So now that you all had some refreshments, so we'll go down the GI track, okay, starting from the esophagus into the stomach. So you heard about the normal anatomy and the physiology part. Now we get into the disease aspects. So the one common disease which you all will encounter, it's called GERD in short, gastroesophageal reflux disease, is basically a reflux set of stomach contents into the esophagus and sometimes even in the oral cavity, I mean people can taste acid. So as I mentioned earlier that this is where you start seeing these breakdown of the sphincter muscles, the lower esophageal sphincter muscles, and I'll come to that. So normally this is what you see when this group of muscles, it's in a closed position, the stomach contents actually do not reflux into the lower end of the esophagus. But time to time you see, as I said, in normal physiology you get this transient relaxation of this group of muscles. But in abnormal cases, these group of muscles are quite a bit, quote unquote, permanently relaxed or not functioning well, then you get these gastric contents going into the esophagus. So again, I'll just go over the normal physiology. As you can see here, we have the food bolus going from the esophagus into the stomach. Now the causes of the gastroesophageal reflux disease include, obviously, anatomic abnormality, certain foods and medications. I think you can see here the C sign, the chocolate. So let me go over, actually, the classic foods, food and beverages also, I have to say, causing abnormal relaxation of these lower esophageal sphincter muscles that all start with C. Cheese, chocolate, carbonated beverage, which is a beverage, then obviously caffeine, probably a lot of you also drink coffee now. But this is mostly in the evening where things get worse, and then you start seeing most of the reflux in the night. And the last C, by the way, is Cabernet wine. So anyway, certain medications also cause this abnormal relaxation. So the symptoms, as you all know, most common heartburn and acid regurgitation, slight difference. People will complain of, as you can see, retrosternal chest pain. Sometimes it confuses with the chest pain of cardiac origin, however we need to distinguish that very carefully, so often we do a cardiac workup, just want to make sure there is no cardiac component to it. And also you can see sometimes acid, or you can have symptoms suggestive of acid regurgitation. Some people complain of acid taste in the mouth. Often you see some erosion of the dental enamels and things like that, people will complain. Less common, you'll see certain symptoms like dysphagia, chronic cough, laryngitis, and asthma. By the way, asthma is another one of the important symptoms people will complain in the case of what we call extraesophageal manifestations of reflux disease. So different types of treatments available. First and foremost, I always talk about the anti-reflux precautions and the lifestyle modifications that you can see here, elevating the head of bed, losing weight, mostly losing the adipose tissue in the trunk, we call it. So less of truncal obesity, so it puts less pressure on the diaphragm. And avoid those C-containing foods and beverages. The product pump inhibitors, the classic ones, have been there for several years now, it's almost over 20 years. A pillar for the treatment of gastroesophageal reflux disease, one of the examples here is omeprazole or Prilosec. Now there's a new protein pump inhibitor, it's not a protein pump, it's a potassium channel acid blocker, or KCAB in short, which is going to be coming to the market, Bonaprazone is the generic name. And you'll hear about that, that's another way of treating the gastroesophageal reflux disease. Then there is finally surgery, although one thing missing here is the endoscopic therapy of anti-reflux, we do quite a bit. It's similar to the Nissen fundoplication, or different variations of this fundoplications that you'll hear. The one we, meaning the interventional endoscopists, perform is called TIF, in short, T-I-F, transoral incisionless fundoplication. And sometimes it's done also in conjunction with the hernia repair, so it's called small C, capital T, capital I, capital F, C-TIF. So esophagitis is the next pathology you'll encounter in the esophagus, it's basically inflammation in the esophagus, mostly from the reflux we talked about, but there are other conditions also of this inflammation that you see in the esophagus. This is where the esophagitis you can see happening. Symptoms are mostly difficulty in swallowing, sometimes with pain. Difficulty is dysphagia, when it is associated with pain, it's called odynophagia. Several causes, as you can see, GERD, infection, medications, radiation, sometimes caustic ingestion, and eosinophilic esophagitis, I think someone mentioned about that, it's another disease which is commonly now seen, especially in the younger folks, and often associated with asthma or allergic conditions also. Perhaps we'll come into that later. Infection, another thing is common, quite commonly we see what we call candida, the fungal infection in the esophagus, in immunosuppressed hosts, or even in diabetics. So this is the LA classification, or Los Angeles classification of esophagitis, this is called the LA grade A, where you can see these small mucosal breaks, which are less than five millimeter in length, and you get more of these breaks, this is the grade B, where