Understanding Gastritis and Peptic Ulcers

What's up Ninja Nerds? In this video today we're going to be talking about stomach disorders that includes both gastritis and peptic ulcer disease. If you guys like these videos, they really help you, they make sense. I think some of the simple ways that you can truly show that appreciation is to support us by hitting that like button, comment down in the comment section, and subscribing. It really goes a long way to help us to keep making these free videos for you guys'enjoyment. Also, for your benefit, if you have the opportunity and the ability to, go down the description box below. There's a link that goes to our website. On our website, we have a lot of amazing things that I think will help to augment your learning process. Things like really amazing notes, illustrations, quiz questions, and we're even developing exam prep courses to streamline your learning process. become a member and check out some of those cool stuff. All right, let's talk a little bit about stomach disorders. So we'll talk first about gastritis, and then we'll finish off with peptic ulcer disease. I think it's really important to talk about these in combination, because oftentimes they can be somewhat difficult to differentiate, because they do have a lot of the same pathophysiology, a lot of the same similar complaints, which is some minor differences, and we'll try to talk about those things. So gastritis is inflammation of the stomach lining, right? So it primarily involves the mucosa. So it's a lot of mucosal inflammation. And we'll represent that gastritis as where it most commonly occurs. And it's usually going to be somewhere along like the antrum. So you're going to have most likely here antral involvement. And so here's a little bit of gastritis. So gastritis primarily occurs within the antrum. Is going to be the most common location. And again we kind of classify this as basically. some inflammation of the stomach lining with associated very small mucosal erosions. So if I were to take a piece of this kind of inflammatory material and kind of zoom in and out on the microscopic level, it's important to remember your layers of the alarminary canal. We have serosa and pink, here in the red one this cheek chunky one is the muscularis externa, the blue one is the submucosa, and then you have these three components of the mucosa, the epithelial layer, this purple maroon color which is the lamina propria and then the muscularis mucosa. Oftentimes when we talk about patients who develop gastritis it's also often classified as kind of generalized inflammation that can cause a couple different things. You may see one particular factor here which is you may see these small little erosions. So here we have some erosions and these erosions don't really extend super deep. They're really shallow and that's really really important. important. That's one big differentiation between gastritis and peptic ulcer disease. Small shallow erosions that usually only extend through the epithelial layer and sometimes into the lamina propria, but they'll never cross the muscularis mucosa and go into the submucosa. If they do, it's no longer gastritis, it's ulcers, peptic ulcers. That's one particular thing. Another thing is that these patients usually also have, when it comes to gastritis, gastritis cause causes generalized inflammation. So a lot of these cells, like your normal cells, like the parietal cells, the actual chief cells, the mucus containing cells, all of these things becomes a little bit inflamed and injured. And another thing that's really important here is that sometimes there's this generalized mucus layer, and there's this mucus layer that's supposed to kind of neutralize the hydrochloric acid that's present inside of the stomach. And what we see in these patients is that they also have this like very thin mucus layer. So they have a thin mucus layer. That's another one. So when I see a patient with a thin mucus layer, I see shallow erosions, and I see a very big characteristic here, which is a lot of just generalized mucosal inflammation. This really, really suggests a patient that has gastritis. So these are the three things at the microscopic level that really suggest this patient having this classic inflammation and erosions in the antrum. The question is, that comes up is what's the classic finding the patients who have gastritis and usually because it's in the stomach and it's in the antrum it often gives this what's called epigastric abdominal pain so oftentimes the classic finding here is epigastric abdominal pain now here's the thing Gastritis has been thought that it could be more related to what we call dyspepsia, meaning that it can be affected by the concept of if we eat food, does it worsen the pain or decrease the pain? And it's actually really interesting because we haven't seen a lot of like relationship, significant relationship between the patient who has epigastric abdominal pain related to gastritis and food making it worse or better. And so it's no really specific thing there. It is really helpful for patients who develop changes in their epigastric abdominal pain when they have food consumption with peptic ulcer disease. And so we'll use that as a differentiating factor. Okay, antral inflammation, erosions, This is the common location epigastric abdominal pain question is what's causing this inflammation, what's causing these shallow erosions, and what's causing this thin mucus layer. So we come over here to the pathophysiology and these are the four most common causes that are going to be tested on in your exam. The first one's NSAIDs and ethanol, and I put more of an emphasis on the NSAIDs. And what happens here is that these drugs will lead to, they inhibit an enzyme. You know they inhibit this enzyme. It's called cyclooxygenase. And cyclooxygenase is supposed to take and convert arachidonic acid into prostaglandins. But if I inhibit that enzyme, can I make prostaglandins? No. And so what happens is my prostaglandin production, and there's many different types of prostaglandins. I think it's a little bit beyond the scope. of this lecture to go over each type, but you will have a drop in the prostaglandin production. This drop in the prostaglandin production leads to two effects. One is prostaglandin production is very acutely tied to the production of hydrochloric acid by these special cells called parietal cells. Whenever there's decreased prostaglandins, prostaglandins is supposed to tamper down the parietal cell production of hydrochloric acid. But if you have... have less of it what happens to the hydrochloric acid it increases and so they develop an increase in hydrochloric acid this hydrochloric acid is what causes inflammation and injury to all the mucosal lining so here we're going to get some inflammation and if it gets really really bad it can lead to erosions where the antrum and will precipitate epigastric abdominal pain this is by the parietal cells here we'll write that down this is called our parietal cells. These are the cells that make two things. One is they make hydrochloric acid and they also make this thing called intrinsic factor. Now when the parietal cells are injured we see that effect but here's the other one. We have these mucus containing cells and these mucus containing cells they almost call are called foveolar cells not necessarily goblet cells they're similar but they produce what's called an alkaline mucus and if you have less prostaglandins you make less alkaline mucus. And so what happens is the alkaline mucus, which is going to be a mucus rich in a lot of bicarbonate, you know what the purpose of the dang mucus is? It's supposed to neutralize the hydrochloric acid and create a thick layer here that protects these cells. If I don't have that, this thing can go uncontrolled and cause more inflammation and erosions. And so this is the primary pathophysiology of why lots of NSAIDs, lots of heavy alcohol use have been tied to patients developing gastritis and sometimes even peptic ulcer disease. So memorize this pathway. Another one is a really, really big one. This is more of an acute cause. It can lead to more chronic gastritis, but this one's a really big one that can also be found in acute and chronic gastritis. H. pylori is a bacteria, and this has two interesting effects. One is the bacteria, through some mechanism, we don't really know how, but it can actually increase the production of, you have specific cells, they're in teraendocrine cells, and they can make a hormone called gastrin. And through some mechanism, we don't really know how, but H. pylori may increase the production the production of gastrin. The thing with gastrin is it does the same thing is it actually has a direct stimulatory effect on parietal cells and if gastrin is in high amounts what it'll do is it'll stimulate these parietal cells and these parietal cells will pump out tons of hydrochloric acid and if they pump out hydrochloric acid and it's very large amounts what do you think it can do we already talked about it it'll lead to inflammation and it'll lead to erosion of the stomach mucosa. The other concept is even a little bit more complicated though, and this is actually the big one. And I think this is really, really pertinent to your actual diagnostics. H. pylori is a bacteria that's really interesting because it can make a very interesting enzyme called urease. And urease is this enzyme that, thus the name, it can break down urea and convert it into what's called ammonia. So that's what will happen. They'll actually make lots of ammonia. ammonia, because there's lots of urea naturally within our stomach contents. So when it makes lots of this ammonia, what it does is it makes the actual pH of the stomach more alkaline, because this is a base. And when you make... The pH more alkaline, it increases H. pylori. Survival. These things can survive longer. And these things have particular types of toxins, like cagade and tabacate toxins that they release that affects the permeability and directly injures the actual cells of the mucosa. And so they induce a... cytotoxicity to these actual cells. When there's an increase in the cytotoxicity, there's more injury to the mucus. mucosal cells, more inflammation, and then thus over time you'll end up with these nasty erosions as well. Okay, so with these patients we now see H. pylori, how this one can cause gastritis. The next one's really interesting and this is called Curling's ulcers. Curling's ulcers and Cushing's ulcers are what we sometimes refer to as stress ulcers. And I think this is a misnomer. And I think it's really important to be able to differentiate. Because when I talk about ulcers, ulcers means that I'm passing into the submucosa. These don't pass into the submucosa. So they're technically a misnomer in their terminology, where it's a Curling's or Cushing's ulcers. They're not really true ulcers. They cause inflammation and small mucosal erosions. Really important thing to differentiate. But Curling's, I want you to think about the classic clinical vignette as a burn. burn, so a curling iron. So patients often get these terrible burns and these burns lead to hypovolemia. So they drop a patient's blood volume because when you get burns, you lose a lot of your actual blood volume, all right, because you cause massive dehydration because you're losing a lot of fluid from cells. This affects your circulatory perfusion. Another common effect is sepsis. And sepsis leads to increased dilation. dilation and capillary permeability. So now these vessels are dilated and also super permeable. The combination of these is you end up with decreased perfusion to tissues. So now if I have decreased perfusion to my tissues, what do you think is going to happen? I'm going to lead to ischemia. And if I lead to ischemia to the actual