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Benign Gastric disease, Dr Athula Withanage

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Summary

This on-demand teaching session is relevant to medical professionals and will cover topics such as the three functions of the vagus nerve and the arterial blockage of the stomach. Professionals will learn how to precisely and accurately answer examination questions and understand the importance and effects of vegas nerve activity on various medical conditions. They will also understand the clinical grade anatomy of the vagus nerve and its followers, as well as the gastric intrinsic factor, details on gastric face and intestinal face, and the role of hormones in digestion.
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Learning objectives

Learning Objectives: 1. Understand the three functions of the vagus nerve 2. Recognize the anatomy of the vagus nerve and its branches 3. Explain the impact of vagus nerve dysfunction on gastric surgery 4. Identify the approaches for dealing with artery blockage in the stomach 5. Analyze the role of various hormones and receptors in the production and release of acid in the stomach
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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Uh brought it right. Um uh You met me uh in Cardiff uh uh few weeks ago uh with I did the intestinal obstruction. Now I'm coming from, I'm on holiday in Senior Lanka. I'm coming from uh the beautiful hospital here. This is known as the Neville Fernando Teaching Hospital and uh also known as uh Colombo East, um Colombo East uh teaching state teaching Hospital. Um and whenever you want to come here for electives or anything, you are quite welcome. Right. Let's uh good afternoon, good morning, good evening, good night. Wherever you are in the world. Ok. We are going to talk about mainly gastric surgery although I uh I did say that uh uh it's a benign condition. So we'll be mentioning the benign condition as we go. So sorry sir to interrupt. Do you mind making it full screen, full screen? Ok, we'll do right. Ok. Um Right. So we can't talk about any gastric disease uh or even surgery or, or even medical treatment without talking about the, the main nerve, which is the vagus nerve and you know, the general functions, the digestion, the heart rate, maintenance, respiratory rate, vasomotor activity, especially in the gut reflex actions such as coughing, sneezing, et cetera. Uh But uh we are more interested in how it uh affects uh our surgical conditions, right? And so, uh normally I sit down and ask uh my colleague, doctors, uh uh uh what are the main three functions of the nerve? And that's an examination question. And if you cannot, uh the thing is that you know everything, but you can't come out with the correct answer. So there are three functions are the secretory activity. We'll discuss that in detail, the motility. Probably you remember from your physiology that uh gastric coal meal. And the uh uh the other thing is uh receptive relaxation and adapt to relaxations, giving the child for the accommodation and all our surgical activity uh is to deal with the three functions of the uh of the uh vagus nerve. And uh so uh you should be able to answer that, you know, what is the function of the for the vagus, the 10th cranial nerve. So, vagus nerve, it's uh around the esophagus. There is an anterior and, and, and uh left and uh uh left vagus and the right vagus, the left one rotates around and become the anterior vagus and the uh the posterior, the, the, the, the right one which is a bit further away, uh uh becomes the uh becomes the uh posterior one here. Uh So it runs parallel uh the vagus nerve, run pa is a parasympathetic nerve supply is run parallel to the lesser curve. And so the left run anteriorly and give uh give the final hepatic branch, the right run posteriorly and give the celiac plexus branch. And the uh the uh the there is tonic fa contraction and eventually making the enteral middle, the peristalsis increase in the distal part of the stomach so that you need to understand. So on the body uh uh of the stomach, the vagus nerve is called the nerve of lethargy. Um Only, only it's important to the surgeon. And the um the uh uh there is the uh gastric intrinsic factor we'll talk about later is there, it's not nothing to do with the nerve itself and it ends in, in, in a branching like a cross foot. We, we call it a cross foot. Um The uh on both letter nerve, the anterior and posterior lethargy nerves. And uh so this is the main. So because when we are talking about the truncal vagotomy, the the selective vagotomy, highly selective vagotomy, we need to know these branches and the endings. And then of course, when you, when you, we talked about this la accommodation, uh receptive relaxation, you can uh because your stomach is, is uh not more than your fist, uh maybe two fist, but you can eat lot more than that. Uh So, uh so that is