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E Zysin. So what these two routes do is they form a portosystemic anastomosis, which is a connection between the portal and systemic venous systems. Ok. So let's look at the lymphatics and innervation. Then the lymphatic drainage of the esophagus is divided into three sections. So you've got the superior third, the middle third and the lower third, superior third consists of your deep cervical lymph nodes. Your middle third consists of the posterior and superior mediastinal nodes. And then the lower third, which consists of the left gastric and celiac nodes. Now, I mean there are more nodes on this image here, but these are the important ones to remember because they're the ones that commonly get affected when there is, you know, something wrong with your esophagus, if we then look at the innervation. So your esophagus is innervated by the esophageal plexus. This is formed by a combination of the parasympathetic vagal trunks and the sympathetic vagal fibers from the cervical and the thoracic sympathetic trunks. The two different types of nerve fibers run in the vagal trunks. So you have the upper esophageal sphincter and the upper striated muscle which originate from the nucleus ambiguus and then you have fibers that supply the lower esophageal sphincter and the smooth muscle of the lower esophagus which arise from the dorsal motor nucleus. Ok. So we looked at the anatomy of the esophagus and we know that the esophagus has many different functions. One of the main functions of the esophagus is its function in swallowing. So the esophagus has three key phases in swallowing. You have the oral preparatory phase, the pharyngeal phase and the esophageal phase, we'll look at all of these three phases in a bit of detail. Then, so the oral preparatory phase is voluntary, we are chewing the food consciously in the mouth. Obviously, I don't know how many people here think about chewing their food when they're normally eating. I know I don't, but it's a, it's a phase that we do consciously. We think about it whilst we're chewing. And once that food bolus is created, we push that food bolus back towards the wall of the pharynx. And once the bolus touches the pharyngeal wall, the next phase then begins the next phase we said was the pharyngeal phase. So this is an involuntary face. So now we don't have any control over this. During this, the soft palate seals off the nasopharynx and the pharyngeal constrictors will push the bolus downwards. Whilst this happens, the larynx elevates which causes the epiglottis to close. And at the same time, the vocal cords will adduct. So this temporarily seizes breathing and the upper esophageal sphincter will now open up, the next phase is then the esophageal phase. So now the food bolus has just crossed the upper esophageal sphincter and it's moving past the upper esophageal sphincter now closes and you have peristaltic waves which carry the food down towards the stomach. This whole process of swallowing takes approximately around um, seven seconds and I say around seven seconds because for me who I'm a slow eater, it takes probably a bit longer. And I know some people who practically inhale their food as well. It's a bit faster process for them. Um ok, so let's have a look at what happens then when things start to go wrong. So we'll start off by looking at the definitions of metaplasia, dysplasia and neoplasia. Now, metaplasia refers to the reversible change in which one somatic cell type replaces another somatic cell type. So for example, if we look in the esophagus, the replacement of squamous epithelial cells by intestinal type, columnar epithelial cells. So when this happens in the esoph esophagus, this is known as Barrett's esophagus. And the reason why this change can occur is mainly due to the chronic exposure of gastroesophageal reflux that causes irritation and inflammation to the esophageal lining. The next is dysplasia. Then so dysplasia is the disordered growth or maturation of cells within a tissue, often considered precursor to cancer. The cells at this stage start to deform. As we can see in this image here and then there is an increased mitotic activity, dysplasia is very, very uh severe. So it's um it's a warning sign essentially because it indicates an increased risk to progression of cancer. If it's left untreated neoplasia, then refers to the abnormal and uncontrolled growth of cells leading to the formation of a tumor or a mass. And you can see that in this image where it's crossed the mucosal layer and is entering into the next layer of the tissue. So you have two types of neoplasms. You can either have a benign neoplasm which is noncancerous or you can have a malignant neoplasm which is cancerous. Now, if we think how this all effects in the formation of Barrett's esophagus and further, then initially you have metaplasia which converts your esophageal squamous epithelium into esophageal intestinal type columnar epithelium. And if that's left untreated, then that can advance further into a lower grade dysplasia, which then continues to a high grade dysplasia and eventually this will lead to esophageal adenocarcinoma. So, on this slide, what I've got is I got a few images of what the esophagus looks like when you put a camera down it, uh the top left image is the normal image for an esophagus and you can see how it's nice and pink. Um and you know, it's not got any difference in color changes. You can't really see any darker areas of inflammation, but we can see the other images. So if we just look at the image to the right of that, which shows Barret's esophagus, you can see there's a clear difference between the two colors. So you've got a darker pink color here or a reddish color, which shows that that part is the part that has changed in the epithelia. So you've gone from a squamous to a columnar type thelium over there and it's quite clear to see on an uh in a camera down the esophagus. And you can see that from the other two images which are actually live images from patients that I've got. And you can clearly see the changes in the two different tissue type with the lighter color and the darker color. So, Barrett's esophagus is uh very, very important to identify and treat because as we know, it can advance further into more sinister things. So, Barrett esophagus will usually be treated surgically um via endoscopic mucosal resection. Um We will look at that procedure a bit later on in this presentation. OK. So what are the differences then between esophageal squamous cell carcinoma and esophageal adenocarcinoma. In terms of location, squamous cell carcinoma is present in the upper and middle thirds of the esophagus. Whereas adenocarcinoma is more on the lower third of the esophagus. Esophageal squamous cell carcinoma is more prevalent in lower and middle income countries. Like we said in the beginning of this presentation, the cause of that is mainly smoking and alcohol consumption that is much more higher in these countries. Whereas if we look at high income countries where