tissue of the stomach, the mucosal lining, so we'll put here, we'll put in like parentheses, mucosal. ischemia, what do you think can start happening? It'll cause massive inflammation from hypoxia and it'll cause mucosal injury and some types of small erosions from maybe minor necrosis there. And so these patients can develop, we'll kind of bring this one over here, kind of same thing, save us some time and space. This will precipitate increased inflammations and erosions due to poor perfusion. So remember, the primary stimulus here is burns and sepsis, okay? Just a different pathophysiological process. But under the umbrella, of critically ill patients we call this Curling's Ulcers. The other one's really interesting, I want you to think cushion, think of brain. There's a lot of kind of cushion within the brain, but what happens is when patients have brain injury, they end up with a very, very high intracranial pressure. And whenever the intracranial pressure is super, super high, through mechanisms that are really really interesting you create these kind of like reflex mechanisms because what happens in your icp is really high you try to increase your blood pressure to perfuse the brain and it creates a vagal reflex and your vagus nerve kind of becomes super hyperactive and if your vagus nerve you may have increased vagus nerve activity this goes back to where you have to understand like basic physiology here do you remember what the vagus nerve releases onto parietal cells you guys remember acetylcholine and so there'll be an increase in acetylcholine release And if there's an increase in acetylcholine on these parietal cells, it's going to cause them to pump out more hydrochloric acid. And if they pump out more and more and more hydrochloric acid, what do you think is going to happen? It's going to cause potentially the same thing. More inflammation because it can damage the tissue, erode the tissue, and cause gastritis. So these are the big things that I really want you to remember. Is if I said patient has epigastric. pain you think it could be gastritis because it's not really changing the food the types of changes you think any NSAID use like chronic alcohol use is there a chance they get a H pylori I have to test for that one could it be induced from really significant stress on the body like burns and sepsis or high intracranial pressure okay that gives us this concept there is one small like subtype I don't want to beat it like a dead horse I don't want to go too crazy but we call this one autoimmune gastritis And it doesn't have the same mechanism. And this one's interesting. Your body generates these antibodies. And these antibodies, they go and they attack those special cells that we've been kind of hitting a lot in pink. What are those cells called? They're called parietal cells. And when they attack the parietal cells, they'll injure the parietal cells. And they'll cause dysfunction of the parietal cells. And the parietal cells not only make hydrochloric acid, but they also make that other thing I told you, which is called B12, an intrinsic factor. And they also make hydrochloric acid. If you damage the parietal cells, you injure them, you'll drop the hydrochloric acid which can lead to some complications and you'll drop the intrinsic factor which can lead to some complications. The only thing is is this cause dysfunction, it causes atrophy. That's really important to remember. This process here leads to atrophy of the actual stomach lining as compared to all of these which leads to inflammation and erosions. And so if someone says I have a patient with autoimmune gastritis this doesn't cause any of these problems. classically cause inflammation and erosions it can cause a weakness kind of like really decreasing kind of like amount of tissue thinning of the tissue but it most commonly affects more around the fundus and so we'll use this in a blue color it affects more around the fundus so if I said fundal involvement of the stomach you think autoimmune but if I said it's more antral involvement you think about these okay now we come down and talk about PUD or peptic ulcer disease. So peptic ulcer disease, same thing, it's involving the stomach, but here's another big differentiating point. You can develop this inflammation in ulcers of the stomach, but guess what's more common? It's more common for you to get ulcers of the duodenum. So there's two locations that now are actually occurring with the stomach. One is the duodenum and one is the antrum. Same thing as we talked about above. And so you can have what's called an antral location, and you can have the duodenum as a location. Between these, which one is actually more common to cause these nasty inflammation and ulcers? It's actually going to be this one. And that's really, really important to remember. Now, one other big thing is because this definitely involves the stomach and it can involve the duodenum. same thing it's gonna produce epigastric abdominal pain that's the classic finding so you'll see a patient who has epigastric abdominal pain we're like Zach so did gastritis and as I can already see over here a lot of these causes are coming up above So how am I supposed to differentiate these? It can be tough. Sometimes it may have to be kind of like a pathological diagnosis that you get from a biopsy or kind of an EGD look. But when it comes to history, this epigastric abdominal pain may lend to you a little bit more help when it comes to the presence of food. So if you introduce food to these patients, it can cause kind of an interesting type of process. Let's say I introduce food to a patient and they have food. have a antral or gastric ulcer. So if it's a gastric ulcer the pain is greater. So that's the way I remember it is gastric or antral location. The gastric ulcer when I introduce food the pain is greater. It increases if you will. Okay so the pain will increase. Duodenal decreases. That's the kind of the best way that I think helps me to remember this. is duodenal will cause the pain to decrease when you introduce food. And I think the concept behind this is really due to the presence of food and the production of hydrochloric acid in the stomach. During that time period it's going to hit the stomach. It won't really actually affect the stomach, the actual duodenum, but then eventually after a couple hours after you've eaten and you dump that food that's actually rich in hydrochloric acid into the duodenum, guess what happens? The pain starts to come. And that's something that you'll see with duodenal ulcers. They won't hurt, they'll actually decrease in pain when you give them food, but then later after the patient stops eating that pain will start to come back and increase okay all right that's the way I want you to remember this when it comes to the location and the classic findings but the other thing that you have to know is at the microscopic level if I take a piece of this ulcer and zoom in on what's the big difference this is the big difference this is a true ulcer okay this is a deep submucosal and beyond ulcer. And that's one really, really big difference between these two. As I told you before, gastritis, if it does cause erosions, it will not break past the submucosa. This one will. There's also going to be the same thing. There's going to be injury to these cells. So there's going to be... inflammation. So it's not just going to be a submucosal and beyond ulcer, you're also going to have lots of inflammation. And then lastly, the same kind of concept as we talked about above in these patients, you're also going to have a thin mucus lining. These cells that are supposed to produce that mucus, that mucus layer is going to be a little bit thin. So as you can kind of see the kind of microscopic difference that really kind of comes in between these two is just the presence of really deep ulcers and then the location and then the pain changes with food. But again pretty similar concept where they're both going to have a very thin mucus layer, they're both going to have inflammation, they both have erosions but one is going to be really deep ulcerations and one's a shallow type of ulceration. Alright these are the big kind of things I want you to understand. Question arises again what's causing this massive degree of inflammation that's causing inflammation and kind of erode this actually nasty ulcers and thin mucus layers that are leading to these ulcers forming particularly within the antrum and the duodenum causing this terrible pain. Well you already kind of know these and I won't go too ham on these I think it should be a quick recap where the insets and ethanol what do they do and then have it the cox enzyme that leads to prostaglandin production I'm gonna put PG that leads to what we said the parietal cells you're gonna lead to a increased hydrochloric acid production a decrease in mucus production and that'll lead to ulcers and inflammation That was a pretty quick recap of that concept. Antibiotic toxin enzyme, decrease the prostaglandins, increase hydrochloric acid from parietal cells, decrease the alkaline mucus, and lead to ulcer formation. All right, cool. So that's the big, big things here to remember. The other concept, and I'd say that this is the second most common cause, this is the most common cause of peptic ulcer disease. Most common. Patients who have H. pylori, they make life really difficult, but it's the same kind of concepts that we talked about above. So again, what happens with this sucker here? What does he do? He causes increased gastrin production. And this can occur in two places. It can occur in the duodenum, it can occur in the stomach. Either way, hydrochloric acid. acid starts to increase. If it increases, it leads to ulcers and inflammation. The other concept is the same thing as we talked about above. It's a good quick recap here, is that what happens is this will cause urease, really important enzyme that breaks down ammonia into, I'm sorry, breaks down urea into ammonia. Ammonia levels will increase, creates an alkaline environment, allows H. pylori to survive. So it increases their survival. If it increases, If H. pylori survives, it can cause direct cytotoxic damage to the mucosal layer and cause nasty ulcers to form and create spaces between the cells which allows for the acid to erode in between the cells into the deeper layers. So it's going to induce cytotoxicity. Now Once all of this kind of happens, cytotoxicity, these patients will start to have these nasty, nasty ulcers and all of these particular problems like massive inflammation. All right, but here is going to be again just that quick. recap, they make lots of urease, increase in pneumonia, increase H. pylori survival, increase cytotoxicity, and we see this particular problem. Okay, quick last one here. So this is the most common cause. The second most common cause of the NSAIDs is ethanol. The last one that I would really want you guys to remember if a patient has refractory duodenal ulcers. So if you hear the term refractory duodenal ulcers, that is refractory. to treatment they just are not getting better I want you to think about a gastronoma this is a tumor that usually sits around the level of the pancreas and what this thing does is it pumps out tons of gastrin and this gastrin will act on a bunch of different cells like parietal cells and pump up a ton of hydrochloric acid that hydrochloric acid will lead to refractory duodenal ulcers and inflammation and I think that is a really really big thing to remember here guys okay so with that being said if I see A potential very high level of gastrin causing increased hydrochloric acid production and the formation of refractory duodenal ulcers. I'm definitely going to want to take into consideration, could this patient have a gastrinoma? This disease we actually kind of call a very