Hey guys, my name is Brad and welcome to nursing.com. And in today’s video, what we’re going to do is we’re going to be discussing peptic ulcer disease, some of the pathophysiology, as well as how we’re going to treat it. Without further ado. Let’s dive in. 

So regarding the pathophysiology of peptic ulcer disease, it’s important to understand that it’s like a chink in the armor, right? Whenever you’re looking at the stomach and you look at the inside lining of the stomach, right? What we actually have is this nice mucosal membrane, right? This mucosal lining on the inside of the stomach. And the entire purpose of this mucosal lining is to protect these sensitive submucosal and muscle layers. These delicate, sensitive tissues from that corrosive hydrochloric acid, right? Remember our stomach produces hydrochloric acid in an attempt to try and chew up and dissolve the food that we consume so that once it passes into the small intestine, we’re able to more effectively remove nutrients. 

Peptic ulcer disease is like a chink in that armor. It is a breakdown in an area of that mucosal lining that would then allow the spillage of hydrochloric acid into that mucosal membrane to then begin to chew away at these sensitive and delicate tissues. This is incredibly problematic, right? We think about hydrochloric acid. We think about acid in general as this liquid substance that’s capable of chewing. It’s being very corrosive and able to chew through anything, right? Well, imagine what would happen if you had a little breakdown, a chink in the armor of that mucosal lining, that’s supposed to protect those sensitive tissues. If you have that breakdown and you lose that protection, that stomach acid is now able to reach these more delicate tissues and it begins to chew away at it. And all of the symptoms that we’re going to see as well as the treatment modalities geared towards working on peptic ulcer disease are all related to that chink in the armor. 

So some of the different causes of peptic ulcer disease. What are some different things that would actually cause that chink in the armor, that disruption, in the mucosal lining that’s supposed to protect our stomach. One of the leading causes that’s important for you to know regarding peptic ulcer disease is H. pylori also known as Helicobacter pylori. And essentially not to get too technical, but what this is, is this an infection that ends up resulting in inflammation of that mucosal lining of the stomach, causing a breakdown in that mucosal lining, which then allows stomach acid to chew through that lining in the stomach, right? Peptic ulcer disease. So an actual infection, H. pylori, causes an inflammatory response in that mucosal lining, allowing hydrochloric acid to start to chew up those stomach tissues.  NSAIDs are another one, right? I’m not going to dive into this cellular process, but just know, or remember, or maybe research NSAIDs work on cyclooxygenase 1 (COX-1) as well as cyclooxygenase 2 (COX-2), right? One is responsible for reducing inflammation. That’s what NSAIDs are responsible for. But one of the other cyclooxygenases actually chews away that protective mucosal lining again, allowing hydrochloric acid to escape into those mucosal and submucosal tissues and start to chew away at our stomach lining. Also smoking as well as alcohol consumption, both also can directly lead to the development of peptic ulcer disease. But it’s important to know that the leading culprits are H. pylori as well as NSAIDs. 

So what are some of the assessment findings that we’re going to see in patients who are experiencing peptic ulcer disease? Well, one is going to be epigastric, stomach pain, right? Stomach pain in that upper abdomen. Again, we have an actual degradation in the lining of that stomach. We have hydrochloric acid, basically. We’re digesting ourselves, we’re digesting our own stomach. So that’s going to cause us epigastric pain. That’s going to cause nausea and vomiting, weight loss as your appetite is going to be greatly decreased. Every time you eat, you’re going to have increased hydrochloric acid production. More hydrochloric acid production, more chewing away at the lining of the stomach, right? It’s a very big problem. Abdominal fullness and hematemesis, right? You can actually have degradation in that lining to the point that you end up bleeding. You ended up producing a GI bleed. It’s not uncommon in peptic ulcer disease, right? 

