S1E11 Gastric Disorders

<v Speaker 1>Today we're gonna be going over gastric disorders, so it's
<v Speaker 1>going to be involving gastritis, peptic ulcer disease, and pyloric stenosis.
<v Speaker 1>And I just want to mention really quick, if you
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<v Speaker 1>So with that being said, let's go ahead and start
<v Speaker 1>with aqte gastritis. So qute gastritis is an inflammation resulting
<v Speaker 1>from gastric mucosal injury. It's important to note that there
<v Speaker 1>is something else called gastropathy, which is going to be
<v Speaker 1>a more superficial mucosal injury with no associated inflammation. So
<v Speaker 1>that's another term that you need to know as well.
<v Speaker 1>As far as eteologies, H pylori most common cause by
<v Speaker 1>far H pylori. Remember this is going to be your
<v Speaker 1>most common cause of acte gastritis.
<v Speaker 2>And H.
<v Speaker 1>Pylori is a GRAM negative bacteria that's very common. It's
<v Speaker 1>actually found in about half of the world's population, So
<v Speaker 1>not everybody gets symptoms from this though, So just because
<v Speaker 1>it's part of your microbio doesn't mean you're gonna have symptoms,
<v Speaker 1>but the people that do develop symptoms. H Pylori infects
<v Speaker 1>the gastric mucosa. It releases certain enzymes and toxins, and
<v Speaker 1>it injures the epithelial cells of the stomach, which leaves
<v Speaker 1>the stomach more vulnerable to the acid that's present and
<v Speaker 1>causes gastritis. It can cause peptic ulcers as well as
<v Speaker 1>pain and a number of other symptoms. So that's how
<v Speaker 1>H bilori causes that. Again, most common cause. That keep
<v Speaker 1>repeating it because it's important. And then your second most
<v Speaker 1>common cause is going to be from n seds and aspirin.
<v Speaker 1>So the way n seds and aspirin and cause gastritis
<v Speaker 1>one way is that it's just from a superficial irritation
<v Speaker 1>of the epithelium of the gastric mucosa. So that can
<v Speaker 1>happen if you take like eight hundred milligrams vibuprof and
<v Speaker 1>you didn't any food with it, and you just have
<v Speaker 1>this stomach pain for a couple hours. But the more
<v Speaker 1>important factor is that n sets inhibit COX one production,
<v Speaker 1>so COX one production is actually responsible for producing prostag landins.
<v Speaker 1>So if you decrease COX one production, decrease production of
<v Speaker 1>prostic landings. Well, why does that matter. It's because prostac
<v Speaker 1>landins actually inhibit gastric acid secretion, so less prostac landins
<v Speaker 1>means more gastric acid and more irritation like gastritis peptic ulcers.
<v Speaker 1>So that's why n sets are really important as a
<v Speaker 1>factor that can cause gastritis. And that's actually why n
<v Speaker 1>sets like celebres, which is also known as celocoxid, were
<v Speaker 1>created because celebres actually targets COX two rather than COX one,
<v Speaker 1>So this leads to less gastric issues and they have
<v Speaker 1>a number of other cardiovascular problems, but that's besides the point.
<v Speaker 1>But that's why they were created because when you don't
<v Speaker 1>target COX one, you don't affect the prostac landids in
<v Speaker 1>the stomach and you have less gastric problems. So that's
<v Speaker 1>why nc's are a big issue here. Some other less
<v Speaker 1>important causes are going to be alcohol, trauma, acute stress,
<v Speaker 1>radiation and things like that, but the ones you need
<v Speaker 1>to know is going to be h pylori and n sets.
<v Speaker 1>Do not forget those H pyloris You're most common and
<v Speaker 1>says you're second most common costs.
<v Speaker 2>So remember those.