esophageal adenocarcinoma is more prevalent. And then the cause of that is actually because of the consequence of metaplastic epithelium. So, having conditions such as go obesity and a high fat intake, which is leading to these metaplastic and dysplastic changes and causing the ca uh cancer. All right. So let's take a look at what the risk factors are for developing esophageal carcinomas. Then the risk factors for esophageal cancer include Gourd and Barrett's esophagus. Like discussed tobacco and alcohol consumption have direct toxic effects on the lining of the esophageal wall and tobacco and alcohol actually have a synergistic effect. So that combined use actually causes more damage than if you were to use either of them by itself. Then if we look at um obesity and diet which causes increased reflux and that can lead to further development of Barrett's esophagus and further. And then you have genetic factors which contribute to the development of esophageal cancer as well. Right. So let's take a look at how esophageal cancers actually develop. What are the cellular level processes that are going on? So, esophageal cancer typically develops through a multistep process involving progressive genetic and cellular changes. There are some key stages. So the process begins with genetic mutations, right. So this is the initiation ST stage. So this is alterations in the DNA of normal esophageal cells. So this can be triggered by certain carcinogens, these cells will then proliferate further if the trigger continues. And if the carcinogen is continued to be present, and then further genetic mutations will lead to the formation of dysplastic cells. And eventually this will advance to cancerous cells. The other way that this cancer can develop is due to chronic inflammation and oxidative stress. So with this persistent inflammation, with conditions like gourd or Barrett's esophagus can lead to continuous tissue damage. Now, what I mean is you get inflammation, the inflammation is starting to be healed. But before it's completely healed, you get gored again. The inflammation continues that process of damage repair, damage repair, basically creates a lot of stress on the esophageal lining which increases the chances of them leading to metaplasia and dysplasia. Then the next thing was oxidative stress. So, in terms of oxidative stress, you have reactive oxygen species that's produced during normal cellular processes or as a normal response to inflammation. Now, this creates oxidative stress. When we have prolonged exposure to oxidative stress, it can lead to the damage of the DNA, the proteins and the lipids and that contributes to the development of esophageal cancer. Finally, we'll take a look at the certain molecular alterations that are present in esophageal cancer. So, these are tp 53 mutations. So this is a tumor suppressor gene. You have the P 16 ink four a alterations. So this is a regulator in the cell cycle. You have the H er two overexpression. So this is the human epidermal growth factor receptor overexpression of this is seen in patients that have esophageal cancer and then you have the epidermal growth factor receptor. So this is also present um in patients that have esophageal cancer. Now knowing these off the top of your head is not exceptionally necessary but having an understanding of what the different molecular alterations are will basically guide for further targeted treatments and focus on personalized therapies for patients as well. Right. So let's look at what happens when a patient presents to your clinic. Now, a patient will come and they will complain of certain symptoms. We don't know what the symptoms are, we don't know what the diagnosis is. But early stage esophageal cancer often lacks well defined symptoms. So many of the symptoms that the patient will actually present with are going to be quite severe or they might present with symptoms at a much later stage of the disease. So the patient might come in saying doctor I have very difficulty swallowing. Now, they might say I'm on, I'm on a liquid diet or I have difficulty swallowing solids. I can't really chew and swallow that well in. So this is dysphagia and it's very, very common presentation for patients that have esophageal cancer. It's quite progressive in nature. So often, like I said, patients will present with difficulty swallowing solids. Um but if a patient ignores the fact um of their dysphasia and presents at a later stage. They could even present at a stage where they might have difficulty swallowing liquids. Patients may also report weight loss. They might also say, um, they have painful swallowing, which is a dinner aphasia. And, um, you know, that's often felt when you're normally drinking something really, really hot or really, really cold. It's the feeling at the back of your throat which causes you to, you know, tense up for a couple of seconds. And that's the feeling that the patients will be constantly be in when they have these symptoms. And finally, the patient may also have hoarseness of voice. Uh depending on about what stage of cancer they're presenting in on clinical examination. Patients may have the signs of recent weight loss, cachexia, signs of dehydration and supraclavicular lymphadenopathy. If the patient is presenting at a much later stage of the disease, we may also see signs of metastatic disease. So, these may include such as jaundice and Hepatomegaly as clinicians. It's very, very important to understand these symptoms and know when these red flag symptoms present so that we can you know, correctly refer further on to wherever the patient needs to go. Ok. So now that we've got a suspected diagnosis of esophageal cancer, what are we going to do further on? Now, any patient that it has suspected esophageal malignancy should be offered urgent upper gi endoscopy. Any malignancy that is seen on an O GD should be biopsied and the specimen should be sent for urgent histology. So if you look at what the current nice guidelines are for upper gi endoscopy, it states that the red flag symptoms for a suspected esophageal malignancy are to any patients with dysphagia and any patient that is greater than 55 year old with weight loss, upper abdominal pain, dyspepsia or reflux. So any of these particular boxes being ticked, the patient needs to be referred for an urgent upper G IO GD patients that are not fit for an O GD then. So they can be offered a ct neck and thorax. Now, this scan is good. However, it's much less sensitive and it's much less specific as well. So an O GD is ideally what you wanna be going for. Um Let's take a look at this image here then. So this is an image of what you would see on a normal O GD. So you can see it's quite uh quite clean. Um You can see some of the spit and saliva that's present in the patient. There's no signs of any inflammation. You've got nice pink, um healthy tissue looking esophagus. You can see the esophagus is quite opened up, there's enough space for food and liquid you travel down in comparison. Then let's look at this image. So this image is