it's greater than five millimeter in length, but not extending between the loops. Now once you start seeing the extension between the loops of more than two folds, that's where you call it LA grade C, and when the mucosal breaks actually encompass more than 75% of the circumference, then it's LA grade D. So I was mentioning about the normal, again, let me repeat, the normal mucosal lining of the esophagus, it's composed of stratified squamous epithelium, okay, stratified squamous epithelium, non-keratinizing, but now in a condition called Barrett's, which again you hear a lot, it's a replacement of that normal lining with the lining which is coming from small intestine. Again I emphasize, it's the columnar lined esophagus, or columnar epithelium, which is replacing the normal lining. The reason it's happening is because you get an injury from the reflux, mostly, and that injury results in death of the normal lining. Now when that happens, there is always a body's quote-unquote healing process, but in this case there is an abnormal healing, meaning in the sense that the replacement of the normal with this columnar line, it's called metaplasia. Meta means change, and this is the change. Now it's again a columnar, but it's a specialized columnar lined epithelium because it has these goblet cells, there's a special goblet cells which has mucus in it, it's actually coming from the small intestine, not stomach. Again I repeat this, very important, it's replaced by the small intestinal type of mucosa. It's a precancerous condition, but I call it precancerous only when the metaplasia I mentioned about, that's just a change, that's just a replacement, changes into a condition called dysplasia. Dysplasia means it's early cancer or precancer in the superficial lining. So that's the precancer condition, and there is an increased risk of developing from dysplasia, and it's again high-grade dysplasia, into the esophageal adenocarcinoma. Low-grade can also progress, but at a very, very low rate. Often you'll see these patients coming in with no symptoms, in fact they don't get any symptoms classic of heartburn or acid regurgitation. So this is the progression I was mentioning about, as you can see. So this is the salmon color projection, as we call it, into this pinkish, and this is also here one island. But this is, so you can see this progression from metaplastic lining, or metaplasia, getting into now so-called low-grade into the high-grade dysplasia, once you start seeing this kind of nodular and then full-blown esophageal adenocarcinoma. Again I repeat, the carcinoma that you develop here, it's adenocarcinoma, not squamous. Squamous is only in the upper one-third, as I mentioned, most of the time, or even in the middle part, but not so much with the barrets. Barrets is always what you develop is the adenocarcinoma in the end. So how do you treat? You heard some of the tools mentioned. So one of the tools here is the RFA, or the radiofrequency ablation technique, where we have the RFA catheter, and now it's through the scope. You can basically go and use the radiofrequency energy. So this is basically the energy which is now converted into the thermal part, and that's where you kind of ablate, see the tissue right here. Basically it's a destruction. So this is what you start seeing post-RFA. So there's another technique. If you start seeing some of those nodules or abnormal areas, we inject. You already saw how we do this procedure called endoscopic mucosal resection, and then we do what we call is a cap-fitted EMR technique, where you just suction out that elevated lesion into the cap and then cut it. Now moving on from this into the different pathophysiology of the motility of the esophagus, there are different motility disorders we encounter, or problems with the movement of the esophagus, mainly peristalsis. And the symptoms you can see are dysphagia, adrenophagia, chest pain, and heartburn. There are different manometry catheters available, and these are done usually by the manometry nurses, and they place the catheter, and they know exactly that it's in the lower end of the esophagus, based on the tracing that you see on the monitor. Different types of disorders you'll encounter. The one commonly we see is the achalasia. Different types, again, there are three types, type 1, 2, and 3. Then there is a nutcracker esophagus, there's a diffuse esophageal spasm, and also sometimes you see ineffective motility with this condition called systemic sclerosis, it's a collagen vascular disorder. So achalasia in Greek, it means doesn't relax, so hallmark you see is absence of peristalsis, and also failure of the lower esophageal sphincter to relax, and you can, this is a classic appearance with the barium, which is called, you can see here, it's a bird's beak appearance. This is a classic type 1 achalasia. It leads to the functional obstruction of the food bolus in the esophagus, so the food keeps accumulating, and eventually the esophagus almost takes the shape of a sigmoid colon, that large. So what do we do with that? Well, in older days, we don't do this often, we used to inject botulinum at the lower esophageal sphincter, we do it in four quadrants, we inject, and this injection is happening at the so-called Z line, at the squamous columnar junction, and what it does, it basically helps in the relaxation of the hypercontractile lower esophageal sphincter. Then we used to also do, and we still