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 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 commment down 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 so 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 often times they can be somewhat difficult to differentiate because they do have a lot of the same pathophysiology a lot of the same similar complaints was just 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 the microscopic level it's important to remember your layers of the alinary canal we have Sosa and pink here in the red one this CH chunky one is the muscularis externa the blue one is the sub mucosa and then you have these three components of the mucosa the epithelial lay this purple maroonish color which is the lamin appropria and then the muscularis mucosa often times when we talk about patients who develop gastritis it's 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 that's one big differentiation between gastritis and peptic ulcer disease small shallow erosions that usually only extend through the epithelia layer and sometimes into the lamon appropriate but they'll never cross the muscularis mucosa and go into the sub mucosa if they do it's no longer gastritis it's ulcers peptic ulcers that's one particular thing another thing is is that these patients usually also have when it comes to gastritis gastritis causes generalized inflammation so a lot of these cells like your you know normal cells like the parietal cells the P the actual Chief cells the mucus containing cells all of these things become a little bit inflamed and injured and another thing that's really important here is that sometimes there's this like generalized mucus layer and there's this mucous layer that's supposed to kind of like neutralize the hydrochloric acid that's present inside of the stomach and what we see in these patients is 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 okay so these are the three things at the microscopic level that really suggest this patient having this classic like inflammation and erosions in the antrum the question that comes up is what's the classic finding that patients who have gastritis and usually because it's in the stomach and it's in the antrum it often gives this uh what's called epigastric abdominal pain so often times 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 a patient who has epigastric abdominal pain related to a 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 Anil inflammation erosions this is the location epigastric abdominal pain question is what's causing this inflammation what's causing these shell erosions and what's causing this thin mucous 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 ineds and ethanol and I put more of an emphasis on the nids and what happens here is that these drugs will lead to they inhibit an enzyme you know they inhibit this enzyme um it's called cyclo oxygenase and and cyc oxygenase is supposed to take and convert arachadonic acid into prostaglandins but if I inhibit that enzyme can I make prostaglandins no and so what happens is my prostag gland in 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 prostag glanded production this drop in the prostag glanded production leads to two effects one is prostag gland and production is very acutely tied to the production of hydrochloric acid by these special cells called parietal cells whenever there's decreased Prost glands prostag glands is supposed to Tamper down the parietal cell production of hydrochloric acid but if you 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 mucosa 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 at beg gastric 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 called are called folar cells not necessarily goblet cells they're similar but they produce what's called an alkaline mucus and if you have less prostate glin 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 that this thing can go uncontrolled and cause more inflammation and erosions and so this is the primary path of physiology of why lots of incets 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 inter Endocrine cells and they can make a hormone called gastrin and through some mechanism we don't really know how but hpylori may increase the production of gastrin the thing with gastron is is it does the same thing is it actually has a direct stimulatory effect on parietal cells and if gastron is in high amounts what it'll will 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 its 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 erosions 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 Urias and Urias is this enzyme that thus the name it can break down Ura and convert into what's called ammonia so that's what will happen they'll actually make lots of ammonia because there's lots of Ura naturally within our stomach contents so when it makes lots of this ammonia what it does is 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 kagay and Tac toxins that they release that affects the permeability and directly injures the actual cells of the mucosa and so that induce a cyto toxic cyto toxicity I got to spell these things right man Cy toxicity to these actual cells when there's an increase in the cytotoxicity there's more injury to the 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 ulcers curling ulcers and Cushing ulcers are what we some sometimes referred 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 uh ulcers ulcers means that I'm passing into the the sub mucosa these don't pass into the sub mucosa so they're technically a misnomer in their terminology where it's a curling or Cushings ulcers they're not really true ulcers they cause inflammation and small mucosal erosions really important thing to differentiate but curling I want you to think about the classic clinical vignette is a 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 you lose a lot of your actual blood 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 increase 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 aeia and if I lead to aeia to the actual tissue of the stomach the mucosal lining so we'll put here we'll put in like parenthesis mucosal aeia 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 increase inflammations and erosions due to poor profusion 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 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 intra cranial pressure and whenever the intracranial pressure is super super high through mechanisms that are really really interesting you create these kind of reflex mechanism because what happens when your ICP is really high you try to increase your blood pressure to profuse the brain and it creates a vagal reflex and your vagus nerve kind of becomes super hyperactive and if your vagus nerve you have increased vagus nerve activity this goes back to where you have to understand like basic physiology here you remember what the vagus nerve releases on De prial cells you guys remember acetal cooline 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 inet use like chronic alcohol use is there a chance they get of 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 prial cells and the pral cells not only make hydrochloric acid but they also make that other I told you which is called B12 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 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 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 anal involvement you think about these okay now we come down to 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 dadum 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 going to produce epigastric abdominal pain that's the classic finding so you'll see a patient who has epigastric