Today we're gonna be going over gastric disorders, so it's going to be involving gastritis, peptic ulcer disease, and pyloric stenosis. And 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 Podcasts, 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 discovered as well. I'd really appreciate that.
So with that being said, let's go ahead and start with aqte gastritis. So qute 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 eteologies, H pylori most common cause by far H pylori. Remember this is going to be your most common cause of acte 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 microbio doesn't mean you're gonna 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 bilori causes that. Again, most common cause. That keep repeating it because it's important. And then your second most common cause is going to be from n seds and aspirin. So the way n seds and aspirin and 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 eight hundred milligrams vibuprof and you didn't any food with it, and you just have this stomach pain for a couple hours. But the more important factor is that n sets inhibit COX one production, so COX one production is actually responsible for producing prostag landins. So if you decrease COX one production, decrease production of
prostic landings. Well, why does that matter. It's because prostac landins actually inhibit gastric acid secretion, so less prostac landins means more gastric acid and more irritation like gastritis peptic ulcers. So that's why n sets are really important as a
factor that can cause gastritis. And that's actually why n sets like celebres, which is also known as celocoxid, were created because celebres actually targets COX two rather than COX one, 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 one, you don't affect the prostac landids in the stomach and you have less gastric problems. So that's
why nc's 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 n sets. Do not forget those H pyloris You're most common and says you're second most common costs.
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 gonna stick out in a vignette, but just these non specific 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 uria 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 pepticals or disease and what they involve, but those so initially you probably test for h uria 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 endoscopy, which would be your best test. And this is going to be patients that are refractory to PPIs, H two
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, you're your breath test or vecal antigen test came back positive. You're going to treat H pylori. So how do you treat H pyloria, whether it's quadruple therapy. Quadruple therapy is going to be a combination of PPIs, bismuth, metronidazol, and tetracycling.
So H pylori positive treat the H pylori with quadruple therapy. You want to discontinue n SAID use if that's what's causing it, and you can also use PPIs and H two blockers, particularly in patients who require the continued use of n SET. So whether it's a cardiovascular patient that requires daily aspirin patient with chronic pain that has to take their ND sets but they develop gastritis, then you can use PPIs and H two blockers as well for
the treatment. So treatment depends on the cause H pylori. Treat the H pylori discontinue n said use if they're using it, and PPIs and H two blockers are going to be your main.
Ways to treat qute gastritis.
As 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 metaplastic 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 a cute gastritis, this isn't going to be from N sets or it's 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 B twelve deficiency as well as this gastritis that these patients have. These patients are also at a high risk of gastric carcinoma.
And one other important thing.
That you need to know is that while acute gastritis most commonly affects the antrum 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 vin yet they may mention that. So remember a QT gastritis affects the antrum, chronic autoimmune is going to most commonly affect the fundus in the body and spares the andantrum. 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 two with gastritis as well. So peptic ulcer disease encompasses both duodenal ulcers and gastric ulcers. So some things that two have in common, some things that help differentiate them. So we'll go over the different things. So let's start with duoden ulcers so duoden 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 edinal carcinoma. So remember that duodenal ulcers usually benign. Gastric ulcers are more commonly associated with gastric adino carcinoma, and duoden ulcers are your more common type as far
as eteologies, 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, N SAIDs an aspirin really easy. You already know this for gastritis, So again hpylori most common. N says an 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 one percent of patients. It's something called Zollinger 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 another a few other things. So again not a very common cause, but something that 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 hpylori is your most common cause overall, but it's going to be more associated with duodeno ulcers, where n sets an asper, your second most common cause overall is going to be more commonly associated with gaster cultures, So just know that,
but again same overlap with gastritis. Hpylori most common, and sayd as an aspirin second most common, and then just know about zolinger ellison just as that oddball that may come up, as well as some of the other factors you know that can lead to pepic ulcers as well. Increased alcohol use, smoking also more common and elderly. Those are the less less important things that you need to know.
But of course hpilor and SAIDs 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 of it and yet, But what you do need to know with this on the history and exam is the different presentation. Do oddinal ulcers are going to get better with food? Gastric ulcers are going to get worse with food. So why does that happen? Well, gastric cultures. When you eat, acids obviously released to help break down the food, and so the
ulcers in the stomach you have pain right away. So as soon as you eat, immediately these patients start having pain, whereas duadinal 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 in 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 duodom. Now these patients start to have pain. So while these patients are eating and they have a duodin 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 gonna have, They're gonna have relief with food. They're gonna see their symptoms improved. Duadinals are going to be better with food. Gastric is gonna be worse with food. The way I remember that duodenal ulcers. Du I remember, dude, give me food?
Do you do?
Just like in dude and duodenal? Dude give me food? So better with food, duodonal 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 duaden ulcers. You may see weight gain because their symptoms get better with food, so they tend to eat more, So it 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 pepsia blah blah blah, to this sudden onset of this sharp, acute abdominal pain. They may have signs of peritonitis 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 in 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 listen 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 that you're going to do 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 urrea breath test or an H. Pylori stool antigen H pylori testing.
