Cram The Pance - S1E11 Gastric Disorders

Episode Date: February 2, 2021

Acute Gastritis, Peptic Ulcer Disease, Pyloric Stenosis review for your Pance, Panre, and Eor’s.►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

Today we're going to be going over gastric disorders. That's going to be involving gastritis, peptic ulcer disease, and pyloric stenosis. I just want to mention really quick. If you do like the podcast, it's helping you, please, please, if you wouldn't mind giving me a review on Apple podcast, Spotify, just let me know that it's helping you. It kind of also gets the word out about the podcast and helps other people discover it as well. I'd really appreciate that. So with that being said, let's go ahead and start with acute gastritis. So acute gastritis is an inflammation resulting from gastric mucosal injury.

It's important to note that there is something else called gastropathy, which is going to be a more superficial mucosal injury with no associated inflammation. So that's another term that you need to know as well. As far as etiology's H. Pylori, most common cause by far. H. Pylori, remember, this is going to be your most common cause of acute gastritis. And H. Pylori is a gram negative bacteria that's very common. It's actually found in about half of the world's population. So not everybody gets symptoms from this, though. So just because it's part of your. in microbiome doesn't mean you're going to have symptoms. But the people that do develop symptoms, H. Pylori infects the gastric mucosa. It releases certain enzymes and toxins, and it injures the epithelial cells of the stomach, which leaves the stomach more vulnerable to the acid that's present and causes gastritis. It can cause peptic ulcers as well as pain and a number of other symptoms. So that's how H.BiLory causes that. Again, most common cause, I keep repeating it because it's important. And then your second most common cause is going to be from inseds and aspirin. So the way inseds and aspirin cause gastritis, one way is that it's just from a superficial

irritation of the epithelium of the gastric mucosa. So that can happen if you take like 800 milligrams vibeprofen, you need any food with it and you just have this stomach pain for a couple hours. But the more important factor is that inseds inhibit Cox 1 production. So Cox 1 production is actually responsible for producing prostate landins. So if you decrease Cox 1, production, you decrease production of prostic glandins. Well, why does that matter? It's because prostate glandins actually inhibit gastric acid secretion. So less prostic landins means more gastric acid and more irritation like gastritis, peptic ulcers. So that's why nseds are really important as a factor that can cause gastritis. And that's actually why nseds like cellobrex,

which is also known as cellocoxib, were created because celibrex actually targets Cox2 rather than Cox So this leads to less gastric issues. And they have a number of other cardiovascular problems, but that's besides the point. But that's why they were created because when you don't target Cox 1, you don't affect the prostate glands in the stomach and you have less gastric problems. So that's why insides are a big issue here. Some other less important causes are going to be alcohol, trauma, acute stress, radiation and things like that. But the ones you need to know is going to be H. Pylori and Ns. Do not forget those H. Pylori is your most common.

and says your second most common cause. So remember those. As far as the patient presentation, some patients initially may be asymptomatic, but as it progresses, you're going to have these non-specific symptoms. It's like epigastric discomfort, also known as dyspepsia. They may have some nausea, loss of appetite, nothing really specific that you need to know that's going to stick out in a vignette, but just these nonspecific epigastric symptoms. Diagnosing, while your test of choice, although it isn't necessarily going to be the first thing you do,

is going to be an upper endoscopy. This is going to be your best test. But initially, you're going to do some testing for H. Pylori, because these are things that are non-invasive. You can do a urea breath test, a fecal antigen test, to test for H. Pylori to see if you need to treat that. I'll go over those tests a little bit in Peptic ulcer disease and what they involve. So initially, you'll probably test for H. Pylori, urea breath test, fecal antigen test. And then eventually, if those tests come back negative, these patients are still having symptoms, you may move on to an upper endoscis. which would be your best test. And this is going to be patients that are refractory to PPI, H2 blockers, things like that.

So some of the ways you can diagnose test for H. Pylori, upper endoscopy. And treatment, well, it all depends on the cause. So if these patients have H. Pylori, your test came back positive. Your Uriam breath test, your fecal antigen test came back positive, you're going to treat H. H. Pylori. So how do you treat H. Pylori?

