DISEASES | Peptic Ulcer Disease

Peptic Ulcer Disease (PUD) is very common in Kashmir and refers to a defect in the gastric or duodenal mucosal wall that extends through the muscularis mucosa into the deeper layers of the submucosa.

Ulcer formation is the net result of a lack of homeostasis between factors within the GI tract responsible for the breakdown of food (e.g., gastric acid and pepsin) and factors that promote mucosal defense and repair (e.g., bicarbonate, mucus secretion, and PGs). The mucus and bicarbonate barrier, through its buffering action, is the primary source of defense against gastric acid. It allows an acidic environment to be maintained on the epithelial lining. PGs inhibit gastric acid secretion, stimulation of mucus and bicarbonate production, increase mucosal blood flow and stimulate epithelial cell regeneration.

   

There are many etiologies of PUD such as:

-H. Pylori infection

-Use of NSAIDs

-Stress-related mucosal damage (SRMD): occurs more frequently in critically ill patients and is due to compromised mesenteric perfusion resulting in mucosal defects

-Zollinger-Ellison syndrome Others (cigarette smoking)

The relatively high incidence of PUD in the elderly may be due to higher NSAID use. H. pylori infection and NSAID use account for most cases of PUD. Ulcers related to H. pylori infection more commonly affect the duodenum. Ulcers related to NSAIDs more frequently affect the stomach.

Gastric ulcer (GU) tends to occur much later: in life than duodenal ulcer (DU), with the peak incidence of GU occurring in patients over 60 years of age. Malignancy is more commonly found with GU than DU.

Patients typically present with early satiety after meals, nausea, vomiting, abdominal pain, and weight loss. Patient requires emergent surgical intervention, and these patients should not undergo endoscopy.

CLASSIFICATION

PUD can be classified as uncomplicated or complicated.

Uncomplicated disease is typically characterized by mild epigastric pain, whereas complicated disease involves acute upper GI complications such as GI bleeding, obstruction, or perforation.

Complications of PUD include gas trointestinal (GI) bleeding, perforation, and obstruction. Complications of untreated or undiagnosed H. pylori infection include gastric cancer and PUD.

DIAGNOSIS

Radiologic and/or endoscopic procedures are usually required to document the presence of ulcers. Because endoscopic testing is invasive and expensive, it is only indicated in patients 60 years of age or older with new-onset dyspepsia.

Patients with dyspepsia who are younger than 60 years may forgo endoscopy but should be tested for H.pylori using noninvasive testing and treated if positive. Those who test negative for H. pylori should be offered a trial (4-8 weeks) of acid suppression therapy or proceed to endoscopy. Persistent dyspepsia despite a trial of acid suppressive therapy warrants upper endoscopy evaluation.

Routine laboratory tests are not helpful in establishing a diagnosis of PUD.

Hematocrit, hemoglobin, and stool guaiac tests are used to detect bleeding.

DIAGNOSTIC TESTS

Diagnostic tests to detect H. pylori presence can be either endoscopic or non endoscopic. Endoscopic diagnosis involves extraction of gastric tissue samples that are subsequently tested for H. pylori

Nonendoscopic testing methods for H. pylori include the urea breath test, serologic testing, and stool antigen assay. These tests are less invasive and less expensive than endoscopy. The urea breath test is usually first, line because of its high sensitivity and specificity and short turnaround time. Concomitant acid suppressive or antibiotic therapy may give false-negative results. The urea breath test can also be used to confirm eradication of H. pylori infection.

Serologic testing provides a quick (within 15 minutes) office-based assessment of exposure to H. pylori, but it cannot differentiate active infection from previously treated infection; patients can remain seropositive for years after eradication. Serologic testing is recommended in patients with recent or current antibiotic or acid-suppressive therapy. Stool antigen assays can be useful for initial diagnosis or to confirm H pylori eradication .They have highest sensitivity and specificity and are affected less by concomitant medication use.

NONPHARMACOLOGIC TREATMENT

Any Patient with PUD should eliminate or reduce psychological stress,cigarette smoking, and use of NSAIDs. Although there is no need for a special diet, patients should avoid foods and beverages that cause dyspepsia or exacerbate ulcer symptoms (eg, spicy foods, caffeine, and alcohol).

Emergency surgery may be required for bleeding, perforation, or obstruction.

INITIAL MANAGEMENT

Treat the underlying etiology.

