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Speaker 1: Today we're gonna be going over gastric disorders, so it's

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going to be involving gastritis, peptic ulcer disease, and pyloric stenosis.

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And I just want to mention really quick, if you

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do like the podcast, it's helping you. Please, please, if

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you wouldn't mind giving me a review on Apple Podcasts, Spotify,

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just let me know that it's helping you. It kind

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of also gets the word out about the podcast and

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helps other people discovered as well. I'd really appreciate that.

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So with that being said, let's go ahead and start

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with aqte gastritis. So qute gastritis is an inflammation resulting

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from gastric mucosal injury. It's important to note that there

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is something else called gastropathy, which is going to be

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a more superficial mucosal injury with no associated inflammation. So

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that's another term that you need to know as well.

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As far as eteologies, H pylori most common cause by

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far H pylori. Remember this is going to be your

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most common cause of acte gastritis.

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Speaker 2: And H.

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Speaker 1: Pylori is a GRAM negative bacteria that's very common. It's

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actually found in about half of the world's population, So

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not everybody gets symptoms from this though, So just because

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it's part of your microbio doesn't mean you're gonna have symptoms,

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but the people that do develop symptoms. H Pylori infects

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the gastric mucosa. It releases certain enzymes and toxins, and

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it injures the epithelial cells of the stomach, which leaves

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the stomach more vulnerable to the acid that's present and

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causes gastritis. It can cause peptic ulcers as well as

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pain and a number of other symptoms. So that's how

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H bilori causes that. Again, most common cause. That keep

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repeating it because it's important. And then your second most

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common cause is going to be from n seds and aspirin.

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So the way n seds and aspirin and cause gastritis

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one way is that it's just from a superficial irritation

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of the epithelium of the gastric mucosa. So that can

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happen if you take like eight hundred milligrams vibuprof and

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you didn't any food with it, and you just have

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this stomach pain for a couple hours. But the more

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important factor is that n sets inhibit COX one production,

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so COX one production is actually responsible for producing prostag landins.

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So if you decrease COX one production, decrease production of

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prostic landings. Well, why does that matter. It's because prostac

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landins actually inhibit gastric acid secretion, so less prostac landins

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means more gastric acid and more irritation like gastritis peptic ulcers.

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So that's why n sets are really important as a

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factor that can cause gastritis. And that's actually why n

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sets like celebres, which is also known as celocoxid, were

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created because celebres actually targets COX two rather than COX one,

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So this leads to less gastric issues and they have

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a number of other cardiovascular problems, but that's besides the point.

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But that's why they were created because when you don't

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target COX one, you don't affect the prostac landids in

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the stomach and you have less gastric problems. So that's

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why nc's are a big issue here. Some other less

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important causes are going to be alcohol, trauma, acute stress,

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radiation and things like that, but the ones you need

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to know is going to be h pylori and n sets.

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Do not forget those H pyloris You're most common and

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says you're second most common costs.

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Speaker 2: So remember those.

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Speaker 1: As far as the patient presentation, some patients initially may

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be asymptomatic, but as it progresses, you're going to have

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these non specific symptoms. It's like epigastric discomfort also known

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as dyspepsia. They may have some nausea, loss of appetite,

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nothing really specific that you need to know that's gonna

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stick out in a vignette, but just these non specific

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epigastric symptoms. Diagnosing while your test of choice, although it

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isn't necessarily going to be the first thing you do,

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is going to be an upper endoscopy. This is going

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to be your best test. But initially you're going to

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do some testing for H pylori because these are things

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that are non invasive. You can do a uria breath test,

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a fecal antigen test to test for H pylori to

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see if you need to treat that. I'll go over

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those tests a little bit in pepticals or disease and

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what they involve, but those so initially you probably test

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for h uria breath test fecal antigen test, and then eventually,

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if those tests come back negative, these patients are still

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having symptoms, you may move on to an upper endoscopy,

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which would be your best test. And this is going

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to be patients that are refractory to PPIs, H two

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blockers things like that. So some of the ways you

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can diagnose test for H pylori, upper endoscopy, and treatment, well,

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it all depends on the cause. So if these patients

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have H pylori, your test came back positive, you're your

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breath test or vecal antigen test came back positive. You're

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going to treat H pylori. So how do you treat

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H pyloria, whether it's quadruple therapy. Quadruple therapy is going

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to be a combination of PPIs, bismuth, metronidazol, and tetracycling.