Well, there's quadruple therapy. Quadruple therapy is going to be a combination of PPI's, Bismith, metronidazole, and tetracycline. So H. Pylori positive, treat the H. Pylori with quadruple therapy. You want to discontinue n-sad use if that's what's causing it. And you can also use PPI's and H-2 blockers, particularly in patients who require the continued use of n-seds. So whether it's a cardiovascular patient that requires daily aspirin, a patient with chronic pain that has to take their inseds, but they develop gastritis. Then you can use PPI's and H-2 blockers as well for the treatment. So treatment depends on the cause.

pylori, treat the H. Pylori, discontinue nsid use if they're using it. And PPI's and H2 blockers are going to be your main ways to treat acute gastritis. Something else that I'm going to go over. It's definitely not very high yield, but you need to know that it exists because it is on the blueprint. It's something called autoimmune metoplastic atrophic gastritis. So again, not high yield, but be aware that it exists. It's a chronic form of gastritis. It's an inherited autoimmune disease. So unlike acute gastritis, this isn't going to be from nseds or its pylori use. It's going to be an autoimmune process. So the immune system is actually attacking the parietal cells, an intrinsic factor in the body. This can lead to B12 deficiency as well as this gastritis that these patients have.

These patients are also at a high risk of gastricarcinoma. And one other important thing that you need to know is that while acute gastritis most commonly affects the anterm of the stomach, chronic or autoimmune gastritis spares the antrum and most commonly affects the fundus or the body. So for real life, maybe not so important, but for a vignette, they may mention that. So remember, acute gastritis affects the aneur. Chronic autoimmune is going to most commonly affect the fundus in the body and spares the antrum. That's really all you need to know for that. Don't go crazy again, not very high yield.

Now, moving on to something that is high yield is peptic ulcer disease. So there's a lot of stuff you need to know on this. Let's go over that. there's going to be some overlap too with gastritis as well. So peptic ulcer disease encompasses both duodenal ulcers and gastric ulcers. There's some things the two have in common, some things that help differentiate them. So we'll go over the different things. So let's start with duodenal ulcers.

So duodenal ulcers are going to be an area of erosion, obviously, in the duodenum. It's going to be your most common type, so much more common, about four times more common than gastric ulcers. And usually it's benign. Gastric ulcers are going to be an area of erosion in the stomach. And these are less prevalent than duodenal ulcers and more commonly associated with gastric adenocarsinoma. So remember that, duodenal ulcers usually benign. Gastric ulcers are more commonly associated with gastric adenocarsinoma. And duodontal ulcers are your more common type.

As far as etiologies, a lot of overlap here with gastritis. Again, H. Pylori, most common cause overall, nothing new that you need to know there. Second most common cause, nseds and aspirin. Really easy. You already know this for gastritis. So again, H. Pylori, most common. N says in aspirin, second most common. And then another odd bowl that you need to know of that's not very common about, you know, like less than 1% of patients is something called Zolinger-Ellison syndrome. And this is a disease that produces high levels of gastrin from a neuroendocrine tumor. And gastrin leads to high levels of acid in the stomach, which can lead to ulcers and gastritis as well as a few other things. So again, not a very common cause, but something that you you do need to know because it may come up in the boards. And just a small factor that you need to know as well. So H. Pylori is your most common cause overall, but it's going to be more associated with

duodenal ulcers, where n-seds and aspirin, your second most common cause overall is going to be more commonly associated with gastric ulcers. So just know that. But again, same overlap with gastritis, H-pilor most common. N-Seds and aspirin second most common. And then just know about Zolinger-Eleason, just as that oddball that may come up, as well as some of the other factors, you know, that can lead to pepiculcers as well, increased alcohol use, smoking, also more common in elderly. Those are the less important things that you need to know. But of course, H. Pellular and Ns know those.