interesting one. It's called Zollinger-Ellison. syndrome so don't forget that if I think the Zollinger-Ellison syndrome I'm looking for a gastronoma okay my friends we covered a lot about stomach disorders talked about gastritis we talked about peptic ulcer disease now what I want to do is I want to say we have a patient who comes in with epigastric abdominal pain, and then on top of that, they develop some scary complications. Let's go into that next. All right, my friends, on to now the complications of stomach disorders. I think the real big thing is that oftentimes gastritis, it's relative. benign and doesn't really cause a lot of complications. It may to some degree cause small mucosal ulcerations that cause a little bit of GI bleeding, but oftentimes it's pretty rare for it to cause pretty profound GI bleeds. With that being said, peptic ulcer disease has a good amount of complications that I think are really important for you to be able to identify and watch out for. So if a patient comes in with epigastric abdominal pain, whether it's a gastric abdominal ulcer that is either greater with food gastric decreases of food duodenal we know that they're having 10 tense epigastric abdominal pain could be due to H pylori big one NSAIDs ethanol or gastronoma when they come in the things that you should be looking for is are they exhibiting any features of a GI bleed one of the reasons why is that as patients start to develop these nasty kind of like ulcers so as they cause lots of inflammation here and it starts to erode through the actual tissue wall especially into the submucosa it can to really get kind of close to some decent vessels that are running within the lesser curvature or in the greater curvature. And so let's say here that it actually does end up causing artery erosion. So it starts to kind of erode. in the arteries. And there's usually two locations. One is it can start to erode into the arteries near the lesser curvature, that's the most common one, and it can kind of erode into the left gastric artery, or near the greater curvature, which is where the gastroduodenal artery is. So this is gonna be the more common one. This will be the second most common one. When it starts to erode via these arteries, bleeding will start to ensue. So you'll start getting blood that'll leak into the stomach. Now, if blood does leak into the stomach, what can happen? It can go two ways. And one way is it will cause the patient, if they do, to vomit out blood. What's that called? Hematemesis. So if I see a patient who is vomiting up blood, that would definitely be making me think about what's called an upper GI bleed. Another way that patients often present with upper GI bleeds is that this blood gets into the stomach, it gets oxidized by the hydrochloric acid, moves through the duodenum, and eventually moves out via the rectum and anus. into the stool and what happens is it causes the stool to become more darker appearing and black kind of appearing and so oftentimes these patients can present with melena And worst case scenario, if you lose enough blood, these patients could go into hypovolemic shock and develop profound anemia. And so worst case scenario, the absolute worst case scenario, so worst case scenario, let's say here, worst case scenario. These patients could lose enough blood where they start to develop signs of hypovolemic or hemorrhagic, which is that subtype of shock with profound anemia. Alright, so this is you the big thing that I would want to watch out for is if a patient has history of peptic ulcer disease and they come in a hypovolemic shock with hematemesis melana definitely start thinking about an upper GI bleed so this can definitely cause an upper GI bleed bleed. All right, what's another potential complication of peptic ulcer disease? And again, it's important to remember that this is actually one of the most common causes of upper GI bleeds, is peptic ulcer disease. A second thing that can also happen here is that this patient could start kind of really eroding through the mucosa, the submucosa, and they start to erode through the serosa. If the patient erodes, so they have what's called serosal erosion, they literally have eaten through all of the walls. So this patient has now caused so much erosion here in the antrum that it has started to completely erode through the serosa, so it went all the way from the mucosa, submucosa, muscularis externa, went all the way down to the serosa, which is the most outer layer, and boom. opens up, allows for any kind of gastric contents that may be here to then easily leak out into the peritoneum. What are some of those contents? It could cause stomach acid to kind of leak out there. It could cause bacteria to leak out here. It could cause air to leak out here. And so what are some of the ways that these patients will present? Whenever there's intense serosal erosion, it may cause perforation. So this is an example of parts of the bowel. This would be a stomach perforation. And whenever they perforate, they can cause things like air to leak out. And this could potentially, if they do cause air to leak out, this could lead to what's called a pneumoperitoneum. A pneumoperitoneum. That's one really, really big thing that you don't want to be able to miss, right? And so oftentimes a pneumoperitoneum, it can present maybe with just increasing abdominal pain, but oftentimes it's more of an intense abdominal pain with peritoneal findings. And another thing that's really interesting is they may present with an x-ray. If you get a KUB, you'll see a little bit of air leaking underneath the actual diaphragm. Oftentimes they'll present not just with an air leak there, but oftentimes they'll also be bacteria. and acid from the stomach that will cause inflammation of the peritoneum. And if it causes inflammation of the peritoneum, this is called peritonitis. So it's called para... tonitis. How do we classify peritonitis? Which is oftentimes these kind of coincide with one another. This is just air that leaked into the peritoneum from a perforation. Peritonitis is there's inflammation of the peritoneum. This is going to cause intense abdominal pain. This is going to cause rigidity. This is going to cause guarding. This is going to cause rebound tenderness. These are all common signs in combination with systemic inflammation, increasing white blood cell count, fever. These are definitely suggestive of perforation with ensuing peritonitis and and pneumoperitoneum. Okay, that's another potential complication. Another one, this is all usually acute. Another one is when patients have this really nasty peptic ulcer disease, and it usually occurs near the antrum, and they get intense antral fibrosis and edema. So let's say that a patient gets intense antral. edema from the kind of the nasty inflammation ulcers and Fibrosis so during the healing process it causes lots of fibrous tissue to be laid down here So usually near the antrum as we kind of go closer here towards the pylorus look you're going to have all of this fibrotic tissue that's kind of being laid down here. And here's all this edematous tissue. And that's because why? Usually nearby, you're having this related kind of ulcer and inflammation. Now, you have obstruction of the gastric outlet. Problem is, is I can't get any of my gastric contents to kind of be released into the actual duodenum. So this process here is being inhibited and it's kind of like a bowel obstruction in a way, except it's not really involving the bowel. And so what happens is these patients will get massive gastric dilation. So that's one big thing. They'll have intense gastric dilation. This will cause a lot of pain and abdominal distension. The other thing is, is that a lot of this content is going to stay in the stomach. And as you start causing gastric dilation, it'll eventually, the stomach will try to keep contracting and pushing and squeezing to push things down into the duodenum. But it's not going to do a good job. And oftentimes, this will cause a lot of vomiting, intense vomiting. So these patients will have very profound vomiting. They'll have intense epigastric abdominal pain because of the gastric dilation. This will increase their pain. pain. And on top of that, here's usually the thing that kind of seals the diagnosis, is whenever you take your stethoscope and you listen over the area of the epigastrium, you'll hear as the stomach really profoundly contracts and it hits this antral area of fibrosis and edema, you'll hear all the contents splash. And that's a very common finding which we call a succussion splash. So if you hear on auscultation this succussion splash, that's usually this fluid from intense gastric contraction because of gastric dilation. It's going to cause it to, boom, squeeze against the antrum and against the pylorus and floosh back. That's a really important thing to look for. If you hear succussion splash, increasing abdominal pain and vomiting in the scenario of a patient who has peptic ulcer disease, usually more chronic, you want to think about goo. I'm not kidding. It's called gastric outlet obstruction, often kind of abbreviated goo. All right, so watch out for perforation with pneumoperitoneum and peritonitis. Watch out for upper GI bleeding and watch out for gastric outlet obstruction. Last one is more of a chronic finding. This is usually as patients develop peptic ulcer disease, there is chronic inflammation. So you can see a little bit of an upper GI bleed in gastritis to a very, very small degree. Very, very minor. In gastritis, you can also see a little bit of this thing as well because it's chronic inflammation. Anytime there is increasing chronic inflammation, which is what you can see in peptic ulcer disease. All right. You will cause cells to have to adapt and they will undergo dysplasia. And as they undergo dysplasia, you increase the risk of this kind of tissue, this inflamed tissue becoming more neoplastic, more cancerous. And this can cause two different types of gastric cancers. One is adenocarcinoma. And the other one is called Malt Lymphoma, which is usually very commonly associated with H. Pylori. What's the most common cause of peptic ulcer disease? H. Pylori. So oftentimes these patients can get Malt lymphoma and adenocarcinoma because of the chronic inflammation causing dysplasia. Now gastric cancer and a patient with underlying peptic ulcer disease you want to look for the classic features. Systemic features, low-grade fevers, weight loss, anemia, these are really really big things to watch out for. So definitely for these watch out for your classic features such as weight loss, anorexia. I think these are usually the big ones and then sometimes maybe like your low-grade fevers, okay? This is the primary complications associated with stomach disorders pertaining to peptic ulcer disease. Again, I don't want you to forget, yes, to assume small degree, gastritis can cause a small little upper GI bleed. In certain types of gastritis, I'll write it here, most particularly atrophic gastritis, there is a pretty high risk. of gastric cancer. So this is the only thing I think that's important. The other thing, I think it's more of a step one topic that you guys should be remembering, more pathology related, but atrophic gastritis can lead to complications like B12 deficiency. It's pretty straightforward. If you produce antibodies against parietal cells, they don't make intrinsic factor. Intrinsic factor binds B12 to aid in absorption. You don't make it, you don't absorb the B12. So watch out for a need. anemia. On top of that, they don't produce hydrochloric acid, so they have achlorhydria. They don't bind iron. They don't absorb iron. Patient develops anemia. So these are the big complications to remember for stomach disorders. Now let's move into the actual diagnostic approach. So we talked a lot about