do often, pneumatic dilation, these are special types of achalasia rigiflex dilators we have, it's a balloon, and we can, you know, inflate that balloon, and essentially what we are doing is opening up the contracted or hypercontracted LES. So you can see here how we go, we put a guide wire in, then we position the balloon, the waist of the balloon should be right at the squamous columnar junction, you then insufflate the balloon, and inflate fully to kind of dilate the lower sphincter. We do this mostly in fluoro, but there are other techniques where we sometimes do it even without the fluoro, just looking in the retroflexion, the G junction. Now more commonly, the surgeons actually started doing this laparoscopic myotomy, where you basically make an incision, as I said, this is basically the muscles that are hypercontractile at the lower end of the esophagus, you make this, you just split open, and that helps in the relaxation of the LES. This is what you see, the mucosa visible through myotomy. Nowadays, more than the laparoscopic, we have a technique called endoscopic myotomy, it's called per-oral endoscopic myotomy, or POEM in short, where you basically dissect into the submucosal space, you know, from using a tunnel, you can see how the tunnel is being formed here, and then once you, and with an orbit jet, and then once we create the tunnel, so this is the tunnel is formed, you get the scoping, and then you start the incision, and basically you start cutting this inner circular, you can see this inner circular muscles, and it all depends how long you want to cut, all this depends on the patients, and also the post-myotomy, people can develop sometimes reflux disease, so again, it all depends on how far you go beyond the squamous columnar junction, and how far also proximal you go above the squamous columnar junction, all this will depend on the case-by-case basis, but, and then there are two different approaches, anterior-posterior, we tend to do more anterior approach, anyway, it doesn't matter, but those are the ways we treat that Echolasia disease. Mostly, it's reserved for type 3 and type 2s, not so much for type 1 Echolasia, just for your information. So then we come to now the disorders in the stomach. The common ones you see is the peptic ulcer disease, where you see ulcer formation, which is nothing other than mucosal breaks in the GI tract. You'll see these ulcer formations, sometimes erosions, we call it, which are the precursors or sometimes healed ulcers noted during endoscopy, commonly seen in the stomach and also as well as in the duodenum, sometimes in the bulb and also in the second part of the duodenum. Now, the causes. These are the two common causes that you should think of when you see ulcer disease. Helicobacter pylori, you still see, although we are slowly and steadily getting away because of improved sanitation. It's a bacteria which loves to hang out in this harsh environment in stomach. It loves acid. And as you can see, these are the bacteria. This is actually in the mucous layer. They're just sitting on the surface, but it's causing this whole ulcer formation. And the other cause is NSAIDs, nonsteroidal anti-inflammatory drugs. For example, ibuprofen, very commonly used, and a lot of other products also in the market, like for example, BC powder. A lot of times people take that for headache and pain, also contain NSAIDs. So you have to be careful about these two because they're the common causes of gastritis and gastric ulcerations and even in the duodenum ulcerations. So what are the symptoms? You see abdominal pain, discomfort. Of course, we see gastrointestinal bleeding. The common ones, we call it hematemesis. Heme, which is blood, and then emesis is vomiting. So you're basically vomiting blood. Sometimes you'll also hear the word coffee ground emesis. It's not exactly blood, but it's like a coffee color material that you're vomiting. So those are just some of these names for essentially bloody vomit. And then you can see melina, which is black tarry, pitch tarry stool. It's really black, pitch tarry stool, which also has a distinct smell. So that's melina, just not any black stool, but it's black tarry stool. So sometimes even you might encounter fresh blood in the stool, too, which we call it hematokinesia. That happens in like 12% to 15% of the cases with bleeding coming out from stomach or proximal part of duodenum. So before the ligament of tritium, you'll hear about that later. The other symptoms include gastric outlet obstruction, nausea, vomiting, obviously, when there is an ulcer disease which is blocking the outlet from the stomach going into the duodenum. And lastly, you might come across conditions with ulcer perforation, where people come in with severe acute abdominal pain, quote unquote acute abdomen, where you need to call the general surgeon right away to take care of it. So this is what you see, the gastric ulcer. We were talking about nice, clean base. And there is a classification also. We call it forest classification. You sometimes hear that. So this is forest 3. And most of the time, we are doing biopsy to rule out helicobacter pylori. And also, if that is negative, then we know that this probably came from overuse of NSAIDs. Most of the time, that's the case. So we treat, obviously, and try to eradicate. Very, very important. It's very, very key that we need to completely eradicate H. pylori, because it's classified