very, very different. Obviously, um you can see there is a growth on the right side which presents that as that white kind of mass. This is actually an image of a patient with a esophageal cancer. And you can see that there is, you know, narrowed lumen, there is mass that's present there. Um, the patient is obviously gonna have some kind of difficulty swallowing and they're gonna present with other symptoms um that are associated with that as well. Mhm. Ok. Now, once the diagnosis of esophageal cancer is confirmed, further investigations are going to be carried out to help plan treatment. So we can have CT chest, abdomen and pelvis and pet ct. Together, these are used uh together to investigate for distant metastases, endoscopic ultrasound to measure the penetration into the esophageal wall and assess the biopsy that um you know, for suspicious mediastinal lymph nodes, you can then do staging laparoscopy. So this assesses for intraperitoneal metastases and looking at any palpable cervical lymph nodes may be investigated via fine needle aspiration. Mm. So now that we've looked down with an O GD scan, we've looked at the size of the tumor and this allows the surgeon or whoever's performing that procedure to start staging the cancer. So we use the TNM stating method to stage esophageal cancer. It involves tumor node and metastasis. So, tumor, there are four stages T one to T four. If we start off with T one, then the cancer is limited to the inner layers of the mucosa and the submucosa. And you can see that in this image here, T two means the cancer has grown into the thick muscle wall of the esophagus. T three, the cancer has spread to the adventitial layer and T four, the cancer is starting to spread outside the adventitial layer into that neighboring organs and structure which you can see here that it's starting to affect the lining of the lung. OK. In terms of node, then, so node describes whether the cancer has spread to the lymph nodes. So again, there are four stages, you have N zero, N one, N two and N three, N zero means there is no lymph node involvement. N one means there is one or two lymph nodes that contain cancerous cells. N 23 to 6, nearby lymph nodes have cancerous cells. And N three means there are seven or more lymph nodes that have cancerous cells metastases then is pretty straightforward. You have M zero and M one M zero being that there is no metastases to other organs. And M one being there is metastases to other organs and structures. So once the cancer has been staged, we can then look at what the treatment options are for that patient. Now, the management of esophageal cancer should be determined by specialist MDT S. So this would include general surgeons, oncologists, specialist nurses, nutritionists, and also palliative care team. The curative treatment comprises of surgical or endoscopic resection, but that entirely depends on tumor size, the stage and patient factors such as general wellbeing and comorbidities. Along with surgery, the patient may or may not require neoadjuvant chemotherapy or chemo radiotherapy. And if you look at squamous cell carcinoma, then the definitive treatment involves chemo radiotherapy and for adenocarcinoma. The definitive treatment involves neoadjuvant chemotherapy followed by its surgical resection. The main surgical procedure for esophageal cancer is esophagectomy. Now, this procedure can be performed as an open surgery or as a minimally invasive procedure. We then have those patients um with metastatic tumors or too unfit for curative therapy. These patients are offered a range of palliative options. These include so esophageal stent for patients that have difficulty swallowing chemotherapy and radiotherapy along with immunotherapy. So all of them can be offered um for any patient to help control the disease. And along with this nutritional support should also be offered to the patient. That's because they're suffering from significant dysphagia and cachexia. And if their dysphasia becomes too significant, then what we can do is we can give them a radiologically inserted gastrostomy. So that's a rig tube. It's a tube that goes directly inserted into your stomach and the patients can be fed through that, right. So, what I've got here is an image of the surgery of that, of what we've just been talking about. So this is how esophagectomy would take place. Multiple open approaches can be performed. This particular image shows um a procedure known as the Va Lewis procedure. Now, this is a, this is an amazing surgery which involves right thoracotomy with laparotomy. This is, this surgery is also known as a two stage esophagectomy. So you can see how part of the esophagus is removed and the stomach is basically pulled up and, you know, connected to the esophagus at the top. We also have another procedure known as the mccowan procedure. That's a three stage esophagectomy. So, this involves an incision in the right thorax and abdominal and neck incisions as well. Ok. Right. So that finishes off looking at part of the esophageal cancer. Um, we'll go through a case study and we'll try and work through everything that we've been through right now. Mm mm. So we've got a 66 year old man who presents to his outpatient with a six week history of increasing dysphasia. Initially, this involved only solids, but he is now also having difficulty with liquids also and describes food as sticking in the middle of his chest. He has also lost 4 kg in weight and his appetite is poor. He is not taking any medication apart from an an acid suspension from the local pharmacy, he is a retired publican and smokes 10 to 15 cigarettes per day and drinks 2 to 3 pints of beer most days. So everyone's got that clinical examination does not reveal significant abnormality. Ok. So I'll keep this up here. I want you all to think about what the potential of differentials could be for this gentleman here. Give you a minute to think about it. If everyone can start posting some answers in the chat, I can't actually see the chat. So I will read out answers. So, if people, um, put what they think is in the chat, we've had adenocarcinoma as one, if you just pop what they want in the chat, um, esophageal cancer, anybody else. So, we've got adenocarcinoma and then esophageal cancer as well. Yeah. Absolutely. So there, there's, there's some great differentials. So, esophageal cancer. Yeah, that would be the top differential for this person for this patient. Then you can have a mediaster mass or it could be Gored as well, potentially achalasia, which is a bit bit of a less chance of it being achalasia. But that's definitely part of the differentials. Um So these are some of the differentials here. Now, what investigations would we like to do then for this gentleman? So again, just stick your answers in the chat and I'll read them out. Um, O GD. We've had anybody else. Absolutely. And I would agree with that. So O GD is your first line investigation that you'd want to carry out with the, you know, signs and symptoms that this gentleman's presenting with. So actually the, the patient