<v Speaker 1>As far as the patient presentation, some patients initially may
<v Speaker 1>be asymptomatic, but as it progresses, you're going to have
<v Speaker 1>these non specific symptoms. It's like epigastric discomfort also known
<v Speaker 1>as dyspepsia. They may have some nausea, loss of appetite,
<v Speaker 1>nothing really specific that you need to know that's gonna
<v Speaker 1>stick out in a vignette, but just these non specific
<v Speaker 1>epigastric symptoms. Diagnosing while your test of choice, although it
<v Speaker 1>isn't necessarily going to be the first thing you do,
<v Speaker 1>is going to be an upper endoscopy. This is going
<v Speaker 1>to be your best test. But initially you're going to
<v Speaker 1>do some testing for H pylori because these are things
<v Speaker 1>that are non invasive. You can do a uria breath test,
<v Speaker 1>a fecal antigen test to test for H pylori to
<v Speaker 1>see if you need to treat that. I'll go over
<v Speaker 1>those tests a little bit in pepticals or disease and
<v Speaker 1>what they involve, but those so initially you probably test
<v Speaker 1>for h uria breath test fecal antigen test, and then eventually,
<v Speaker 1>if those tests come back negative, these patients are still
<v Speaker 1>having symptoms, you may move on to an upper endoscopy,
<v Speaker 1>which would be your best test. And this is going
<v Speaker 1>to be patients that are refractory to PPIs, H two
<v Speaker 1>blockers things like that. So some of the ways you
<v Speaker 1>can diagnose test for H pylori, upper endoscopy, and treatment, well,
<v Speaker 1>it all depends on the cause. So if these patients
<v Speaker 1>have H pylori, your test came back positive, you're your
<v Speaker 1>breath test or vecal antigen test came back positive. You're
<v Speaker 1>going to treat H pylori. So how do you treat
<v Speaker 1>H pyloria, whether it's quadruple therapy. Quadruple therapy is going
<v Speaker 1>to be a combination of PPIs, bismuth, metronidazol, and tetracycling.
<v Speaker 1>So H pylori positive treat the H pylori with quadruple therapy.
<v Speaker 1>You want to discontinue n SAID use if that's what's
<v Speaker 1>causing it, and you can also use PPIs and H
<v Speaker 1>two blockers, particularly in patients who require the continued use
<v Speaker 1>of n SET. So whether it's a cardiovascular patient that
<v Speaker 1>requires daily aspirin patient with chronic pain that has to
<v Speaker 1>take their ND sets but they develop gastritis, then you
<v Speaker 1>can use PPIs and H two blockers as well for
<v Speaker 1>the treatment. So treatment depends on the cause H pylori.
<v Speaker 1>Treat the H pylori discontinue n said use if they're
<v Speaker 1>using it, and PPIs and H two blockers are going
<v Speaker 1>to be your main.
<v Speaker 2>Ways to treat qute gastritis.
<v Speaker 1>As something else that I'm going to go over, it's
<v Speaker 1>definitely not very high yield, but you need to know
<v Speaker 1>that it exists because it is on the blueprint. It's
<v Speaker 1>something called autoimmune metaplastic atrophic gastritis, so again not high yield,
<v Speaker 1>but be aware that it exists. It's a chronic form
<v Speaker 1>of gastritis. It's an inherited autoimmune disease, so unlike a
<v Speaker 1>cute gastritis, this isn't going to be from N sets
<v Speaker 1>or it's pylori use. It's going to be an autoimmune process.
<v Speaker 1>So the immune system is actually attacking the parietal cells,
<v Speaker 1>an intrinsic factor in the body. This can lead to
<v Speaker 1>B twelve deficiency as well as this gastritis that these
<v Speaker 1>patients have. These patients are also at a high risk
<v Speaker 1>of gastric carcinoma.
<v Speaker 2>And one other important thing.
<v Speaker 1>That you need to know is that while acute gastritis
<v Speaker 1>most commonly affects the antrum of the stomach, chronic or
<v Speaker 1>autoimmune gastritis spares the antrum and most commonly affects the
<v Speaker 1>fundus or the body. So for real life maybe not
<v Speaker 1>so important, but for a vin yet they may mention that.
<v Speaker 1>So remember a QT gastritis affects the antrum, chronic autoimmune
<v Speaker 1>is going to most commonly affect the fundus in the
<v Speaker 1>body and spares the andantrum. That's really all you need
<v Speaker 1>to know for that. Don't go crazy again, not very
<v Speaker 1>high yield.
<v Speaker 2>Now moving on.
<v Speaker 1>To something that is high yield is peptic ulcer disease.
<v Speaker 1>So there's a lot of stuff you need to know
<v Speaker 1>on this. Let's go over that. There's going to be
<v Speaker 1>some overlap two with gastritis as well. So peptic ulcer
<v Speaker 1>disease encompasses both duodenal ulcers and gastric ulcers. So some
<v Speaker 1>things that two have in common, some things that help
<v Speaker 1>differentiate them. So we'll go over the different things. So
<v Speaker 1>let's start with duoden ulcers so duoden ulcers are going
<v Speaker 1>to be an area of erosion obviously in the duodenum.