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So H pylori positive treat the H pylori with quadruple therapy.

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You want to discontinue n SAID use if that's what's

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causing it, and you can also use PPIs and H

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two blockers, particularly in patients who require the continued use

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of n SET. So whether it's a cardiovascular patient that

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requires daily aspirin patient with chronic pain that has to

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take their ND sets but they develop gastritis, then you

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can use PPIs and H two blockers as well for

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the treatment. So treatment depends on the cause H pylori.

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Treat the H pylori discontinue n said use if they're

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using it, and PPIs and H two blockers are going

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to be your main.

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Speaker 2: Ways to treat qute gastritis.

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Speaker 1: As something else that I'm going to go over, it's

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definitely not very high yield, but you need to know

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that it exists because it is on the blueprint. It's

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something called autoimmune metaplastic atrophic gastritis, so again not high yield,

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but be aware that it exists. It's a chronic form

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of gastritis. It's an inherited autoimmune disease, so unlike a

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cute gastritis, this isn't going to be from N sets

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or it's pylori use. It's going to be an autoimmune process.

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So the immune system is actually attacking the parietal cells,

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an intrinsic factor in the body. This can lead to

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B twelve deficiency as well as this gastritis that these

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patients have. These patients are also at a high risk

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of gastric carcinoma.

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Speaker 2: And one other important thing.

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Speaker 1: That you need to know is that while acute gastritis

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most commonly affects the antrum of the stomach, chronic or

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autoimmune gastritis spares the antrum and most commonly affects the

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fundus or the body. So for real life maybe not

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so important, but for a vin yet they may mention that.

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So remember a QT gastritis affects the antrum, chronic autoimmune

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is going to most commonly affect the fundus in the

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body and spares the andantrum. That's really all you need

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to know for that. Don't go crazy again, not very

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high yield.

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Speaker 2: Now moving on.

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Speaker 1: To something that is high yield is peptic ulcer disease.

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So there's a lot of stuff you need to know

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on this. Let's go over that. There's going to be

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some overlap two with gastritis as well. So peptic ulcer

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disease encompasses both duodenal ulcers and gastric ulcers. So some

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things that two have in common, some things that help

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differentiate them. So we'll go over the different things. So

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let's start with duoden ulcers so duoden ulcers are going

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to be an area of erosion obviously in the duodenum.

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It's going to be your most common type, so much

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more common, about four times more common than gastric ulcers,

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and usually it's benign. Gastric Ulcers are going to be

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an area of erosion in the stomach, and these are

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less prevalent than duodenal ulcers and more commonly associated with

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gastric edinal carcinoma. So remember that duodenal ulcers usually benign.

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Gastric ulcers are more commonly associated with gastric adino carcinoma,

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and duoden ulcers are your more common type as far

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as eteologies, a lot of overlap here with gastritis. Again

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h pylori most common cause overall, nothing new that you

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need to know there, Second most common cause, N SAIDs

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an aspirin really easy. You already know this for gastritis,

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So again hpylori most common. N says an aspirin second

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most common. And then another odd bowl that you need

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to know of that's not very common about you know,

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like less than one percent of patients. It's something called

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Zollinger Ellison syndrome and This is a disease that produces

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high levels of gastrin from a neuroendocrine tumor, and gastrin

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leads to high levels of acid in the stomach, which

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can lead to ulcers and gastritis as well as another

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a few other things. So again not a very common cause,

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but something that you do need to know because it

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may come up in the boards, and just a small

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factor that you need to know as well. So hpylori

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is your most common cause overall, but it's going to

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be more associated with duodeno ulcers, where n sets an asper,

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your second most common cause overall is going to be

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more commonly associated with gaster cultures, So just know that,

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but again same overlap with gastritis. Hpylori most common, and

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sayd as an aspirin second most common, and then just

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know about zolinger ellison just as that oddball that may

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come up, as well as some of the other factors

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you know that can lead to pepic ulcers as well.