peptic ulcer disease. We talked a lot about gastritis. The next thing is to do is to talk about, okay, how do I go about diagnosing gastritis, the causes, and how do I go about diagnosing peptic ulcer disease, and that one more particularly and its causes. Well, the first thing is to do is to do a lot of research. So let's start with first thing is I have to make sure that the patient is not super, super sick because if they perforated, this is a big deal. I need to focus on that first. So what do I look for? I look for very severe abdominal pain, rigidity. I look for rebound tenderness. I look for fevers, maybe even a little bit of a white count, a leukocytosis. That's enough for me to say, I need to kind of really evaluate these patients. Maybe let's get an abdominal x-ray. And if I do that, look, remember I told you that they'll have what's called air underneath their diaphragm? That's indicative of a pneumoperitoneum. This patient's really sick. I need to get these patients more particularly to an OR, and I'll kind of do a diagnostic evaluation there. So I'll do what's called a laparotomy. And that's going to be the most important thing to identify. If they do not have a pneumoperitoneum, then I can kind of go and take a little bit of a more calculated approach, if you will. The first thing is I have to ask myself the question is, does this patient have epigastric abdominal pain without any alarm features? In other words, they have no complications. So do they have any evidence of GI bleeding, hematemesis, melanoma, anemia? Okay, they don't? All right, good. Do they have any evidence of weight loss? That would suggest maybe they have some potentially a cancer or do they have a gastric outlet obstruction? All right, they don't. Okay, good. Do they have any nausea and vomiting? Could that suggest a gastric outlet obstruction as well? So it's important for me to think about that to see if... if they have any complications related to their peptic ulcer disease. If they don't have any of those, but you still have a high degree of suspicion that they have peptic ulcer disease, then you can start testing them for H. pylori, since that's oftentimes the most common cause of peptic ulcer disease, and even to some degree, gastritis. So when I do this, I do it a couple different ways. One is I can test the antigens in their stool. So H. pylori will have antigens on it. And what I'll do is I'll take those antigens and I'll actually, you know, apply antibodies to see if they bind to those antigens. Because I know which type of antibodies I can actually utilize to bind to the H. pylori antigens. If they have H. pylori in their stool, meaning it came from their stomach, they'll have a positive stool antigen test. Because, again, it would have to pass from their stomach down into the duodenum, down into the large intestine, and it'll be in their stool. We'd have that and it would be positive. If that is the case, that adds to them saying that they could have. an infection with H. pylori. The other thing here is I can do what's called a urea breath test. A urea breath test is oftentimes one of the easier tests. What you do is you give them urea, all right? If it gets into their stomach and they have H. pylori, it will convert the urea into ammonia. If that also is present, it'll also make lots of CO2. When you have them breathe, they're going to have lots of CO2 that they would actually breathe out. And the higher that CO2 level is, the more likely it suggests that there's potentially a bacteria in their stomach with the urease enzyme helping to convert a lot of the urea into ammonia and CO2. And that's a really pretty good test. The other one is serology titers. These are not very good tests. This looks for potentially antibodies that your body has tried to develop against the H. pylori. But the problem is that they're often IgG antibodies. And that doesn't tell you if a patient has an active infection. So it's not super helpful at all. Oftentimes, the best non-invasive test is the urea breath test and the stool antigen test. Usually for diagnostics, urea breath test is better. For stool antigen test, we oftentimes use it to test patients as they're being treated to see if they eradicated the bacteria or not. But if they come up positive, it's probably maybe... H. pylori gastritis or peptic ulcer disease. Either way, you're going to treat them the same. If the stool antigen test came back negative, the urea breath test came back negative, the serology antibodies were negative, which again, not super helpful, but at least gives you an idea. It's unlikely that they have any H. pylori. And so therefore, I should look for another cause. What's the other one that I really don't want to miss? A Zollinger-Ellison syndrome. So then what I'll do is I'll obtain a serum gastrin level because in these patients, it's going to be exceedingly high. And if it is really high, then I got to do it one more test. I'm going to give them secretin. Now secretin is supposed to help to play a role in kind of suppressing the gastrin levels. If I give them secretin and the tumor is just pumping out gastrin regardless of secretin is present or not, then I would know. But here, if I give them secretin continuously high, that means that this tumor is not under regulation. It's likely Zollinger-Ellison syndrome. And so that would help me to add the diagnosis. So high gastrin levels that don't suppress with secretin would really give me the answer. And that's how I would go about diagnosing potentially the cause of H. pylori, gastritis, or peptic ulcer disease. And if it's not that, how do I determine if it's Zollinger-Ellison syndrome related to PUD? Now, what if they do have alarm features? Alright, so they have GI bleeding, they have anemia, weight loss, nausea, vomiting. Well, then I'm concerned about a complication. I really should get an EGD. All the time, when you have alarm features, get an EGD. Because what it may show me is, look at this narrowing of their gastric outlet. That's a gastric outlet obstruction. It may show me the evidence of a GI bleed. And that's why they're having hematemesis, melanoma, anemia. And also, it may show really, really large ulcers that are kind of concerning here. I think it's important if you see an ulcer, you should always try to biopsy that ulcer. And the reason why is if I get a biopsy, it'll help me to determine, is this really showing me some abnormal cells that look more of a malignant type of nature? That's a big, big thing. And I got to go down the cancer route. But if it actually shows me that the cytology is not abnormal for cancer cells, then I should really go the route of testing for H. pylori, which is going to be really good testing. And it's going to be something I can treat. So First one that we would do is the urease test. So if I get a piece of tissue, which has the H. pylori in it, I'm going to drop it into this test tube. And then what I'm going to do is I'm going to put a medium of urea. Alright, you already see where this is going. It'll turn pink if the actual bacteria is present. The reason why is the bacteria will have that... urease enzyme that'll chew up the urea and convert it into ammonia which will then help to turn the indicator on which gives it that pinkish color and that'll be one test that I could really use to say oh they definitely have H. pylori. The other test that I could do which is the gold standard test is I could actually take a piece of that tissue look at it under the microscope and use what's called a GM cysteine and you'll be able to highlight all of these like little bacteria and usually this is done by a pathologist. So this would be some testing that I'd be able to see as a potential way of saying, oh, they definitely have H. pylori. All right. And again, if they have H. pylori, it's really the look of the actual EGD that tells me, is it gastritis, which is small little mucosal ulcer, small little mucosal erosions, or if it's peptic ulcer disease, is these deep ulcers that go beyond the actual mucosa into the submucosa. All right. So that's how we would go about diagnosing these stomach disorders such as gastritis. and peptic ulcer disease, but more particularly saying, how do I identify any complications? And how do I identify if it's H. pylori or not? How do I identify if it's H. pylori or not? All right, my friends, we move on to the next step here, which is how do we treat these stomach disorders? You treat them all the same, regardless of its gastritis or if it's peptic ulcer disease. With this one, acid suppression therapy is going to be key. You really want to try to reduce a lot of the hydrochloric acid production, all right? The reason why is you don't want to worsen a lot of these ulcers or worsen a lot of the inflammation of the stomach lining. And so PPIs would be kind of your first go-to treatment here. The other thing is it's actually kind of beneficial to maybe pump up. So you want to reduce hydrochloric acid and maybe increase the alkaline mucus barrier. And so sometimes we actually may add on some drugs that helps to be able to increase those foveolar cells to make a lot of alkaline mucus and give you a thick barrier there. And this is going to be things like sucralfate or misoprostol. So again, reduce hydrochloric acid, thicken up the alkaline barrier. Another thing that you have to identify is do they have H. pylori? If they have H. pylori, you have to eradicate the infection. And oftentimes it's giving them clarithromycin and amoxicillin. All right. So it's usually clarithromycin, amoxicillin, and a PPI. We call that CAP therapy. If they have an allergy potentially to penicillin, then you switch it to metronidazole clarithromycin, all right, a PPI, and oftentimes you'll add in something like bismuth subsalicylate, which is like quadruple therapy. The other thing is that when you give them something to treat their H. pylori, you want to make sure that you're eradicating the H. pylori. And so you actually will test their stool antigen test. You could also do the urea breath test, but stool antigen test is actually relatively easy. And you're looking to see, hey, Have we given enough antibiotics for about 14 days that it's actually cleared out this infection? And that's the ways that we would do that. It's also important to remember that peptic ulcer disease comes with some pretty hefty complications, pretty scary ones. You have to be able to identify a GI bleed. And if they have alarm features, you need to get an EGD. And oftentimes the EGD will be enough to diagnose it and also at the same time, treat them by cauterizing it, using epi into the area and getting rid of that bleeding source. It's also important to remember that if they have evidence of a perforation, maybe there's a, you know, you do a KUB or an abdominal x-ray and you say, oh, shoot, they have a pneumoperitoneum and then features of peritonitis. I need to do a surgery. Usually it's a laparotomy. And they'll come in and what they'll do is they say, oh, he perforated right here on the antrum or he perforated around the duodenum. I'm going to take a part of the greater omentum. And what they do is they wrap it right over that. They use it as like a patch. Over where the area of the perforation is and they suture it down. That's called a gram patch. And then lastly, do they have gastric outlet obstruction that's evident on their EGD? Oh, they do? Okay, let's actually pass down this little dilator, expand and stretch open the gastric outlet, and then allow for food and fluid to easily flow so they don't have as much nausea, vomiting, weight loss, and the succussion splash that they may present with. All right, my friends, that talks about the treatment. And that finishes up our lecture on stomach disorders. I really hope that made sense and I hope that you guys enjoyed it. As always, until next time.