<v Speaker 1>It's going to be your most common type, so much
<v Speaker 1>more common, about four times more common than gastric ulcers,
<v Speaker 1>and usually it's benign. Gastric Ulcers are going to be
<v Speaker 1>an area of erosion in the stomach, and these are
<v Speaker 1>less prevalent than duodenal ulcers and more commonly associated with
<v Speaker 1>gastric edinal carcinoma. So remember that duodenal ulcers usually benign.
<v Speaker 1>Gastric ulcers are more commonly associated with gastric adino carcinoma,
<v Speaker 1>and duoden ulcers are your more common type as far
<v Speaker 1>as eteologies, a lot of overlap here with gastritis. Again
<v Speaker 1>h pylori most common cause overall, nothing new that you
<v Speaker 1>need to know there, Second most common cause, N SAIDs
<v Speaker 1>an aspirin really easy. You already know this for gastritis,
<v Speaker 1>So again hpylori most common. N says an aspirin second
<v Speaker 1>most common. And then another odd bowl that you need
<v Speaker 1>to know of that's not very common about you know,
<v Speaker 1>like less than one percent of patients. It's something called
<v Speaker 1>Zollinger Ellison syndrome and This is a disease that produces
<v Speaker 1>high levels of gastrin from a neuroendocrine tumor, and gastrin
<v Speaker 1>leads to high levels of acid in the stomach, which
<v Speaker 1>can lead to ulcers and gastritis as well as another
<v Speaker 1>a few other things. So again not a very common cause,
<v Speaker 1>but something that you do need to know because it
<v Speaker 1>may come up in the boards, and just a small
<v Speaker 1>factor that you need to know as well. So hpylori
<v Speaker 1>is your most common cause overall, but it's going to
<v Speaker 1>be more associated with duodeno ulcers, where n sets an asper,
<v Speaker 1>your second most common cause overall is going to be
<v Speaker 1>more commonly associated with gaster cultures, So just know that,
<v Speaker 1>but again same overlap with gastritis. Hpylori most common, and
<v Speaker 1>sayd as an aspirin second most common, and then just
<v Speaker 1>know about zolinger ellison just as that oddball that may
<v Speaker 1>come up, as well as some of the other factors
<v Speaker 1>you know that can lead to pepic ulcers as well.
<v Speaker 1>Increased alcohol use, smoking also more common and elderly. Those
<v Speaker 1>are the less less important things that you need to know.
<v Speaker 1>But of course hpilor and SAIDs know those. Don't forget
<v Speaker 1>that as far as the history and exam, these patients
<v Speaker 1>are going to have some again non specific epigastric pain, burning, nausea,
<v Speaker 1>they may have early satiety.
<v Speaker 2>Those things aren't that important.
<v Speaker 1>It's not going to help you differentiate on of it and yet,
<v Speaker 1>But what you do need to know with this on
<v Speaker 1>the history and exam is the different presentation. Do oddinal
<v Speaker 1>ulcers are going to get better with food? Gastric ulcers
<v Speaker 1>are going to get worse with food. So why does
<v Speaker 1>that happen? Well, gastric cultures. When you eat, acids obviously
<v Speaker 1>released to help break down the food, and so the
<v Speaker 1>ulcers in the stomach you have pain right away. So
<v Speaker 1>as soon as you eat, immediately these patients start having pain,
<v Speaker 1>whereas duadinal ulcers obviously a little bit further down the
<v Speaker 1>GI tract. As you're eating, the food's kind of shut down,
<v Speaker 1>it's clamped off, it's churning up in there trying to
<v Speaker 1>break down the food. So all the acids in the stomach,
<v Speaker 1>but it's not until about two to five hours later
<v Speaker 1>that the food starts to be released from the stomach
<v Speaker 1>enters the duodom. Now these patients start to have pain.
<v Speaker 1>So while these patients are eating and they have a
<v Speaker 1>duodin ulcer. They have some relief for about two to
<v Speaker 1>five hours while the acids still sitting in the stomach.
<v Speaker 2>Once it starts to come out, then they have pain.
