me pause when I don't think there's something, but if I have seen it comes back as Bayer's, and I kind of have to, I'm proud of myself that I saw it, but then also kind of nervous that, you know, did I miss it on someone else? But anyhow, Bayer's esophagus will be seen as kind of what we call, we describe as salmon colored mucosa. So the mucosa of what looks like the stomach kind of creeping up the esophagus. And this is a really good schematic. So it kind of shows the progression from normal all the way to cancer. And then underneath it, you have kind of potentially what the histology would look like as well. So on the far left, obviously you see that normal Z line, that normal squamous columnar line. And then as you move to the right, you start seeing that irregular Z line, the salmon colored mucosa creeping up the esophagus, the Z line, or the actual, the natural gastroesophageal line with high junctions down here, and you see the salmon colored mucosa kind of up here. You also see the demarcations a little bit more irregular. You might call this thing a tongue. We kind of have descriptors for what we're looking at in describing the change in the mucosa, and then maybe an island right there. And then as you continue to move to the right, you start seeing nodularity, you have a low grade dysplasia that develops into high grade dysplasia, and then ultimately it could develop into a full cancer. We describe Barrett's a lot of times endoscopically based on how long it is from the G junction, its circumference, and then kind of what other abnormalities are we seeing. Are we seeing nodularity, edema, strictures, obviously a mass. And if we find Barrett's esophagus, generally we will follow endoscopically depending on what the biopsies show, every one to three years. So if you're found to have Barrett's esophagus, and you're found to have a high grade dysplasia, there are different types of treatment that we can use. So there are different techniques. So we don't usually treat low grade dysplasia at this time, although that's a little bit controversial as well, I would say. But generally if you're found to have high grade dysplasia, there's now a lot of different treatment choices. And they can include things like cryoablation, photodynamic therapy, but radiofrequency ablation is really the most common that we use. And radiofrequency ablation uses radiofrequency energy that's delivered by a balloon, as shown here, or sometimes even a paddle, and it has these really closely spaced electrodes that then ablate the Barrett's esophagus, or the Barrett's mucosa. And it generates this like really uniform circumferential thermal injury that has a very limited depth of destruction. And so you can tell here, after the energy has been applied, you see that nice circumferential kind of ablation of that first layer of the mucosa. And this is really nice because it shows pretty circumferential depth here. If a visible lesion or nodularity is seen, then RFA really won't be effective for a lot of different reasons. At the very least, it won't have that full contact with the mucosa, but then secondly, it probably won't have that depth that you need for destruction. And so when RFA is not an option, when you have that nodularity, you really want to do and you want to make sure that you biopsy, you want to make sure that we're not dealing with cancer. But if we're dealing with high-grade dysplasia alone, the preferred method of treatment really in these cases would be endoscopic resection, either with endoscopic mucosal resection, as seen here, or even endoscopic semi-mucosal dissection. And endoscopic resection, I know Bill kind of went over this a little bit, but just to go over it one more time, it really involves the excision of a larger segment in blocks, so all together. That way, you're not leaving little bits of tissue behind. And the technique of it is really similar to the technique for, for example, like removing a really large polyp. And so you're going to identify the lesion, and then using a needle, inject an injectant underneath the lesion in the semi-mucosa to raise that lesion off of that semi-mucosal layer. This is showing saline. There's some different injectants that we can use. And then you have, we have these devices, they're specifically made for this, but it's a distal end cap that's attached to the scope with a band that's already attached. And then you can suction up the lesion into the distal end cap, and then resect it in that fashion. The goal, again, is to really get that on-block resuction, so you're not leaving any tissue behind. Okay, so moving on to esophageal motility. So we talked a lot about GERD and its sequelae, which is really defined a lot by, you know, mucosal abnormalities. But we're going to talk about this abnormal motility, which oftentimes you might not see any mucosal abnormalities, and we're really talking about a function of abnormality of the movement of the muscle in the esophagus. The symptoms of esophageal motility can include dysphagia, which