Peptic Ulcer Disease Ncbi

[Rode Strawther]

Thesite is secure.

The ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

The rapidly declining prevalence of Helicobacter pylori infection and widespread use of potent anti-secretory drugs means peptic ulcer disease has become substantially less prevalent than it was two decades ago. Management has, however, become more challenging than ever because of the threat of increasing antimicrobial resistance worldwide and widespread use of complex anti-thrombotic therapy in the ageing population. Peptic ulcers not associated with H pylori infection or the use of non-steroidal anti-inflammatory drugs are now also imposing substantial diagnostic and therapeutic challenges. This Seminar aims to provide a balanced overview of the latest advances in the pathogenetic mechanisms of peptic ulcers, guidelines on therapies targeting H pylori infection, approaches to treatment of peptic ulcer complications associated with anti-inflammatory analgesics and anti-thrombotic agents, and the unmet needs in terms of our knowledge and management of this increasingly challenging condition.

Peptic ulcer disease continues to be a source of significant morbidity and mortality worldwide. Approximately two-thirds of patients found to have peptic ulcer disease are asymptomatic. In symptomatic patients, the most common presenting symptom of peptic ulcer disease is epigastric pain, which may be associated with dyspepsia, bloating, abdominal fullness, nausea, or early satiety. Most cases of peptic ulcer disease are associated with Helicobacter pylori infection or the use of nonsteroidal anti-inflammatory drugs (NSAIDs), or both. In this review, we discuss the role of proton pump inhibitors in the management of peptic ulcer disease, highlight the latest guidelines about the diagnosis and management of H. pylori, and discuss the latest evidence in the management of complications related to peptic ulcer disease, including endoscopic intervention for peptic ulcer-related bleeding. Timely diagnosis and treatment of peptic ulcer disease and its sequelae are crucial in order to minimize associated morbidity and mortality, as is prevention of peptic ulcer disease among patients at high risk, including those infected with H. pylori and users of NSAIDs.

Peptic ulcer disease is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. It may involve the lower esophagus, distal duodenum, or jejunum. This activity reviews the cause, pathophysiology, and presentation of peptic ulcer disease and highlights the role of the interprofessional team in its management.

Objectives:Review the causes of peptic ulcer disease.Describe the presentation of a patient with peptic ulcer disease.Summarize the treatment options for peptic ulcer disease.Review the importance of improving care coordination among interprofessional team members to improve outcomes for patients affected by peptic ulcer disease.Access free multiple choice questions on this topic.

Peptic ulcer disease (PUD) is characterized by discontinuation in the inner lining of the gastrointestinal (GI) tract because of gastric acid secretion or pepsin. It extends into the muscularis propria layer of the gastric epithelium. It usually occurs in the stomach and proximal duodenum. It may involve the lower esophagus, distal duodenum, or jejunum. Epigastric pain usually occurs within 15-30 minutes following a meal in patients with a gastric ulcer; on the other hand, the pain with a duodenal ulcer tends to occur 2-3 hours after a meal. Today, testing for Helicobacter pylori is recommended in all patients with peptic ulcer disease. Endoscopy may be required in some patients to confirm the diagnosis, especially in those patients with sinister symptoms. Today, most patients can be managed with a proton pump inhibitor (PPI) based triple-drug therapy.

H. pylorus is a gram-negative bacillus that is found within the gastric epithelial cells. This bacterium is responsible for 90% of duodenal ulcers and 70% to 90% of gastric ulcers. H. pylori infection is more prevalent among those with lower socioeconomic status and is commonly acquired during childhood. The organism has a wide spectrum of virulence factors allowing it to adhere to and inflame the gastric mucosa. This results in hypochlorhydria or achlorhydria, leading to gastric ulceration.

Nonsteroidal anti-inflammatory drugs use is the second most common cause of PUD after H. pylori infection.[2][3] The secretion of prostaglandin normally protects the gastric mucosa. NSAIDs block prostaglandin synthesis by inhibiting the COX-1 enzyme, resulting in decreased gastric mucus and bicarbonate production and a decrease in mucosal blood flow.

Peptic ulcer disease (PUD) is a global problem with a lifetime risk of development ranging from 5% to 10%.[4][5] Overall, there is a decrease in the incidence of PUD worldwide due to improved hygienic and sanitary conditions combined with effective treatment and judicious use of NSAIDs.[5] Duodenal ulcers are four times more common than gastric ulcers. Also, duodenal ulcers are more common in men than in the woman.