as a class A carcinogen by WHO. So you don't want to have 70%, 80% eradication rate. We try to achieve at least 95% and above, if possible. And we are getting there. And then there are medications like, as I mentioned, protein pump inhibitors. And there will be these other potassium channel acid blockers, which will also help in the healing of these ulcers. Upper GI bleeding, as I was just mentioning, that bleeding from the GI tract before the ligament of trites. Now, ligament of trites is the position where the duodenum curves around and gets into a proximal jejunum. You probably saw that in the anatomy slide before. So that's the definition. And what you see, I mentioned, hematemesis or coffee ground emesis in the stool. As I said, 10% to 12%, sorry, 12% to 15% of the time, you'll see hematokizia, bright red blood prolactin, and melina. So these are the different causes. Nice pictures here. So let me quickly go over. So these are the esophageal varices. Again, common cause of massive upper GI bleeding. These are just the erosions. You see these. So it's called erosive gastropathy. Some of them can have healed ulcer. For S3, we call it gastropathy. You'll hear the word a lot. It's not gastritis, itis in Latin. It's mainly inflammation. But opathy, gastropathy, duodenopathy, entropathy, that means there is an abnormal condition. And in this case, the abnormal condition is basically congestion. It's a sub-epithelial congestion. So we call it reactive gastropathy. You'll hear these words. Post-bariatric surgery, sometimes you'll see a lot of bile reflux. So you'll get this bile reflux gastropathy. This is a nice ulcer in the duodenal bulb. And sometimes you'll see this bile stain. So that's what the color is from. You can see these tears. That's at the Mallory-Weiss tear at the squamo-columnar junction. Just to be careful, sometimes we see a hadal hernia sac where we do see tears. Because that hadal hernia, which is basically the herniated portion of the stomach going into the esophagus. So you heard before the top of the gastric fold. The top of the gastric fold is now quite higher. Squamo-columnar junction and the diaphragmatic pinch, they are not at the same place. That's the hernia. Now, this area is extremely vascular, and you get tears. And that's called sometimes Cameron's erosions or ulcers or just a gastric mucosal tears. Mallory-Weiss tear, classically, at the squamo-columnar junction when there is no hernia. This is a classic condition called GAVE or gastric enteral vascular ectasia. And you can see these stripes, almost like a watermelon. So it's otherwise known as watermelon stomach. These are the varices in the fundus of the esophagus. That's called the gastric varices. And this is what you see. It's otherwise known as angio-dysplasia. I prefer the word angioectasia, where it's a dilated vessel. So how do you manage? First thing is always ABCs. You resuscitate the person. Then you start them on proton pump inhibitors. That's what we have most of the time, IV. And then you switch to oral. And then you start doing a lot of these hemostasis techniques. You probably saw, again, with the tools that we use, nowadays, it's mostly either two or three modalities, meaning you do epinephrine. We use one in 10,000, mostly, injections. Then we do the thermal therapy using this bipolar or multipolar. This is called the gold probe. And then after that, we use these clips. These are called hemoclips to close the defect. And sometimes we have also put bands. It mostly happens in the esophageal varices, but also sometimes in a condition called nodular GAVE. You saw that we can put these bands, too. Now we do have another modality where we do hemospray, where we spray after doing all these endoscopy, if there is some oozing of blood, those hemostatic powders. So gastric outlet obstruction, mechanical obstruction, as I was mentioning, at the pyloric junction. As you can see, different causes, benign causes. Often we see peptic ulcer related or malignant when you see gastric or pancreatic cancer invading and causing this narrowing of the channel. Symptoms are pretty straightforward, nausea, vomiting, pain, abdominal distention, weight loss, and early satiety. These are some of the x-ray pictures. You can see how dilated the stomach can get, okay? Because there's a risk of aspiration after that. And when you do the endoscopy, you see a pinhole opening almost at the pyloric channel. So you put an NG, decompress the stomach first, and then you start putting stents. And this is one of the stent placements. You can see this during a wall flex stent across the pylorus. There is also, now we do US guided. Okay, so this is the stent. We basically check it with the post this fluoro exam. And this is what it looks like. So before we get to the surgery, there's also now US endoscopic ultrasound guided gastroenterostomy. It's very similar to the surgical techniques. But what we do is, instead of, obviously here they're cutting. We go through the stomach into a loop of distal duodenum or jejunum and put an axial stent. So that's the US guided gastroenterostomy. And we secure it. So this is the Bill Roth II gastrojejunostomy, where you basically have an obstruction right here. You bypass it, so you do a section here. And you bring this loop of the proximal jejunum. And then you suture it with the stomach. So this is a gastrojejunostomy. So this is the, basically we call it the biliopancreatic limb. And