I think some of the simple ways that you can truly show that appreciation is to support us by hitting that like button, comment down in the comment section, and subscribing. It really goes a long way to help us to keep making these free videos for you guys'enjoyment. Also, for your benefit, if you have the opportunity and the ability to, go down the description box below. There's a link that goes to our website. On our website, we have a lot of amazing things that I think will help to augment your learning process.

Things like really amazing notes, illustrations, quiz questions, and we're even developing exam prep courses to streamline your learning process. become a member and check out some of those cool stuff. All right, let's talk a little bit about stomach disorders.

So we'll talk first about gastritis, and then we'll finish off with peptic ulcer disease. I think it's really important to talk about these in combination, because oftentimes they can be somewhat difficult to differentiate, because they do have a lot of the same pathophysiology, a lot of the same similar complaints, which is some minor differences, and we'll try to talk about those things. So gastritis is inflammation of the stomach lining, right? So it primarily involves the mucosa. So it's a lot of mucosal inflammation.

And we'll represent that gastritis as where it most commonly occurs. And it's usually going to be somewhere along like the antrum. So you're going to have most likely here antral involvement. And so here's a little bit of gastritis. So gastritis primarily occurs within the antrum.

Is going to be the most common location. And again we kind of classify this as basically. some inflammation of the stomach lining with associated very small mucosal erosions.

So if I were to take a piece of this kind of inflammatory material and kind of zoom in and out on the microscopic level, it's important to remember your layers of the alarminary canal. We have serosa and pink, here in the red one this cheek chunky one is the muscularis externa, the blue one is the submucosa, and then you have these three components of the mucosa, the epithelial layer, this purple maroon color which is the lamina propria and then the muscularis mucosa. Oftentimes when we talk about patients who develop gastritis it's also often classified as kind of generalized inflammation that can cause a couple different things.

You may see one particular factor here which is you may see these small little erosions. So here we have some erosions and these erosions don't really extend super deep. They're really shallow and that's really really important. important.

That's one big differentiation between gastritis and peptic ulcer disease. Small shallow erosions that usually only extend through the epithelial layer and sometimes into the lamina propria, but they'll never cross the muscularis mucosa and go into the submucosa. If they do, it's no longer gastritis, it's ulcers, peptic ulcers. That's one particular thing.

Another thing is that these patients usually also have, when it comes to gastritis, gastritis cause causes generalized inflammation. So a lot of these cells, like your normal cells, like the parietal cells, the actual chief cells, the mucus containing cells, all of these things becomes a little bit inflamed and injured. And another thing that's really important here is that sometimes there's this generalized mucus layer, and there's this mucus layer that's supposed to kind of neutralize the hydrochloric acid that's present inside of the stomach.

And what we see in these patients is that they also have this like very thin mucus layer. So they have a thin mucus layer. That's another one. So when I see a patient with a thin mucus layer, I see shallow erosions, and I see a very big characteristic here, which is a lot of just generalized mucosal inflammation.

This really, really suggests a patient that has gastritis. So these are the three things at the microscopic level that really suggest this patient having this classic inflammation and erosions in the antrum. The question is, that comes up is what's the classic finding the patients who have gastritis and usually because it's in the stomach and it's in the antrum it often gives this what's called epigastric abdominal pain so oftentimes the classic finding here is epigastric abdominal pain now here's the thing Gastritis has been thought that it could be more related to what we call dyspepsia, meaning that it can be affected by the concept of if we eat food, does it worsen the pain or decrease the pain? And it's actually really interesting because we haven't seen a lot of like relationship, significant relationship between the patient who has epigastric abdominal pain related to gastritis and food making it worse or better.

And so it's no really specific thing there. It is really helpful for patients who develop changes in their epigastric abdominal pain when they have food consumption with peptic ulcer disease. And so we'll use that as a differentiating factor. Okay, antral inflammation, erosions, This is the common location epigastric abdominal pain question is what's causing this inflammation, what's causing these shallow erosions, and what's causing this thin mucus layer.

So we come over here to the pathophysiology and these are the four most common causes that are going to be tested on in your exam. The first one's NSAIDs and ethanol, and I put more of an emphasis on the NSAIDs. And what happens here is that these drugs will lead to, they inhibit an enzyme.

You know they inhibit this enzyme. It's called cyclooxygenase. And cyclooxygenase is supposed to take and convert arachidonic acid into prostaglandins. But if I inhibit that enzyme, can I make prostaglandins? No.

And so what happens is my prostaglandin production, and there's many different types of prostaglandins. I think it's a little bit beyond the scope. of this lecture to go over each type, but you will have a drop in the prostaglandin production. This drop in the prostaglandin production leads to two effects.

One is prostaglandin production is very acutely tied to the production of hydrochloric acid by these special cells called parietal cells. Whenever there's decreased prostaglandins, prostaglandins is supposed to tamper down the parietal cell production of hydrochloric acid. But if you have... have less of it what happens to the hydrochloric acid it increases and so they develop an increase in hydrochloric acid this hydrochloric acid is what causes inflammation and injury to all the mucosal lining so here we're going to get some inflammation and if it gets really really bad it can lead to erosions where the antrum and will precipitate epigastric abdominal pain this is by the parietal cells here we'll write that down this is called our parietal cells.

These are the cells that make two things. One is they make hydrochloric acid and they also make this thing called intrinsic factor. Now when the parietal cells are injured we see that effect but here's the other one.

We have these mucus containing cells and these mucus containing cells they almost call are called foveolar cells not necessarily goblet cells they're similar but they produce what's called an alkaline mucus and if you have less prostaglandins you make less alkaline mucus. And so what happens is the alkaline mucus, which is going to be a mucus rich in a lot of bicarbonate, you know what the purpose of the dang mucus is? It's supposed to neutralize the hydrochloric acid and create a thick layer here that protects these cells. If I don't have that, this thing can go uncontrolled and cause more inflammation and erosions.

And so this is the primary pathophysiology of why lots of NSAIDs, lots of heavy alcohol use have been tied to patients developing gastritis and sometimes even peptic ulcer disease. So memorize this pathway. Another one is a really, really big one.

This is more of an acute cause. It can lead to more chronic gastritis, but this one's a really big one that can also be found in acute and chronic gastritis. H. pylori is a bacteria, and this has two interesting effects.

One is the bacteria, through some mechanism, we don't really know how, but it can actually increase the production of, you have specific cells, they're in teraendocrine cells, and they can make a hormone called gastrin. And through some mechanism, we don't really know how, but H. pylori may increase the production the production of gastrin. The thing with gastrin is it does the same thing is it actually has a direct stimulatory effect on parietal cells and if gastrin is in high amounts what it'll do is it'll stimulate these parietal cells and these parietal cells will pump out tons of hydrochloric acid and if they pump out hydrochloric acid and it's very large amounts what do you think it can do we already talked about it it'll lead to inflammation and it'll lead to erosion of the stomach mucosa.

The other concept is even a little bit more complicated though, and this is actually the big one. And I think this is really, really pertinent to your actual diagnostics. H. pylori is a bacteria that's really interesting because it can make a very interesting enzyme called urease.

And urease is this enzyme that, thus the name, it can break down urea and convert it into what's called ammonia. So that's what will happen. They'll actually make lots of ammonia. ammonia, because there's lots of urea naturally within our stomach contents.

So when it makes lots of this ammonia, what it does is it makes the actual pH of the stomach more alkaline, because this is a base. And when you make... The pH more alkaline, it increases H. pylori.

Survival. These things can survive longer. And these things have particular types of toxins, like cagade and tabacate toxins that they release that affects the permeability and directly injures the actual cells of the mucosa.

And so they induce a... cytotoxicity to these actual cells. When there's an increase in the cytotoxicity, there's more injury to the mucus. mucosal cells, more inflammation, and then thus over time you'll end up with these nasty erosions as well.

Okay, so with these patients we now see H. pylori, how this one can cause gastritis. The next one's really interesting and this is called Curling's ulcers. Curling's ulcers and Cushing's ulcers are what we sometimes refer to as stress ulcers.

And I think this is a misnomer. And I think it's really important to be able to differentiate. Because when I talk about ulcers, ulcers means that I'm passing into the submucosa. These don't pass into the submucosa.

So they're technically a misnomer in their terminology, where it's a Curling's or Cushing's ulcers. They're not really true ulcers. They cause inflammation and small mucosal erosions.

Really important thing to differentiate. But Curling's, I want you to think about the classic clinical vignette as a burn. burn, so a curling iron.

So patients often get these terrible burns and these burns lead to hypovolemia. So they drop a patient's blood volume because when you get burns, you lose a lot of your actual blood volume, all right, because you cause massive dehydration because you're losing a lot of fluid from cells. This affects your circulatory perfusion. Another common effect is sepsis.

And sepsis leads to increased dilation. dilation and capillary permeability. So now these vessels are dilated and also super permeable.

The combination of these is you end up with decreased perfusion to tissues. So now if I have decreased perfusion to my tissues, what do you think is going to happen? I'm going to lead to ischemia.

And if I lead to ischemia to the actual tissue of the stomach, the mucosal lining, so we'll put here, we'll put in like parentheses, mucosal. ischemia, what do you think can start happening? It'll cause massive inflammation from hypoxia and it'll cause mucosal injury and some types of small erosions from maybe minor necrosis there.

And so these patients can develop, we'll kind of bring this one over here, kind of same thing, save us some time and space. This will precipitate increased inflammations and erosions due to poor perfusion. So remember, the primary stimulus here is burns and sepsis, okay? Just a different pathophysiological process.

