Peptic Ulcer Disease: Mechanisms and Treatment | Lecturio Medical

[00:00] Our topic now brings us into peptidylcholism, a peptidylcholism disease. You divide this into that disease or erosion that's taking place in the stomach versus that type of erosion that might be taking place into adenome. By far in the US, the most common type of peptidylcholism disease

[00:20] would be the type that's taking place in the duodenum. However, for learning purposes, we need to make sure that we cover both sets of pectacosa disease and then, importantly, we will go through the symptoms of your patient so that you're able to distinguish one from the other. Mechanism of injury. If there's direct mucosa damage,

[00:40] due to toxins, ethanol, and NSAIDs, M-P-L-H. Now for the most part, you can think of pectacosis disease taking place in the stomach as really not due to increased acid production. Remember that the stomach is extremely effective with protecting the lining of the stomach from

[01:00] the acid due to all that bicarbonate, prostaglandins and such, so therefore, protecting its stomach from all that acid. However, if the lining of the stomach has been compromised where it could take place due to, let's say, NSAIDs, which is then inhibiting your COX pathway.

[01:20] Then you might then inhibit the formation of the prostaglandin necessary to properly protect or contribute to the protection of the stomach. Or if there's actual chemical damage taking place to the lining of the stomach due to bile that might then regurgitate back into the stomach. Remember bile.

[01:40] is being released or secreted from your gallbladder into the second part of the duodenum. So therefore, there must be some kind of method by which the bile is retrograde flow back in the stomach causing damage.

[02:00] In the end, you have the stomach and from henceforth, whenever you deal with H. pylori, you should be thinking either the distal end of the stomach or the first part of the duodenum as being its place of residence. In the stomach, the H. pylori, if you remember from micro, then has an enzyme called urease.

[02:20] Therefore, it will take the urea and it will create a force field for itself. That force field that H. pylori then creates in the abdomen and stomach is then made up of ammonia. Amazing, isn't it? At some point in time, it can then burrow into the lining of the stomach and is therefore weakening the lining, resulting in

[02:40] pectic ulcer disease, H. pylori, bowel, NSAIDs, alcohol. Prostitaglantin inhibition, like we just said, with NSAIDs or steroids, even with pathologies such as Cushing, in which you would have excess cortisol, hypercorizolism, is then knocking out your phospholipase A2.

[03:00] you don't have the necessary prostaglandin to protect the lining of the stomach as such against the acid. Increased acid production could be a cause, but more importantly, the most important pathogenesis for peptidosis disease of the stomach would be damaged or lining. Whereas if it is,

[03:20] pathogenesis, public ulcer disease of the duodenum, then in fact there would be increased acid. For example, if you do Zolinger-Ellison syndrome and with the gastronoma, with all that acid which is then coming out like a huge wave out of the stomach and into the duodenum, there is no way that the duodenum can properly be used.

[03:40] protect itself against all that acid. Mycosus ischemia is always a possibility. Whenever there is infarction that's taking place, then at some point in time, you might then be hurting or injuring the lining of the stomach. Beptic ulcer disease, if it is in the stomach, the pain is.

[04:00] patient here is going to be complaining of epigastric pain. However, this time around, with pectacosis disease in the stomach, you would not find in the patient would not be complaining of pain that's radiating to the back. Is that clear? On your step and on your wards, if the pain is radiating to the back,

[04:20] Then this gives you the high suspicion and differential of pancreatic damage. However, if it's not, then you're thinking about peptidosis disease. Also, with this erosion that's taking place, remember you have not perforated. Ulceration means ulceration. It's a clean, punched-out lesion in the stomach.

[04:40] and a clean punched-out lesion here with bleeding taking place may result in hematemesis. With all this blood that's now being released, either from the stomach or maybe perhaps the duodenum, you can only imagine that, as I told you earlier, that the stool has an opportunity to completely

[05:00] saturate itself with blood. So therefore, by the time it's evacuated here, the stool in fact is going to look black and tarry. Ametemesis, ametrochis, iron deficiency, anemia, all of these, well, all part of bleeding. Next, if there's perforation that's taking place,

[05:20] places, especially if you have the duodenum type of peptidosis disease. It is then perforated and then it will then affect different organs or blood vessels. If it is peptidosis disease of the stomach, which is usually found in the lesser antiretment of the stomach, and if it is to perforate, then you are then going to

[05:40] or the perforation is going to affect the left gastric artery. Whereas if the perforation takes place down in the duodenum, then the perforation then causes damage to the gastric duodenum artery. Gastric outlet obstruction due to parapyloric scar formation is an important complication.

[06:00] At some point in time, when there is enough damage that is taking place, any type of damage, at some point, the body wishes to respond with the repair process. This repair process that you are looking for at some point with fibrosis taking place may actually then cause gastric outlet problems because of the

[06:20] More or less, think of it as being a stricture formation or a scar formation and therefore decreasing the emptying of the stomach. Gastricosis may be malignant, while duodenalcers are basically never. Once again, pectacosis disease, keep in mind that if it's the stomach.