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Increased alcohol use, smoking also more common and elderly. Those

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are the less less important things that you need to know.

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But of course hpilor and SAIDs know those. Don't forget

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that as far as the history and exam, these patients

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are going to have some again non specific epigastric pain, burning, nausea,

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they may have early satiety.

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Speaker 2: Those things aren't that important.

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Speaker 1: It's not going to help you differentiate on of it and yet,

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But what you do need to know with this on

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the history and exam is the different presentation. Do oddinal

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ulcers are going to get better with food? Gastric ulcers

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are going to get worse with food. So why does

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that happen? Well, gastric cultures. When you eat, acids obviously

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released to help break down the food, and so the

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ulcers in the stomach you have pain right away. So

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as soon as you eat, immediately these patients start having pain,

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whereas duadinal ulcers obviously a little bit further down the

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GI tract. As you're eating, the food's kind of shut down,

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it's clamped off, it's churning up in there trying to

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break down the food. So all the acids in the stomach,

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but it's not until about two to five hours later

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that the food starts to be released from the stomach

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enters the duodom. Now these patients start to have pain.

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So while these patients are eating and they have a

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duodin ulcer. They have some relief for about two to

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five hours while the acids still sitting in the stomach.

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Speaker 2: Once it starts to come out, then they have pain.

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Speaker 1: So duodenal ulcers they're gonna have, They're gonna have relief

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with food. They're gonna see their symptoms improved. Duadinals are

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going to be better with food. Gastric is gonna be

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worse with food. The way I remember that duodenal ulcers.

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Du I remember, dude, give me food?

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Speaker 2: Do you do?

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Speaker 1: Just like in dude and duodenal? Dude give me food?

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So better with food, duodonal ulcers and gastric.

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Speaker 2: Is worse with food.

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Speaker 1: And that's why patients with gastric ulcers that the pain

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gets worse with eating. A lot of times you'll see

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weight loss in these individuals compared to duaden ulcers. You

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may see weight gain because their symptoms get better with food,

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so they tend to eat more, So it makes sense.

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Speaker 2: One other thing to be.

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Speaker 1: Mindful of is that peptic ulcers can bleed and they

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can also perforate, So you need to know that peptic

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ulcers are actually peptic ulcer disease is the most common

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cause of an upper GI bleed. Peptic Ulcer disease most

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common cause of an upper GI bleed. And in the

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case that they do perforate, these patients are going to

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go from this kind of vague epigastric pain pepsia blah

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blah blah, to this sudden onset of this sharp, acute

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abdominal pain. They may have signs of peritonitis like rebound

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tenderness guarding. So know that these peptic ulcers can perforate,

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they can bleed, and the presentation is going to be

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much different. It's obviously a much more serious situation as

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far as diagnosing. Ultimately, your most sensitive and specific test

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is going to be in an endoscopy, But there's a

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few things you want to do before you get to

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an endoscopy. But remember, if an endoscopy is on the

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answer listen it says what is your best test endoscopy,

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it's always going to be the endoscopy. But in real life,

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there's a few things that you're going to do first

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and a few other tests. So if it says what's

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your initial test, you may go with some other things.

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So let's go over that Initially you're probably going to

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test for H. Pylori, So you can do that a

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couple of different ways. You can do a urrea breath

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test or an H. Pylori stool antigen H pylori testing.

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When you do a uria breath test, what you need

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to know about this is is that H. Pylori produces

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an enzyme called urease, which breaks down urrea into ammonia

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and carbon dioxide. So the way this test works is

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that during the test, the patient is given a pill

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containing urea and then they blow into this bag. They

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blow into the bag, they close off the bag, it's

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sent to a lab, and then they test for the

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amount of exhaled carbon dioxide. And remember again they were

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given urea, and as I said before, H pylori turns

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urea into carbon dioxide and ammonia. So if there's an

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increase in all this carbon dioxide that's in this bag,

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then obviously this is gonna be a positive test for H.

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Speaker 2: Pylori.

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Speaker 1: So that's how a urrea breath test works. H Pylori

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stool intogen is straightforward. It's literally just checking for a

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stool antigen of H.

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Speaker 2: Pylori.