is that difficulty swallowing, odoniphagia, painful swallowing, chest pain, and heartburn. And as you might note, these are sometimes very similar to the same symptoms we just discussed of GERD. So sometimes when we're talking about esophageal motility, it's difficult to differentiate the two just by clinical assessment. So and since the mucosa looks normal oftentimes when we're discussing esophageal motility, the endoscopic exam of the esophagus may not always be beneficial or be helpful. And instead, we need some sort of other evaluation to really look at how the muscles are moving. And we use esophageal manometry, which looks at the intraluminal pressure of the esophagus, the peristalsis, the contractions, the strength of them, the number of them, how effective they are, the muscle coordination. And then it also really looks at that lower esophageal sphincter and tells us if that's appropriately working. The procedure is usually done as an outpatient, like awake. Usually the patient's awake and they need to be cooperative, or it's helpful if they are. And the nurses will place this electrode catheter down through the nose. They help swallow it into the esophagus, and then it goes into the stomach. And then they will have the patient take very small sips of water. And as that water goes, travels down from the mouth into the stomach, this electrode will then monitor all those things that we were talking about. There are four different types of or classifications of esophageal motility. So we have achalasia, which is due to inadequate LES relaxation. We have nutcracker esophagus, which is due to a hypertensive or a really tight lower LES. Diffuse esophageal spasm, which is due to an uncoordinated esophageal contractions. And then systemic sclerosis, you might hear it as scleroderma. That's like ineffective esophageal motility. And you just have pretty diffused esophageal hypocontraction, where really the muscles of the esophagus really aren't working to move that bolus down. So achalasia, from the Greek word does not relax, is referring to the progressive degeneration of these ganglion cells in the myenteric plexus in the esophageal wall. And it leads to the really failure relaxation of that LES. And it's accompanied by a complete loss of peristalsis throughout the esophagus. It's kind of uncommon. I feel like we see it a lot just because maybe we're at a tertiary referral center. But generally in the community, it's not a common, common problem. But it leads to this gradual onset of dysphagia, this feeling like that patients cannot swallow. And you get this functional obstruction, meaning that there's not really a mass sitting there. But because the LES is so tight, nothing's getting through. And this is a classic and pathognomonic barium esophagram showing this really massively dilated esophagus. And then where it should be emptying into the stomach, you can't. This actually, it's a little bit hard to see here, but it's called a bird beak sign, where you see just like a trickle of barium kind of trickling down through that LES down into the stomach. And that's caused from that persistently contracted LES. It's interesting because a lot of these patients, it's so slow and gradual in onset that a lot of times they come in and their esophagus is full of food and liquid. And you're like, why didn't you come in earlier? And it's amazing what your bodies are able to just kind of tolerate. I can't see that sometimes. OK, so how do we treat achalasia? It's really aimed at decreasing that resting pressure in the LES. And the choice of treatment really depends on the patient's quality of how fit they are for surgery, what their surgical risk is. So if patients are not a surgical candidate or declined surgery and doesn't want really aggressive intervention, Botox injection has been a really effective way in improving swallowing. So it's done endoscopically. And yes, it is the same Botox that we like to use elsewhere. But you inject a total of 100 units in a four quadrant, kind of like circumferentially around the LES. The goal is that it decreases that resting or that basal LES pressure. It's a really easy procedure to perform. It doesn't take a ton of skill. And it has a really good safety margin, really few complications overall. It's practiced pretty frequently. It has a really good immediate response. You know, sometimes it's been reported up to like 90% effectively, effective. But the duration of the response can be really short-lived. And it's not the greatest in younger patients and in patients with certain types of achalasia. But it is a good treatment option. There are some concerns that if you are planning on doing surgery or doing a POEM, which we'll talk about in a minute, that the Botox may not be the first-line therapy that you would go to, because that might actually affect those future subsequent surgeries. But so what would be another way that we can treat achalasia? Pneumatic dilation is something that we could consider, especially if someone is a surgical