<v Speaker 1>So duodenal ulcers they're gonna have, They're gonna have relief
<v Speaker 1>with food. They're gonna see their symptoms improved. Duadinals are
<v Speaker 1>going to be better with food. Gastric is gonna be
<v Speaker 1>worse with food. The way I remember that duodenal ulcers.
<v Speaker 1>Du I remember, dude, give me food?
<v Speaker 2>Do you do?
<v Speaker 1>Just like in dude and duodenal? Dude give me food?
<v Speaker 1>So better with food, duodonal ulcers and gastric.
<v Speaker 2>Is worse with food.
<v Speaker 1>And that's why patients with gastric ulcers that the pain
<v Speaker 1>gets worse with eating. A lot of times you'll see
<v Speaker 1>weight loss in these individuals compared to duaden ulcers. You
<v Speaker 1>may see weight gain because their symptoms get better with food,
<v Speaker 1>so they tend to eat more, So it makes sense.
<v Speaker 2>One other thing to be.
<v Speaker 1>Mindful of is that peptic ulcers can bleed and they
<v Speaker 1>can also perforate, So you need to know that peptic
<v Speaker 1>ulcers are actually peptic ulcer disease is the most common
<v Speaker 1>cause of an upper GI bleed. Peptic Ulcer disease most
<v Speaker 1>common cause of an upper GI bleed. And in the
<v Speaker 1>case that they do perforate, these patients are going to
<v Speaker 1>go from this kind of vague epigastric pain pepsia blah
<v Speaker 1>blah blah, to this sudden onset of this sharp, acute
<v Speaker 1>abdominal pain. They may have signs of peritonitis like rebound
<v Speaker 1>tenderness guarding. So know that these peptic ulcers can perforate,
<v Speaker 1>they can bleed, and the presentation is going to be
<v Speaker 1>much different. It's obviously a much more serious situation as
<v Speaker 1>far as diagnosing. Ultimately, your most sensitive and specific test
<v Speaker 1>is going to be in an endoscopy, But there's a
<v Speaker 1>few things you want to do before you get to
<v Speaker 1>an endoscopy. But remember, if an endoscopy is on the
<v Speaker 1>answer listen it says what is your best test endoscopy,
<v Speaker 1>it's always going to be the endoscopy. But in real life,
<v Speaker 1>there's a few things that you're going to do first
<v Speaker 1>and a few other tests. So if it says what's
<v Speaker 1>your initial test, you may go with some other things.
<v Speaker 1>So let's go over that Initially you're probably going to
<v Speaker 1>test for H. Pylori, So you can do that a
<v Speaker 1>couple of different ways. You can do a urrea breath
<v Speaker 1>test or an H. Pylori stool antigen H pylori testing.
<v Speaker 1>When you do a uria breath test, what you need
<v Speaker 1>to know about this is is that H. Pylori produces
<v Speaker 1>an enzyme called urease, which breaks down urrea into ammonia
<v Speaker 1>and carbon dioxide. So the way this test works is
<v Speaker 1>that during the test, the patient is given a pill
<v Speaker 1>containing urea and then they blow into this bag. They
<v Speaker 1>blow into the bag, they close off the bag, it's
<v Speaker 1>sent to a lab, and then they test for the
<v Speaker 1>amount of exhaled carbon dioxide. And remember again they were
<v Speaker 1>given urea, and as I said before, H pylori turns
<v Speaker 1>urea into carbon dioxide and ammonia. So if there's an
<v Speaker 1>increase in all this carbon dioxide that's in this bag,
<v Speaker 1>then obviously this is gonna be a positive test for H.
<v Speaker 2>Pylori.
<v Speaker 1>So that's how a urrea breath test works. H Pylori
<v Speaker 1>stool intogen is straightforward. It's literally just checking for a
<v Speaker 1>stool antigen of H.
<v Speaker 2>Pylori.
<v Speaker 1>So that's another test that you can do as well.
<v Speaker 1>And then ultimately, like I said before, the gold standard
<v Speaker 1>test is going to be your endoscopy. That's going to
<v Speaker 1>be to diagnose. You can visualize the ulcer and you
<v Speaker 1>can take biopsies if needed, and then treatment depends on
<v Speaker 1>the cause. So let's start with H pylori. If this
<v Speaker 1>patient is H pylori positive, again, just like in guesstritis,
<v Speaker 1>you're going to do quadruple therapy. The way I remember
<v Speaker 1>quadruple therapy for an hpylori positive patient is I remember
<v Speaker 1>these patients have belly pain. They want you to treat
<v Speaker 1>their belly pain so they can get better. So they
<v Speaker 1>say to you, treat my belly, please, treat my belly please.