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Speaker 1: So that's another test that you can do as well.

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And then ultimately, like I said before, the gold standard

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test is going to be your endoscopy. That's going to

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be to diagnose. You can visualize the ulcer and you

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can take biopsies if needed, and then treatment depends on

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the cause. So let's start with H pylori. If this

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patient is H pylori positive, again, just like in guesstritis,

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you're going to do quadruple therapy. The way I remember

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quadruple therapy for an hpylori positive patient is I remember

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these patients have belly pain. They want you to treat

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their belly pain so they can get better. So they

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say to you, treat my belly, please, treat my belly please.

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TMBP that stands for tetracycling, metronideisol, bismyth subseliciy, and PPIs

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treat my belly please. Tetracycling, metronide, is al, bismuth, subselicily,

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and P. Those are for your H. Pylori positive patients. Now,

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if these patients are hpylori negative, how do you treat

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their peptic ulcer disease? Well, first, treat the underlying cause.

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If they're taking nsids, they're smokers, they drink a bunch

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of alcohol. You're going to discontinue all those things obviously,

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and then you're going to give them PPIs as well.

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You can also use H two blockers, but realistically, anytime

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you have an option of a PPI or an H

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two blocker, unless there's some contraindication of PPIs, always use PPIs.

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Why is that PPIs are much more effective, and that's because,

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I mean, just really quickly break down the way these

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work and just to give you a little bit about

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the may of the mets. So you have a parietal

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cell in the stomach. The parietal cell has a proton pump.

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That's what shoots out all the hydrochloric acid into the stomach.

283
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That's where all of your acid in the stomach comes from.

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So how is your prietal cell activated. Well, acetylcholine, histamine,

285
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and gastrin all activate the prietal cell to pump out

286
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this acid. An H CH two blocker obviously blocks H

287
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two and that's histamine, So that's a histamine blocker, So

288
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it blocks just histamine, but you still have acetocholine and

289
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gastrine that can activate the parietal cell. So while it

290
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helps because you stop the histamine from activating the paryal cell.

291
00:14:16,039 --> 00:14:18,840
Stylcholine and gastrine are still working there to pump out acid,

292
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so there's still some acid production, Whereas a proton pump

293
00:14:22,159 --> 00:14:26,200
inhibitor actually completely shuts off the proton pump, so it

294
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doesn't matter how much is stylcholine, how much histamine, how

295
00:14:28,679 --> 00:14:32,120
much gastrine is activating that parietal cell. The pump is

296
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shut off, so no acids coming out. So PPIs are

297
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much more effective. So remember, if you have an option

298
00:14:37,519 --> 00:14:40,159
of a PPI or hto blocker, use the PPI. So

299
00:14:40,200 --> 00:14:44,080
again H pylor negative, treat the underlying cause, give them PPIs.

300
00:14:44,360 --> 00:14:47,279
That's the treatment. If they're H pylori positive, treat the

301
00:14:47,399 --> 00:14:50,639
H pylori very easy treatment. And then there's one other

302
00:14:50,679 --> 00:14:54,480
treatment option that you should probably know. For refractory patients.

303
00:14:54,519 --> 00:14:58,679
The PPIs aren't working, you discontinued all the ensis, et cetera,

304
00:14:58,960 --> 00:15:01,320
and they're still having SIN, you can do something called

305
00:15:01,320 --> 00:15:04,519
the parietal cell veagotomy, which is where they sever the

306
00:15:04,600 --> 00:15:09,000
vagual nerve, which essentially shuts down the portion of the

307
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stomach where the parietal cells are located. And this obviously

308
00:15:12,519 --> 00:15:15,759
leads to decreased acid by about seventy five percent, So

309
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pretty effective procedure, but it's invasive. Obviously, there's a lot

310
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of things you want to try before you get to

311
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a parietal cell vegotamin. This is just going to be

312
00:15:22,240 --> 00:15:25,080
for your refractory patients. So those are the treatments. Let's

313
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move on to the home stretch here. The last thing

314
00:15:26,879 --> 00:15:28,039
we're going to go over, and that's going to be

315
00:15:28,039 --> 00:15:30,720
pyloric stenosis. So this is going to be a condition

