Thank you very much, Sarah, for that kind introduction. Day two of a fantastic course, which we have seen already, and it's my privilege to talk about one of my favorite topics, which is gastroesophageal reflux disease, Barrett's esophagus, and endoscopic eradication therapy for Barrett. So these are my disclosures. The objectives for my talk are presented here on the slide. I'll first go over in the first section, really, the pathophysiology of GERD, how we establish diagnosis, and then kind of lead into the more complex GERD complications. And that brings us to Barrett's, which is one of the complications of reflux disease. And then identify which patients with Barrett's are good candidates for endoscopic therapy. I'll review some of the limitations of the current regimens, go over a little bit of the literature, and then end up with practice polls. So that's the overview. So it's really one talk, but has two components, first one focused on reflux, and the second one more focused on Barrett's esophagus. So as we all know, by now, especially with the last lecture in place, reflux is a common problem, and it is fairly prevalent with about 10 to 20 percent of the population having weakly symptoms, and the percentage of that has more significant and more frequent symptoms. The classic symptoms are heartburn, and there's the feeling of a water brash, or some people will feel some atypical chest pain as well. But a percentage of patients will have dysphagia as well, which we'll talk about down the road in terms of complications. The prevalence is equally there in males and females, and there tends to be a higher incidence of esophagitis in older people and smokers. We will reflect on some of the atypical symptoms of GERD as the discussion goes along. A brief moment to review the pathophysiology of GERD. These have been well-defined, the elements that contribute to the development of reflux in one individual compared to another who doesn't have it. So the primary issue in GERD is the impairment of the overall function of the LES, and this is impacted upon by other elements, such as increased intra-abdominal pressure, such as when you are lifting heavy weights, for example, the development of a hiatal hernia, which is basically the stomach moving into the thoracic cavity to some extent. There is also in some patients a defective esophageal clearance, so that fluid that comes up doesn't move back and so forth. There could be other areas of esophageal dysmortility, which would make reflux worse, such as in patients with scleroderma, for example. And then finally, one of the areas that is not looked at very commonly in routine clinical practice is the concept of delayed gastric emptying. A percentage of these patients will have an abnormal emptying of the stomach so that more content sits in the stomach and is at risk for refluxing back into the esophagus, as shown in the graphic here. So a variety of reasons why reflux develops in a patient compared to another. As I mentioned, the symptomatology of GERD can be fairly classic in terms of heartburn and patients feeling that acid or food content is refluxing back into the chest cavity, especially in and around the lower chest and the epigastrium. But a number of patients will have atypical symptoms, and those are listed here. Some of these symptoms are more commonly seen in the GI clinic, such as sore throat and voice hoarseness and cough. Others are seen in other specialty clinics, such as those patients who have asthma that is not presenting or behaving typically to asthma therapy. And aspiration pneumonia, of course, is a kind of a late complication related directly to aspiration of content. A small percentage of patients will have a globus sensation. Sometimes these patients can be very difficult to reassure that there is not a tumor or a real mass that is leading to that lump-like sensation. But if it happens to be the case that they are not already on PPI therapy, this globus population would be a good therapeutic trial for you to try PPI therapy and lifestyle modification for GERD and see if it works, then it would have been an atypical symptom from reflux. There's a fair amount of data on reflux disease management and the guidelines out there. Some of those are listed here. This is the ACG, clinical practice guideline, from very recently. And the AG also has what they call clinical practice updates. Now, CPUs or clinical practice updates are actually very good documents because they kind of fall in between two major guidelines and reflect enhancements in knowledge that are more recent, more current, and will make it to the guidelines in the next iteration. So look out for these CPUs that are coming out more frequently around many disease states. And there's one that exists for GERD. The diagnosis of GERD, it looks busy, but I'll try to walk through this algorithm in a lucid fashion. So you have a patient with heartburn coming in with or without alarm symptoms. And these symptoms do occur with some degree of frequency. That's why they are being seen in a referral clinic, such as a GI clinic. So typically, you'll see them, and if you're convinced that the symptoms are related to reflux, you'll go with an eight-week trial of PPI once a day. If there