[06:40] You should be monitoring or should be thinking, hmm, there's a possibility of a primary gastric cancer developing. Duodenum, almost never. On the left, peptic ulcer disease is in the duodenum. You'll notice that you have a clean, punched-out lesion. Whereas a gastric ulcer, you also have a gastric ulcer.

[07:00] also have a clean punched out lesion, endoscopy, esophageal gastrodoidontoscopy would be your best measure or best method of diagnosis. With this ulceration, at some point remember, keep your ulceration and perforation completely separate.

[07:20] Management of peptidosis disease, antacids. Because of the burning sensation that's taking place, magnesium and albumin cause long-term toxicity. Be careful with antacids, magnesium and aluminum. Mochacla syndrome due to prolonged use of calcium is something that you want to keep in mind with antacids.

[07:40] Once again, milk alkaline syndrome due to prolonged use of calcium.

[08:00] protect the lining of the stomach. Avoid an renal insufficiency though and that's a big deal. So the drugs that I've given here for management, I've given you as to what it does objectively and then things that you want to keep in mind as side effects because these patients will be on these drugs for quite a bit of time.

[08:20] time.

[08:40] to document the healing. The management, remember, H. pylori highly associated with both of these issues. So therefore, the importance of eradicating H. pylori cannot be understated, responsible for developing lymphomas perhaps, and maybe even our intestinal type of

[09:00] of gastric primary adenocarcinoma. Now we have two types of treatment. So you want to either think quadruple, bismuth, and the quadruple therapy would include bismuth, metronazole, tetracycline, and proton pump inhibitor. Or you could have clorithromycin-based triple therapy, which would then be called clorithromycin.

[09:20] consist of amoxicillin, clarithromycin, and your PPI.

[09:40] I've been taking this over decades and with 10-seds, as we mentioned earlier, if the prostaglandins are then lost within the stomach, the lining of the stomach in fact now becomes vulnerable to the acid abuse and so therefore may bring about erosion of the lining, resulting in pectacosar disease of the stomach.

[10:00] the stomach. The first case that you're going to find with pectacosis disease is the stomach, with long-term use, you consider this to be acute. It's not like you take one aspirin or you take one ibuprofen and then all of a sudden you're the patient develops pectacosis disease. That makes no sense.

[10:20] taking these drugs over a long period of time. Also, keep in mind though, if NSAIDs have been taken over a long period of time, that in the kidney, with prostaglandin is responsible for keeping the afferent arteriole open, if NSAIDs are taken, you take out the prostaglandin.

[10:40] You're at risk of vasoconstricting the afferent and over a long period of time here as well, you're worried about chronic kidney injury. Is that clear? Two major organ systems that are extremely vulnerable to attack with NSAID use and really because of the easy accessibility of these.

[11:00] drugs by the patient over the counter, you have to properly educate your patient because they're going to be popping pills all of the time whenever they feel pain and I'm talking popping pills excessively for a long period of time and they may or may not even tell you, right? Increased risk of bleeding with low

[11:20] dose and high dose aspirin through the increased risk of dose dependencies of what you're worried about. Exactly what I was saying, the patients are in pain. They might be taking aspirin and they might be increasing the dosage without you ever knowing. It's important that you establish in your practice exit rapport.

[11:40] with your patient so that they're being transparent between you and your patient. Enteric coating does not reduce the risk of bleeding. Do not allow the advertisements and the commercials to fool you. High rate of mortality for NSAID associated with GI bleeding.

[12:00] Who's your patient? With NSAID, associated with Peptococcus disease, greater than 70. Higher dose of NSAIDs. Often associated with H. pylori and concomitant corticosteroids. Remember please, with NSAIDs, they might very well be in pain.

[12:20] and if they are, they're probably taking prednisone as well. My goodness, a combination of NSAIDs and corticosteroids definitely compromises the production of your prostate gland and therefore increases the risk of pectacosor disease further. Also, anticoagulants and prior

[12:40] history of pepidococcal disease, NSAIDs, what does it do? Inhabitoplastic landin, management, PPI, and removed NSAIDs. At some point in time, if pepidococcal disease has kicked in, remove the offending agent, educate your patient properly, and PPI.

[13:00] Always feature H. pylori, highly indicated, gastric or duodenum. H. pylori, for the most part, you assume is present. Prophylaxis, mesoprostol, aprostaglandin, it's a prostaglandin E derivative and combats the effect.

[13:20] effects of NSAIDs. Diarrhea is a dose-emitting side effect, however, and abseacontra indicated in pregnancy. Prophylaxis, PPI, superior to H2 blockers we've talked about when it comes to acid control.

[13:40] COX-2 inhibitors might be a possible alternative, lacks cardiovascular protective effect, and can cause protective effect loss for concomitantly baby aspirin use. So COX-2 inhibitors, you've heard of cell coccib, so on and so forth.

[14:00] might be alternatives that you're looking for when dealing with NSAID-associated peptid-calcy disease.

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