316
00:15:30,960 --> 00:15:33,879
commonly in newborns. About three to six weeks is going

317
00:15:33,919 --> 00:15:36,279
to be your most common age range, and it's a

318
00:15:36,320 --> 00:15:42,000
thickening hypertrophy, a thickening or hypertrophy of the pyloris, which

319
00:15:42,039 --> 00:15:45,080
is the sphincter, the muscular valve between the stomach and

320
00:15:45,120 --> 00:15:49,399
the duodenum, so it prevents gastric emptying. Risk factors are

321
00:15:49,440 --> 00:15:52,399
going to be males four times more common in male,

322
00:15:52,480 --> 00:15:55,200
so definitely know that males are going to be much

323
00:15:55,200 --> 00:15:58,279
more common. Look at your vignette. If it's a female,

324
00:15:58,720 --> 00:16:00,519
you know for a vignette probably and that's so common

325
00:16:00,519 --> 00:16:03,000
that it's going to be pylar scinosis. Three to six

326
00:16:03,039 --> 00:16:05,360
weeks is going to be your most common age of presentation.

327
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Sometimes they'll say three to twelve, but generally three to

328
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six is the most common. And then first born patients

329
00:16:11,519 --> 00:16:13,240
are also going to be at a higher risk. And

330
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then the last thing too, not as you know, not

331
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as big of a risk as the other ones, but

332
00:16:17,799 --> 00:16:22,279
macrolide antibiotics, in particular erythromycin within the first two weeks

333
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of birth can also lead to pyloric stenosis. And this

334
00:16:26,360 --> 00:16:29,600
is the way it's explained, is most likely due to

335
00:16:29,639 --> 00:16:33,840
the increased gastric motility with macrolight antibiotics. Erythromycin, even a

336
00:16:33,919 --> 00:16:37,240
zythromycin can cause this. So the increased gastric motility in

337
00:16:37,279 --> 00:16:40,279
these drugs can lead to hypertrophy from the pyloris basically

338
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just being overworked. And it's the same reason that we

339
00:16:43,320 --> 00:16:47,360
use erythromycin and gastroparesis because it increases the gimotility. So

340
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if you have a patient under two weeks they give

341
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them a erythromycin, this may lead to pyloric stenosis. So

342
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risks again males first born three to six weeks of

343
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life and macrolide antibiotics in particular erythromycin. All right, So

344
00:16:59,519 --> 00:17:02,559
as far as the history and the exam. They may

345
00:17:02,600 --> 00:17:06,599
have some non specific symptoms weight loss, dehydration doesn't matter.

346
00:17:06,680 --> 00:17:08,319
You don't care about that stuff because it's not going

347
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to help you differentiate it in Yet, what you need

348
00:17:11,119 --> 00:17:14,079
to know for pylor ex stenosis, there's two really big

349
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things you cannot forget. So pilar stenosis non bilious projectile

350
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vomiting after feeding. That is going to be your vignette

351
00:17:22,240 --> 00:17:24,400
right there. You can just go ahead and circle pilar stenosis.

352
00:17:24,480 --> 00:17:26,440
That's gonna be your answer. So you see non bilious

353
00:17:26,440 --> 00:17:29,839
projectile vomiting after feeding pilar stenosis. So why is it

354
00:17:29,960 --> 00:17:33,599
non bilious? Well, remember this is an obstruction at the stomach.

355
00:17:33,640 --> 00:17:36,519
It's at the pylorus, so we're not into the area

356
00:17:36,519 --> 00:17:38,759
where the bile is coming from the common bioduct. It's

357
00:17:38,799 --> 00:17:41,880
not evolves. It's an unomal rotation of the small bowel,

358
00:17:41,920 --> 00:17:43,559
so we're not in the area where the bile is

359
00:17:43,599 --> 00:17:46,839
being excreted. So it's gonna be non bilious. It's in

360
00:17:46,880 --> 00:17:50,200
the stomach, So non bilious projectile vomiting after feeding that

361
00:17:50,359 --> 00:17:53,359
is going to be pathonomoonic, almost as pathonomonic as The

362
00:17:53,400 --> 00:17:55,119
second thing you need to know for the exam and

363
00:17:55,160 --> 00:17:58,000
that's going to be an olive shaped mass. So on

364
00:17:58,079 --> 00:18:01,720
physical exam, we talked about the the pyloris being hypertropheed.