Don't forget that. As far as the history and exam, these patients are going to have some, again, non-specific epigastric pain, burning, nausea, they may have early satiety. Those things aren't that important. It's not going to help you differentiate on a vignette. But what you do need to know with this on the history and exam is the different presentation. duodinal ulcers are going to get better with food. Gastric ulcers are going to get worse with food. So why does that happen? Well, gastric ulcers, when you eat, acids obviously release to help break down the food. And since the ulcers in the stomach, you have pain right away. So as soon as you eat, immediately these patients start having pain.

Whereas duodenal ulcers, obviously a little bit further down the GI tract, as you're eating, the food's kind of shut down, it's clamped off. It's churning up and there trying to break down the food. So all the acids in the stomach, but it's not until about two to five hours later that the food starts to be released from the stomach, enters the duodenum, now these patients start to have pain. So while these patients are eating and they have a duodenal ulcer, they have some relief for about two to five hours while the acids still sitting in the stomach. Once it starts to come out, then they have pain. So duodenal ulcers, they're going to have relief with food. They're going to see their symptoms improve. Duodinoles are going to be better with food. gastric is going to be worse with food.

The way I remember that, duodenal ulcers, DU, I remember dude give me food, just like in dude and duodinal, dude give me food. So better with food, duodinal ulcers and gastric is worse with food. And that's why patients with gastric ulcers that the pain gets worse with eating, a lot of times you'll see weight loss in these individuals compared to duodinal ulcers, you may see weight gain because their symptoms get better with food, so they tend to eat more. makes sense. One other thing to be mindful of is that peptic ulcers can bleed and they can also perforate. So you need to know that peptic ulcers are actually, peptic ulcer disease is the most

common cause of an upper GI bleed. Peptic ulcer disease, most common cause of an upper GI bleed. And in the case that they do perforate, these patients are going to go from this kind of vague epigastric pain, dyspepsia, blah, blah, blah, to this sudden onset of this sharp acute abdominal pain. They may have signs of parotinitis like rebound tenderness guarding. So know that these peptic ulcers can perforate. They can bleed. And the presentation is going to be much different. It's obviously a much more serious situation. As far as diagnosing, ultimately, your most sensitive and specific test is going to be an endoscopy. But there's a few things you want to do before you get to an endoscopy. But remember, if an endoscopy is on the answer list and it says, what is your best test?

Endoscopy. It's always going to be the endoscopy. But in real life, there's a few things you're going to first and a few other tests. So if it says what's your initial test, you may go with some other things. So let's go over that. Initially, you're probably going to test for H. Pylori. So you can do that a couple of different ways. You can do a urea breath test or an H. Pylori stool antigen. H. Pylori testing when you do a urea breath test, what you need to know about this is, is that H. Pylori produces an enzyme called uriase, which breaks down urea into ammonia and carbon dioxide. So the way this test works is that during the test, the patient is given a pill containing urea, and then they blow into this bag. They blow into the bag, they close off the bag, it's sent to a lab,

and then they test for the amount of exhaled carbon dioxide. And remember, again, they were given uria, and as I said before, H. Pylori turns uria into carbon dioxide pneumonia. So if there's an increase in all this carbon dioxide that's in this bag, then obviously this is going to be a positive test for H. So that's how a urea breath test works. H. Pylori stool intogen is strong. straightforward. It's literally just checking for a stool antigen of H. Pylori. So that's another test that you can do as well. And then ultimately, like I said before, the gold standard test is going to be your endoscopy. That's going to be to diagnose. You can visualize the ulcer. You can take biopsies if needed. And then treatment depends on the cause. So let's start with H. Pylori. If this patient is

H. Pylori positive, again, just like in gastritis, you're going to do quadruple therapy. The way I remember quadruple therapy for an H. Pylori positive patient is I remember these patients, have belly pain. They want you to treat their belly pain so they can get better. So they say to you, treat my belly please. Treat my belly please. Tmbp. That stands for tetracycline, metronidazole, bismuth, subcellicillate and PPI's. Treat my belly please, tetracycline, metronidazole, bismith, subcellicillate, and PPI's. Those are for your H. Pylori positive patients. Now, if these patients are H. Pylori negative, how do you treat their Peptic ulcer disease? Well, first, treat the underlying cause.

