Peptic ulcer disease (PUD) is defined by a discontinuity in the gastrointestinal inner lining brought on by pepsin or gastric acid release. Usually occurring in the stomach or proximal duodenum, peptic ulcers are acid-induced lesions of the digestive system depicted by denuded mucosa with damage extending into the muscularis propria or submucosa.
Patients with gastric ulcers often have epigastric discomfort 15 to 30 minutes after eating; in contrast, patients with duodenal ulcers typically experience pain 2 to 3 hours after eating meals.
Epidemiology
With a lifetime development risk of between 5% and 10%, peptic ulcer disease is widespread. Globally, peptic ulcer disease incidence has decreased due to improved hygienic and sanitary settings, competent medical care, and prudent NSAID use. Additionally, men are more likely than women to develop duodenal ulcers.
Anatomy
Pathophysiology
The protective mucosal lining of the stomach and duodenum is damaged, which leads to the ulcerogenic process. It is well understood that H. pylori infections, the use of NSAIDs, and low-dose aspirin cause mucosal lining damage. Both bacterial causes and the host’s inflammatory response have a role in the cost to the mucosal lining in the context of an H. pylori infection.
Mucosal damage caused by the use of NSAIDs results from the suppression of prostaglandins produced by the enzyme cyclooxygenase 1 (COX-1), which are essential for preserving mucosal integrity. The ulcerative process begins when the mucosal layer is damaged, exposing the stomach epithelium to acid. If the situation persists, the ulcer will develop until it reaches the serosal layer.
Etiology
NSAID-induced
Nonsteroidal anti-inflammatory drugs are the second most frequent cause of peptic ulcer disease. Prostaglandin is often secreted to protect the stomach mucosa. By inhibiting the COX-1 enzyme, NSAIDs prevent the creation of prostaglandins, which lowers the production of gastrointestinal mucus, bicarbonate, and mucosal blood flow.
H. pylori associated Peptic Ulcer
The stomach epithelial cells contain the gram-negative bacillus H. pylorus. These bacteria lead on 90% of duodenal ulcers and 70% of stomach ulcers. Lower socioeconomic status individuals are more likely to have H. pylori infection, frequently acquired during childhood. The bacteria may attach to and inflame the stomach mucosa due to a broad spectrum of virulence factors.
In addition to NSAIDs, corticosteroids, bisphosphonates, potassium chloride, and fluorouracil have all been linked to PUD’s pathogenesis. Smoking tends to be associated with duodenal ulcers; however, the relationship is not linear. Alcohol can trigger acidity by irritating the stomach mucosa.
Genetics
Prognostic Factors
After the condition’s underlying cause is adequately managed, the prognosis for peptic ulcer disease is favorable. The ulcer’s recurrence may be avoided by practicing proper hygiene and avoiding NSAIDs, alcohol, and smoking.
However, recurrence is frequent, with rates in most cases reaching 60%. Gastric perforation spurred on NSAIDs occurs in one patient every year at a rate of 0.3%. However, peptic ulcer disease death rates have declined.
Peptic ulcer disease (PUD) is defined by a discontinuity in the gastrointestinal inner lining brought on by pepsin or gastric acid release. Usually occurring in the stomach or proximal duodenum, peptic ulcers are acid-induced lesions of the digestive system depicted by denuded mucosa with damage extending into the muscularis propria or submucosa.
Patients with gastric ulcers often have epigastric discomfort 15 to 30 minutes after eating; in contrast, patients with duodenal ulcers typically experience pain 2 to 3 hours after eating meals.
With a lifetime development risk of between 5% and 10%, peptic ulcer disease is widespread. Globally, peptic ulcer disease incidence has decreased due to improved hygienic and sanitary settings, competent medical care, and prudent NSAID use. Additionally, men are more likely than women to develop duodenal ulcers.
The protective mucosal lining of the stomach and duodenum is damaged, which leads to the ulcerogenic process. It is well understood that H. pylori infections, the use of NSAIDs, and low-dose aspirin cause mucosal lining damage. Both bacterial causes and the host’s inflammatory response have a role in the cost to the mucosal lining in the context of an H. pylori infection.
Mucosal damage caused by the use of NSAIDs results from the suppression of prostaglandins produced by the enzyme cyclooxygenase 1 (COX-1), which are essential for preserving mucosal integrity. The ulcerative process begins when the mucosal layer is damaged, exposing the stomach epithelium to acid. If the situation persists, the ulcer will develop until it reaches the serosal layer.