was unable to tolerate an O GD. So you went, underwent a barium swallow. Um I'll show you an image of the barium swallow on the next slide. So if we can have what you think the likely diagnosis is now this is the image of the barium swallow. OK. Has this changed? What people think the diagnosis would be? What do we think based on this image? OK. So, and I assume it might be a bit difficult to interpret. Uh We've got a question. Is it upper esophagus? Where the upper body is? It is? Yes. So upper middle esophagus, it could be SCC someone said brilliant. Yeah. So what, what this x-ray is actually showing, it's, it's showing that there is an extensive polypoidal and ulcerating tumor in the mid esophagus. So it's the upper and mid esophagus. And what we, what we've got here, this is an image of a barium swallow and you can actually see some n uh narrowings in the esophageal area and that's due to esophageal cancer. So, following his barium swallow, he has another O GD under general anesthetic. Endoscopy biopsy confirms esophageal adenocarcinoma. So who said that? Absolutely correct. So what investigations then are used in staging esophageal carcinoma? So, you've identified via an O GD that it's this what we're going to, what investigations would we like to do next again? Pop your answers in the chat. We've got an ultrasound and also a staging CT Yeah. So staging CT definitely, we've also had P at scan as well. Absolutely. Yeah. So CT, chest, abdomen, pelvis. Absolutely. Endoscopic ultrasound. Brilliant. And pet scan. So you've covered all three of the ones I've got here. So, these are some important scans that you'd want to do to check if a patient um you know, and help for managing um organizing management plans. So in this patient, then staging investigations revealed enlarged nodes in the mediastinum and an enlarged supraclavicular node likely to be metastatic. What would be appropriate treatment for this patient? Then what do you think again? Thank you everyone for being so receptive to all the questions pop, keep popping your answers in the chat as well. I'm finding this very helpful to go through for myself as well. Anybody have any idea on treatments? We've had a neo adjuvant chemotherapy and es esopha. So surgery. Yeah. Um definitely up there with some of the management options that we could potentially think of. So if we go back to looking at the case for this patient, I think I should have just put it on the slide there. Um You know, this patient has a six week issue of dysphasia. Um, initial size, he's lost 4 kg of weight. He's 66 year old and he's retired. He drinks 2 to 3 pints of beer, beer most lately, uh most dates. So in terms of treatment, I absolutely agree. So you could potentially think of um surgery or you could go on the lines of palliative. What I've got here is I think the patient would actually require some palliative chemotherapy and then we would have to focus on, um, you know, improving quality of life for this patient. So that could be a radiological insertion of esophageal stent, which would help try and ease his dysphasia. Obviously, if the dysphasia continues, we would then er continue further with maybe a rig tube, et cetera and we could try and do a laser treatment of the esophageal lesion to try and reduce the pain that the patient might be in because of the presence of the mass. Ok. Um Great work, everyone. Um Thank you for your input. I think that's the end of this case study. Yes. Um So I hope, you know, the top of your cancer, that part of the presentation was useful. We'll move swiftly on with gastric cancer. Um Yeah. Is that OK? Yeah. Go for it. Cool. Um Yeah, I was just wondering if we wanted to take a minute break or something but I think I'll make a start on this just bearing in mind the time. Ok. Ok. So gastric cancer, the next, the next part of this presentation. Um Once again, let's take a look at why gastric cancer is a significant health concern worldwide. So I think actually going through the er global impact in epidemiology is very, very important before we actually move on to looking at the clinical understanding of the cancer. It just puts it into perspective of why it is so important of actually going through these uh you know, conditions and why it's important for us to understand why these conditions are so severe. Gastric cancer is a significant health concern worldwide in terms of mortality and morbidity rates. Gastric cancer is one of the leading causes of cancer related deaths worldwide, um particularly in lower and middle income countries. So the mortality of gastric cancer remains quite high actually because of late stage diagnosis and limited treatment options for advanced stage disease in terms of clinical challenges. This is this is probably the most important reason why they um it's such a big clinical challenge um that gastric cancer poses. And since the patients present at such a much later stage, many patients become ineligible for surgery. And I instantly just thought about for palliative management, gastric cancer and its treatments can significantly impact a patient's quality of life. So, symptoms such as abdominal pain, dysphagia, fatigue can affect physical and emotional wellbeing, you then also have treatment related side effects. So this includes nausea, vomiting, hair loss, and you know, this this all comes together to further diminish the quality of life. You also have complications of surgery. So this impacts the functional status of the patient overall. When we think about, you know, the patient's diagnosis, it's very, very important to take all of these things into account before moving on with the medicine and the surgery to actually take a step back and think about how will this affect the quality of life for this patient and do it for the patient's best interest. Finally, then, in terms of public health perspective, we've already mentioned the high mortality rates and this creates a significant um significant public health challenge. Prevention strategies will focus on addressing risk factors such as um h pylori infections, that's helicobacter pylori infections, tobacco smoking and dietary factors. Furthermore, early detection and screening programs will aim to identify gastric cancer at earlier stages when treatment is more effective. Other public health init initiatives also include emphasis on health education, raising awareness about signs and symptoms of gastric cancer and promoting a healthy lifestyle. Ok, so we said gastric cancer was one of the leading causes of cancer related deaths worldwide. Well, actually gastric cancer is the fifth most commonly diagnosed cancer globally and it's the second highest cause of cancer related deaths, mostly due to the patients presenting in advanced disease. We can look at the graph on the right. So this graph here is taken from 2018 glo data and it shows over 1 million cases of gastric cancer are diagnosed each year around the world with prevalence rate being just over 1.5 million. Um Yeah. So you can see that in this graph over here, gastric cancer is