due to the, the receptive and adaptive relaxation. And if you take away that function. What happens, you know, you do a vagotomy suddenly it becomes a pouch which has no function and uh causing problems, stasis. So, stasis when there is stasis, you have to make a ate procedure. So that is the that is the importance of that. So you can do for the stomach, either pyloroplasty or gastroenterostomy, right. So uh uh the the so it is divided functionally into proximal region and the and the distal distal region, the distal region is mainly peristalsis is the work work area. It is the factory area. It is where, where the acid is secreted as well and also it retains uh and then peristalsis work at the same time and and treat to rate and empty eventually and also prevent bile coming in because the bile reflux also may cause gastritis. So that function of vagus nerve is also important, right? So secondary activity as uh Yvonne Petrovich Palos describe it uh the phallic face, the gastric face and the intestinal face, external phase, not much to do with the Vegas. But we still we always talk about when we talk about Vegas, we talked about all the three. So the catholic phase, the respond to sight, you know, you probably remember the sham feeding techniques um done by uh paler and the uh making a hole in the, in the in the pharynx, the esophagus, the stomach, the saliva is secreted. So that is the site of smell, taste of food uh that is mediated definitely through vagal activity. So directly, uh it also directly stimulate the parietal cells and release gastrin. And of course, you know what causes gastrin cause uh the uh uh the release of a acid. So gastric face, the food actually comes into the stomach and it distends and increase the pressure slightly and the contact with the food is important. So it releases gastrin uh from the antrum. Uh So the intestinal phase is started by introduction of the acidic kind into the duodenum into the sucres enteric. That is a word we use from Gannon, the uh uh the physiology book. So you should remember what is Sarcos enteric. It is the alkaline fluid uh liquidy uh uh stuff in the duodenum. And the also uh not only just the time entering the duodenum there, already some of the peptides being absorbed into the portal circulation also try and stop the acid secretion. And there are other uh other hormones involved. So it's mainly a kind of hormonal rather than uh the vagus activity. Uh So, because all this happens even in a uh they've done experiments even in the, when the Vegas is denervated. So, in this phase, although we described on the Vegas, it is not uh uh that important there, that's what they say. OK. Right. So, so the um a the arterial blockage of stomach is so important to the surgeon. Why? Because number one is the patient is bleeding and is mainly bleeding from the first inch of the duodenum from the gastroduodenal artery. That will be asked from you what artery bleeds. Uh When you have a duodenal observation, normally, it's the first uh inch of the duodenum, uh the bulb of the duodenum. Uh and the uh uh gastroduodenal artery is horrendous bleeding. You can see the spur uh through the endoscope. And also it's not just the gastroduodenal artery, although it's not indicated in this picture, there is another artery going uh towards the pancreas called trans pancreatic artery. So it's a trifurcation almost uh because there will be back bleeding from the pancreatic artery as well, transverse pancreatic artery. And using that, we call it three point ligation. So we ligate the proximal part of the gastroduodenal artery, the the uh distal part. And also you must uh ligate the uh the uh transverse pancreatic artery. So, uh although it is not indicated in this picture, and then of course, these arteries and I'm not going to go through all the branches of the celiac plexus, uh the left gastric artery, there's splenic artery and the right uh the hepatic artery which gives eventually the right gastric artery which arcades with the uh left gas artery. Then it it, it is the gastroepiploic arteries coming from the left gastric uh left gastroepiploic and then from the gastroduodenal artery divides into superior uh pancreatic coo artery and the uh uh the gastric api like right artery, see these arteries. So when we are doing a gastrectomy, that's why it's so important. This arcade, we have to lift. This tonsil is a resection. You have to lift this up into the, into the, into the thorax and you have to have a blood supply because all these will be resected at the top. And this blood supply depends. It is based the the the the stomach conduit is based on the blood supply uh of the uh uh o of the uh right gastric and gastroepiploic arteries. So you should not because even if you touch these arteries, it get damaged. So handling these arteries are very important because it has to rise up. Otherwise you will have end up with putting up a, a small bowel which is not very uh uh uh uh uh yeah, confidently, you