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peptic ulcer
Tuesday 6 March 2012
gastric peptic ulcer
A “peptic ulcer”refers to any deep mucosal break resulting from exposure to gastric acid or pepsin.
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gastric mucosal ulceration / gastric ulcer
These ulcers develop adjacent to sites containing oxyntic mucosa.
Rarely, they arise in the acid-secreting mucosa itself.
Peptic ulcers fall into several major etiologic groups
Those resulting from acidhypersecretion,as in Zollinger-Ellison syndrome;
those due to NSAIDs;
those associated with HP infection.
Previously, most peptic ulcers resulted from HP infections.
Urease and other factors produced by the HP break the mucosal barrier, allowing ulcers to develop.
Not all HP infections lead to ulcer development.
VacA- and CagA-positive HP are more likely to produce peptic ulcers than VacA- and CagA- negative HP.
Specifically,colonization with vacA2m2/cag A-positive HP strains correlates with peptic ulcer disease (PUD) risk.
Smoking also increases ulcerincidence.
In Western countries the importance of HP in gastric PUD has declined and has been replaced by NSAID use.
Multiple environmental and genetic factors associate with peptic ulcer risk.
The incidence of gastric ulcers variesdepending on geographic locale, age, and sex.
Evidence supporting a genetic contribution to gastric and duodenal peptic ulcers include increased family aggregation (more for blood relatives than spouses), twin studies, blood group studies, and elevated pepsinogen levels among relatives.
A marked decline in peptic ulcers has resulted from decreased smoking, a decreased incidence of HP infections, and the widespread use of aggressive acid suppressive therapies.
Today in Western countries, peptic ulcers tend to affect the elderly using NSAIDs.
The probability ofdeveloping a peptic ulcer is highest in middle-aged men (age 41 to 60) with chronic antral gastritis or chronic pangastritis.
Peptic ulcers also develop as sporadic lesions, in patients with gastrinomas or systemic mastocytosis (due to increased histamine secretion), and in rare genetic syndromes including multiple endocrine neoplasia type 1 (MEN1).
A specific pepsinogen C gene polymorphism maypredict gastric ulcer risk.
Peptic injury may also complicate any disorder in which the mucosal barrier is compromised and mucosal ulcers form including infectious or drug injury.
Prepyloric and duodenal ulcers arise in the setting of increased acid secretion and antral gastritis, whereas gastric ulcers associate with decreased gastric acid secretion and diminished mucosal defenses.
There is a close association between the ulcer site and the severity ofthe gastritis.
Antral ulcers most commonly develop along the lesser curve; with increasing severity of corpus gastritis, the ulcer location moves proximally.
The further a gastric ulcer is from the pylorus, the more likely one is to find atrophic gastritis involving the body.
This contrasts with duodenal and prepyloric ulcers, which associate with an antral-predominant gastritis without progressive body gastritis.
Episodic epigastric pain that is aggravated by meals or alcohol, often occurring at night, is the most prominent clinical feature of PUD.
Bleeding develops in about 20% of patients and is massive in 5%. Bleeding is particularly likely in older individuals on NSAIDs.
Endoscopic visualization of a bleeding vessel or other signs of recent hemorrhage predict further bleeding and increased mortality.
Juxtapyloric ulcers cause obstruction due to coexisting edema and pyloric stenosis as the ulcer heals and fibrosis develops.
Ulcer depth varies; it may perforate through the wall, extending into adjacent structures.
The risk ofperforation is increased in those who smoke and the risk correlates with the number ofcigarettes smoked.
Gastric ulcers are usually solitary, although about 30% of patients have associated duodenal ulcers and 6% to 13% have multiple gastric ulcers.
Gastric peptic ulcers arise anywhere in the stomach, but they typically develop on its lesser curvature, usually at the antral–corpus junction.
The consequences of peptic ulceration include hemorrhage secondary to vascular erosion, perforation, ulcer penetration into contiguous structures, and pyloric outlet obstruction due to inflammation or scarring.
Perforations typically appear as a round hole in the ulcer base.
The serosal surface appears congested and fibrinous adhesions may be present.
Occasionally, a large gastric ulcer high on the lesser curvature heals to produce a scarred, constricted, hourglass-shaped stomach (hourglass stomach).
Less commonly, gastric ulcers extend along the lesser curvature from the cardia to the incisura, forming a “trench ulcer”.