is complete relief of symptoms, you will discontinue the PPI. And that is the current kind of recommendation. Obviously, if the symptoms recur, in practice, I can tell you most patients will be placed back on PPI, but the algorithm suggests that you will then proceed to EGD and see what's going on. Now, on the other arm, if you have started with an eight-week trial and you have incomplete relief or no relief, then you're going to go to an EGD, which, of course, we would do. And this would be typically attempted to be done without PPI therapy on board. And from there, you have two arms. Either you will have a normal EGD or minimal esophagitis. At that point, you are looking for reflux monitoring off of therapy. And if that's normal, you will consider other causes for the symptoms. On the other hand, if the endoscopy reveals that there is more significant esophagitis or that there is a complication known as Barrett's, which we will define later on in the talk, then you know that this is reflux disease, one way or the other, and now you got to just figure out how you're going to manage this particular condition. So that's kind of the overall algorithm. It starts with the PPI trial, and you get a one-on-one relief. You're all set. If you don't get relief, then you go one of these routes, and one of these routes will confirm good. If you have severe esophagitis, you don't have esophagitis, so relatively normal EGD, and you got to look at other things, and we'll talk about those other things in a few minutes. Now one thing that's important for us when we see patients in clinic, and typically the GERD consult is an outpatient consult, is to emphasize to the patient that we actually can give you any amount of medication, but unless and until you're not modifying your lifestyle, your diet, and several of the aspects listed here on this slide, you're not going to get much traction with this disease state. So this is a very important counseling point, and I personally find one of the more difficult ones for patients to follow through, at least in the early relationship of their management. So there are trigger foods. Everybody's foods may be different, but these are generally recognized to be very strong trigger foods for reflux. At night, nocturnal reflux is a special entity that we really can't get into details, but in general, suffice it to say that raising the head of the bed, however you do it, whether you have an electronic mattress or you place a couple of cinder blocks under the headboard, the concept is that this does help. Smoking is a very important cause of persistent reflux, and it directly relates to acid generation and inability to control healing in cases with the reverse of suffagitis. And of course, it makes sense, especially for those patients who have any degree of gastric dysmotility, which I referred to earlier, that they should not eat within three hours of laying down, and in general, it's not good practice to have a large dinner and then go to bed. So lifestyle modification is very important, but the other important thing is also the question comes up is, when should we perform upper endoscopy for GERD? This is an early teaching for all our trainees who are in fellowship, and this is also an important point for all providers who are seeing these patients on a regular basis. So one of the concepts we talk about is the importance of recognizing alarm symptoms, and of course, alarm symptoms can come in various shapes and sizes, which are listed here in this red box. So melanoma, which is bleeding, dysphagia, non-cardiac chest pain, and feeling of obviously a mess, whether it's on physical exam or imaging, and then of course, unintentional weight loss, especially in older patients. So these are all alarm symptoms. You need to ask these questions. Sometimes the patient will tell you themselves, so that's important. Inadequate response to a treatment, like I mentioned in the algorithm previously, when the patient is not responding, you go to an EGD. Recurrence of symptoms after discontinuing PPI, we talked about that in the algorithm. Although this is the case as per the current guidelines, I'll tell you in practice, a lot of the patients will want to go back on the PPI and do like a repeat trial, which is okay as well, as long as there are no alarm symptoms. There are multiple risk factors for Barrett's esophagus in some patients, and for example, in a family history of esophageal cancer in Barrett's and one or more individuals. And there are also certain syndromic conditions where foregut malignancies are at elevated risk, so these are special populations where an operandoscopy threshold might be lower than in the average person. Now an important early complication of GERD is esophagitis, and it is listed here. This is the so-called LA classification, and it goes with grade A, B, C, and D, A being the most mild form and D being the most severe form of esophageal inflammation, basically corrosion of the mucosa from acid. And in grade A, the erosions are focal, they don't meet each other, they're less than 5 millimeters. Grade B, they're about larger than 5 millimeters, but they're not meeting each other as well. In grade C, the erosions are now confluent, they meet each other, but