can't do that. Uh But with stomach, uh it is easy to do that. So that is one thing. So I uh that, so uh the the gastroduodenal artery bleeding, we definitely will ask you in the exam and also uh uh vascular a case. I don't think many people uh will ask anything from a medical student from the doc, but the doctors, they will ask that question. Right. Um Right, you probably have seen this picture somewhere. This is the uh the uh the parietal cell and there are three receptors. Remember the muscarinic receptor, the H two receptor and the gastrin receptor. So, the fine pathway. Um it is uh is a hydrogen potassium A TPS pathway. Uh uh is the one to produce the, finally the acid dehydrogenate iron. And uh in Sri Lanka, I used to call it hypos. Sorry. Uh it, it doesn't apply to you all. OK. Right. So uh histamine is relaxed. Uh is I uh I is the one which, which uh act on the histamine receptor. And that's why we block it by uh by using H two receptor antagonist, like like raNITIdine. Then of course, uh it is stimulated by uh ga uh the uh enterochromaffin cells and the uh uh and also it is directly stimulated uh uh by uh by uh uh the vagus nerve. So also the mainly the way the stimulates the muscarinic acetycholine res uh receptor and also gastrin act directly on the. But uh PP I is the uh uh we, we block the uh the uh the pro the pro uh proton pump. What, what do you call that uh pro proton pump inhibitor? Uh I is is acting at this level. Um and the uh S two receptor antagonist act right here, right? OK. So that is an important diagram uh about the uh uh uh about the uh release of acid. Uh It is the same thing I don't need to go through that mainly uh the body and the fundus uh is uh acid and Pepsin is like secreted initially. Pepsin or then is ed it converts into uh pepsin in the, in the presence of acid. And then of course, the anim and the pylorus mucus and gastrin is secreted because you have to chew up all these and break this and titer, the uh substance uh in the distal part of the stomach, right? This is the uh uh the gastric gland, normally the top end of the gastric gland, sometimes this confuses because we think they are all they are on the flat mucosa. All these glands are but gastric gland, I it is within the gastric gland. All these important cells are. So mucous glands are very important because the mucosal barrier is important for us. And also peral cell which uh uh which uh gastrin act which, which produces the, the acid and the chief ones that I used to remember it as G peptic. So chief uh cells uh normally produces pepsin or then uh converted into Pepsin. And then of course, uh in uh uh enterochromaffin cell, the other one also produces acid, right. So there is the same thing again, the parietal cells, the uh uh uh uh uh secrete the acid in the gastric crypts and the uh in the base of the down in the bottom of the uh uh gastric gland, there is pepsinogen secreting uh uh cells and the uh uh entero and then enter produces as the G cells produces gastrin on the way that we said that it will be stimulated uh So uh the uh uh in the duodenum, the D cells produce somatostatin negatively act this is the intestinal phase and also cholecystokinin, right. So, uh uh so it is uh uh a war between the uh acid pepsin and the mucosal barrier. So, because you will be asked how are the ulcers are formed, so that it is, it is it is the uh interaction of the uh acid pepsin and other injurious factors uh uh with the uh uh mucosal barrier. So it is important, important to protect that. So uh what uh what is this barrier? It continuous bicarbonate and mucus secret situation. Gastric mucosal cells also have epical membrane, tight junction. It is impermeable to back diffusion of acid into the cell. So, reconstitution of epithelial cells, they migrate over the basement membrane and replace the damaged cells. So, in order to protect the uh underlying uh mucosa, uh you usually replace those cells and also prostaglandin stimulate blood flow and uh and secretion of mucus and bicarbonate. So the perfect blood flow is very, very important. So um uh gastric mucus is a viscid layer of mucopolysaccharide, which is the one which protects the stomach and is a real barrier mucosal defense versus the injurious factor. So that is your answer for formation of ulcer because uh you can't just say H pylori and this and that you have to say what happens uh with all these injurious factors, you know how it affects it. So mucosal defense versus injurious factor including helicobacter pylori. So, buffering capacity is due to the bicarb I, many factors break down uh the great uh uh mucosal barrier, gastric mucosal barrier. And uh uh the, the ones are uh the bile bile reflux may cause problems. Alcohol, uh NSA I DS uh because of the prostaglandin production stops. Uh and trauma, trauma is mainly due to shock here and your blood supply will be uh less and uh the the uh and smoking and shock due to ischemia during hypovolemic insult. That's why