more prevalent in males. So in developed countries, gastric cancer is 2.2 times more common and likely to be diagnosed in males compared to females. If we then take a look at this map over here, it shows the estimated age standardized incidence rate. For stomach cancer worldwide. So again, this is the 2018 data from GLO as well. The dark blue areas uh show where the incidence rates are the highest. So we can see that in the East and Central Asia along with some of Latin America as well. Korea actually has the highest national incidents. So with almost 60 per 100,000 new cases annually for males, right? So let's take a look at the anatomy of the stomach. We'll start off with the inner layers first and then we'll move on to looking at the bigger picture, the gastric wall is made up of four layers. So again, from the outside, you have the cirrhosa or the adventitia layer, then you have the muscle layer, the submucosa and then the mucosa, the mucosa comes into direct contact with the food and it has three layers of its own, the innermost layer being the epithelial layer. So the epithelial layer is involved in absorbing and secreting. Um you know, mucous. Um the middle layer then is the lamina propria, it has your blood, your lymphatic vessels, the um it has your mucosa associated lymph lymphoid tissue. So, malt uh which contains lymphocytes and these are, you know involved in eliminating pathogens that pass through the epithelial layer. And then the outermost layer of the inner layer of the mucosa is the muscularis mucosa. So this is a smooth muscle layer that contracts and it helps with the breakdown of food, if you take a look at the image on the right. So that's a just a zoomed in image of what the epithelial layer looks like. So you can see that there is um dips in the stomach lining which form the gastric pits. These pits are continuous with gastric glands below which contain various epithelial cell types. Each secreting certain substances. For example, you have your surface mucous cells. So these are also known as foveolar cells and these secrete mucous, you then have your um parietal cells. So these are present in the body and the fundus of the stomach which we will look at in the next slide. Um these secrete hydrochloric acid and they help maintain an acidic ph in the stomach. There are also chief cells that are present in this layer as well. So, these secrete pepsinogen which help digest proteins. And then there are g cells, g cells actually have multiple functions. So this includes uh secretion of gastrin and er stimulating parietal cells to inc increase to secrete hydrochloric acid. We move out slightly and take a look at the stomach as a whole. So like I said, the stomach um is an intraperitoneal organ which is located between the esophagus and the beginning of the duodenum. It primarily lies in the epigastric and the umbilical regions. There are four divisions of the stomach as seen in the image on the left. So you have your cardia, the fundus, the body and the pylori, the medial and lateral borders of the stomach are curved. These form the lesser and greater curvatures. The greater curvature forms the long convex lateral border of the stomach and it curves to the right as it continues medially to reach the pyloric antrum. The lesser curvature forms the shorter concave middle surface of the stomach. Um and the lesser curvature gives attachment to the hepatogastric ligament. There are two sphincters of the stomach that are located at each orifice. So one just above the cardia and one just after pylori. So you have the lower esophageal sphincter, which is at the level of t 11. This marks the transition point between the esophagus and the stomach. And then you have the pyloric sphincter. So this is the first part um of the duodenum just, you know, be just before the first part of the duo duodenum. Mhm. Ok. Let's take a look at the vasculature around the stomach. So the arterial supply to the stomach comes from your celiac trunk and its branches, anastomoses form along the lesser curvature of the right and left gastric arteries and along the greater curvature by the right and left gastro mental arteries, the right gastric artery and its branches. Um So this involves the proper hepatic artery and the left gastric artery which arises directly from the celiac trunk. We then have the right gastro omental artery, which is the terminal branch of the gastroduodenal artery and the left gastro omental artery, which is the branch of your splenic artery. The veins of the stomach run parallel to the arteries. So you have the right and left gastric veins which directly drain into the hepatic portal vein. You have the short gastric vein, uh the left and right gastro mental veins, which all ultimately drain into the superior mesenteric vein. And I look quite a lot of um, anatomy to go through, but I'm hoping it's just a bit of recap. Ok. If we then move on to looking at the lymphatics and the innervation. So the gastric lymphatic vessels travel with the arteries along the greater and lesser curvatures of the stomach. We can see that in this image on the left. So the lymph fluid will drain into the gastric and the gastro and mental lymph nodes that are found at each curvature. We have the efferent lymphatic vessels from these nodes that connect to the celiac lymph nodes. And these are located at the posterior abdominal wall in terms of the innervation, then. So the image on the right, we've the stomach receives innervation from the autonomic nervous system. So, the parasympathetic nerve supply arises from the anterior and posterior vagal trunks. This is derived from the vagus nerve and the sympathetic nerve supply arises from the T six to the T nine spinal cord segments and it passes through the celiac plexus via the greater splanchnic nerve. This also carries some pain, transmitting fibers. Ok. So once again, we've been through the impact and the anatomy. So start, let's start looking at what happens when things start to go wrong in the stomach. Now, there are four types of cancers that we will look at regarding gastric cancer. These include adenocarcinoma, gist, which are gastrointestinal stromal tumors, primary gastric lymphoma and stomach neuroendocrine tumors. Of course, adenocarcinoma comprises of the majority of the tumors in the stomach. Um and the rest of the presentation will focus on adenocarcinoma. But for now, we will also look at these other types of cancers. Ok. So, adenocarcinoma, nearly all cancers that start in the stomach are adenocarcinomas. They develop in the gland cells which um produce mucus in the innermost lining of the stomach. Adenocarcinoma can be split into two types. So you have gastric cardia cancer. So this begins in, in the top inch of the stomach where the cardia is and um you know where it meets the be below the esophagus, basically. And then you have noncardia gastric cancer. So this cancer begins in all other areas of the stomach that is not the cardia. Got a mini uh got a histology section here which shows what adenocarcinoma would look like under the