they don't cover more than three-fourths of the esophageal circumference. In grade D, the erosions are persistent and they are confluent and nearly cover the entire circumference of the esophagus. So these are common entities, and these need to be recognized on endoscopy by the operator. Now we go to the testing component. How do you test for GERD? There are two basic mechanisms if we want to prove acid reflux or non-acid reflux for that matter as well. One of the mechanisms is by placing this probe, so to speak, that basically attaches onto the endoscope and has a suction anchoring mechanism built in. So you go into the metesophagus or a certain level above the GE junction and you suction down the esophagus. There's a suction mechanism attached to this thing here, which is a Bravo pH probe. And miraculously, it sticks to the esophageal wall just long enough so we can do our test. And this is typically performed off of PPI for the diagnosis of reflux, and the patient can go about their day. There's nothing hanging out of their face or through their nose. Now there's another test known as the pH plus the impedance study. The pH study, of course, tests for acid reflux. The impedance study tests for non-acid reflux. And this is a little bit more invasive from a patient perspective. There's a tube that goes down the nose. It may be placed with or without endoscopy, depending on the situation, and there's stuff hanging off the patient. So it's not very popular, but it is used, diagnosed GERD, and performed off of PPI. It also tells you about non-acid content coming back, which is known as the impedance study. So still being practiced, but you can imagine the patients probably prefer this more often than the impedance study for obvious reasons. Now we come to the concept of managing a persistent GERD, the so-called failed medical management. Failed medical management does still exist. In part, you know, the non-adherence and non-compliance may be a reason as well. But a lot of these patients have other things going on. They have lifestyle issues that are persistent. There are anatomical constraints that are not able to be overcome by medical therapy or a variety of other reasons. So these patients are good candidates to be deferred to our surgical, so-called esophageal and foregird surgery colleagues. In the big parts of the country, general surgery is doing these procedures. And these are listed here. The classic would be innocent fundoplication with some form of modification. There's also the LINX procedure, which is the magnetic sphincter augmentation procedure, and a surgical colleague doing a CTIF procedure as well. On the endoscopic side, the new advancement has been this development of the transoral incisionless fundoplication, which is an endoscopic procedure. It does require some time to learn this. There's a fairly robust instrument that goes down the throat, but it's all done endoscopically, and there's no surgery involved unless you do a CTIF repair along with the surgeon in the OR. There used to be a device known as STRETA. It's still around, which is basically ablating the sphincter and creating fibrosis. I do not know how popular it is right now, but we can have a conversation around that. But mostly, the endoscopic interventions are relying around the TIF procedure at this time. And the whole concept of these procedures is to strengthen the LES and re-establish the barrier for reflux. Complications of GERD, which will lead us directly into the next section, which is Barrett's, are listed here. So, peptic strictures are fibrotic narrowings of the esophagus, typically at the lower end of the esophagus, created by acid. Another form of obstruction is the so-called Schatzky's ring, which is relatively easy to disrupt with an endoscopic dilation. Bleeding and iron deficiency does occur if you have significant erosive esophagitis and you have slow, ongoing bleeding. And it's a common finding in many of our inpatients who come in with anemia and melanoma or GI bleeding. And then finally, of course, last but not the least, is Barrett's esophagus with esophageal adenocarcinoma as a potential complication, and we'll talk about that in more detail soon. This slide with pictures represents, of course, very severe examples of erosive esophagitis here as well as here. You can see here these erosions are confluent, so this would be a good example of a grade D LA esophagitis. And then up here you have what we call high-definition white light endoscopy image of a patient with Barrett's esophagus. I'll just go through this real quick here. This is the so-called top of the gastric fold or the anatomical GE junction. You can see the gastric fold here, if you can see my cursor. And then we have mapped out, just artificially here, the extent of the columnar line mucosa, which constitutes Barrett's esophagus. And it's much easier seen in this picture where we have a button on the endoscope which starts a blue light of a certain wavelength known as narrowband imaging. So it just provides a sharp contrast between the normal squamous mucosa and the Barrett's mucosa shown here. So this is all intestinal metaplasia of the specialized type and is the definition of, at least the European definition of Barrett's