we, we review uh uh various uh uh PP I SS to the patient going to the intensive care unit, right? So I just put this uh there for you too because suddenly the the examiners get clever enough. What is sarcastic? And so it is the alkaline intestine and contains it was in the physiology book, you can say no. And it contains water mucus proteins, bicarb uh hydrogen bicarb carbonate ions from the duodenum and pancreatic juices as well. OK. Right. So what are the history I'm talking to you from the endoscopy unit? Typing uh uh esophagus, we normally call it OGD esophagus, the uh ga gastric and duodenal uh looking at them with the endoscope. Um So flexible endoscopy and uh you it is always diagnostic and also therapeutic. So you need to know those two words, diagnostic and therapeutic. So therap uh so diagnostic is your diagnose an ulcer. Uh And of course you do you have a differential diagnosis because barium, swallow and meal, that's what we call the barium study. Uh, barium swallow and meal will not show you uh, something like mall waste tear because it is right. E even when we do surgery, open the stomach, we still can't see it because it's right at the esophagogastric junction and uh very difficult to see. Of course, therapeutic methods. You inject various ulcers around it. You take of course you for diagnostic reasons, you take biopsy, especially gastric ulcer. So flexible endoscopy or gastroscopy is an important investigation, right. So uh endoluminal ultrasound and is looking for the depth of invasion that is mainly for cancer treatment. So it's a radial echo endoscopy with rotating transducer, you can see all the layers. So if it is cancer, you can see whether it is T one T two T two T three or or T four, right. So, uh uh so uh that is an important investigation. And then of course, you could do normal uh contrast and and ct for the stomach. And of course, you have to do uh if it is cancer, you have to do positron emission tomography, we call it pet scan. And uh so I it is the uh uh glucose metabolism. We use 18 fluorodeoxyglucos which which converts in the pathway, but there is nothing to convert it back. So it get trapped in the cell. So it's a metabolic is known as metabolic trapping. And you are looking mainly at the lymph nodes. So, it is important to know whether the, especially for gastric, uh we are not doing that today. Gastric carcinoma. Uh you have to know if there are gone to the lymph nodes. There is really no point of uh uh doing major surgery better to do palliative bypass type operation and, and the uh and not to mutilate the patient unnecessarily, that's the one jar and the surgeons use. So, uh the metabolic trapping is important looking at the cancer. Uh and then the barium and so and mal now is outdated. We do only if we uh if we suspect there is a, a pharyngeal pouch, uh you must not introduce, as I, I think I may have said that before you must not introduce AAA endoscope. Uh because you may perforate the pouch and cause terrible problems and facial problems. So, so only the patient get uh difficulties in swallowing. So it's a almost a pharyngeal problem. Uh because uh pharyngeal pouch is in the pharynx. No, although we think it is in the esophagus, it is not in the esophagus. So uh you mu you must be very careful putting an endoscope through a pharyngeal pouch. So, right. So Helicobacter pylori, everybody talks about it. Uh because who class it as one of the carcinogens, uh main carcinogens uh affecting uh causing cancer. Uh and uh uh and it causes gastritis cancer and ulceration. So, so cancer is here. Very important. It hydrolyzes urea to produce carbon dioxide. Plus ammonia is a strong alkali and ammonia on enteral G cell does produce gastrin hypergastrinemia occurs and you know what happens after that acid hypersecretion. So, a activity we use that for breath test dye for diagnosis. And the uh uh various isotopes use 13 C and 14 C. I don't think we are going to ask you any questions from those and the flow test, we may, we may ask what is flow test. So it is a urease test. It's a Campylobacter like organisms produced. So that's why it's called flow test. Campylobacter like organism. And uh there's also now available fecal antigen test, but I don't think we are going to ask you that. And the uh helicobacter produces two types of toxins and the surgeon's jargon is, is a tale of two toxins. So, cytotoxin associated DNA product and VAC aid, which is C A and vac A vacuolated cytotoxin a product. So, uh it cause vacuolation and destruction of the cells in the epithelial layer and cause gastritis, ulceration and neoplasia. So we said gastritis cancer and ulcer. So remember those three what eli bacter causes and the tale of two toxins cag A and B A, right. So uh uh the the same thing is H pylori protease and lipase degrade gastric mucosa. So, break the barrier, disrupt apical epithelial cell surface, break the barrier cell injury and back diffusion of HCL H pylori increases acid secret in patients