candidate, only because it does carry risk. And you want to make sure that if there were a potential complication, that the patient would be able to adequately go to surgery if there were one. Pneumatic dilation, again, the purpose of it is to weaken that LAS. It causes this circumferential stretching of the muscle fibers. And then you want to tear it, but do it in a controlled fashion. It's done endoscopically and under fluoroscopic guidance. I don't actually do this, but this is how you do it. From the picture and from what I know from my training. But you'll go endoscopically, identify the LAS, and then you want to mark the LAS either by injecting a little tattoo that can be radiopaque and seen on fluoroscopy. Some people put external markers on the patient, which is a little bit, I don't know, wary. You put a guide wire that goes through the LAS into the stomach. You withdraw everything. And so now everything's done fluoroscopically, and you put this balloon. It's a rigid balloon, so it's a noncompliant balloon. And they are in like 30, 35, 40 millimeters, so they're pretty big. And then you advance it under fluoroscopic guidance. You want to position it, ideally, right in the middle of where your LAS is. And then you slowly inflate it. And as you inflate it, you'll see this, what we call waste. So you know that the balloon is appropriately situated. And you keep inflating it until that waste goes away. So you inflate it slowly and constantly, so you're getting that pressure, stretching those fibers, tearing them appropriately. And then you hold it for 60 seconds, and then you deflate everything, take it out. And then I think most people do a relook endoscopy where they go back down and make sure that everything has been opened and torn appropriately, but not torn too much, not perforated. This is pretty effective. In like 70 to 90% of people, people do well, but then how long does it last? And so that leads to the Heller myotomy, a surgical myotomy, which is another way, it's a primary alternative to pneumatic dilation for treatment, primary surgical treatment for achalasia. And it's usually performed laparoscopically. This is surgery, so this is not something that your gastroenterologist will be doing, this particular one. And since the LAS disruption, you may be smart, but doesn't that disrupt the ability of the LAS to control GERD? You're right, it does. And so oftentimes it's paired then with an anti-reflux procedure, like a Nissen fundamentation, and sometimes they do a partial Nissen. But what can we do in GI? So let's say we wanna do something that can kind of help treat this achalasia. We can do something called peroral endoscopic myotomy, or POM, which is a form of that natural orifice transluminal endoscopic surgery, the notes that we've talked about. And it's an endoscopic method of performing myotomy during the LAS. I also don't do this myself, but I've seen it, tried it on some animals. During POM, it's really a cool procedure. So the endoscopist makes an incision into that submucosal space and then tunnels down the esophagus, so they're in that third space, going all the way down to the lower esophageal sphincter, and then using really specific scalpels that are endoscopic of sorts, they kind of cut the muscle of the muscularis propria to weaken that LAS, and then they tunnel back up and then close the defect, and then all is good. It's awesome. And when they were first doing it, it took a couple hours, and now I think people that do this regularly can have it down to 30 minutes or something like that, maybe even less. So it's the long-term data is promising. We still are waiting for longer-term data to come in, but really good results have been reported, especially in certain patients that don't respond to the conventional therapy. So certain types of achalasia respond better to this, and then obviously patients that have failed other endoscopic surgeries. Oh, sorry. So that's creating the tunnel, tunneling all the way down. And then cutting the muscle fibers. Okay, so we made it through the esophagus on to peptic ulcer disease. So peptic ulcer disease is one of the most common entities that afflict the GI physicians, primary care physicians, patients. Peptic ulcers are really defined as the defects in the gastric or duodenal mucosa, and it extends through the muscularis mucosa. They develop and persist as a function of constant peptic acid activity. Excuse me. And it really remains a really important cause of morbidity for patients. The natural history of peptic ulcers range from healing without any intervention to kind of progressive development of complications with the potential of a lot of problems, including bleeding, perforation, pain, and there's a cancer risk related to some ulcers. But peptic ulcer disease is associated with two main entities, H. pylori infection and NSAIDs. And they are independent risk factors, but synergistically they're really bad for the creation of peptic ulcers. H. pylori really affects a number of aspects of GI physiology. It