NSAID-induced
Nonsteroidal anti-inflammatory drugs are the second most frequent cause of peptic ulcer disease. Prostaglandin is often secreted to protect the stomach mucosa. By inhibiting the COX-1 enzyme, NSAIDs prevent the creation of prostaglandins, which lowers the production of gastrointestinal mucus, bicarbonate, and mucosal blood flow.
H. pylori associated Peptic Ulcer
The stomach epithelial cells contain the gram-negative bacillus H. pylorus. These bacteria lead on 90% of duodenal ulcers and 70% of stomach ulcers. Lower socioeconomic status individuals are more likely to have H. pylori infection, frequently acquired during childhood. The bacteria may attach to and inflame the stomach mucosa due to a broad spectrum of virulence factors.
In addition to NSAIDs, corticosteroids, bisphosphonates, potassium chloride, and fluorouracil have all been linked to PUD’s pathogenesis. Smoking tends to be associated with duodenal ulcers; however, the relationship is not linear. Alcohol can trigger acidity by irritating the stomach mucosa.
After the condition’s underlying cause is adequately managed, the prognosis for peptic ulcer disease is favorable. The ulcer’s recurrence may be avoided by practicing proper hygiene and avoiding NSAIDs, alcohol, and smoking.
However, recurrence is frequent, with rates in most cases reaching 60%. Gastric perforation spurred on NSAIDs occurs in one patient every year at a rate of 0.3%. However, peptic ulcer disease death rates have declined.
Peptic ulcer disease (PUD) is defined by a discontinuity in the gastrointestinal inner lining brought on by pepsin or gastric acid release. Usually occurring in the stomach or proximal duodenum, peptic ulcers are acid-induced lesions of the digestive system depicted by denuded mucosa with damage extending into the muscularis propria or submucosa.
Patients with gastric ulcers often have epigastric discomfort 15 to 30 minutes after eating; in contrast, patients with duodenal ulcers typically experience pain 2 to 3 hours after eating meals.
With a lifetime development risk of between 5% and 10%, peptic ulcer disease is widespread. Globally, peptic ulcer disease incidence has decreased due to improved hygienic and sanitary settings, competent medical care, and prudent NSAID use. Additionally, men are more likely than women to develop duodenal ulcers.
The protective mucosal lining of the stomach and duodenum is damaged, which leads to the ulcerogenic process. It is well understood that H. pylori infections, the use of NSAIDs, and low-dose aspirin cause mucosal lining damage. Both bacterial causes and the host’s inflammatory response have a role in the cost to the mucosal lining in the context of an H. pylori infection.
Mucosal damage caused by the use of NSAIDs results from the suppression of prostaglandins produced by the enzyme cyclooxygenase 1 (COX-1), which are essential for preserving mucosal integrity. The ulcerative process begins when the mucosal layer is damaged, exposing the stomach epithelium to acid. If the situation persists, the ulcer will develop until it reaches the serosal layer.
NSAID-induced
Nonsteroidal anti-inflammatory drugs are the second most frequent cause of peptic ulcer disease. Prostaglandin is often secreted to protect the stomach mucosa. By inhibiting the COX-1 enzyme, NSAIDs prevent the creation of prostaglandins, which lowers the production of gastrointestinal mucus, bicarbonate, and mucosal blood flow.
H. pylori associated Peptic Ulcer
The stomach epithelial cells contain the gram-negative bacillus H. pylorus. These bacteria lead on 90% of duodenal ulcers and 70% of stomach ulcers. Lower socioeconomic status individuals are more likely to have H. pylori infection, frequently acquired during childhood. The bacteria may attach to and inflame the stomach mucosa due to a broad spectrum of virulence factors.
In addition to NSAIDs, corticosteroids, bisphosphonates, potassium chloride, and fluorouracil have all been linked to PUD’s pathogenesis. Smoking tends to be associated with duodenal ulcers; however, the relationship is not linear. Alcohol can trigger acidity by irritating the stomach mucosa.
After the condition’s underlying cause is adequately managed, the prognosis for peptic ulcer disease is favorable. The ulcer’s recurrence may be avoided by practicing proper hygiene and avoiding NSAIDs, alcohol, and smoking.
However, recurrence is frequent, with rates in most cases reaching 60%. Gastric perforation spurred on NSAIDs occurs in one patient every year at a rate of 0.3%. However, peptic ulcer disease death rates have declined.
https://www.ncbi.nlm.nih.gov/books/NBK534792/
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