with, especially with du break the back break the grade barriers. It cause autoimmune damage to the gastric epithelial cell. Again, break the the grade barrier TNF alpha and ammonia released during H pylori gastritis. Uh So it is an after effect rather than it is due to breaking of the barrier. So patients with d 95% have H pylori in the enter. So, so when you do a gastroscopy, you, you take a sample biopsy and do the flow test on the spot. So that is important and you can send the same sample or another sample for histology looking for the same thing uh H pylori. OK. So gastritis, autoimmune, there, there are type A and type B. Those are the ones that you need to know autoimmune is it causes atrophy of the parietal cell mass, acid mass. So you get alo hydria and uh uh so and also it destroys the, the uh the intrinsic factor as well. You know what happens B 12 is not absorbed from the ileum. So uh uh so and it could because of ahya and, and, and, and this uh pan gastritis, you get gastric cancer. So uh type B uh so type A will autoimmune type B BAC I I put bacteria for you to remember easily. So, bacteria, diabetes due to bacteria, what bacteria, it's helicobacter associated pan gastritis again cause intestinal metaplasia. Remember I was talking about when I did colorectal cancer about uh dysplasia cancer sequence and uh and an adenoma cancer sequence, the gel stain model. And now we have got the third one metaplasia cancer sequence in the stomach. So, and the other one is erosive gastritis. Uh due to NSA ID, I don't need to go through explaining that uh inhibition of cox one receptor enzyme reducing cy to protective prostaglandin. So try to protect your prostaglandin. There are uh other medication now available. Um The junior doctors know more about it than me. Uh because I'm not a physician. So stress gastritis, reduction of mucosal blood supply. Um uh uh because of low BP, uh hence IC U patients are always given PPIs if bleeding occurs due to ulceration, a barrier agent such as Sucralfate can be used as well. So for this one, because this cos I'll I'll explain to you a bit later. Sucralfate, what is it? Cushing's ulcer is a single deep ulcer due to brain uh in injury or, or, or after neurosurgery. So that is the type of ulcer you get after neurosurgery, but you can get a ulcer called curling's ulcer due to burns. We'll be talking about burns, I think next week to you. So, so they are the ones get curling ulcer and I will never forget it because as when I was in Seo, there was a, a chap who was trying to plant a bomb in northern Ireland brought to my hospital and he was burned all over. He was thrown away by his colleagues uh with guns and I had to take it over in the middle of the night. It was a horrible experience for me, but I had to obey them. So I took the patient in. But uh uh we did everything possible. We didn't know anything about A TLS those days. So we just put out drips took blood and cross match and gave him uh Ranitidin. There was no PPIs then. Uh but the patient suddenly during the consultant go around, uh the vomited blood and died. And the consultant immediately said curling salsa. So I will never forget that. That's a horrible experience. And the other one is a menus disease. Uh uh uh uh uh it's a form of gastritis. It cause hypertrophy of the gastro gastric mucosal folds. Uh uh and the uh overexpression of TG uh uh uh TGF uh alpha and the uh all these cytokines uh uh and it's a premalignant condition. It causes a lot of mucus coming through. And also they are losing potassium at the same time, but it's a premalignant condition. The only treatment is uh removing the stomach total gastrectomy, right? And the uh I love this uh slide. I got it from uh from a uh some advertisement. And actually, um my professor used to say the old Indian doctors, Jargon, Harri Curry and Bori is no longer applied but in fact, uh, I disagreed with him. Uh, yeah, it may not be the only reason but there is something in that and worry, uh, uh, I would say that yes, there is something in it but also there are Helicobacter Pylori and other NSA ID now. So things have changed. But, uh, I like, like that, uh, Harry and body and the patients like it as well. They laugh when I say this. Ok. So peptic ulcer disease, I think, you know all about this. I think I have given you the most important ones. Um uh H pylori are very important. Uh The duodenal ulcers are benign. Normally it benign and uh uh but gastric ulcers are not. So that's what you don't start. Somebody comes to you with the, the this is the take home message today. Somebody come to you and you will start him on PPIs and send him home and forget about it. That paper died uh can die within the year. Uh because you have not done a gastroscopy OGD. Uh Gastroscopy is a must. So don't start the patient and discharge the patient will be happy. No further pain. Becau because any ulcer could be from the beginning uh uh a cancerous. So that, that's why it has be