When you do a uria breath test, what you need to know about this is is that H. Pylori produces an enzyme called urease, which breaks down urrea 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 urea, and as I said before, H pylori turns urea into carbon dioxide and ammonia. So if there's an increase in all this carbon dioxide that's in this bag, then obviously this is gonna be a positive test for H.
Pylori.
So that's how a urrea breath test works. H Pylori stool intogen is 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 and 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 guesstritis,
you're going to do quadruple therapy. The way I remember quadruple therapy for an hpylori 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 tetracycling, metronideisol, bismyth subseliciy, and PPIs treat my belly please. Tetracycling, metronide, is al, bismuth, subselicily,
and P. Those are for your H. Pylori positive patients. Now, if these patients are hpylori negative, how do you treat their peptic ulcer disease? Well, first, treat the underlying cause. If they're taking nsids, 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 PPIs as well.
You can also use H two blockers, but realistically, anytime you have an option of a PPI or an H two blocker, unless there's some contraindication of PPIs, always use PPIs. Why is that PPIs are much more effective, and that's because, I mean, just really quickly break down the way these work and just to give you a little bit about the may of the mets. 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 prietal cell activated. Well, acetylcholine, histamine, and gastrin all activate the prietal cell to pump out this acid. An H CH two blocker obviously blocks H two and that's histamine, So that's a histamine blocker, So it blocks just histamine, but you still have acetocholine and gastrine that can activate the parietal cell. So while it helps because you stop the histamine from activating the paryal cell.
Stylcholine and gastrine 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 is stylcholine, how much histamine, how much gastrine 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 hto blocker, use the PPI. So again H pylor negative, treat the underlying cause, give them PPIs. 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 ensis, et cetera, and they're still having SIN, you can do something called the parietal cell veagotomy, which is where they sever the vagual 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 seventy five percent, So 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 vegotamin. 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 pyloris, which is the sphincter, 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 male, 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 and that's so common that it's going to be pylar scinosis. Three to six weeks is going to be your most common age of presentation. Sometimes they'll say three to twelve, but generally three to six is the most common. And then first born 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 macrolight antibiotics. Erythromycin, even a
zythromycin 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 gastroparesis because it increases the gimotility. So if you have a patient under two weeks they give them a erythromycin, this may lead to pyloric stenosis. So risks again males first born three to six weeks of life and macrolide antibiotics in particular erythromycin. All right, So
as far as the history and the exam. They may have some non specific symptoms weight loss, dehydration doesn't matter. You don't care about that stuff because it's not going to help you differentiate it in Yet, what you need to know for pylor ex stenosis, there's two really big things you cannot forget. So pilar stenosis non bilious projectile vomiting after feeding. That is going to be your vignette right there. You can just go ahead and circle pilar stenosis.
That's gonna be your answer. So you see non bilious projectile vomiting after feeding pilar stenosis. So why is it non bilious? Well, remember this is an obstruction at the stomach. It's at the pylorus, so we're not into the area where the bile is coming from the common bioduct. It's not evolves. It's an unomal rotation of the small bowel, so we're not in the area where the bile is
being excreted. So it's gonna be non bilious. It's in the stomach, So non bilious projectile vomiting after feeding that is going to be pathonomoonic, almost as pathonomonic 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 the pyloris being hypertropheed. It's enlarged, and on physical exam, normally you're not gonna
be able to feel the pylorus. But these patients, because it's hypertrop feed, 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 pathdomonic 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 mass, they would go right to surgery, you know, after you treated them with fluids and things like that. So physical exam no non bilious 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 ninety seven to ninety nine percent 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 seven eighteen millimeters. Don't worry about those numbers, but I just want to throw that out there so you know that's how you actually have a positive ultrasound.
But ultra sound is gonna 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 ultrasounds inconclusive, the physical exam is 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 pyloxynosis, 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 of barium because that hypertro feed 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 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 and that's a railroad sign on upper GI. So again in real life, probably not going to do an UPPERGI, but you do need to know for the exams because they like to throw out these key terms of string sign and railroad track sign on what you'll see on UPPERGI. And then as far as labs, they're vomiting up all the stomach acids, so you may have this hypochloromic metabolic acidosis.
They may also have hypokalmia, and this is just because the kidney's compensating and flushing out all of the renal potassium excretion. So hypochloromic metabolic acidosis may be seen. And then they also may have hypokalemia 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 HYPOKLEMICX you want to replace the potassium, may give them some dextros IV fluids and things like that. Once they're euvulymic, then you get to the actual procedure that needs to be done in these patients. And this is called the pyloral miotomy is the name of the procedure that you want to do once they're stable their euvolemic 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 contents can flow through
this area, so that again it's called a pyloromiotomy. Pyloromotomy is going to be the treatment of choice once these patients are stable and euvolemic, 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 panry, your ear, and good luck in PA school and