abdominal pain where you're like Zach so did gastritis and as I can already see over here a lot of these causes are cing 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 EG 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 the kind of an interesting type of process let's say I introduce food to a patient and they 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 anol location the gastric ulcer when I introduce food the pain is greater it increases if you will okay so the pain will increase dadal 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 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 stom 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 dual 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 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 sub mucosa 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 sub 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 inflamm the both have erosions but one is going to be really deep ulcerations and one's a shallow type of ulceration all right 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 Ero this actual nasty ulcers and thin mucous layers that are leading to these ulcers forming particularly within the antrum and the dadum 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 ineds and ethanol what do they do they inhibit the Cox enzyme that leads to prostag gland in production I'm going to put PG that leads to what we said the parietal cells you're going to lead to a increase hydrochloric acid production a decrease in mucous production and that'll lead to ulcers and inflammation right that was a pretty quick recap of that concept inhibit the Cox enzyme decrease the prostaglandins increase hydrochloric acid from parial cells decrease the alkaline mucus and lead to ulcer formation all right cool so that's some 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 concept 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 dadum it can occur in the stomach either way hydrochloric 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 Urias really important enzyme that breaks down ammonia into I'm sorry breaks down Ura into ammonia ammonia levels will increase it creates an alkaline environment allows H pylori to survive so it increases their survival 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 cyto toxicity now once all of this kind of happens cytotoxicity these patients will start to have these nasty nasty ulcers and all these particular problems like massive inflammation all right but here is going to be again just that quick recap they make lots of uas increase in pneumonia increase H pylor survival increase cytotoxicity and we see this particular problem okay quick last last one here so this is the most common cause the second one that I the second most common cause will be inets and ethanol the last one that I would really want you guys to remember if a patient has refractory refractory dadal ulcers so if you hear the term refractory dadal 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 gastron and this gastron 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 dual 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 gastron causing increased hydrochloric acid production and the formation of refractory dualin ulcers I'm definitely going to want to take into consideration could this patient have a gastronoma this disease we actually kind of call a very interesting one it's called Zinger Ellison syndrome so don't forget that if I think Zinger Ellison syndrome I for a gastronoma okay my friends we covered a lot about stomach disorders we talked about gastritis we talked about peptic uler disease now what I want to do is I want to say we have a patient who comes in with that beg gastric 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 relatively benign and doesn't really cause a lot of complications it made to some degree cause small mucosal ulcerations that cause a little bit of GI bleeding but often times 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 up with epigastric abdominal pain whether it's a gastric dwad ulcer that e these either greater with food gastric decreases with food dadal we know that they're having tense gastric abdominal pain could be due to H pylori big one ineds 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 sub mucosa it can 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 like 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 going to be the more common one this would 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 right 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 often times these patients can present with Melina in worst case scenario if you lose enough blood these patients could go into hypovolemic shock and develop Pro found 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 all right so this is usually the big thing that I would want to watch out for is if a patient has history of peptic uler disese and they come in hypmic shock with hematemesis Melena definitely start thinking about an upper GI bleed so this can definitely cause an upper GI 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 jabl 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 sub mucosa and they start to erode through the Sosa if the patient erodes so they have what's called sosal erosion they literally have eaten through all of the walls so this patient has now caused so much erosion here in the Anum that it has started to completely erode through the Sosa so went all the way from the mucosa sub mucosa muscularis externa went all the way down to the Sosa which 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 perenium 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 sosal 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 numo parium a numo parium that's one really really big thing that you don't want to be able to miss right and so often times a numa parium they can present maybe with just increasing abdominal pain but often times it's more of an intense abdominal pain with peronal findings and another thing that's really interesting is they may present with on an an x-ray if you get a KU you see a little bit of air leaking underneath the actual diaphragm often times they'll present not just with an air leak there but often times they'll also be bacteria and acid from the stomach that will cause inflammation of the perenium and if it causes inflammation of the parium this is called peritonitis so it's called par tontis how do we classify peritonitis which is often times these kind of coincide with one another this is just area that leaked into the perum from a perforation peritonitis is there's inflammation of the perum 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 and in combination with systemic inflammation increasing white blood so count fever these are definitely suggestive of perforation with ins suing peritonitis and pneum perenium 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 anal fibrosis and edema so let's say that a patient gets intense antral edema from the um 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 Anum as we kind of go closer here towards the pyloris look you're going to have all of this fibrotic tissue that's kind of being laid down here and here's all this emitus 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 dadum 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 Mass 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 contents 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 dadum but it's not going to do a good job and often times this will cause a lot of vomiting and tend 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 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 antal 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 oscilation 