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Peptic Ulcer Disease

by Carlo Raj, MD
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    Our topic now brings us into Peptic Ulcer Disease. With peptic ulcer 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 in duodenum. By far in the U.S., the most common type of peptic ulcer disease 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 peptic ulcer 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 mucosal damage due to toxins, ethanol, NSAIDS, bile or <i>H. pylori</i>. Now for the most part, you can think of peptic ulcer disease taking place in the stomach is really not due to increased acid production. Remember that the stomach is extremely effective with protecting the lining of the stomach from the acid and due to all that bicarbonate, prostaglandins and such so therefore protecting the stomach from all that acid. However, if the lining of the stomach has been compromised where it could take place due to, let’s says, NSAIDs which is then inhibiting your COX pathway 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 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. <i>H. pylori </i>in the stomach would be residing...

    About the Lecture

    The lecture Peptic Ulcer Disease by Carlo Raj, MD is from the course Stomach and Duodenum Diseases.


    Included Quiz Questions

    1. Gastric outlet obstruction.
    2. Perforation of the ulcer.
    3. Iron deficiency anemia.
    4. Malignancy.
    5. GERD.
    1. Reflux of acid into the esophageal mucosa.
    2. Mucosal damage due to Helicobacter pylori and NSAIDs.
    3. Loss of blood supply to mucosa.
    4. Increased acid production.
    5. Inhibition of prostaglandins.
    1. Rupture of the left gastric artery.
    2. Peri-pyloric scar formation.
    3. Malignancy.
    4. Rupture of the gastroduodenal artery.
    5. Pancreatic bleeding.
    1. Warfarin toxicity due to inhibition of cytochrome P450 by cimetidine.
    2. Toxicity of the antacids.
    3. Mucosal ischemia due to previous MI.
    4. Interaction with proton pump inhibitors.
    5. Interaction with sucralfate.
    1. Malignancy due to gastric ulcer disease and antibiotics for H. pylori with follow up EGD.
    2. Duodenal ulcer and proton pump inhibitors.
    3. Gastro esophageal reflux disease and antacids.
    4. Inflammation of the stomach and PPI.
    5. Perforated ulcer and endoscopy.

    Author of lecture Peptic Ulcer Disease

     Carlo Raj, MD

    Carlo Raj, MD


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