Eradication of Helicobacter pylori (H. pylori)_ Patients with peptic ulcers should be tested for infection with H. pylori and treated accordingly. Eradication of H. pylori in patients with peptic ulcer disease is associated with higher healing rates in patients with duodenal and gastric ulcers. In addition, eradication of H. pylori infection is associated with lower ulcer recurrence rates in patients with gastric and duodenal ulcers who are not placed on maintenance antisecretory therapy. Discontinue nonsteroidal anti-inflammatory drugs (NSAIDs).

Patients with peptic ulcers should be advised to avoid NSAIDs. NSAIDs, including aspirin, increase the risk of peptic ulcer disease and are associated with an increased risk of complications from a peptic ulcer.

RARE OR UNCLEAR CAUSE

Rare causes of ulcer disease (eg, infections, Crohn disease, and ischemia) should be addressed and treated. In patients with peptic ulcer disease of unclear etj. ology, additional evaluation is needed to exclude other rare causes of peptic ulcer.Initial antisecretory therapy. Choice of therapy – All patients with peptic ulcers should receive antisecretory therapy with a proton pump inhibitor (PPI) (eg, omeprazole 20 to 40 mg daily or equivalent) to facilitate ulcer healing. PPI use results in faster control of peptic ulcer disease symptoms and higher ulcer healing rates as compared with H2RA as a consequence of stronger acid suppression. PPIs also heal NSAID-related ulcers more effectively as compared with H2RAS.

DURATION

The duration of initial antisecretory Therapy varies based on the ulcer characteristics, the underlying etiology (H. pylori, NSAID use) and the presence of ulcer complications (eg, bleeding, perforation, penetration, or gastric outlet obstruction).

(a)
Treatment of H. Pylori-Associated Ulcers

All patients with evidence of active infection with H. pylori should be offered treatment. Goal of H. pylori therapy: complete eradication. Antisecretory therapy in H. pylori. positive ulcer.

Uncomplicated ulcer – In patients with uncomplicated ulcers, PPI (eg, omeprazole 20 mg twice daily) given for 14 days, along with the antibiotic regimen to treat .pylori, is usually adequate to induce healing.

Complicated ulcer All patients with complicated peptic ulcers (ulcers with bleeding, perforation, penetration, or gastric outlet obstruction) should initially receive acid suppressive therapy with an intravenous PPI. Once patients are tolerating oral medications, they should be switched to an oral PPI at high-dose twice daily to enhance healing (eg, omeprazole 40 mg twice daily). Dosing should generally be reduced to once daily after four weeks. However, in patients with bleeding, the intravenous PPI can be switched to a lower oral dose (eg, 20 mg omeprazole once daily) 72 hours after endoscopy, provided there is no evidence of recurrent bleeding.

The duration of treatment depends on the location and cause of the ulcer, but is typically between 4 and 12 weeks in total.

PRECAUTIONS

Avoid spicy and processed foods, stress, smoking, drinking and consumption of large doses of caffeine. All of these contribute to or even worsen dyspepsia and also do not allow the ulcer to heal because of the constituents these foods contain. Stress stimulates HCl secretion, thereby causing or worsening stomach ulcers.

EVALUATION OF THERAPEUTIC OUTCOMES

-Monitor patients for symptomatic relief of ulcer pain, potential adverse drug effects, and drug interactions.

-Ulcer pain typically resolves in a few days when NSAIDs are discontinued and within 7 days upon initiation of antiulcer therapy.

-Patients with uncomplicated PUD are usually symptom free after treatment with any of the recommended antiulcer regimens.

-Persistent or recurrent symptoms within 14 days after the end of treatment suggests failure of ulcer healing or H. pylori eradication or presence of an alternative diagnosis such as gastroesophageal reflux disease.

-Most patients with uncomplicated HP-positive ulcers do not require confirmation of ulcer healing or HP eradication.

-Monitor patients taking NSAIDs closely for signs and symptoms of bleeding, obstruction, penetration, and perforation.

-Follow-up endoscopy is justified in patients with frequent symptom recurrence, refractory disease, complications, or suspected hyperse cretory states.

The author is B.Sc Nursing from Pacific Institute Of Medical Sciences Udaipur and Gold Medalist from Sai Tirupati University

Disclaimer: The views and opinions expressed in this article are the personal opinions of the author.

The facts, analysis, assumptions and perspective appearing in the article do not reflect the views of GK.

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