But under the umbrella, of critically ill patients we call this Curling's Ulcers. The other one's really interesting, I want you to think cushion, think of brain. There's a lot of kind of cushion within the brain, but what happens is when patients have brain injury, they end up with a very, very high intracranial pressure.

And whenever the intracranial pressure is super, super high, through mechanisms that are really really interesting you create these kind of like reflex mechanisms because what happens in your icp is really high you try to increase your blood pressure to perfuse the brain and it creates a vagal reflex and your vagus nerve kind of becomes super hyperactive and if your vagus nerve you may have increased vagus nerve activity this goes back to where you have to understand like basic physiology here do you remember what the vagus nerve releases onto parietal cells you guys remember acetylcholine and so there'll be an increase in acetylcholine release And if there's an increase in acetylcholine on these parietal cells, it's going to cause them to pump out more hydrochloric acid. And if they pump out more and more and more hydrochloric acid, what do you think is going to happen? It's going to cause potentially the same thing.

More inflammation because it can damage the tissue, erode the tissue, and cause gastritis. So these are the big things that I really want you to remember. Is if I said patient has epigastric.

pain you think it could be gastritis because it's not really changing the food the types of changes you think any NSAID use like chronic alcohol use is there a chance they get a H pylori I have to test for that one could it be induced from really significant stress on the body like burns and sepsis or high intracranial pressure okay that gives us this concept there is one small like subtype I don't want to beat it like a dead horse I don't want to go too crazy but we call this one autoimmune gastritis And it doesn't have the same mechanism. And this one's interesting. Your body generates these antibodies. And these antibodies, they go and they attack those special cells that we've been kind of hitting a lot in pink.

What are those cells called? They're called parietal cells. And when they attack the parietal cells, they'll injure the parietal cells. And they'll cause dysfunction of the parietal cells.

And the parietal cells not only make hydrochloric acid, but they also make that other thing I told you, which is called B12, an intrinsic factor. And they also make hydrochloric acid. If you damage the parietal cells, you injure them, you'll drop the hydrochloric acid which can lead to some complications and you'll drop the intrinsic factor which can lead to some complications.

The only thing is is this cause dysfunction, it causes atrophy. That's really important to remember. This process here leads to atrophy of the actual stomach lining as compared to all of these which leads to inflammation and erosions. And so if someone says I have a patient with autoimmune gastritis this doesn't cause any of these problems. classically cause inflammation and erosions it can cause a weakness kind of like really decreasing kind of like amount of tissue thinning of the tissue but it most commonly affects more around the fundus and so we'll use this in a blue color it affects more around the fundus so if I said fundal involvement of the stomach you think autoimmune but if I said it's more antral involvement you think about these okay now we come down and talk about PUD or peptic ulcer disease.

So peptic ulcer disease, same thing, it's involving the stomach, but here's another big differentiating point. You can develop this inflammation in ulcers of the stomach, but guess what's more common? It's more common for you to get ulcers of the duodenum. So there's two locations that now are actually occurring with the stomach.

One is the duodenum and one is the antrum. Same thing as we talked about above. And so you can have what's called an antral location, and you can have the duodenum as a location.

Between these, which one is actually more common to cause these nasty inflammation and ulcers? It's actually going to be this one. And that's really, really important to remember.

Now, one other big thing is because this definitely involves the stomach and it can involve the duodenum. same thing it's gonna produce epigastric abdominal pain that's the classic finding so you'll see a patient who has epigastric abdominal pain we're like Zach so did gastritis and as I can already see over here a lot of these causes are coming up above So how am I supposed to differentiate these? It can be tough.

Sometimes it may have to be kind of like a pathological diagnosis that you get from a biopsy or kind of an EGD look. But when it comes to history, this epigastric abdominal pain may lend to you a little bit more help when it comes to the presence of food. So if you introduce food to these patients, it can cause kind of an interesting type of process. Let's say I introduce food to a patient and they have food. have a antral or gastric ulcer.

So if it's a gastric ulcer the pain is greater. So that's the way I remember it is gastric or antral location. The gastric ulcer when I introduce food the pain is greater. It increases if you will. Okay so the pain will increase.

Duodenal decreases. That's the kind of the best way that I think helps me to remember this. is duodenal will cause the pain to decrease when you introduce food.

And I think the concept behind this is really due to the presence of food and the production of hydrochloric acid in the stomach. During that time period it's going to hit the stomach. It won't really actually affect the stomach, the actual duodenum, but then eventually after a couple hours after you've eaten and you dump that food that's actually rich in hydrochloric acid into the duodenum, guess what happens?

The pain starts to come. And that's something that you'll see with duodenal ulcers. They won't hurt, they'll actually decrease in pain when you give them food, but then later after the patient stops eating that pain will start to come back and increase okay all right that's the way I want you to remember this when it comes to the location and the classic findings but the other thing that you have to know is at the microscopic level if I take a piece of this ulcer and zoom in on what's the big difference this is the big difference this is a true ulcer okay this is a deep submucosal and beyond ulcer.

And that's one really, really big difference between these two. As I told you before, gastritis, if it does cause erosions, it will not break past the submucosa. This one will. There's also going to be the same thing.

There's going to be injury to these cells. So there's going to be... inflammation. So it's not just going to be a submucosal and beyond ulcer, you're also going to have lots of inflammation. And then lastly, the same kind of concept as we talked about above in these patients, you're also going to have a thin mucus lining.

These cells that are supposed to produce that mucus, that mucus layer is going to be a little bit thin. So as you can kind of see the kind of microscopic difference that really kind of comes in between these two is just the presence of really deep ulcers and then the location and then the pain changes with food. But again pretty similar concept where they're both going to have a very thin mucus layer, they're both going to have inflammation, they both have erosions but one is going to be really deep ulcerations and one's a shallow type of ulceration. Alright these are the big kind of things I want you to understand. Question arises again what's causing this massive degree of inflammation that's causing inflammation and kind of erode this actually nasty ulcers and thin mucus layers that are leading to these ulcers forming particularly within the antrum and the duodenum causing this terrible pain.

Well you already kind of know these and I won't go too ham on these I think it should be a quick recap where the insets and ethanol what do they do and then have it the cox enzyme that leads to prostaglandin production I'm gonna put PG that leads to what we said the parietal cells you're gonna lead to a increased hydrochloric acid production a decrease in mucus production and that'll lead to ulcers and inflammation That was a pretty quick recap of that concept. Antibiotic toxin enzyme, decrease the prostaglandins, increase hydrochloric acid from parietal cells, decrease the alkaline mucus, and lead to ulcer formation. All right, cool.

So that's the big, big things here to remember. The other concept, and I'd say that this is the second most common cause, this is the most common cause of peptic ulcer disease. Most common. Patients who have H. pylori, they make life really difficult, but it's the same kind of concepts that we talked about above.

So again, what happens with this sucker here? What does he do? He causes increased gastrin production. And this can occur in two places. It can occur in the duodenum, it can occur in the stomach.

Either way, hydrochloric acid. acid starts to increase. If it increases, it leads to ulcers and inflammation. The other concept is the same thing as we talked about above. It's a good quick recap here, is that what happens is this will cause urease, really important enzyme that breaks down ammonia into, I'm sorry, breaks down urea into ammonia.

Ammonia levels will increase, creates an alkaline environment, allows H. pylori to survive. So it increases their survival.

If it increases, If H. pylori survives, it can cause direct cytotoxic damage to the mucosal layer and cause nasty ulcers to form and create spaces between the cells which allows for the acid to erode in between the cells into the deeper layers. So it's going to induce cytotoxicity.

Now Once all of this kind of happens, cytotoxicity, these patients will start to have these nasty, nasty ulcers and all of these particular problems like massive inflammation. All right, but here is going to be again just that quick. recap, they make lots of urease, increase in pneumonia, increase H.

pylori survival, increase cytotoxicity, and we see this particular problem. Okay, quick last one here. So this is the most common cause.

The second most common cause of the NSAIDs is ethanol. The last one that I would really want you guys to remember if a patient has refractory duodenal ulcers. So if you hear the term refractory duodenal ulcers, that is refractory. to treatment they just are not getting better I want you to think about a gastronoma this is a tumor that usually sits around the level of the pancreas and what this thing does is it pumps out tons of gastrin and this gastrin will act on a bunch of different cells like parietal cells and pump up a ton of hydrochloric acid that hydrochloric acid will lead to refractory duodenal ulcers and inflammation and I think that is a really really big thing to remember here guys okay so with that being said if I see A potential very high level of gastrin causing increased hydrochloric acid production and the formation of refractory duodenal ulcers.

I'm definitely going to want to take into consideration, could this patient have a gastrinoma? This disease we actually kind of call a very interesting one. It's called Zollinger-Ellison.

syndrome so don't forget that if I think the Zollinger-Ellison syndrome I'm looking for a gastronoma okay my friends we covered a lot about stomach disorders talked about gastritis we talked about peptic ulcer disease now what I want to do is I want to say we have a patient who comes in with epigastric abdominal pain, and then on top of that, they develop some scary complications. Let's go into that next. All right, my friends, on to now the complications of stomach disorders. I think the real big thing is that oftentimes gastritis, it's relative.

benign and doesn't really cause a lot of complications. It may to some degree cause small mucosal ulcerations that cause a little bit of GI bleeding, but oftentimes it's pretty rare for it to cause pretty profound GI bleeds. With that being said, peptic ulcer disease has a good amount of complications that I think are really important for you to be able to identify and watch out for.