endoscopic imaging. And then finally here is Barrett's gone really bad. This is endoscopic appearance of endosophageal cancer. And typically the adenocarcinoma that's associated with Barrett's starts at the distal esophagus level as opposed to squamous cell carcinoma, which can start anywhere and typically in the metasophagus. So practice pills for GERD are listed here. Typically a patient comes in with classic symptoms. You go with a PPI trial. Patients can present with typical or atypical symptoms. And then the evaluations we have discussed will include endoscopy as well as pH and impedance testing. Lifestyle modification is extremely important for all patients to go through that and medical therapy alone may not be enough. Endoscopy should be performed for patients with alarm symptoms and wherever it belongs in the algorithm that we reviewed. And one should have a low threshold, especially in older patients who are developing these symptoms that are vague and don't quite fit the classic pattern. Non-responders should be evaluated for gastric dysmotility. And then both endoscopic and surgical options exist now for patients with persistent symptoms, refractory GERD, and those who have failed medical therapy for one reason or another. Now moving to the next section here is Barrett's esophagus, which is a precancerous condition, a direct complication of chronic longstanding esophageal reflux. And this is defined a little interestingly. So in the USA, we do need that column of columnar-lined epithelium at least one centimeter with biopsies showing specialized intestinal metaplasia. In Europe, the endoscopic appearance is good enough, and that's one of the differences between the two continents. Short segment Barrett's is defined as Barrett's that's less than three centimeters, and anything that's three centimeters or longer is long segment. And it has implications for surveillance, which we'll talk about. Barrett's esophagus is a precancerous condition with the annual risk of progression listed here at 0.3, which is pretty stable throughout the literature there. Risk factors are listed here. Chronic reflux is one of the main risk factors, but Caucasian, race, central obesity, male gender, smoking, they're all risk factors there, and certainly an older patient. The concept of family history, genetics, familial basis is still being explored. We don't quite yet have a gene for esophageal cancer, but this is where the science is moving in the current time, and maybe in 5 to 10 years we'll have a little better understanding of the genetic predisposition, although there are certain tests available commercially now that aim to predict your probability of developing cancer in a five-year time period based on molecular markers modifications. Alcohol consumption does not increase the risk of Barrett's, and that's important to note, but smoking does. Now the natural history of Barrett's is listed here. When we see these patients first in the clinic, we do talk to them that, you know, you had a normal esophagus to start with, and then at some point you have developed what we call nondisplastic Barrett's, and this is the sequence of events going down here, this path, that could develop depending on your natural history and your genetic profile and your molecular mechanisms that create cancer from Barrett's. Not every patient will develop this, but this is the natural history of this disease in its worst case. So here are the numbers listed for risk of cancer progression based on the literature. So if you'd only have just Barrett's, your risk is relatively low on a year-by-year basis for developing cancer, but once you move through the layers of dysplasia here, low grade is 0.7, but high grade is 10 times that at 7% per year, but obviously once you have established carcinoma, that patient will require more aggressive and definitive management. So that's kind of an overview of where things stand in terms of the risk progression for Barrett's esophagus. Now I mentioned some of the risks for Barrett's, but here are the risks for developing neoplasia, advancing age, obviously increasing length of BE has been looked at as well, smoking and the lack of PPIUs. A recent study again confirmed that PPIUs has some degree of chemoprevention elements built into it such that patients with Barrett's are strongly recommended to stay on it. Now who should be treated for Barrett's? It's clear that patients who have high grade dysplasia, early carcinoma are good candidates for endoscopic therapy. Those who have more invasive cancer are great candidates for surgery, especially if they are early in the disease and are surgically fit. The only question is here on the left side where you have patients for indefinite for dysplasia and non-dysplastic Barrett's, particularly some of those patients who have low grade dysplasia who are at low risk, we may be able to survey them. So I'll get a little deeper into this in the next few slides. So management of low grade dysplasia is something that will come up in all of your practices if you're seeing these patients. And these are patients who have a relatively low risk of progression to cancer. We reviewed that just now, it's 0.7 per year at worst. There's a low rate of progression, there's a