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Peptic Ulcer Disease

by Carlo Raj, MD
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    00:01 Our topic now brings us into Peptic Ulcer Disease.

    00:04 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.

    00:15 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.

    00:23 However, for learning purposes, we need to make sure that we cover both sets of peptic ulcer disease.

    00:29 And then importantly, we will go through the symptoms of your patient so that you’re able to distinguish one from the other.

    00:36 Mechanism of Injury If there’s direct mucosal damage due to toxins, ethanol, NSAIDS, bile or <i>H. pylori</i>.

    00:46 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.

    00:55 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.

    01:08 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.

    01:30 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.

    01:39 Remember bile is being released or secreted from your gallbladder into the second part of the duodenum.

    01:48 So therefore, there must be some kind of method by which the bile is retrograde flow back in the stomach causing damage.

    01:56 <i>H. pylori </i>in the stomach would be residing where? In the antrum of the stomach.

    02:02 And from henceforth whenever we deal with <i>H. pylori</i>, you should be thinking either the distal end of the stomach or the first part of the duodenum as being its place of residence.

    02:15 In the stomach, the <i>H. pylori</i> if you remember from micro that has an enzyme called urease.

    02:20 They’ll fully take the urea and they will create a force field for itself.

    02:25 That force field that the <i>H. pylori</i> then creates in the antrum of the stomach is then made up of ammonia.

    02:31 Amazing, isn’t it? At some point in time, it could then burrow into the lining of the stomach and so therefore weakening the lining resulting in peptic ulcer disease.

    02:41 <i>H. pylori</i>, bile, NSAIDs, alcohol.

    02:46 Prostaglandin inhibition like we just said with NSAIDs or steroids even with pathologies such as Cushing in which you would have excess cortisol, hypercortisolism, 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.

    03:07 Increased acid production could be a cause.

    03:11 But more importantly, the most important pathogenesis for peptic ulcer disease of the stomach would be damage to the lining.

    03:19 Whereas, if it is pathogenesis for peptic ulcer disease of the duodenum then in fact there would be increased acid.

    03:26 For example, if you do a Zollinger−Ellison syndrome and with the gastrinoma, 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 protect itself against all that acid.

    03:44 Mucosal ischemia is always a possibility whenever there is an infarction that’s taking place and at some point in time you might then be hurting or injuring the lining of the stomach.

    03:57 Peptic ulcer disease, if it is in the stomach, the patient here is going to be complaining of epigastric pain.

    04:04 However, this time around, with peptic ulcer disease in the stomach, you would not find and the patient would not be complaining of pain that’s radiating to the back.

    04:12 Is that clear? On your step and on your words, if the pain is radiating to the back then this gives you the high suspicion and differential of pancreatic damage.

    04:25 However if it’s not then you’re thinking about peptic ulcer disease.

    04:29 Also with this erosion that’s taking place, remember, you have not perforated.

    04:33 Ulceration means ulceration.

    04:35 It’s a clean, punched−out lesion in the stomach.

    04:40 In a clean, punched−out lesion, here, with bleeding taking place may result in hematemesis.

    04:49 With all those 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 saturate itself with blood.

    05:02 So therefore by the time that’s evacuated, here the stool in fact is going to look black and tarry.

    05:10 Hematemesis, hematochezia, iron deficiency anemia, all of these, well, all part of bleeding.

    05:17 Next, if there’s perforation that’s taking place especially of duodenal type of peptic ulcer disease, it will then perforate and then it will then affect different organs or blood vessels.

    05:31 If it is peptic ulcer disease of the stomach which is usually found in the lesser antrum of the stomach and if it is to perforate then you are then going to or the perforation is going to affect the left gastric artery.

    05:45 Whereas if the perforation takes place down in the duodenum, then the perforation then causes damage to the gastroduodenal artery.

    05:55 Gastric outlet obstruction due to peri−pyloric scar formation is an important complication.

    06:01 At some point in time when there's enough damage that's taking place, any type of damage at some point, the body wishes to respond with the repair process.

    06:09 This repair process that you’re looking for at some point with fibrosis taking place, may actually then cause gastric outlet problems because of the more or less think of it as being a stricture formation or a scar formation and therefore decreasing the emptying of the stomach.

    06:29 Gastric ulcers may be malignant while duodenal ulcers are basically never.

    06:35 Once again, peptic ulcer disease, keep in mind that if it's the stomach you should be monitoring or should be thinking, hmm, there’s possibility of a primary gastric cancer developing and duodenal almost never.

    06:52 On the left, the peptic ulcer disease is in the duodenum.

    06:55 You’ll notice that you have a clean, punched−out lesion.

    06:58 Whereas in gastric ulcer, you also have a clean, punched−out lesion.

    07:02 Endoscopy, Esophagogastro− duodenoscopy, would be your best measure or best method of diagnosis.

    07:11 With this ulceration at some point, remember, keep your ulceration and perforation completely separate.

    07:21 Management of Peptic Ulcer Disease Antacids Because of the burning sensation that’s taking place, magnesium and aluminum cause long−term toxicity.

    07:30 Be careful with antacids, magnesium and aluminum.

    07:34 Milk alkali syndrome due to prolonged use of calcium.

    07:37 A symptom that you want to keep in mind with antacids.

    07:40 Once again, milk alkali syndrome due to prolonged use of calcium.

    07:46 H2 Blockers Here once again, you block your receptors on histamine for H2 and decrease acid production if in fact that is one of your concerns with peptic ulcer disease.

    08:02 H2 blockers, however, does inhibit the cytochrome P450 system in the liver so therefore may then cause decreased metabolism with certain drugs.

    08:11 So drug−drug interactions become an important side effect, an interaction that you want to keep in mind for H2 blockers.

    08:21 Proton Pump Inhibitors Extremely effective in terms of decreasing the amount of hydrogen that you’re pumping into the stomach.

    08:30 Irreversible blockage of your hydrogen−potassium pump.

    08:33 However, if you are using this, keep in mind that because you're decreasing acidity within the stomach, here once again, you might then cause interference of absorption of other drugs.

    08:44 Drug−drug interactions become incredibly important here.

    08:47 Sucralfate It stimulates endogenous prostaglandin productions so that it helps to then protect the lining of the stomach.

    08:56 Avoid in renal insufficiency and that's a big deal.

    09:01 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.

    09:16 Duration of Therapy If it’s duodenal, about 4 to 6 weeks.

    09:21 Gastric, 6 to 8 weeks.

    09:23 But because you’re worried about the risk of developing cancer, you want to do or every once a month repeat Esophagogastro− duodenoscopies.

    09:35 Treatment here always either case of peptic ulcer disease, gastric or duodenum, with duodenum being much more common than gastric by far, by leaps and bounds; in both however, you must when you do an endoscopy, do a biopsy.

    09:52 And <i> H. pylori </i>is indicated 80−85% of your gastric and almost 100% with duodenal.

    10:01 It is important that you know in great detail how to properly manage and eradicate the organism called <i>H. pylori</i>.

    10:09 And why the boards loved this and why the wards loved this is because literally with antibiotics, getting rid of <i>H. pylori</i>, you might actually prevent or even treat certain cancers in the stomach such as your intestinal type of gastric cancer (primary) or perhaps even a lymphoma, a B−type.


    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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