So if a patient comes in with epigastric abdominal pain, whether it's a gastric abdominal ulcer that is either greater with food gastric decreases of food duodenal we know that they're having 10 tense epigastric abdominal pain could be due to H pylori big one NSAIDs ethanol or gastronoma when they come in the things that you should be looking for is are they exhibiting any features of a GI bleed one of the reasons why is that as patients start to develop these nasty kind of like ulcers so as they cause lots of inflammation here and it starts to erode through the actual tissue wall especially into the submucosa it can to really get kind of close to some decent vessels that are running within the lesser curvature or in the greater curvature. And so let's say here that it actually does end up causing artery erosion. So it starts to kind of erode.

in the arteries. And there's usually two locations. One is it can start to erode into the arteries near the lesser curvature, that's the most common one, and it can kind of erode into the left gastric artery, or near the greater curvature, which is where the gastroduodenal artery is. So this is gonna be the more common one. This will be the second most common one.

When it starts to erode via these arteries, bleeding will start to ensue. So you'll start getting blood that'll leak into the stomach. Now, if blood does leak into the stomach, what can happen? It can go two ways.

And one way is it will cause the patient, if they do, to vomit out blood. What's that called? Hematemesis.

So if I see a patient who is vomiting up blood, that would definitely be making me think about what's called an upper GI bleed. Another way that patients often present with upper GI bleeds is that this blood gets into the stomach, it gets oxidized by the hydrochloric acid, moves through the duodenum, and eventually moves out via the rectum and anus. into the stool and what happens is it causes the stool to become more darker appearing and black kind of appearing and so oftentimes these patients can present with melena And worst case scenario, if you lose enough blood, these patients could go into hypovolemic shock and develop profound anemia.

And so worst case scenario, the absolute worst case scenario, so worst case scenario, let's say here, worst case scenario. These patients could lose enough blood where they start to develop signs of hypovolemic or hemorrhagic, which is that subtype of shock with profound anemia. Alright, so this is you the big thing that I would want to watch out for is if a patient has history of peptic ulcer disease and they come in a hypovolemic shock with hematemesis melana definitely start thinking about an upper GI bleed so this can definitely cause an upper GI bleed bleed.

All right, what's another potential complication of peptic ulcer disease? And again, it's important to remember that this is actually one of the most common causes of upper GI bleeds, is peptic ulcer disease. A second thing that can also happen here is that this patient could start kind of really eroding through the mucosa, the submucosa, and they start to erode through the serosa.

If the patient erodes, so they have what's called serosal erosion, they literally have eaten through all of the walls. So this patient has now caused so much erosion here in the antrum that it has started to completely erode through the serosa, so it went all the way from the mucosa, submucosa, muscularis externa, went all the way down to the serosa, which is the most outer layer, and boom. opens up, allows for any kind of gastric contents that may be here to then easily leak out into the peritoneum.

What are some of those contents? It could cause stomach acid to kind of leak out there. It could cause bacteria to leak out here. It could cause air to leak out here. And so what are some of the ways that these patients will present?

Whenever there's intense serosal erosion, it may cause perforation. So this is an example of parts of the bowel. This would be a stomach perforation. And whenever they perforate, they can cause things like air to leak out. And this could potentially, if they do cause air to leak out, this could lead to what's called a pneumoperitoneum.

A pneumoperitoneum. That's one really, really big thing that you don't want to be able to miss, right? And so oftentimes a pneumoperitoneum, it can present maybe with just increasing abdominal pain, but oftentimes it's more of an intense abdominal pain with peritoneal findings. And another thing that's really interesting is they may present with an x-ray.

If you get a KUB, you'll see a little bit of air leaking underneath the actual diaphragm. Oftentimes they'll present not just with an air leak there, but oftentimes they'll also be bacteria. and acid from the stomach that will cause inflammation of the peritoneum. And if it causes inflammation of the peritoneum, this is called peritonitis. So it's called para...

tonitis. How do we classify peritonitis? Which is oftentimes these kind of coincide with one another. This is just air that leaked into the peritoneum from a perforation.

Peritonitis is there's inflammation of the peritoneum. This is going to cause intense abdominal pain. This is going to cause rigidity.

This is going to cause guarding. This is going to cause rebound tenderness. These are all common signs in combination with systemic inflammation, increasing white blood cell count, fever.

These are definitely suggestive of perforation with ensuing peritonitis and and pneumoperitoneum. Okay, that's another potential complication. Another one, this is all usually acute. Another one is when patients have this really nasty peptic ulcer disease, and it usually occurs near the antrum, and they get intense antral fibrosis and edema. So let's say that a patient gets intense antral.

edema from the kind of the nasty inflammation ulcers and Fibrosis so during the healing process it causes lots of fibrous tissue to be laid down here So usually near the antrum as we kind of go closer here towards the pylorus look you're going to have all of this fibrotic tissue that's kind of being laid down here. And here's all this edematous tissue. And that's because why?

Usually nearby, you're having this related kind of ulcer and inflammation. Now, you have obstruction of the gastric outlet. Problem is, is I can't get any of my gastric contents to kind of be released into the actual duodenum. So this process here is being inhibited and it's kind of like a bowel obstruction in a way, except it's not really involving the bowel.

And so what happens is these patients will get massive gastric dilation. So that's one big thing. They'll have intense gastric dilation. This will cause a lot of pain and abdominal distension.

The other thing is, is that a lot of this content is going to stay in the stomach. And as you start causing gastric dilation, it'll eventually, the stomach will try to keep contracting and pushing and squeezing to push things down into the duodenum. But it's not going to do a good job.

And oftentimes, this will cause a lot of vomiting, intense vomiting. So these patients will have very profound vomiting. They'll have intense epigastric abdominal pain because of the gastric dilation. This will increase their pain. pain.

And on top of that, here's usually the thing that kind of seals the diagnosis, is whenever you take your stethoscope and you listen over the area of the epigastrium, you'll hear as the stomach really profoundly contracts and it hits this antral area of fibrosis and edema, you'll hear all the contents splash. And that's a very common finding which we call a succussion splash. So if you hear on auscultation this succussion splash, that's usually this fluid from intense gastric contraction because of gastric dilation.

It's going to cause it to, boom, squeeze against the antrum and against the pylorus and floosh back. That's a really important thing to look for. If you hear succussion splash, increasing abdominal pain and vomiting in the scenario of a patient who has peptic ulcer disease, usually more chronic, you want to think about goo. I'm not kidding. It's called gastric outlet obstruction, often kind of abbreviated goo.

All right, so watch out for perforation with pneumoperitoneum and peritonitis. Watch out for upper GI bleeding and watch out for gastric outlet obstruction. Last one is more of a chronic finding. This is usually as patients develop peptic ulcer disease, there is chronic inflammation.

So you can see a little bit of an upper GI bleed in gastritis to a very, very small degree. Very, very minor. In gastritis, you can also see a little bit of this thing as well because it's chronic inflammation.

Anytime there is increasing chronic inflammation, which is what you can see in peptic ulcer disease. All right. You will cause cells to have to adapt and they will undergo dysplasia.

And as they undergo dysplasia, you increase the risk of this kind of tissue, this inflamed tissue becoming more neoplastic, more cancerous. And this can cause two different types of gastric cancers. One is adenocarcinoma. And the other one is called Malt Lymphoma, which is usually very commonly associated with H. Pylori.

What's the most common cause of peptic ulcer disease? H. Pylori.

So oftentimes these patients can get Malt lymphoma and adenocarcinoma because of the chronic inflammation causing dysplasia. Now gastric cancer and a patient with underlying peptic ulcer disease you want to look for the classic features. Systemic features, low-grade fevers, weight loss, anemia, these are really really big things to watch out for.

So definitely for these watch out for your classic features such as weight loss, anorexia. I think these are usually the big ones and then sometimes maybe like your low-grade fevers, okay? This is the primary complications associated with stomach disorders pertaining to peptic ulcer disease.

Again, I don't want you to forget, yes, to assume small degree, gastritis can cause a small little upper GI bleed. In certain types of gastritis, I'll write it here, most particularly atrophic gastritis, there is a pretty high risk. of gastric cancer.

So this is the only thing I think that's important. The other thing, I think it's more of a step one topic that you guys should be remembering, more pathology related, but atrophic gastritis can lead to complications like B12 deficiency. It's pretty straightforward. If you produce antibodies against parietal cells, they don't make intrinsic factor. Intrinsic factor binds B12 to aid in absorption.

You don't make it, you don't absorb the B12. So watch out for a need. anemia. On top of that, they don't produce hydrochloric acid, so they have achlorhydria. They don't bind iron.

They don't absorb iron. Patient develops anemia. So these are the big complications to remember for stomach disorders.

Now let's move into the actual diagnostic approach. So we talked a lot about peptic ulcer disease. We talked a lot about gastritis. The next thing is to do is to talk about, okay, how do I go about diagnosing gastritis, the causes, and how do I go about diagnosing peptic ulcer disease, and that one more particularly and its causes.

Well, the first thing is to do is to do a lot of research. So let's start with first thing is I have to make sure that the patient is not super, super sick because if they perforated, this is a big deal. I need to focus on that first. So what do I look for?