365
00:18:01,759 --> 00:18:04,960
It's enlarged, and on physical exam, normally you're not gonna

366
00:18:04,960 --> 00:18:07,119
be able to feel the pylorus. But these patients, because

367
00:18:07,119 --> 00:18:10,599
it's hypertrop feed, you're actually going to feel this olive

368
00:18:10,640 --> 00:18:14,440
shaped mass in the epigastric area and it's going to

369
00:18:14,480 --> 00:18:16,759
feel like a small round mass and it's described as

370
00:18:16,799 --> 00:18:20,559
an olive shaped mass. If you see this on a vignette,

371
00:18:20,680 --> 00:18:22,559
you see this or you feel this in real life,

372
00:18:22,599 --> 00:18:25,640
this is really pathdomonic for the disease. And actually, years ago,

373
00:18:25,720 --> 00:18:29,680
before ultrasound was around, this would be the only way

374
00:18:29,680 --> 00:18:31,720
you would diagnose it. If you felt this olive shaped mass,

375
00:18:31,720 --> 00:18:34,000
they would go right to surgery, you know, after you

376
00:18:34,119 --> 00:18:36,720
treated them with fluids and things like that. So physical

377
00:18:36,759 --> 00:18:41,119
exam no non bilious projectile vomiting and no olive shaped mass.

378
00:18:41,119 --> 00:18:42,440
So those are the two things you need to know

379
00:18:42,559 --> 00:18:45,319
as far as diagnosing. Ultrasound is going to be your

380
00:18:45,359 --> 00:18:48,240
test of choice. It's ninety seven to ninety nine percent

381
00:18:48,400 --> 00:18:50,079
sensitive no radiation.

382
00:18:50,160 --> 00:18:50,920
Speaker 2: These are newborns.

383
00:18:50,920 --> 00:18:52,440
Speaker 1: You really don't want to radiate them if you don't

384
00:18:52,480 --> 00:18:54,400
have to. And then on the ultrasound, you're going to

385
00:18:54,440 --> 00:18:58,119
see some pyloric muscle thickness over four millimeters and the

386
00:18:58,160 --> 00:19:00,960
pyloric canal length will be over seven eighteen millimeters. Don't

387
00:19:00,960 --> 00:19:03,079
worry about those numbers, but I just want to throw

388
00:19:03,119 --> 00:19:05,200
that out there so you know that's how you actually

389
00:19:05,400 --> 00:19:06,559
have a positive ultrasound.

390
00:19:06,559 --> 00:19:08,200
Speaker 2: But ultra sound is gonna be your test of choice.

391
00:19:08,240 --> 00:19:09,839
Speaker 1: The only reason I'm even going to mention an upper

392
00:19:09,839 --> 00:19:11,559
GI series not so much that you're going to use

393
00:19:11,559 --> 00:19:12,920
it in real life. It's really only going to be

394
00:19:12,920 --> 00:19:17,079
if ultrasounds inconclusive, the physical exam is inconclusive. But you

395
00:19:17,160 --> 00:19:18,960
need to know for the exam because on an upper

396
00:19:18,960 --> 00:19:21,000
GI series, there's a couple of key terms.

397
00:19:21,200 --> 00:19:22,759
Speaker 2: There's one called a string sign.

398
00:19:22,799 --> 00:19:26,200
Speaker 1: It's not specific only to pyloxynosis, but if you do

399
00:19:26,279 --> 00:19:28,559
see it in this vignette, this is going to be

400
00:19:28,599 --> 00:19:32,000
a narrowed area of barium flow. It's literally going to

401
00:19:32,079 --> 00:19:35,160
look like a string of barium because that hypertro feed

402
00:19:35,160 --> 00:19:37,960
area only allowing a small amount of barium through. So

403
00:19:37,960 --> 00:19:40,319
that's a string sign and upper GI. And there's another

404
00:19:40,400 --> 00:19:43,559
one called a railroad track sign, and this is due