<v Speaker 1>TMBP that stands for tetracycling, metronideisol, bismyth subseliciy, and PPIs
<v Speaker 1>treat my belly please. Tetracycling, metronide, is al, bismuth, subselicily,
<v Speaker 1>and P. Those are for your H. Pylori positive patients. Now,
<v Speaker 1>if these patients are hpylori negative, how do you treat
<v Speaker 1>their peptic ulcer disease? Well, first, treat the underlying cause.
<v Speaker 1>If they're taking nsids, they're smokers, they drink a bunch
<v Speaker 1>of alcohol. You're going to discontinue all those things obviously,
<v Speaker 1>and then you're going to give them PPIs as well.
<v Speaker 1>You can also use H two blockers, but realistically, anytime
<v Speaker 1>you have an option of a PPI or an H
<v Speaker 1>two blocker, unless there's some contraindication of PPIs, always use PPIs.
<v Speaker 1>Why is that PPIs are much more effective, and that's because,
<v Speaker 1>I mean, just really quickly break down the way these
<v Speaker 1>work and just to give you a little bit about
<v Speaker 1>the may of the mets. So you have a parietal
<v Speaker 1>cell in the stomach. The parietal cell has a proton pump.
<v Speaker 1>That's what shoots out all the hydrochloric acid into the stomach.
<v Speaker 1>That's where all of your acid in the stomach comes from.
<v Speaker 1>So how is your prietal cell activated. Well, acetylcholine, histamine,
<v Speaker 1>and gastrin all activate the prietal cell to pump out
<v Speaker 1>this acid. An H CH two blocker obviously blocks H
<v Speaker 1>two and that's histamine, So that's a histamine blocker, So
<v Speaker 1>it blocks just histamine, but you still have acetocholine and
<v Speaker 1>gastrine that can activate the parietal cell. So while it
<v Speaker 1>helps because you stop the histamine from activating the paryal cell.
<v Speaker 1>Stylcholine and gastrine are still working there to pump out acid,
<v Speaker 1>so there's still some acid production, Whereas a proton pump
<v Speaker 1>inhibitor actually completely shuts off the proton pump, so it
<v Speaker 1>doesn't matter how much is stylcholine, how much histamine, how
<v Speaker 1>much gastrine is activating that parietal cell. The pump is
<v Speaker 1>shut off, so no acids coming out. So PPIs are
<v Speaker 1>much more effective. So remember, if you have an option
<v Speaker 1>of a PPI or hto blocker, use the PPI. So
<v Speaker 1>again H pylor negative, treat the underlying cause, give them PPIs.
<v Speaker 1>That's the treatment. If they're H pylori positive, treat the
<v Speaker 1>H pylori very easy treatment. And then there's one other
<v Speaker 1>treatment option that you should probably know. For refractory patients.
<v Speaker 1>The PPIs aren't working, you discontinued all the ensis, et cetera,
<v Speaker 1>and they're still having SIN, you can do something called
<v Speaker 1>the parietal cell veagotomy, which is where they sever the
<v Speaker 1>vagual nerve, which essentially shuts down the portion of the
<v Speaker 1>stomach where the parietal cells are located. And this obviously
<v Speaker 1>leads to decreased acid by about seventy five percent, So
<v Speaker 1>pretty effective procedure, but it's invasive. Obviously, there's a lot
<v Speaker 1>of things you want to try before you get to
<v Speaker 1>a parietal cell vegotamin. This is just going to be
<v Speaker 1>for your refractory patients. So those are the treatments. Let's
<v Speaker 1>move on to the home stretch here. The last thing
<v Speaker 1>we're going to go over, and that's going to be
<v Speaker 1>pyloric stenosis. So this is going to be a condition
<v Speaker 1>commonly in newborns. About three to six weeks is going
<v Speaker 1>to be your most common age range, and it's a
<v Speaker 1>thickening hypertrophy, a thickening or hypertrophy of the pyloris, which
<v Speaker 1>is the sphincter, the muscular valve between the stomach and
<v Speaker 1>the duodenum, so it prevents gastric emptying. Risk factors are
<v Speaker 1>going to be males four times more common in male,
<v Speaker 1>so definitely know that males are going to be much
<v Speaker 1>more common. Look at your vignette. If it's a female,
<v Speaker 1>you know for a vignette probably and that's so common
<v Speaker 1>that it's going to be pylar scinosis. Three to six
<v Speaker 1>weeks is going to be your most common age of presentation.