I look for very severe abdominal pain, rigidity. I look for rebound tenderness. I look for fevers, maybe even a little bit of a white count, a leukocytosis.

That's enough for me to say, I need to kind of really evaluate these patients. Maybe let's get an abdominal x-ray. And if I do that, look, remember I told you that they'll have what's called air underneath their diaphragm?

That's indicative of a pneumoperitoneum. This patient's really sick. I need to get these patients more particularly to an OR, and I'll kind of do a diagnostic evaluation there. So I'll do what's called a laparotomy. And that's going to be the most important thing to identify.

If they do not have a pneumoperitoneum, then I can kind of go and take a little bit of a more calculated approach, if you will. The first thing is I have to ask myself the question is, does this patient have epigastric abdominal pain without any alarm features? In other words, they have no complications.

So do they have any evidence of GI bleeding, hematemesis, melanoma, anemia? Okay, they don't? All right, good.

Do they have any evidence of weight loss? That would suggest maybe they have some potentially a cancer or do they have a gastric outlet obstruction? All right, they don't. Okay, good.

Do they have any nausea and vomiting? Could that suggest a gastric outlet obstruction as well? So it's important for me to think about that to see if... if they have any complications related to their peptic ulcer disease. If they don't have any of those, but you still have a high degree of suspicion that they have peptic ulcer disease, then you can start testing them for H.

pylori, since that's oftentimes the most common cause of peptic ulcer disease, and even to some degree, gastritis. So when I do this, I do it a couple different ways. One is I can test the antigens in their stool.

So H. pylori will have antigens on it. And what I'll do is I'll take those antigens and I'll actually, you know, apply antibodies to see if they bind to those antigens. Because I know which type of antibodies I can actually utilize to bind to the H. pylori antigens.

If they have H. pylori in their stool, meaning it came from their stomach, they'll have a positive stool antigen test. Because, again, it would have to pass from their stomach down into the duodenum, down into the large intestine, and it'll be in their stool. We'd have that and it would be positive.

If that is the case, that adds to them saying that they could have. an infection with H. pylori.

The other thing here is I can do what's called a urea breath test. A urea breath test is oftentimes one of the easier tests. What you do is you give them urea, all right? If it gets into their stomach and they have H.

pylori, it will convert the urea into ammonia. If that also is present, it'll also make lots of CO2. When you have them breathe, they're going to have lots of CO2 that they would actually breathe out. And the higher that CO2 level is, the more likely it suggests that there's potentially a bacteria in their stomach with the urease enzyme helping to convert a lot of the urea into ammonia and CO2.

And that's a really pretty good test. The other one is serology titers. These are not very good tests. This looks for potentially antibodies that your body has tried to develop against the H.

pylori. But the problem is that they're often IgG antibodies. And that doesn't tell you if a patient has an active infection. So it's not super helpful at all. Oftentimes, the best non-invasive test is the urea breath test and the stool antigen test.

Usually for diagnostics, urea breath test is better. For stool antigen test, we oftentimes use it to test patients as they're being treated to see if they eradicated the bacteria or not. But if they come up positive, it's probably maybe... H. pylori gastritis or peptic ulcer disease.

Either way, you're going to treat them the same. If the stool antigen test came back negative, the urea breath test came back negative, the serology antibodies were negative, which again, not super helpful, but at least gives you an idea. It's unlikely that they have any H.

pylori. And so therefore, I should look for another cause. What's the other one that I really don't want to miss?

A Zollinger-Ellison syndrome. So then what I'll do is I'll obtain a serum gastrin level because in these patients, it's going to be exceedingly high. And if it is really high, then I got to do it one more test.

I'm going to give them secretin. Now secretin is supposed to help to play a role in kind of suppressing the gastrin levels. If I give them secretin and the tumor is just pumping out gastrin regardless of secretin is present or not, then I would know. But here, if I give them secretin continuously high, that means that this tumor is not under regulation.

It's likely Zollinger-Ellison syndrome. And so that would help me to add the diagnosis. So high gastrin levels that don't suppress with secretin would really give me the answer. And that's how I would go about diagnosing potentially the cause of H.

pylori, gastritis, or peptic ulcer disease. And if it's not that, how do I determine if it's Zollinger-Ellison syndrome related to PUD? Now, what if they do have alarm features?

Alright, so they have GI bleeding, they have anemia, weight loss, nausea, vomiting. Well, then I'm concerned about a complication. I really should get an EGD.

All the time, when you have alarm features, get an EGD. Because what it may show me is, look at this narrowing of their gastric outlet. That's a gastric outlet obstruction.

It may show me the evidence of a GI bleed. And that's why they're having hematemesis, melanoma, anemia. And also, it may show really, really large ulcers that are kind of concerning here. I think it's important if you see an ulcer, you should always try to biopsy that ulcer. And the reason why is if I get a biopsy, it'll help me to determine, is this really showing me some abnormal cells that look more of a malignant type of nature?

That's a big, big thing. And I got to go down the cancer route. But if it actually shows me that the cytology is not abnormal for cancer cells, then I should really go the route of testing for H.

pylori, which is going to be really good testing. And it's going to be something I can treat. So First one that we would do is the urease test. So if I get a piece of tissue, which has the H.

pylori in it, I'm going to drop it into this test tube. And then what I'm going to do is I'm going to put a medium of urea. Alright, you already see where this is going. It'll turn pink if the actual bacteria is present.

The reason why is the bacteria will have that... urease enzyme that'll chew up the urea and convert it into ammonia which will then help to turn the indicator on which gives it that pinkish color and that'll be one test that I could really use to say oh they definitely have H. pylori. The other test that I could do which is the gold standard test is I could actually take a piece of that tissue look at it under the microscope and use what's called a GM cysteine and you'll be able to highlight all of these like little bacteria and usually this is done by a pathologist.

So this would be some testing that I'd be able to see as a potential way of saying, oh, they definitely have H. pylori. All right.

And again, if they have H. pylori, it's really the look of the actual EGD that tells me, is it gastritis, which is small little mucosal ulcer, small little mucosal erosions, or if it's peptic ulcer disease, is these deep ulcers that go beyond the actual mucosa into the submucosa. All right. So that's how we would go about diagnosing these stomach disorders such as gastritis.

and peptic ulcer disease, but more particularly saying, how do I identify any complications? And how do I identify if it's H. pylori or not?

How do I identify if it's H. pylori or not? All right, my friends, we move on to the next step here, which is how do we treat these stomach disorders? You treat them all the same, regardless of its gastritis or if it's peptic ulcer disease. With this one, acid suppression therapy is going to be key.

You really want to try to reduce a lot of the hydrochloric acid production, all right? The reason why is you don't want to worsen a lot of these ulcers or worsen a lot of the inflammation of the stomach lining. And so PPIs would be kind of your first go-to treatment here.

The other thing is it's actually kind of beneficial to maybe pump up. So you want to reduce hydrochloric acid and maybe increase the alkaline mucus barrier. And so sometimes we actually may add on some drugs that helps to be able to increase those foveolar cells to make a lot of alkaline mucus and give you a thick barrier there.

And this is going to be things like sucralfate or misoprostol. So again, reduce hydrochloric acid, thicken up the alkaline barrier. Another thing that you have to identify is do they have H.

pylori? If they have H. pylori, you have to eradicate the infection.

And oftentimes it's giving them clarithromycin and amoxicillin. All right. So it's usually clarithromycin, amoxicillin, and a PPI. We call that CAP therapy.

If they have an allergy potentially to penicillin, then you switch it to metronidazole clarithromycin, all right, a PPI, and oftentimes you'll add in something like bismuth subsalicylate, which is like quadruple therapy. The other thing is that when you give them something to treat their H. pylori, you want to make sure that you're eradicating the H.

pylori. And so you actually will test their stool antigen test. You could also do the urea breath test, but stool antigen test is actually relatively easy. And you're looking to see, hey, Have we given enough antibiotics for about 14 days that it's actually cleared out this infection?

And that's the ways that we would do that. It's also important to remember that peptic ulcer disease comes with some pretty hefty complications, pretty scary ones. You have to be able to identify a GI bleed.

And if they have alarm features, you need to get an EGD. And oftentimes the EGD will be enough to diagnose it and also at the same time, treat them by cauterizing it, using epi into the area and getting rid of that bleeding source. It's also important to remember that if they have evidence of a perforation, maybe there's a, you know, you do a KUB or an abdominal x-ray and you say, oh, shoot, they have a pneumoperitoneum and then features of peritonitis. I need to do a surgery. Usually it's a laparotomy.

And they'll come in and what they'll do is they say, oh, he perforated right here on the antrum or he perforated around the duodenum. I'm going to take a part of the greater omentum. And what they do is they wrap it right over that.

They use it as like a patch. Over where the area of the perforation is and they suture it down. That's called a gram patch. And then lastly, do they have gastric outlet obstruction that's evident on their EGD?

Oh, they do? Okay, let's actually pass down this little dilator, expand and stretch open the gastric outlet, and then allow for food and fluid to easily flow so they don't have as much nausea, vomiting, weight loss, and the succussion splash that they may present with. All right, my friends, that talks about the treatment. And that finishes up our lecture on stomach disorders.

I really hope that made sense and I hope that you guys enjoyed it. As always, until next time.

Transcript for:Understanding Gastritis and Peptic Ulcers

Transcript for:
Understanding Gastritis and Peptic Ulcers