405
00:19:43,640 --> 00:19:49,240
to the pyloric mucosa compressing and pushing causing this double

406
00:19:49,319 --> 00:19:52,359
canal where you're going to see two small tracks of

407
00:19:52,400 --> 00:19:54,599
barium flowing through. It kind of looks like a railroad

408
00:19:54,759 --> 00:19:57,000
and that's a railroad sign on upper GI. So again

409
00:19:57,039 --> 00:19:59,160
in real life, probably not going to do an UPPERGI,

410
00:19:59,279 --> 00:20:01,240
but you do need to know for the exams because

411
00:20:01,279 --> 00:20:02,960
they like to throw out these key terms of string

412
00:20:03,039 --> 00:20:05,920
sign and railroad track sign on what you'll see on UPPERGI.

413
00:20:06,079 --> 00:20:08,240
And then as far as labs, they're vomiting up all

414
00:20:08,240 --> 00:20:13,359
the stomach acids, so you may have this hypochloromic metabolic acidosis.

415
00:20:13,519 --> 00:20:17,079
They may also have hypokalmia, and this is just because

416
00:20:17,279 --> 00:20:20,720
the kidney's compensating and flushing out all of the renal

417
00:20:20,759 --> 00:20:26,200
potassium excretion. So hypochloromic metabolic acidosis may be seen. And

418
00:20:26,240 --> 00:20:29,400
then they also may have hypokalemia on labs. But your

419
00:20:29,480 --> 00:20:31,519
key for diagnosis is going to be your ultrasound. But

420
00:20:31,559 --> 00:20:34,000
know these things as well. So as far as treatment,

421
00:20:34,599 --> 00:20:38,039
initially these patients can be kind of sick. They're volume depleted,

422
00:20:38,359 --> 00:20:40,519
so before you get to any intervention, you need to

423
00:20:40,559 --> 00:20:44,200
start with some fluids. You want to do electrolyte replacement.

424
00:20:44,240 --> 00:20:46,680
Remember again I said they may be HYPOKLEMICX you want

425
00:20:46,680 --> 00:20:49,759
to replace the potassium, may give them some dextros IV

426
00:20:49,839 --> 00:20:52,720
fluids and things like that. Once they're euvulymic, then you

427
00:20:52,759 --> 00:20:54,799
get to the actual procedure that needs to be done

428
00:20:54,799 --> 00:20:57,599
in these patients. And this is called the pyloral miotomy

429
00:20:57,839 --> 00:20:59,440
is the name of the procedure that you want to

430
00:20:59,480 --> 00:21:03,640
do once they're stable their euvolemic and this is normally

431
00:21:03,640 --> 00:21:08,400
done laparoscopically. The surgeon makes this longitudinal incision into the

432
00:21:08,400 --> 00:21:12,759
pylorus and once they make this longitudinal incision, that hypertrophied

433
00:21:12,880 --> 00:21:16,319
muscle kind of pops out through this incision that they made.

434
00:21:16,480 --> 00:21:19,920
And once it pops up through this area of the incision,

435
00:21:20,480 --> 00:21:23,960
now beneath the area of the incision, there's this canal

436
00:21:24,000 --> 00:21:26,319
that opened up this new space because all the muscle

437
00:21:26,400 --> 00:21:29,000
kind of tunneled up through this incision, and they actually

438
00:21:29,160 --> 00:21:32,480
have this area where the stomach contents can flow through

439
00:21:32,480 --> 00:21:36,839
this area, so that again it's called a pyloromiotomy. Pyloromotomy

440
00:21:37,000 --> 00:21:39,440
is going to be the treatment of choice once these

441
00:21:39,440 --> 00:21:43,000
patients are stable and euvolemic, so that's what you need

442
00:21:43,039 --> 00:21:45,640
to know. Those are the main things. I feel like

443
00:21:45,640 --> 00:21:48,200
I kind of touched on all the high yield stuff.

444
00:21:48,400 --> 00:21:51,559
I hope that was helpful. And as always, good luck

445
00:21:51,640 --> 00:21:54,480
on your pants, your panry, your ear, and good luck

446
00:21:54,519 --> 00:22:00,039
in PA school and