<v Speaker 1>Sometimes they'll say three to twelve, but generally three to
<v Speaker 1>six is the most common. And then first born patients
<v Speaker 1>are also going to be at a higher risk. And
<v Speaker 1>then the last thing too, not as you know, not
<v Speaker 1>as big of a risk as the other ones, but
<v Speaker 1>macrolide antibiotics, in particular erythromycin within the first two weeks
<v Speaker 1>of birth can also lead to pyloric stenosis. And this
<v Speaker 1>is the way it's explained, is most likely due to
<v Speaker 1>the increased gastric motility with macrolight antibiotics. Erythromycin, even a
<v Speaker 1>zythromycin can cause this. So the increased gastric motility in
<v Speaker 1>these drugs can lead to hypertrophy from the pyloris basically
<v Speaker 1>just being overworked. And it's the same reason that we
<v Speaker 1>use erythromycin and gastroparesis because it increases the gimotility. So
<v Speaker 1>if you have a patient under two weeks they give
<v Speaker 1>them a erythromycin, this may lead to pyloric stenosis. So
<v Speaker 1>risks again males first born three to six weeks of
<v Speaker 1>life and macrolide antibiotics in particular erythromycin. All right, So
<v Speaker 1>as far as the history and the exam. They may
<v Speaker 1>have some non specific symptoms weight loss, dehydration doesn't matter.
<v Speaker 1>You don't care about that stuff because it's not going
<v Speaker 1>to help you differentiate it in Yet, what you need
<v Speaker 1>to know for pylor ex stenosis, there's two really big
<v Speaker 1>things you cannot forget. So pilar stenosis non bilious projectile
<v Speaker 1>vomiting after feeding. That is going to be your vignette
<v Speaker 1>right there. You can just go ahead and circle pilar stenosis.
<v Speaker 1>That's gonna be your answer. So you see non bilious
<v Speaker 1>projectile vomiting after feeding pilar stenosis. So why is it
<v Speaker 1>non bilious? Well, remember this is an obstruction at the stomach.
<v Speaker 1>It's at the pylorus, so we're not into the area
<v Speaker 1>where the bile is coming from the common bioduct. It's
<v Speaker 1>not evolves. It's an unomal rotation of the small bowel,
<v Speaker 1>so we're not in the area where the bile is
<v Speaker 1>being excreted. So it's gonna be non bilious. It's in
<v Speaker 1>the stomach, So non bilious projectile vomiting after feeding that
<v Speaker 1>is going to be pathonomoonic, almost as pathonomonic as The
<v Speaker 1>second thing you need to know for the exam and
<v Speaker 1>that's going to be an olive shaped mass. So on
<v Speaker 1>physical exam, we talked about the the pyloris being hypertropheed.
<v Speaker 1>It's enlarged, and on physical exam, normally you're not gonna
<v Speaker 1>be able to feel the pylorus. But these patients, because
<v Speaker 1>it's hypertrop feed, you're actually going to feel this olive
<v Speaker 1>shaped mass in the epigastric area and it's going to
<v Speaker 1>feel like a small round mass and it's described as
<v Speaker 1>an olive shaped mass. If you see this on a vignette,
<v Speaker 1>you see this or you feel this in real life,
<v Speaker 1>this is really pathdomonic for the disease. And actually, years ago,
<v Speaker 1>before ultrasound was around, this would be the only way
<v Speaker 1>you would diagnose it. If you felt this olive shaped mass,
<v Speaker 1>they would go right to surgery, you know, after you
<v Speaker 1>treated them with fluids and things like that. So physical
<v Speaker 1>exam no non bilious projectile vomiting and no olive shaped mass.
<v Speaker 1>So those are the two things you need to know
<v Speaker 1>as far as diagnosing. Ultrasound is going to be your
<v Speaker 1>test of choice. It's ninety seven to ninety nine percent
<v Speaker 1>sensitive no radiation.