that, that, that is shown by the chronicity, especially gastric ulcer. So, so you do not start PPI S if you do not have chance to get a gastroscopy done, I tell my, all my junior doctors don't do that because actually I lost the patient. Uh, it's so partly, uh, due to patient's con uh, noncompliance, but partly due to that, we didn't convince the patient, uh, you know, you, she will come with pain and she, uh, she was only 48 at the time and, uh, it was too late afterwards. So, chronic gastric ulcers. Now we do total gas, uh partial gastrectomy for chronic ulcer because we cannot, we can do biopsies. They say do 10 biopsies, adequate biopsies. But uh we still miss a cancer spot in that ulcer. So a nonhealing gastric ulcer, almost a cancer. So remember that. So, chronicity causes pyloric stenosis and the other glass deformity and various things, pyloric stenosis, uh you know, the classic condition uh where the you have projectile vomiting. And also uh you have the classic uh biochemical changes uh which is uh hypo uh alkalosis and it doesn't happen anymore because we are using PPS. So, especially in cancer patients with pyloric stenosis because pyloric stenosis can come from uh contraction due to ulceration and it can come from, come from uh uh come from uh cancer of the patient, uh Pyloric pylorus. And also it can come from uh you know that they are the, there's a child, children's case, the uh uh the congenital hypertrophy of the pylorus, uh firstborn male infant uh normally has that and they have the same projectile vomiting, et cetera and the treatment is pyloromyotomy. So, that's different. Uh the chronicity causes pyloric stenosis. Um So the clinical features is, is uh severe pain, uh comes and goes vomiting and uh sometimes you can see the wave of peristalsis uh cause like we call it golf play and they may have anemia due to microcytic anemia, due to ulceration, every ulcer bleeds. So they all, so you have to always do a full blood count. So OD the biopsy is very important and uh uh especially to exclude serious pathology, right? So, treatment is lifestyle change, stop smoking and that is very important, stop smoking. Just ask for arterial disease and change your diet, whatever the patient knows better than the doctor that uh uh uh any irritation. Uh uh uh what, what are the diets they irritate? Of course, the main two drugs of treatment are anti seeds, starts with Ancid uh and the S two receptor antagonist and the PPIs stop smoking. So that's the main treatment, medical treatment, right? Um And this is another message I want to give when H pylori and NSA I DS are not responsible. And also there is an ulcer because 95% of duodenal ulcer comes in the first part of the duodenum, the first inch of the duodenum. And uh normally there are kissing ulcers, the anterior ulcer perforates posterior ulcer, uh bleeds from the gastroduodenal artery, right? So, uh medical treatment, um uh I think we, we, we but not me, my lifestyle changes, avoidance and abstinence. So remember those words, avoidance and abstinence, avoid smoking and also abstinence from irritating food. And if possible, because some arthritics, you may not be uh possible to get rid of NSA ID. Uh But they say if the ulcer is less than five millimeters in diameter on endoscopy, uh you can continue with the N A IIS uh uh with the uh with the omeprazole or whatever you're using for that. So, antacids are important that it, it promotes the gastric mucosal defenses, the barrier that we were talking about and the uh uh uh S two receptor antigen, it inhibits histamine H two receptor in the parietal cell. 75% heal in four weeks, eight plus 8. Uh uh 89% heals in uh eight weeks. But omeprazole obviously catching the all the three receptors. Remember that picture of the parietal cells, it heals uh uh in two weeks, there's no, there is uh uh 69% healing and in four weeks, uh the 93% healing and there are other drugs called protective barrier drugs. Um uh I'll see my time. Ok. Protective uh Sucralfate is one AOL of sulfate and aluminum hydroxide. We usually use in the IC U, especially for stress, ulcers, dissociates in dis solution. And this causes a barrier prevents Pepsin acid bile cells diff diffusing and epi uh through the epithelium. So, bismuth compounds are also uh antibacterial against H pylori. So that is important to know and there are various anti helicobacter regimes. It, it changes from country to country. Uh So I'm not going to go through all that. The triple therapy with, with the PPIs and 22 antibotic and it, it varies. And the quadruple therapy you add on metroNIDAZOLE as well. The patients don't like very much. Uh Right. I, I put this one on because when we ask the medical students, what is Gaviscon? And uh nobody uh seem to be able to uh answer this question. Do you know what's Gavis? You can't say Gaviscon is a syrup. I'm uh I'm asking uh a medical student. Yeah. OK. So uh Right. OK. So it is a sodium algate it, it's, it almost like the, the sucralfate. It