microscope. We then have gastrointestinal strong or tumors. So these are a type of soft tissue sarcoma that occur in the gi tract. Um they begin in the nerve cells that are present in the wall of the stomach, more specifically, it comes from the interstitial cells of C um which you can see in the image here. So these are present in the muscular wall um which is in the myenteric plexus of the muscularis propria. So, it's much more common in adults. It's very, very rare in Children. Approximately, only 1 to 2% of all gastrointestinal stromal tumors are seen in pediatric patients. The third type of stomach cancer then is primary gastric lymphoma. So this is a type of non hodgkin lymphoma that forms in the stomach. A common subtype being um large b cell lymphoma and the other common subtype being mucosa associated lymphoid tissue, which is also known as malt. So, uh primary gastric lymphoma accounts for approximately 1 to 5% of all gastric malignancies. The development of MT lymphoma is normally associated with chronic inflammation of the gastric mucosa. So, this chronic inflammation is occurring because of h pylori infection, h pylori. What it does is it activates B lymphocytes in the gastric mucosa resulting in the proliferation of malt and the eventual development of lymphoma. And we've got two images here of histology of what primary gastric lymphoma would look like under a microscope. And finally, let's look at stomach neuroendocrine tumors. The neuroendocrine tumors um of the stomach are also known as gastric net or gastric carcinoids. They are relatively rare tumors that arise from neuroendocrine cells in stomach gastric nets represent a small proportion of all gastric tumors which account for approximately 3 to 5% of all nets. The incidence rate of net has been increasing in the recent years. This is a good thing because that shows that there is improved diagnostic technique and increased awareness of this kind of tumor, which is why the incidence rate is going up. So those are the four cancers um that are, you know, that commonly occur in the stomach. We've gone through them quite briefly, but hopefully, it's, it, it's just for understanding purposes. So what happens next is how do these cancers actually develop? What's the risk factors that causes the development of these cancers being male? So we said being male was one of the most important ones. So there is a 2 to 1 ratio er in gastric cancers between male and female. Unfortunately, um H pylori infection. So this is a bacterium that infects the lining of the stomach. Chronic infection can lead to inflammation, which over time leads to gastric cancer. Then we have increasing age, smoking and alcohol consumption, which are all er equal risk factors as well. High salt diets. So this can lead to the formation of something known as nitrosamines and nitrosamines are known carcinogens when they are present in high quantities. Family history is also an important risk factor and then pernicious anemia. So this is a condition that is characterized by the deficiency in vitamin B12. This is due to impaired absorption of Vitamin D B12 when gastric cancer. Um you know, is present. So let's once again, look at the pathogenesis that's behind gastric cancer. It's quite similar to esophageal cancer. However, there are slight differences that we need to talk about. So, once again, gastric cancer evolves through a multistep process involving a series of genetic and cellular alterations. It involves initiation which is a genetic mutation occurring in normal gastric epithelium. So these initiated cells will then undergo proliferation if the trigger continues to maintain. And furthermore, it then can lead to the progression which is continuous exposure of that trigger and mutations lead to a precancerous state. These initiated cells can eventually then transform into cancerous cells. The progression may involve the alterations in tumor suppressor genes and oncogenes which disrupt normal cellular functions and regulatory pathways. The second type then chronic inflammation. So we said that was due to h pylori infection once again being infected and then treating that infection. But getting the infection continuously has severe impacts on the stomach lining. And this can then cause metaplasia. And if left untreated, if you know repeated infections keep occurring, that metaplasia can lead to dysplasia, which can then ultimately cause cancer. Oxidative stress once again works in the same way. So you have reactive oxygen species, which is generated during normal cellular inflammatory processes. This oxidative stress when present for long periods of times can cause damage to the DNA proteins and the lipids. Then the molecular alterations in gastric cancer. So we have TP 53 mutations. So these are your tumor suppressor genes, her two overexpression and for stomach cancer, you also have something known as E cadherin inactivation. So, e cadherin is an important molecule that is present in the gastric epithelium. And when stomach cancer does develop, this molecule gets inactivated. Once again, it's very, very important to understand these different molecular alterations because it helps us in developing targeted therapies for patients. Right. So let's look at the clinical presentation of a patient. Then normally gastric cancer, what um is not detected in the early stage and most patients will present in the later stage symptoms can be vague and nonspecific. So it's very, very important to identify the red flag symptoms that are present. Um In this advanced stage. These symptoms can include dyspepsia, dysphasia, early satiety. So being full quite quickly, vomiting melena and other nonspecific cancer symptoms such as weight loss, night sweats as well. The signs that would be seen on clinical examination would include an epigastric mass. You would see the trois signs. A Reier sign is um an enlargement of your left supraclavicular lymph node that sign is normally present for this cancer as well. And then if there, if the cancer is developed into an advanced age, you might see other signs of metastatic malignancies. So this would be hepatomegaly ascites and jaundice. Any patient that presents with these symptoms will be on the suspected list for gastric cancer and the investigations would be as follows. So first of all, any ca any patient with gastric cancer that is presenting with hematemesis or melena will warrant urgent bloods, which would include your FBC S LFT se et cetera. You then want to do O GD, which would be the primary investigation for suspected gastric cancer. This would allow direct visualization of any malignancies that are present and then suspect and then, you know, subsequent biopsies can then be carried out. Biopsies are important because they will allow for three things. So, histology, for classification and grading of any neoplasia that's present, you have the CL O test. Um So this is important as it detects the presence of H pylori and then you have the H er two of no protein expression, which is the targeted monoclonal therapies. If present