<v Speaker 2>These are newborns.
<v Speaker 1>You really don't want to radiate them if you don't
<v Speaker 1>have to. And then on the ultrasound, you're going to
<v Speaker 1>see some pyloric muscle thickness over four millimeters and the
<v Speaker 1>pyloric canal length will be over seven eighteen millimeters. Don't
<v Speaker 1>worry about those numbers, but I just want to throw
<v Speaker 1>that out there so you know that's how you actually
<v Speaker 1>have a positive ultrasound.
<v Speaker 2>But ultra sound is gonna be your test of choice.
<v Speaker 1>The only reason I'm even going to mention an upper
<v Speaker 1>GI series not so much that you're going to use
<v Speaker 1>it in real life. It's really only going to be
<v Speaker 1>if ultrasounds inconclusive, the physical exam is inconclusive. But you
<v Speaker 1>need to know for the exam because on an upper
<v Speaker 1>GI series, there's a couple of key terms.
<v Speaker 2>There's one called a string sign.
<v Speaker 1>It's not specific only to pyloxynosis, but if you do
<v Speaker 1>see it in this vignette, this is going to be
<v Speaker 1>a narrowed area of barium flow. It's literally going to
<v Speaker 1>look like a string of barium because that hypertro feed
<v Speaker 1>area only allowing a small amount of barium through. So
<v Speaker 1>that's a string sign and upper GI. And there's another
<v Speaker 1>one called a railroad track sign, and this is due
<v Speaker 1>to the pyloric mucosa compressing and pushing causing this double
<v Speaker 1>canal where you're going to see two small tracks of
<v Speaker 1>barium flowing through. It kind of looks like a railroad
<v Speaker 1>and that's a railroad sign on upper GI. So again
<v Speaker 1>in real life, probably not going to do an UPPERGI,
<v Speaker 1>but you do need to know for the exams because
<v Speaker 1>they like to throw out these key terms of string
<v Speaker 1>sign and railroad track sign on what you'll see on UPPERGI.
<v Speaker 1>And then as far as labs, they're vomiting up all
<v Speaker 1>the stomach acids, so you may have this hypochloromic metabolic acidosis.
<v Speaker 1>They may also have hypokalmia, and this is just because
<v Speaker 1>the kidney's compensating and flushing out all of the renal
<v Speaker 1>potassium excretion. So hypochloromic metabolic acidosis may be seen. And
<v Speaker 1>then they also may have hypokalemia on labs. But your
<v Speaker 1>key for diagnosis is going to be your ultrasound. But
<v Speaker 1>know these things as well. So as far as treatment,
<v Speaker 1>initially these patients can be kind of sick. They're volume depleted,
<v Speaker 1>so before you get to any intervention, you need to
<v Speaker 1>start with some fluids. You want to do electrolyte replacement.
<v Speaker 1>Remember again I said they may be HYPOKLEMICX you want
<v Speaker 1>to replace the potassium, may give them some dextros IV
<v Speaker 1>fluids and things like that. Once they're euvulymic, then you
<v Speaker 1>get to the actual procedure that needs to be done
<v Speaker 1>in these patients. And this is called the pyloral miotomy
<v Speaker 1>is the name of the procedure that you want to
<v Speaker 1>do once they're stable their euvolemic and this is normally
<v Speaker 1>done laparoscopically. The surgeon makes this longitudinal incision into the
<v Speaker 1>pylorus and once they make this longitudinal incision, that hypertrophied
<v Speaker 1>muscle kind of pops out through this incision that they made.
<v Speaker 1>And once it pops up through this area of the incision,
<v Speaker 1>now beneath the area of the incision, there's this canal
<v Speaker 1>that opened up this new space because all the muscle
<v Speaker 1>kind of tunneled up through this incision, and they actually
<v Speaker 1>have this area where the stomach contents can flow through
<v Speaker 1>this area, so that again it's called a pyloromiotomy. Pyloromotomy
<v Speaker 1>is going to be the treatment of choice once these
<v Speaker 1>patients are stable and euvolemic, so that's what you need
<v Speaker 1>to know. Those are the main things. I feel like
<v Speaker 1>I kind of touched on all the high yield stuff.
<v Speaker 1>I hope that was helpful. And as always, good luck
<v Speaker 1>on your pants, your panry, your ear, and good luck
<v Speaker 1>in PA school and