this is the different limb going all the way down to the distal part of the small bowel. Finally, we have a condition called gastroparesis, delayed emptying of the stomach without any mechanical obstruction. And this is mostly functional, the motility disorder of the stomach, we call it. It can be caused by diabetes, it can be post-infectious, post-surgery. But most of the time, we don't know, idiopathic. Nausea, vomiting, early satiety, again the same. But one of the classic ones here, yeah, you get this feeling of bloating and weight loss, obviously, because you're not being able to eat. So you do this gastric emptying study, usually a four-hour study, rather than two hours. Here, they're showing two hours how, it's a nuclear medicine study where you ingest a test meal, and then you see the movement of that solid meal with radio tracer over time. So this is what you see, 0, 30, 90, and 120, and they calculate and tell you that this patient has most of the radio tracer containing meal sitting in the stomach after two hours, so four hours is ideal. The treatment is small, frequent meals, pro-kinetics, anti-emetics. Most of the time, the only pro-kinetic we have now available, which works is the medical bromide, but it only works for a few days. So we are in need, this is one area where we need different agents. There is a new pro-kinetic also now available, pro-calopride, which we can use, and also a gastric pacemaker is being tried for this type of conditions. Finally, quickly, I'll go through some of these bulges or mass in the GI tract, sub-epithelial masses, we call it, meaning they are below the lining. So most of the time, they are intramural, and sometimes they are also outside the GI tract or extramural. Most of them are benign, as you can see, they're different ones. You don't know whether they're smooth muscle tumor, we just call it sub-epithelial mass. And then we do endoscopic ultrasound with FNA, which Dr. Kumar mentioned, and that's the way we kind of diagnose them histopathologically. Some sub-epithelial lesions you can diagnose just by the look, like when you have, this is called pancreatic rest, where you have an umbilication. And sometimes you see a little more yellowish tinge to these sub-epithelial bumps, then we think it's more of a lipoma. But this is what basically leads us to the diagnosis. As you can see, I went through this. So essentially, using this, this is a transducer you see here. So this is a transducer, and then you can start seeing the five layers. And then there are different pathologies based on which layer these sub-epithelial lesions are arising from, and we do an FNA and diagnose them. Any questions? I know I ran one minute and 50 seconds. It's a lot to digest, but anything, any burning questions in the pathological conditions of esophagus and stomach? Yes, sir. Mm-hm. You surgery, I mean, they're tired of taking the. Correct. So how, will it help them 100%? I mean, what's the, so, you know, I mean, what's the percentage? Is it better to, to, to keep taking Pralosec, or is it, try the surgery? So, good question. So this is so we see this now quite a bit. People on medicines like Pralosec, these are proton pump inhibitors for years, right, so we look at the age, how long you have been taking. And most importantly, we look for whether they are responding to Pralosec, meaning they have been pretty much symptom free on Pralosec, okay? And some people will come and say, doc, I've been taking this for five, ten, you know, years. So we do our necessary testing, the usual pH and impedance, just want to make sure. And also manometry to make sure we are not missing out on any other pathophysiology conditions. But after that, we do recommend now endoscopic therapies for anti, for reflux. And the reason is that you don't want them to keep taking it for the next 20, 30 years with obvious adverse effects we know of. Obviously, if the person comes who's 90 year old, you know, then we think differently, but it's mostly for people we know that they are going to take it for longer. Yes, we definitely now consider these alternative strategies. And these are pretty, pretty good, and there's nothing 100% in medicine, so 78% is our success rate. They've been off PPI, they may use very rarely or occasionally on demand. But otherwise, 78 to 80%, they've been pretty okay. And the people who are also going back on PPIs after these kind of anti-reflux surgeries, most of them will take it very infrequently. Maybe once or twice a week at the most, but that's about it, not on a routine, regular basis. Yes? I just pushed in the bottom, yeah. You talked a little bit about H. pylori. If that's left untreated, can that lead to gastric cancer? Correct. So there are two different types of, you know, infection-induced inflammation that H. pylori cause. One, it's a very classic, we call it gastritis and ulcer. The other side, there is too much, so it causes different type of gastritis called atrophic gastritis. And that's the one which is a precursor, eventually, when they undergo changes. Remember the changes I talked about in Barrett, so similar here. We have intestinal metaplasia, and then they develop into cancer. So yes, but we don't know who will develop what. So that's why WHO classified H. pylori as classic carcinogen. It needs to be eradicated, period.

gastrointestinal tract

GERD

treatment options

esophagitis

ulcers

gastric outlet obstruction

Helicobacter pylori