for treatment planning, all patients will then need a CT chest abdomen and pelvis scan and a staging laparoscopy to look for peritoneal metastasis. Pet scans are actually quite rarely used for gastric cancers. The reason being that gastric cancers actually don't take up the radioactive tracer that well. So that's why pet scans are quite rarely used. So once we've done the investigations again, we come back to staging the cancer. This will, this will be done via the TNM staging. So we'll look at tumor once again, tumor has four main stages like previously T one to T four. However, in this case, in gastric cancer, T one is split into two stages. T one A and T one B. This is important because it, in, because when we're planning treatment for the patient, it's important to identify whether the patient is one A or one B one A basically means that the cancer is limited to the mucosa and one B is that the cancer has spread to the sub mucosa. T 23 and four are all the same as esophageal cancer. Then we have node. So node is the node. Again, you have N zero, N one, N two and N three, N zero. Meaning there is no lymphatic spread. N one being 1 to 3, lymph nodes are affected by um cancer N two, meaning 3 to 6 N three is split into two. So you have three A and three B which is unlike esophageal cancer. So three A is 7 to 15 lymph nodes that are involved with cancerous cells. And it makes sense that it's split into two parts because there is a lot more lymph nodes that surround the stomach in this case. And you can see that in this image that is present here. So three A is 7 to 15 lymph nodes that have cancerous cells. And three B is anything that is 16 plus lymph nodes that has cancerous cells, metastases is quite self explanatory. So that is M zero, no metastases and M one being metastases to nearby organs um particularly the liver. So let's look at the treatment for a patient for this kind of patient. Then all patients should be discussed at a specialist upper gi cancer MDT meeting with definitive management plans which includes potential palliation decisions as well. We need to ensure adequate nutrition is established. Therefore, each patient will undergo a nutritional status assessment and be reviewed by a dietician. If necessary, many patients will need definitive um support both pre or post treatment. This can be done via a nasogastric tube or a rig tube. The mainstay treatment for gastric adenocarcinoma is surgery. So patients who are fit enough should be offered um preoperative chemotherapy and then surgery. So, the aim of surgery is to achieve local regional control by removing the tumor and its local lymph nodes. So for proximal gastric cancers, total gastrectomy is offered to the patients and for distal gastric cancers, subtotal gastrectomy is preferred, the distal pancreas and the spleen can also be removed sometimes if there is direct invasion um or involvement of these organs. Um and there is a and there is still a chance of curing from the cancer completely. So the most commonly used method is reconstructing the elementary anatomy and this is via the route on wi reconstruction. And another way is that patients who have early t one A tumors. So this is a tumor that is confined to the mucosal layer. Specifically, they may be offered endoscopic mucosal resection or endoscopic mucosal dissection. Let's have a look at the root on Y reconstruction surgery. So we've got two images, we've got A and B. So this diagram shows the total gastrectomy with the root on Y esophageal gins, which is image A and image B which is a proximal gastrectomy with a double tract uh reconstruction. So what we can see in image A is that the entire stomach has been removed, part of the jejunum has then been been taken up and you formed an anastomosis with the beginning of the esophagus and the jin with image B only partially. So the proximal stomach has been removed, the distal stomach still remains. We've got two anastomosis here. So we've got one with the esophagus and the jejunum. And we've got another anastomosis if we can see my mouse right here between the juju and the stomach as well. So these are two types of procedures which both involve er room wire reconstruction. The other procedure then is endoscopic mucosal resection. Now, this is this is a really, really good procedure. Um and you know, carrying out this procedure means that the patient is actually in a very, very early stage of the cancer. So it's often curative. This procedure is a minimally invasive procedure um for removing gi cancers and precancerous lesions. It's done by using an endoscope. So the growths are removed with the help of an electrical snare, which is this black wire that you can see going around the mass and the way it works is that you form a loop at the end which tightens around the tumor and then you pass an electrical current through the wire, that electrical current will allow the separation of the tumor. And at the same time, it cauterizes the wound. The procedure is very, very useful for removing er polyps as well as well as other small growths um that might be present in the gi tract. And depending on which part of the gi tract we are in the procedure can either be done through the mouth or through the anus. Now, for us, um with, you know, focus on upper gi this procedure will be done through the mouth. Um It is a great curative procedure for tumors that are less than two centimeters in diameter or like I said before, um they are t one a category. So with all surgery comes its complications and this is as I as important as explaining the positives of the surgery. So every patient needs to know this. So there is a 2.5% of death during surgery which can be due to various reasons. Quality of life remains poor for up to six months, post surgery. Sometimes this is longer. If there are other complications that come about during this period, there is a 5 to 10% chance of an anastomotic leak. So this leak, um basically is of Luminal contents leaking into the abdominal cavity. This is quite severe and needs to be looked at urgently because this can cause contamination of the abdominal cavity, which can then progress to severe sepsis. You then have dumping syndrome. So for anyone that doesn't know who dumping syndrome is, this is when um food is quickly moved from the stomach into the intestine. Um So it's like like like, you know, dumping the food into the intestine. It is quite common after gastroesophageal surgery and it requires specific diet control to prevent from happening. You can also get impacted um you know, vitamin b12 deficiency. So again, you know, post surgery, this this vitamin b12 deficiency is very, very common, it can occur. So patients will often need to be given supplements for this and lastly reoperation, which is another complication of surgery. So, bearing that in mind, um you know, bearing all of those complications, the 10 year survival rate for gastric cancer overall is around 15%. And that's also very, very stage dependent. Most gastric cancers, like I said, present in a much later stage of the