And so some of the ways that we’re going to be able to diagnose whether a patient has a chink in the armor or not, is things such as an upper EGD, right? Where they actually would take a scope, feed it in through the mouth, down into the tummy and actually take a look at the stomach itself, actually visualize the mucosal lining of that stomach to see if there’s any chink in the armor. While they’re in there, right, this is kind of bleeding a little bit into therapeutic management or how we’re going to treat, but while they’re in there, they, if there is an active bleed in that lining that chink in the armor, they can also cauterize while they’re there. H. pylori testing. If we suspect that a patient may have peptic ulcer disease, we may very well undergo H. pylori testing. Remember that this is one of the leading causes of peptic ulcer disease, as well as a barium swallow, which is important. Should a patient be having this epigastric pain? Should they have evidence of peptic ulcer disease? A barium swallow is not uncommon. Also, as the patient swallows contrast, which is then highlighted through diagnostic imaging, which could be reflective and show whether we have hydrochloric acid actually spilling out of the stomach or not. Or if we have contrast spilling out of the stomach or not, basically a lot of different diagnostic indicators to tell us whether a patient has peptic ulcer disease or not. 

So what are some of the different things that we’re going to use in order to treat patients with peptic ulcer disease? But one is, of course we know H. pylori is one of the leading causes. So we’re going to treat H. pylori. usually through a combination of antibiotics, as well as PPI’s remember, these are Proton Pump Inhibitors, right? These are medications such as omeprazole, which end in -prazole, all right? These are medications that actually affect that hydrogen potassium pump in the stomach as a proactive means to try and reduce the amount of hydrochloric acid our stomach is producing.  Also H2 antagonist. Medications that again are a proactive attempt to reduce the overall hydrochloric acid produced. We’re going to discontinue NSAIDs as we know, these are common causes of a breakdown or a chink in the armor. Again, this is an actual ulceration, peptic ulcer diseases, an ulceration in that lining of the stomach, right? So what can happen is, you can have bleeding as we’ve already alluded to. It’s not uncommon to see blood transfusions occur as the patient’s hemoglobin is dropping. Something, I actually wasn’t aware of, is, there is a treatment modality called a vagotomy, which is an actual clipping of that vagus nerve. They actually clip the vagus nerve, which innervates the stomach and actually reduces the amount of hydrochloric acid produced. Very interesting, but has side effects, as you imagine, clipping a vagus nerve would. And then another possible treatment as a partial gastrectomy. If you have a patient who has recurrent peptic ulcers, they continue to occur, and as a result, you continue to have bleeding, it’s an actual problem. What may actually occur is they may actually take a portion of the stomach, surgically remove it to try and prevent that weakened chink in the armor to prevent those bleeds from continually reoccurring. 

Some of the patient education that we’re going to go over as well for patients with peptic ulcer disease, similar to patients experiencing GERD, right? But we know NSAIDs are one of the common causes of peptic ulcer disease. So making sure that we encourage them to stop using NSAIDs. We want to stop that breakdown in the cyclooxygenase process, so reducing that mucosal lining of the stomach and therefore continually causing ulceration in that stomach. Stopping smoking. We know that that also leads to peptic ulcer disease. Medication adherence, right? Those PPI’s, those H2 blockers. Anything that we’re prescribing to treat H. pylori. Medication adherence is paramount, as well as any kind of dietary adherence, right? Similar to GERD, reducing food intake is going to cause additional hydrochloric acid production within the stomach, citrus, chocolate, coffee, spicy foods, all of these things that lead to increased hydrochloric acid production. 

And so going over some of the key points surrounding peptic ulcer disease, remember it is like a chink in the armor. It is an actual degradation or break down in that mucosal lining of the stomach that’s supposed to protect our underlying tissues from that corrosive hydrochloric acid. We actually have digestion of our own stomach, basically. Remembering that a lot of the causes, primarily, H. pylori infections, but also overuse of NSAIDs breaking down that mucosal lining. Knowing that all of our assessment findings, again, are related to that hydrochloric acid, hitting that chink in the armor causing pain, causing possible bleeding, indigestion, nausea, vomiting, et cetera. And knowing that all of our therapeutic managements are directly geared at either treating an H. pylori infection or reducing the total amount of stomach acid in our tummy, or blood transfusions, things to actually treat that ulceration in the stomach. And all of the patient education that we just went over. 

Guys, that was peptic ulcer disease. I hope that that helped bring a little bit more understanding to the disease process. I hope that you guys go out there and be your best selves today. And as always, happy nursing.