With peptic ulcers, there is usually a defect in the mucosa that extends to the muscularis mucosa. Once the protective superficial mucosal layer is damaged, the inner layers are susceptible to acidity. Further, the ability of the mucosal cells to secrete bicarbonate is compromised.

Gastric ulcers are most commonly located on the lesser curvature, whereas duodenal ulcers are most common at the duodenal bulb. The ulcer is round to oval with a smooth base. Acute ulcers have regular borders, while chronic ulcers have elevated borders with inflammation. An ulcer extends beyond the muscularis mucosa.

Signs and symptoms of peptic ulcer disease may vary depending upon the location of the disease and age. Gastric and duodenal ulcers can be differentiated from the timing of their symptoms in relation to meals. Nocturnal pain is common with duodenal ulcers. Those with gastric outlet obstruction commonly report a history of abdomen bloating and or fullness.

Diagnosis of PUD requires history taking, physical examination, and invasive/non-invasive medical tests. A careful history should be obtained and noted for the presence of any complications. Patient reporting of epigastric abdominal pain, early satiety, and fullness following a meal raise suspicion of PUD. The pain of gastric ulcers increases 2 to 3 hours after a meal and may result in weight loss, whereas the pain of duodenal ulcers decreases with a meal which can result in weight gain. Any patient presenting with anemia, melena, hematemesis, or weight loss should be further investigated for complications of PUD, predominantly bleeding, perforation, or cancer. A physical exam may reveal epigastric abdominal tenderness and signs of anemia.

6. Computerized tomography of the abdomen with contrast is of limited value in the diagnosis of PUD itself but is helpful in the diagnosis of its complications like perforation and gastric outlet obstruction.

Antisecretory drugs used for peptic ulcer disease (PUD) include H2-receptor antagonists and the proton pump inhibitor (PPIs). PPIs have largely replaced H2 receptor blockers due to their superior healing and efficacy. PPIs block acid production in the stomach, providing relief of symptoms and promote healing. Treatment may be incorporated with calcium supplements as long-term use of the PPIs can increase the risk of bone fractures. NSAIDs induced PUD can be treated by stopping the use of NSAIDs or switching to a lower dose. Corticosteroids, bisphosphonates, and anticoagulants should also be discontinued if possible. Prostaglandin analogs (misoprostol) are sometimes used as prophylaxis for NSAID-induced peptic ulcers. First-line treatment for H. pylori-induced PUD is a triple regimen comprising two antibiotics and a proton pump inhibitor. Pantoprazole, clarithromycin, and metronidazole, or amoxicillin are used for 7 to 14 days.[7] Antibiotics and PPIs work synergistically to eradicate H. pylori.[8] The antibiotic selected should take into consideration the presence of antibiotic resistance in the environment. If first-line therapy fails, quadruple therapy with bismuth and different antibiotics is used.

Surgical treatment is indicated if the patient is unresponsive to medical treatment, noncompliant, or at high risk of complications. A refractory peptic ulcer is one over 5 mm in diameter that does not heal despite 8-12 weeks of PPI therapy. The common causes are persistent H.pylori infection, continued use of NSAIDs, or significant comorbidities that impair ulcer healing or other conditions like gastrinoma or gastric cancer. If the ulcer persists despite addressing the above risk factors, patients can be candidates for surgical treatment. Surgical options include vagotomy or partial gastrectomy.[9]

The prognosis of peptic ulcer disease (PUD) is excellent after the underlying cause is successfully treated. Recurrence of the ulcer may be prevented by maintaining good hygiene and avoiding alcohol, smoking, and NSAIDs. Unfortunately, recurrence is common with rates exceeding 60% in most series. NSAID-induced gastric perforation occurs at a rate of 0.3% per patient per year. However, unlike in the past, mortality rates for peptic ulcer disease have decreased significantly.

Patients with peptic ulcer disease (PUD) should be counseled about potentially injurious agents like nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin, alcohol, tobacco, and caffeine. If it is necessary to use NSAIDs use the lowest possible dose and also consider prophylaxis for patients who use NSAIDs. Obesity has a strong association with peptic ulcer disease, and patients should be asked to lose weight. Stress reduction counseling can be helpful in some cases.

3a8082e126