cause it's an algen uh seaweed. So it's 250 mg inactive ingredient and form a protective layer that floats on top of the contents. And there is sodium bicarbonate and also calcium carbonate for and to see the uh function though because we any drug you give it to a patient, you should, especially a simple drug like score, you should be able to answer uh the examiner because you can't say well, it is a syrup or anything, you know. So be careful. So I'm just warning you because it's uh uh for the exam. Uh Right. So our famous vagus nerve is back. Uh So uh so various uh various truncal vagotomy, which is the one that we used to enjoy as a registrant uh 30 40 years ago. And the uh then of course, the consultant will do the selective vagotomy uh uh leaving the branch going to the pylorus. So then you don't have to do a pyloroplasty because the pylorus is innervated. So, although you are not also not damaging the crossed foot on either side, on uh either lethargic nerves, highly selective. You just need these branches going right on to the stomach. Uh The, the recurrence rate is very high in the tranquil vagotomy. And you have to send a, a sec segment of that for histology to prove that you have done the right thing, not just some branch, uh little, little uh uh band, you divide it. So uh you have to prove yourself that you have done the correct operation. So you have to send that two segments for histology. So it is very important. So if you do uh uh do AAA uh uh uh take of taken off the motility, obviously, you need a drainage procedure. So the famous drainage procedure is pyloroplasty. You, you divide it longitudinally and stitch it transversely. So it becomes bigger. So, or if that is if two fibroids because of the duodenal ulceration, you and it's not cancer, you go and do a uh uh gastroenterostomy retro Coly because you don't go to anywhere near that. If it is a cancer because cancer spread that area in the stomach. So we go and pick all. So um it's not important for you, but it's nice to know about it. OK. Right. So Vagotomy and the uh one we already described uh remember to send the histology and of course, build Roth one and build Roth two. It's simply this. So, Ruth one you resect that segment, the acid bearing segment, uh or ulcer bearing segment and do a gastro uh duodenal anastomosis. That's it. OK. That is Ruth one, bro, two is uh here it is done. An anti anastomosis is uh close, both ends and then do a gastroenterostomy. Uh So uh uh you taken away the ulcer beating area or ulcer producing area, uh or, or acid producing area and that's road two and do antico anastomosis. But normally most people do a retro for benign conditions. So that is that uh and then of course, these uh complications uh uh did I miss something there anyway, sequelae of gastric surgery. I will just name it. A recurrent ulceration is number one, especially after vagotomy, uh uh Stal vagotomy, uh loss of receptive relaxation. Uh So you get a gas bout syndrome when the patient come to you afterwards, it gets, it gets better after a while bile vomiting because you left a long rou and Y loop. You know the uh the uh the ascending loop and the uh you have to do a uh entero entero anastomosis to get rid of that bile carrying segment. So, early dumping and late dumpling dumping. So it is an osmotic load given to the Jejunum. Suddenly uh all the fluid comes in and you get a AAA hypovolemic problems, you get the patient to lie down and the uh uh uh patients get better. And if the patient's BP is very low, then of course, you can got uh IV infusion. If a leg dumping after 24 hours, you get, it is due to the previous uh uh uh uh the uh the meal, uh carbohydrates uh containing meal. And then of course, you get rebound uh uh hypo uh hypoinsulinemia and then rebound hypoglycemia. So uh due to rebound, hyperinsulinism, yeah, osteo trite does help, but also you can use some sugar as well. Get the patient to lie down. Uh post omy, diarrhea is only 5% and this normally get better carcinoma of the stomach. The cause of Adria. You may get, if you leave a very short stomach, you can get uh uh sto a cancer of the stomach weight loss. Uh uh and anemia and tuberculosis may light up uh because of poor nutrition and uh and uh loss of B 12, obviously. And osteoporosis, uh you can treat with calcium and various things. Vitamin uh D vitamin B 12, et cetera and you may get gallstones because you denervated the whole system. So, uh so that is the problem. OK. Perforation and there. So sometimes you may get a, uh, we recently had a 56 year old patient admitted with some onset epigastric pain. Um, and the uh uh uh and the uh, perforation I is a terrible situation. The patient will not move, will lie down. And the specific thread about perforation is so, stabbing pain, sudden onset, stabbing pain board, like rigidity of the abdomen and disappearance of the liver dullness or in the x-ray, free gas under the hemidiaphragm on erect chest x-ray. So you must get a ee