disease. So they have a five year survival of less than 5%. And those patients that present at at a much later stage will be then be offered palliative management. So these you know, these uh involve chemotherapy, less supportive care and stenting and palliative surgery can also be used sometimes when stenting fails. So usually the surgery that is offered to patients for palliative management is distal gastrectomy which is offered um for relief of pain and better quality of life. Ok. So earlier on the presentation, we talked about the public health perspective on gastric cancers and what can be done to detect it early. So that that slide directly um reflects on this slide which is prevention, screening. So patients should be advised about lifestyle changes, especially if they are experiencing symptoms such as abdominal pain, reflux or painful, swallowing, uh chemoprevention. So this is for any patient that is at a higher risk um of developing cancer or they are at suspected um you know, early stage cancer. So, chemoprevention can be given to these patients and obviously, h pylori eradication as well. Secondary prevention involves regional and nationwide screening programs and then treating premalignant lesions or early stage cancer. Ok. So that completes the gastric cancer part of the presentation. We'll have a look at another case study for gastric cancer. Um Hopefully everyone's still awake to get involved with this, right. So a 67 year old man attends his GP with a six week history of upper abdominal discomfort. His symptoms are vague and he describes them as indigestion but they appear to relate to the epigastrium. He also has noticed he has lost his appetite and lost 2 kg in weight. He has no dysphagia and has not experienced nausea, vomiting or hematosis. He has been taking antacid suspension and also an H two blocker for over the counter at the pharmacy with minor alleviation of symptoms, no other medication or history of note. So this so he is an alcohol drinker and smokes. So sorry, sorry, he's not an alcohol drinker but smokes 5 to 10 cigarettes per day. He has recently retired from his job as an office manager on examination. He looks pale but is not jaundiced. Chest and respiratory examination is normal. Some small hard non tender nodes are present in the left supraclavicular fossa, but no other nodes are palpable and no definite mass or organomegaly is present in the abdomen. Ok. So I hope everyone's got that once again. Um Oh, so before that, we've got blood results from the GP. So blood results show. So the hemoglobin is low, the M CV count is low and the E sr is increased. Everything else using these LFT S white cell count platelets, they're all within the normal range. So, what do you think the differentials are for this patient? Again, if you just stick your answers in the chat, I will read them out. Uh We've got stomach cancer. Yeah. So that would be the top of the list for adenocarcinoma. Absolutely. See if there's any more. So, your stomach cancer and adenocarcinoma. Yeah. So gastric carcinoma, that would be the top of the list for me as well. Uh We could also have peptic ulcer disease, gord, um gallstone disease and even chronic pancreatitis. We're trying to stretch it a bit. Um depends. So these are all differential diagnosis for this patient. So, what investigations then would we like to carry out? So, you've already seen the blood report from the GP O GD again? Absolutely. Yeah. So I'd go for bloods. So we've got the bloods already for, from the GP. Um, O GD would be the first line investigation. And then you can also do a CT chest abdomen pelvis as well. That depends on whether the patient is able to tolerate the O GD or not. So, the patient was able to tolerate the O GD and it demonstrated a large probable malignant ulcer on the greater curvature of the stomach and biopsies confirm malignancy what would be the most appropriate next investigation. Then after this, we've got ac Act tap, not sure what a tap is, but CT so I'm thinking that's a thorax, abdomen pelvis. Ok. Another pet scan maybe so uh pet scan is definitely there as well. Obviously, we know that pet scan is not that useful for gastric cancers. Um But absolutely. So CT chest abdomen pelvis. Yeah, definitely there. So actually, I've got an image of the CT chest abdomen and pelvis. Um and I've labeled it here so we can talk through what each thing is. So what we can see on the right side, it's label A is the right lobe of the liver B shows the left kidney C is the hepatic flexure colon. So that's quite, that's the bright white um thing you see then you have D which is the paraaortic adenopathy. E is a thick walled stomach and f is your aorta. So the CT confirms a probable metastatic disease in the peritoneum and the paraaortic nodes. Um probable liver metastases are also present not on this image, but they are present bearing that in mind. What treatment would you then consider for this patient? Um palliative treatment. Yeah, maybe chemo good. Yeah. Um palliative treatment, chemotherapy both then just the first line. Brilliant. Um Yeah, that's absolutely what you'd want to go for for this patient. You can also do stenting, um which will help for mechanical obstruction. This patient is at a, you know, late stage of the disease. Um and most likely surgery won't really help unless you're trying to relieve painful patient, palliative would be the way forward for this person. Ok. Um That is the end of the presentation. Uh Thank you, everyone. Um who got involved and uh thank you for getting involved in the case as well. Hope you enjoyed it. If you have any questions, please let me know. Thank you so much for such an amazing talk of going through those two conditions and cases in so much detail, really helpful, especially for me as well. Um And thank you to everybody who answered questions in the chat. It's amazing when the audience actually gets involved. Um I've just put the feedback form in the chat. If you guys can fill that in, you'll get a copy of the slides and you'll also get access to the recording once it's processed, it may not happen straight away. It takes a bit of time, but our next session is on Thursday or is it tomorrow night? I can't remember but subscribe to med all on, um, subscribe to us on Medal. So it's a follow up done. You'll get notified whenever we have um teaching sessions. Also follow us on Facebook and also Instagram. We will also post some Mc Qs at the end of the week for you guys to test your um knowledge massive. Thank you once again to our sponsors and also for Hussein, our amazing speaker this evening. Um without you guys, you wouldn't be able to hold this lecture series. So honestly, thank you so much. So big round of applause for you. Any questions, please place them in the chats, but otherwise have an amazing evening. You've, I think you can see the chat now you've had some. Next, next session is at Thursday at 6 p.m. There we go. Thank you, Rohita helpful. As always for saving my back. So, there we go. Thank you so much as well. Thank you, Florence. All right, bye-bye.