If they're taking inseds, they're smokers, they drink a bunch of alcohol, you're going to discontinue all those things, obviously. And then you're going to give them PPI as well. You can also use H2 blockers, but realistically, any time you have an option of a PPI or an H2 blocker, unless there's some contraindication of PPI's, always use PPI's. Why is that? PPIs are much more effective. And that's because, let me just really quickly break down the way these work and just to give you a little bit about the MOLF. way of the meds. So you have a parietal cell in the stomach. The parietal cell has a proton pump. That's what

shoots out all the hydrochloric acid into the stomach. That's where all of your acid in the stomach comes from. So how is your parietal cell activated? Well, acetylcholine, histamine, histamine, all activate the parietal cell to pump out this acid. So an H2 blocker obviously blocks H2 and that's histamine. That's a histamine blocker. So it blocks just histamine, but you still have acetycholone. and gastrin that can activate the parietal cell. So while it helps because you stop the histamine from activating the parietal cell, Cetocoline and gastrin are still working there to pump out acid. So there's still some acid production, whereas a proton pump inhibitor actually

completely shuts off the proton pump. So it doesn't matter how much acetylcholine, how much histamine, how much gastrin is activating that parietal cell, the pump is shut off. So no acids coming out. So PPIs are much more effective. So remember if you have an option of a PPI or H2 blocker, use the PPI. So again, H. Pilari negative, treat the underlying cause. Give them PPI's. That's the treatment. If they're H. Pylori positive, treat the H. Pylori. Very easy treatment. And then there's one

other treatment option that you should probably know for refractory patients. The PPIs aren't working. You discontinued all the insides, et cetera, and they're still having symptoms. You can do something called a parietal cell vagotomy, which is where they sever the vagal nerve, which essentially shuts down the portion of the stomach where the parietal cells are located, and this obviously leads to decreased acid by about 75%. So a pretty effective procedure, but it's invasive, obviously. There's a lot of things you want to try before you get to a parietal cell vagotomy. This is just going to be for your refractory patients. So those are the treatments. Let's move on to the home stretch here. The last thing we're going to go over, and that's going to be pyloric stenosis. So this is going to be a condition commonly in newborns.

About three to six weeks is going to be your most common age range. And it's a thickening, hypertrophy, a thickening or hypertrophy of the pylorus, which is the sphincter or the muscular valve between the stomach and the duodenum. So it prevents gastric emptying. Risk factors are going to be males, four times more common in males. So definitely know that males are going to be much more common. Look at your vignette. If it's a female, you know, for a vignette, probably not so common that it's going to be pyloracinosis. Three to six weeks is going to be your most common age of presentation. Sometimes they'll say three to 12, but generally three to six is the most common. And then firstborn patients are also going to be at a higher risk. And then the last thing, too, not as, you know,

not as big of a risk as the other ones, but macrolide antibiotics, in particular erythromycin within the first two weeks of birth can also lead to pyloric stenosis. And this is, the way it's explained, is most likely due to the increased gastric motility with macrolide antibiotics, erythromycin, even azithromycin. can cause this. So the increased gastric motility in these drugs can lead to hypertrophy from the pyloris, basically just being overworked. And it's the same reason that we use erythromycin and gastroporesisus because it increases the GI motility. So if you have a patient under two weeks, they give them erythromycin. This may lead to pyloracinosis. So risks again, males firstborn, three to six weeks of life and macrolide antibiotics, in particular erythromycin. All right. So as far as the

the history and the exam, they may have some nonspecific symptoms, weight, loss, dehydration, doesn't matter. You don't care about that stuff because it's not going to help you differentiate a vignette. What you need to know for pyloric stenosis, there's two really big things you cannot forget. So pyloric stenosis, non-billious projectile vomiting after feeding. That is going to be your vignette right there. You can just go ahead and circle pyloric stenosis. That's going to be your answer. So you see non-billus projectile vomiting after feeding pyloric stenosis. So why is it non-bilius? Well, remember, this is an obstruction at the stomach. It's at the pyloris. So we're not into the area where the bile is coming from the common bile duct.