significant amount of inter-observer variation amongst pathologists as to what constitutes low grade dysplasia. So for those reasons, automatic ablation therapy is not recommended for this population. So what are the considerations of patients who you might want to treat? So if a patient is confirmed by an expert pathologist to have low grade dysplasia, that's important. If the patient has history of Barrett's, multiple family members, esophageal cancer in the family, that might be the way to go if the patient has a lot of comorbidities now, which are expected to get worse down the road, may not be a great candidate for long-term surveillance, that might be a good discussion to have patients with persistent low grade dysplasia that's multifocal in a long segment of Barrett's and have had a history of other GI cancers, it might be good candidates for that, especially if they are motivated. And then ultimately, it's a shared decision making. It's a very nuanced topic. We spend a lot of time on this in the clinic. And in fact, because it is so controversial, you can go in one of each way with ablation versus surveillance. There is a NIH funded trial on this question that we are also now part of, known as the SURVENT trial, S-U-R-V-E-N-T, which is looking at this question as a primary endpoint. Should we do surveillance or should we do ablation? So that's the importance of low grade dysplasia. How do you determine appropriate therapy once you've decided to treat? So it's an interesting thing because not all patients automatically become candidates. So the first step you need to know is confirm what you're treating. This is an interesting study that came out a few years ago where they looked at 293 patients with low grade dysplasia, and they were submitted as all of them having low grade dysplasia. But clearly, when they looked at these patients in detail, only about a percentage, 73% of these were downstaged to a non-dysplastic barrett's by an expert pathologist. So 73% of established low grade patients were downstaged. So that's important that you be very careful that low grade dysplasia is confirmed by an expert pathologist, and only once it's confirmed should you offer treatment. And even then, surveillance is still an option. The second step is when you do perform an endoscopy and you're committed to endoscopic ablation, one of the guiding mantras in endoscopic therapy is to identify and look for what we call nodular mucosa or a raised focal lesion in the barrett's. So this is like a polyp in the barrett's, and if you see one, they're more likely to harbor high grade dysplasia and cancer, and the recommendation there is to resect this lesion. So endoscopic resection techniques have been established. And if the pathology shows that the lesion is limited to the mucosa, you can continue with endoscopic therapy. If the pathology shows that the lesion now extends into the submucosa, then you need to take this patient to the tumor board and then decide whether endoscopic therapy is okay or whether we need to go for esophagectomy. So endoscopic eradication therapy options are listed here, endoscopic resection techniques, endoscopic submucosal dissection, and then of course, for flat barretts, you have radiofrequency ablation, cryoablation, or a variety of other thermal techniques that exist. Many patients may require multimodal therapy, and we had a paper on that a few years ago, that whatever it takes to bring the patient to justice is good. Patients must commit to a six to eight-week sequential treatment session commitment, and they need to know this up front in the clinic visit and continue with their PPI so that we can have acid control that promotes healing in between treatment sessions. So here's an example to break the monotony of a video of a raised focal lesion, which has been marked here with cautery, and this is the band EMR apparatus that loads onto the scope. We suction this nodule into this barrel, and we fire a band, just like a variceal band, and then we snare, resect this lesion, either above or below the band, and the snare passes right through the channel of this endoscope. So you can watch how the snare will take what this pseudopolyp that we created and resect it using standard cautery. It's pretty safe and does not typically lead to perforation. You can see the intact muscle wall of the esophagus right there, and making sure that there's no bleeding and perforation in this setting. And then this test then goes to the pathologist and they determine whether endoscopic therapy is good enough, if it's limited to the mucosa, or if the patient needs to go to the tumor board. The next technique here is GAP EMR. It's a little more involved because the lesions typically that we use this for are larger. There is a submucosal injection, which is a requirement for this. It's a dedicated plastic cap with a snare that comes in a kit, and as you can see here, the cap allows us to suction a larger area of the esophageal tumor, and the snare is ready at the base to snare it and choke it and then cut it. This particular intervention does carry a higher risk for complications, but it should only be done with exactly the same technique that I described here, and after an endoscopic ultrasound, it's