includes gastric, it increases gastric acid secretion. It really decreases the mucosal defense mechanisms. And the prevalence of H. pylori both, I would say, in the population as a whole is really decreasing in developed regions, and we think it's because of increased better hand hygiene and less transmission early on. And NSAID use is associated with a fourfold increase in the risk of peptic ulcer disease, so while we love NSAIDs, feel like it's anti-inflammatory, I love it for my headaches, it really can do a number to the GI system. NSAIDs are also, I'm sorry, other risk factors for peptic ulcer disease would include things like smoking, alcohol intake, like there's some other genetic issues. Okay, so symptoms of peptic ulcer disease include abdominal pain, discomfort, postprandial, belching, epigastric fullness, early satiety, and you can get more complications that are more aggressive, such as bleeding that can be manifest as hematemesis, where you're throwing up blood, or melanin, which is digested blood that comes out from below. You can actually get gastric outlet obstruction that can occur when the ulcer is located, the pylorus, and that can cause delayed gastric emptying and can cause symptoms of gastric outlet obstruction, nausea, vomiting, again, early satiety, bloating, and then when they're really severe, they can actually just continue to progress and go deeper and actually lead to a perforation, which would then be an emergency. Okay, the mainstay of diagnosis of peptic ulcer disease is with endoscopy. A lot of patients I'll see say, oh, I had an ulcer, but then never had an endoscopy, so what they mean is that they've had some sort of symptoms that were bad enough that someone said, maybe you have an ulcer, but the way to actually diagnose it is to take a look endoscopically and look, and it's kind of advantageous, because not only can you identify it, but you can actually grade it as far as how severe it is, and then take a biopsy to make sure that we're not dealing with any H. pylori effect on it or anything else that could contribute to an ulcer. And when we look at the ulcers endoscopically, we're really looking at not only the size, but the depth, and if there's any stigmata, bleeding, if there's any visible vessels or pigmented spots or adherent clots that could maybe change the risk of bleeding. And then additionally, gastric ulcers, not peptic ulcers, but gastric ulcers could be a sign of malignancy, and so if we don't know what's causing the ulcer, we assume that it's acid, and they have all the risks, but a lot of times when we look at these ulcers, we wanna make sure that we're not missing some underlying malignancy as well. And so we can oftentimes biopsy it as well. I don't think the clock is working, just FYI, because it said six minutes the whole entire time, I just realized. So I have no idea how I'm doing with time, I'm sorry. So moving on. To treat H. pylori, if there is H. pylori, you wanna treat it and eradicate it, which is a whole separate topic of antibiotics and resistance and whatnot, but really important to not only treat it, but to prove that you've treated it. And then if they're taking NSAIDs, to stop the NSAIDs, which can be really difficult in a lot of patients that have arthritis, and that is their mainstay of treatment, and they don't wanna do narcotics or opioids, I should say, so that can be a lot easier said than done, but those are by far the two things that you wanna do. And then, of course, we have PPIs. So PPIs are really important in treating peptic ulcer disease. Okay, and then since peptic ulcer disease can lead to GI bleeding, we have a good segue to talk about upper GI bleeding in general. It's defined as anything bleeding from anything proximal to the ligament atrites. I know Gauri talked a little bit about that transition from the duodenum into the jejunum, but anything that is above that ligament atrites is considered upper GI bleeding, which makes sense. You're not gonna be throwing up blood if you're bleeding from the colon, or at least, I mean, that would be pretty dramatic. So since blood in the GI tract includes hematemesis, which is bright red blood, like obviously bloody vomitus, or it can actually look like coffee ground emesis, which looks like coffee grounds, but it's really like digested old blood in the stomach that's coming up. And then from below, it can look, again, frankly bloody, hematekesia, which is bright red blood, or it can look like melanoma, which is, melanoma is really interesting. And so, I mean, once you've seen melanoma, you'll never not see it or not smell it. It's very distinctive. But it's like this black stool, but it's really tarry. I mean, it looks like tar, it's sticky, and it smells like death. And it's very different than just dark stool, which a lot of patients will be like, I think I have black stool, because it's really dark. But in any case, it's important, though, to distinguish. Yes, question. So I'm just sitting here as a dad of three. Is that like the infant