It's not a volvialis. It's an animal rotation of the small bowel. So we're not in the area where the bile is being excreted. So it's going to be non-billus. It's in the stomach. So non-billus projectile vomiting after feeding. That is going to be pathognomic, almost as pathognomic as the second thing you need to know for the exam. And that's going to be an olive-shaped mass. So on physical exam, we talked about the pylorus being hypertrophied.

It's enlarged. And on physical exam, normally you're not. going to be able to feel the pylorus. But these patients, because it's hypertrophied, you're actually going to feel this olive-shaped mass in the epigastric area, and it's going to feel like a small round mass, and it's described as an olive-shaped mass. If you see this on a vignette, you see this or you feel this in real life, this is really pathonomonic for the disease. And actually years ago, before ultrasound was around, this would be the only way you would diagnose it. If you felt this olive-shaped mask, they would go right to surgery, but you know after you treated them with fluids and things like that so physical exam no non-billus

projectile vomiting and no olive-shaped mass so those are the two things you need to know as far as diagnosing ultrasound is going to be your test of choice it's 97 to 99% sensitive no radiation these are newborns you really don't want to radiate them if you don't have to and then on the ultrasound you're going to see some pyloric muscle thickness over four millimeters and the pyloric canal length will be over 17 millimeters don't worry about those numbers but i just wanted to throw that out there so you know that's how you actually have a positive ultrasound. But ultrasound is going to be your test of choice. The only reason I'm even going to mention an upper GI series, not so much that you're going to use it in real life. It's really only going to be if ultrasound's

inconclusive. The physical exam was inconclusive. But you need to know for the exam because on an upper GI series, there's a couple of key terms. There's one called a string sign. It's not specific only to pylorchitis. But if you do see it in this vignette, this is going to be a narrowed area of barium flow. It's literally going to look like a string. It's not a string. ring of barium because that hypertrophied area only allowing a small amount of barium through. So that's a string sign and upper GI. And there's another one called a railroad track sign. And this is due to the the pyloric mucosa compressing and pushing causing this double canal where you're

going to see two small tracks of barium flowing through. It kind of looks like a railroad. That's a railroad sign on upper GI. So again, in real life, probably not going to do an upper GI, but you do need to know for the exams because they like to throw out these key terms. So string sign and railroad track sign of what you'll see in an upper GI. Then as far as labs, they're vomiting up all the stomach acid. So you may have this hypochloremic metabolic acidosis.

They may also have hypokalemia. And this is just because the kidneys compensating and flushing out all of the renal potassium excretion. So hypoglymic metabolic acidosis may be seen. And they also may have hypochalemia on labs. But your key for diagnosis is going to be your ultrasound, but know these things as well. So as far as treatment, initially these patients can be kind of sick. They're volume depleted.

So before you get to any intervention, you need to start with some fluids. You want to do electrolyte replacement. Remember, again, I said they may be hypokalimics. You want to replace the potassium. They give them some dextrose IV fluids and things like that. Once they're eulamic, then you get to the actual procedure that needs to be done in these patients. And this is called a pyloral myotomy is the name of the procedure that you want to do once

they're stable, they're eaulymic. and this is normally done laparoscopically. The surgeon makes this longitudinal incision into the pylorus. And once they make this longitudinal incision, that hypertrophied muscle kind of pops out through this incision that they made. And once it pops up through this area of the incision, now beneath the area of the incision, there's this canal that opened up this new space because all the muscle kind of tunneled up through this incision. And they actually have this area where the stomach content, can flow through this area. So that again, it's called a pyloromyotomy. Pyloromyotomy is going to be the

treatment of choice once these patients are stable and eovelymic. So that's what you need to know. Those are the main things. I feel like I kind of touched on all the high yield stuff. I hope that was helpful. And as always, good luck on your pants, your panery, your EOR, and good luck in PA school.