typically suggested that the muscle layer is free. So you can see here, it takes a little bit more effort to get this off, and it's a much larger specimen, and we inspect the specimen, inspect the base, no perforation, and we continue with the resection. I still have a little more tumor to remove down there, but in the interest of time, I'll move forward. ESD, or endoscopic submucosal dissection, has emerged even in the Western world as an option for Barrett's and Barrett's-related cancer. This meta-analysis of 11 studies told us basically that there's a higher rate of complete removal, so-called R0 resection with this technique, but the average procedure time is up to two hours. Those cases that I just showed you were performed in 10, 15, 20 minutes. ESD takes much longer. The other thing that we learned is that obviously it takes a longer time for the endoscopist to learn this technique, but that the perforation and bleeding rates are also higher than those related with EMR. But it's an option now, and it is, if performed well for larger lesions, it may be a better option than EMR because of the oncologic specimen that you get out is more complete. Now, endoscopic ablation is two primary modalities, radiofrequency ablation and cryotherapy. The concept of ablation is to obliterate the dysplastic Barrett's and create this neo-squamous epithelium. We were born with squamous epithelium, and our aim is to return the esophagus back to that with these techniques. A variety of techniques are available, which I'll show you next. Contraindications to Barrett's ablation are listed here, which makes sense. And typically, most patients will be eligible for this unless they have one of these issues. Let's see here next, if the slide moves. The ideal ablation technique basically takes care of the entire Barrett's segment. It's easy to administer, well-tolerated by the patient, is durable, and has an excellent safety profile, and we're lucky that right now the two commercially available techniques for this fulfill all these criteria with a very low stricture rate. This is RFA and the pivotal trials that were done. It is a bipolar energy delivery system developed by a company in the past known as Barrett's Medical, but now owned by Medtronic. The long-term outcomes for removing all Barrett's and definitely removing all dysplasia are pretty good, and these set the bar for what needs to be achieved with any ablation technology going forward. So here's a video showing a Barrett's radiofrequency ablation pedal that is also loaded onto the endoscope. You can see here, this is the top of the gastric fold, and that's our starting point. And then when we hit the pedal, we get an electrocoagulation type of phenomenon, and this is dead mucosa now, and when it regrows, it'll regrow as squamous mucosa. Moving on to cryotherapy. Cryotherapy is basically freezing the tissue and changing it from Barrett's to squamous based on freezing techniques. Two commercially available techniques are available now, liquid nitrogen cryotherapy and nitrous oxide based cryotherapy, and these are very effective, and there is data to support these as well. This is a liquid nitrogen platform, you know, it does require some capital investment. It is very cold at minus 196 degrees centigrade. That's four times colder than the North Pole, and it is very interesting because it destroys cells but doesn't damage the matrix or the collagen. That's why the stricture rates are much lower and the pain thresholds are also not felt that much. So it's very well tolerated and quite effective in both Barrett's as well as in cancer. This is a video showing cryotherapy here. You can see the sprays coming out and coating, sort of spraying the entire segment at risk. There are many indications for this which we can talk about in the discussion and get some clarity on that. Complications of course have to be discussed. The most important intra-procedural complications are sedation related, bleeding, and perforation. Thankfully, perforation occurs extremely rarely in these procedures. Bleeding with EMR can occur but again is surprisingly low compared to colonic EMR bleeding. And nowadays with sophisticated anesthesia protocols, these issues are relatively small. Post-procedure, the patients will have chest pain, typically a little bit more with radiofrequency ablation than with cryotherapy. And these other complications are relatively rare. Challenging scenarios in Barrett's endotherapy is persistent esophagitis, which I mentioned earlier. There is acid control in these patients and that can be a problem in some of these patients. Difficult anatomy, especially in older patients, getting things and devices past strictures and difficult UES anatomy is very difficult. I do find that patient non-adherence can be a problem. These patients need to show up and sometimes they get tired of a sequential ablation protocol and that can be a problem as well. These are the key considerations for older patients. I won't get too much into it, but a lot of these older patients will present with a dysplastic Barrett situation. We do invoke shared decision-making a lot in these patients and sometimes, particularly for low-grade dysplasia, I will continue to monitor them rather than