test done to see the free gas under the diaphragm. So, erect chest is important even in intestinal obstruction and supine film abdomen is important. Uh So for that, so the remember the trial, the the stabbing pain, both like rigidity and the uh uh uh absence of labor, dullness and free gas under the diaphragm hematosis and melena. Uh there is no time to go through. It's a, it's a different subject, gastrointestinal bleeding. And that we mentioned already about mallory was tear stop the NSA ID. And you may have an unusual because I'm a vascular surgeon as well. So I have seen many aorto enteric fistula, especially after aortic grafting the top end of anastomosis get attached to the duodenum. And this is a terrible uh uh big operation you have to do to save these patients because uh nothing will help uh until you re graft that patient. Uh So uh various gastrointestinal stromal tumors we talked about that already and now it's called uh uh uh leiomyoma. Uh We used to call it um Anyway, the pyloric stenosis, we talked about it. And the pyloric remember to see uh remember the splash how to do it. You must know how to do it. And you, most people shake the abdomen. But uh the proper way to do is get someone to put the finger and tap on one side and feel from the other side. Some people use the stethoscope as well, but depends on what you have been told in your own medical college. Uh But I like someone uh uh I, I used to say, ask the examiner to put that hand in the middle and you tap from one side and uh uh and uh he will feel himself as well. Ok. So nonhealing tronic gastric ulcer, we'll have to have a gastrectomy as well. So remember that. So remember treating a gastric ulcer is a, is a great ability for any doctor. So, uh like you to rebleed. Uh I like to play with this and I tell it is over 60/100 under 100 under 10. So what are they? So over 60 is a patient over 60/100 is tachycardia under 100 is low BP under 10 is, is already bled and the HB is 10 and they are more likely to bleed. And also when the patient come to the hospital, somebody has witnessed the bleeding that is also important because they are, if you have seen that yourself, you are we likely to rebleed. So get the endoscopy as soon as possible. And also uh uh there is a comorbidity is important and also signs of hypertension, the SP and evi cap medicine and all that is important. Uh So uh the post endoscopy, the stigma of recent bleed, I think it's in every book. Uh I think the best to read the, the protocol given in coma and clock. Uh it is uh whose protocol is that? Uh I've forgotten now. Sorry about that. Uh The team, I know him as I've forgotten the name Tim Pro Pro pro. You don't, do you, do you know that? No. OK. Sorry. Anyway, I'll tell you in the next uh next next lecture and the be other benign condition that we need to finish that. Now, only five minutes left on the stomach, fixed in two places or stomach rotates and the hole of the omentum and the colon goes up is known as the organo axial rotation. And of course, it looks like per per uh gas under the diaphragm because your trans spon is under the under the left hemi right hemi dig and the acute gastric dilatation, you have to be very careful because the patient may uh may, may, may, may, may die from aspiration. So you have to put in an NG tube. And I told you how to manage the NG tube properly. The two hourly aspirate, the free drainage. Don't forget all that and try to bear and phy Tobar, especially after gastrectomy. You may get that and the uh uh foreign bodies and uh in females shouldn't say female psychiatric patient out and feel Dula for malformation. Uh It is the one that examiners like what is DU LA four malformation. It is a submucous bleeding uh due to when you uh a small, small capillaries under the, but when it's not bleeding, you can see that's the problem and it can be anywhere in the gut. So, Duo malformation, right? Uh uh uh I think uh that's all I want to say. Uh this is c of the stomach. I did not plan to do that. Right. Right. So, next thing will be uh the wound care and management and the uh uh this is uh my book and uh the PDF you should be in any library. So uh uh uh or else you can get down the book. Uh So that will be the lecture next Tuesday at 12 o'clock. Uh And then I followed by burns. I will do both lectures, right? Thank you very much. Any questions. So, no questions in the chart. So, any questions? Thank you very much. I hope that I have delivered enough material uh because it is very difficult to read about gastric and all that. All these autoimmune uh gastritis and all that Uh, so I think I have given the main sub, main uh, information to you. Thank you very much. So, uh, this is from Lanka. Uh, I was given that from Cardiff in the past. Um, and we will meet again in the sunny Sri Lanka. It's not sunny today. Uh, uh, from, uh, from teaching hospital. Uh, you can come here for electives if you want to and we can arrange that. Yes. Thank you and goodbye. Bye.