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 pyloris and Flo back that's a really important thing to look for if you hear succussion Splat increasing abdominal pain and vomiting in the scenario of a patient who has peptic Ula 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 num Partin 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 bleeding 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 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 Ado carcinoma and the other one is called malt lymphoma which is usually very commonly associated with H pylori what's the most common cause of eptic Ulcer Disease H pylori so off the times these patients can get malt lymphoma and adoc carcinoma 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 lowgrade 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 a small deg degree gastritis can cause a small little upper GI bleed and certain types of gastritis I'll write it here most particularly at trophic 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 remember more path pathology related but a trophic 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 make it you don't absorb the B12 so watch out for anemia on top of that they don't produce hydrochloric acid so they have achlorhydria they don't bind iron they don't B 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 in its causes well the 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 remember I told you that they'll have what's called air underneath their diaphragm that's indicative of an Numa parium this patient's really sick I need to get these patients more particularly to an O 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 num numo parum all right then I can kind of go and take a little bit of a more uh 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 Melena anemia okay they don't all right good what do they have any evidence of weight loss that would suggest maybe they have some uh 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 up ruction as well so it's important for me to think about that to see 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 often times 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 hpylori antigens if they have hpylori in their stool meaning it came from their stomach they'll have a positive stool antigen test because this again it would have to pass from their stomach down into the dadum down to the large intestine and it'll be in their stool we'd have that and it would be positive if that is the the case that adds to them saying that they could have an infection with hpylori the other thing here is I could do what's called a Ura breath test a Ura breath test is often times one of the easier tests what you do is you give them Ura right if it gets into their stomach and they have hpylori it will convert the urhea into ammonia if that also is present it'll also make lots of CO2 when you have them breathe 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 uas enzyme helping to convert a lot of the Ura into ammonia and CO2 and that's a really pretty good test the other one is uh corology tighters these are not very good tests this looks for potentially antibodies that your body is tried to develop against the hpylori but the problem is that they're often IGG an antibodies and that doesn't tell you if a patient has an active infection um so it's not super helpful at all often times the best non-invasive test is the Ura breath test and the stool antigen test usually for Diagnostics Ura 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 ARA 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 aoling or Ellison syndrome so then what I'll do is I'll obtain a serum gastron level because in these patients it's going to be exceedingly high and if it is really high then I got got to do it one more test I'm going to give them secreton now secreton is supposed to help to play a role in kind of suppressing the gastron levels if I give them secretin and the tumor is just pumping out gastron regardless if secreton is present or not then I would know but here if I give them secret and the gastron levels are continuously high that means that this tumor is not under regulation it's likely Zinger Ellison syndrome and so that would help me to add the diagnosis so high gastron levels that don't suppress with would really give me the answer and that's how it go about diagnosing potentially the cause of HPI gastritis or peptic ulcer disease and if it's not that how do I determine if it's Zink or Ellison syndrome related PUD now what if they do have alarm features right 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 EG 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 hemimysis molinaa anemia and also it may show really really large ulcers that are kind of concerning here and 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 rout 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 yurias 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 Ura all right you already see where this is going it'll turn pink if the actual bacteria's present the reason why is the bacteria will have that uas enzyme that'll chew up the Ura and convert it into amonia 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 pilori 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 Zain 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 pilori all right and again if they have hpylori it's really the look of the actual EGD that tells me is it gastritis which it's small little mucosal ulcer small mucosal erosions or if it's peptic ulcer disease is these deep ulcers that go beyond the actual mucosa into the sub mucosa 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 hpylori or not how do I identify if it's hpylori 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 if it's gastritis or if it's peptic alar disease with this one acid suppression therapy is going to be key you really want to try to reduce a lot of the hydroc IC 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 fvol cells to make a lot of alkal mucus and give you a thick barrier there and this is going to be things like sucrate or misoprostol so again reduce hydrochloric acid thicken up the alkaline barrier the another thing that you have to identify is do they have hpylori if they have hpylori you have to eradicate the infection and often times it's giving them chloromycin and Amoxicillin all right so it's usually chloromycin amoxicilin and a PPI we call that cap therapy if they have an allergy potentially to uh penicillin then you switch it to met ridol chloromycin all right a PPI and often times you'll add in something like bismuth sub calicy which is like quadruple therapy the other thing is that when you give them something to treat their hpylori you want to make sure that you're eradicating the hpylori and so you actually will test their stool antigen test you could also do the Ura 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 me remember that peptic ulcer disease comes with some pretty hefty complications pretty scary ones you have to be able to identify g a GI bleed and if they have alarm features you need to get an EGD and oftentimes the EG 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 do a KUB or an abdominal X-ray and you say oh shoot they have an Numa perenium and then features of peritonitis I need to do a S surgery usually it's a laparotomy um and they'll come in and what they'll do is they say oh he perforated right here on the antrum or he perforated on the dadum I'm going to take a part of the greater mum 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 suure it down that's called a gram patch and then lastly do they have gastric Outlet of stru stru 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 [Music]