offer a cumbersome treatment protocol. There are very well-defined indications for surgical therapy. This is an important slide. Every time you have invasive carcinoma, you need to make sure we go to the tumor board. Some of these features, poorly differentiated tumors, lymphovascular inflation are red flags and they need to be managed immediately with the appropriate protocols, typically surgery and chemotherapy, depending on the stage of the disease. Nodular long-segment Barretts that is refractory to endotherapy need to have a shared decision-making and send them to surgery because you want to treat the disease state and not just hang around and find metastatic cancer down the road. So there are significant number of still indications for surgery and we recognize them early and move patients along the treatment pathway in line with patient-centric care. There are some newer technologies for Barretts evaluation. This is the CDX brush biopsy. There are swallowable capsules and sponges that are detecting DNA and methylation markers. There is a predictive analytics test which is taking a biopsy and sending it off for molecular analysis which tells you in five years what's going to be your risk. AI is just entering the field and there are some early studies going on to find cancer in Barretts and so forth. More to come on that. And then of course there are also magnetic available capsules. So a lot of this is early. But the goal for these sponges and capsules is potentially, maybe, that in the future a primary care provider, a physician or an APP, could have a patient swallow these and they could be sent off for DNA analysis and the patients could be told whether they have Barretts and if they have Barretts, what's their risk of cancer. So interesting stuff that's being developed now. So I'll refer to the guideline. I think one of the things that's important to note in the Barretts management is multidisciplinary team approaches. It's important to know that these procedures be done by an experienced endoscopist. You should have experienced thoracic surgery access. The tumor board is a big part of this discussion and really emphasize the importance of well-trained expert pathologists. And if they're not available on site, these slides need to be sent outside for the second opinion that I mentioned previously. So it's a team sport as well. And that's why there are some centers of excellence for this disease state that have laid down the parameters of how this should be done. So what's the role of the APPs in Barretts practice? That's listed here. These slides are available to you as enduring material. They're all involved at least in our practice in the initial evaluation of these patients in the PERI procedure management support. Also involved and facilitate the GI tumor board discussions and any recommendations that come out from the tumor board. Frequently we'll have medication requirements around ablation therapy and they definitely help us with managing that as well. So one of the things that I've always talked about and we are doing as well is participation of APPs in Barretts related research and of course, engagements with industry events whenever they're educational and aimed at enhancing the field. Municipals in Barretts are basically saying that newer devices are available on the horizon but established therapy is multimodal, very effective for dysplasia management and early cancer management. Patients who achieve complete remission and neosquamous mucosa will be surveilled indefinitely as of now. Asset control is an important longstanding part of this whole paradigm and is a big partner in getting these patients to normalcy. Any patient who has invasive disease should go to the tumor board and I do believe as it is in our practice and many others that the APPs have a pivotal role in Barretts practice both from the clinical spectrum all the way to research and academic productivity. Thank you very much. Actually I do have a couple of polling questions which we'll do really quickly. Endoscopic eradication therapy is all of these procedures except, this is an except question, radiofrequency ablation, fine needle aspiration, endoscopic mucosal resection and cryoablation. So which of these is not one of the endoscopic eradication therapies? Wow, look at that. FNA is not. FNA is an EUS procedure which we reviewed yesterday and the others are. The next question here is a patient is referred with Barretts two centimeter segment pathology shows intestinal metaplasia without dysplasia, no dysplasia, just Barretts. Which of the following is the best current practice recommendation that is supported by the guidelines? Single best answer. Offer endoscopic ablation, offer surveillance, offer referring to the thoracic surgery or all of the above. Offer surveillance endoscopy. This is great. I like that. This is a difficult choice to make when patients are referred thinking that they'll get treated but it is the right choice and at this time supported by the guidelines. Thank you very much. Great, great, great job everybody. Thank you.

gastroesophageal reflux disease

GERD

Barrett's esophagus

endoscopic eradication therapy

diagnosis methods

complications

lifestyle modifications

ablation therapy