poop? No, meconium is not melanoma, but that's a good, it is kind of blackish as well. But yes, no, it's very different. I should be able to talk more about meconium. I don't know if anyone else wants to chime in. I also just had a baby with meconium, but no, it's very, very different. It looks totally worse than what that looks like. It is smellier, stickier, and you just think it's wrong. Like, that should not be coming out of me, which maybe you think about for your baby, but anyhow, it's different. Ahem. What was I gonna say? I was gonna say something. By the way, the bad smell of melanin, it's not people's smell. It has a distinct smell to it. But it's this black, tarry stickiness that's distinct. You can walk into an emergency room, and if there's a patient with a GI bleeder with melanin, you know it as soon as you walk in the emergency room. It's just pervasive throughout the ER. Yeah. If you see hematemesis or coffee-grown emesis, you know you're having a GI bleed. Again, I'm sorry, an upper GI bleed. You know it's coming from before the ligament trite somewhere. I mean, almost 99.9%, that's the case. It could be coming from the, there's other things. But anyhow, if you see hematokizia, you wanna say you think it's coming from the lower GI tract or the colon, but it could also potentially be coming from a very, very brisk upper GI bleed. And if you think that there's, you know, if you're seeing bright red blood coming out in your stool, and the patient is really hemodynamically unstable, they're very sick, they need to be in the ICU, that type of picture, then you must be thinking it's a really, really major GI bleed, and it could be coming from an upper GI source, such as an ulcer or esophageal varices or something else. Bright red blood coming from the colon, don't quote me on this, but oftentimes isn't that dramatic. They don't get that sick that quickly. They can, but just generally. Melanin, when you see it coming down, we often wanna say that we think of it coming from the upper GI source as well, because we think digested blood. But it can actually be coming not only from the upper GI, meaning proximal to the ligament trites, but it could be coming also from anywhere in the small intestine, because it's still gonna be digested. And it can actually even come from the right colon. So you could have a slow right colonic bleed that takes forever to come out, and by the time it comes out, it looks like melanin. So things that come up from below sometimes are not as straightforward as things that come out from above, if that makes sense. Okay, and then besides ulcers, what else causes GI bleeds? So esophageal varices, and gave, erosions, ulcers, gastropathy, duodenal ulcers unrelated to peptic ulcer disease, a Mallory-Weiss tear, which is a little tear at the GE junction from increased pressure, and then angio-dysplasia. I was gonna say esophageal varices and gastric varices are almost always associated with cirrhosis or end-stage liver disease. You might have gastric varices related to a spleen vein clot. These are other causes, and they kind of vary as far as their degree of severity or how they present with bleeding. And then management always for a GI bleed is always, always resuscitation. So always make sure your patient's stable, make sure they have fluids, make sure they have two large IVs before you even start assessing whether or not, or how you're gonna treat the bleed, what's causing the bleed. And then after you get through resuscitation, PPIs are really important in the management of at least peptic ulcer bleeds. And we have IV forms and oral forms, and there's a lot of studies on PPIs and how effective they are, and they don't really change morbidity, or mortality, I should say. But there is a lot of evidence that if you use PPIs prior to an endoscopy, it downstages the grades of the ulcer and decreases the need for endoscopic management. And so they're really important in our management of peptic ulcer disease. If a patient's found to have high-risk stigmata on an endoscopy when we find an ulcer, so if they have a visible vessel, if it's actively bleeding, we usually continue to treat them with IV PPIs for about 72 hours after, then transition them after that to orals. If they are found to have a low-risk ulcer, clean-based, no stigmata, not actively bleeding, we can sometimes get away with just doing oral PPI therapy. It has no change. But let's say they are high-risk at the time of endoscopy, or they are actually bleeding. There's endoscopically lots of different tools that we can use to achieve hemostasis. I know that we just heard about some of them, but epinephrine injection, thermal therapy, hemoglobin band ligation, these are all very exciting. These are kind of our mainstays. This is partly why some of us go into GI, because we can actually physically do something right then and there. And we'll have time to play with all of these tools in the lab later in a little bit. And then finally, I just want to end on gastroparesis. I am really sorry about time, guys. Gastroparesis is delayed emptying of the stomach in the absence of a mechanical obstruction. Diabetes is one of the most common offenders for causing gastroparesis. But you can see this post-surgically, post-infectious, which is actually really common and frustrating for patients, because it's like if I started having gastroparesis after the spring cold, that'd be annoying. And then idiopathic. And symptoms are really, it's nausea, vomiting, early satiety, abdominal pain, bloating, weight loss. The same symptoms that you might see with a gastric outlet obstruction related to the gallbladder ulcer at the pyloric channel. And this can be pretty debilitating, these symptoms, because they're just always feeling full. They feel like they can't eat. They always feel like they have to throw up. Treatments, or diagnosis. So the diagnosis for gastric emptying is a nuclear medicine study where a patient is given this meal. It's kind of gross. It's like low-fat egg whites on toast. And then they follow it with imaging and see how quickly that meal is moving out of the stomach. And they look at it at time zero, one hour, two hours, four hours after they ingest this meal. So if you have greater than 10% at four hours left of that meal, or over 60% at two hours of this low-fat meal, that's really considered indicative of a delayed gastric emptying. Okay, I'm sorry. So this is showing normal, the food bowls, it's moving through, and then you have your delayed gastric emptying where nothing is really moving into the small intestines, all just staying in the stomach there. Treatment for gastroparesis is fairly limited at this time. We really kind of try to focus on kind of food choices and trying to stay away from really roughish-based food, just really increase the time that the food stays in the stomach. We often recommend they take small frequent meals throughout the day rather than two to three large meals that we're all used to. Give the stomach time to digest, break down what's in there, and try to move it forward before putting more food in there. Sorry. And there are some medications that we can use, the prokinetics erythromycin and metoclopramide, which can try to help contract the stomach and, again, move that food bolus into the small intestine. We use antimedics, which doesn't really do anything for the gastroparesis, but it helps with the symptoms of nausea. And then gastric pacemakers can be placed at certain centers of excellence and are considered kind of compassionate treatments for patients with refractory symptoms, especially if it's really, really bad nausea. And then the final topic for me is epithelial masses or lesions, which can be seen in the GI tract. And, again, these are arising from within the GI tract, so it can either be, or they're not mucosal-based. They're not on the inside of the stomach, but they're either arising from within the walls of the GI tract, or they could be even extrinsic outside of the GI, just pushing in. You don't know until you examine further. The most common would be a lipoma, which is a fatty tumor, or a leiomyoma, or a pancreatic arrest. Those are, by far, the most common causes of this. But they can also be a more premalignant or malignant etiology, such as a gist or a carcinoid. And so when we see these, oftentimes they're referred for further workup with endoscopic ultrasound, where we can actually look through the layers, assess the size, the depth, what layer it's coming from, which could help guide us in terms of identifying what type of lesion this is, and then taking a fine needle aspiration if it's big enough, and then we can actually decide what to do, and if we need to resect it, refer a surgery, or just watch it. Okay, and I made it. I'm done. Any questions? Yeah. Maybe in simple terms, describe what is the third space? The third space, I think in its simplest term, is when we're working in not the luminal part of the GI tract, but we're going inside those wall layers and working in one of those submucosal layers would be the best way, I think, to describe it. So for example, POM, where we're actually going, I mean, it's like, I think the scariest thing ever. You have a wall that's like five millimeters, and you're literally putting the scope inside the middle of the layers and going all the way down the esophagus. So that's third space. That's in the submucosa. That's third space. Beyond the mucosa. Yeah. Beyond the mucosa, but not outside of the wall of the GI tract. So you can think of it as the first space is inside the lining. The second space is maybe surgery on the outside. This is the third space in the middle. So that's what we're talking about in the first space. Wall of the digestive tract that we're doing all the work. And we're doing a lot of submucosal dissection, kind of like working in that third space, but also be another example. I'm so sorry. I talk so much. I'm sorry.

esophagus

stomach

GERD

achalasia

peptic ulcer disease

endoscopy

upper gastrointestinal bleeding

gastroparesis