Chronic duodenitis: pathogenesis
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Pathogenesis of secondary chronic duodenitis
The pathogenesis of the primary chronic duodenitis is not completely known. It assumes the role of immune mechanisms, violations of neurohumoral regulation of the function of the duodenum, the direct effect of etiological factors on the mucosa of the duodenum.
Pathogenesis of secondary chronic duodenitis
One of the main etiological factors of secondary chronic duodenitis is Helicobacter pylori infection. Chronic duodenitis develops, as a rule, against a background of chronic Helicobacter pylori and metaplasia of the gastric epithelium in the duodenum. H. Pylori colonizes areas of metaplastic gastric epithelium in the duodenum and causes an inflammatory process. The centers of the metaplastic epithelium are easily damaged by acidic gastric contents, and erosions develop in the areas of metaplasia. Duodenitis caused by H. Pylori, as a rule, is localized in the bulb of the duodenum. With gastric ulcer secondary chronic duodenitis develops due to the damaging effect of the aggressive acid-peptic factor and H. Pylori on the mucosa of the duodenum. In chronic hepatitis and chronic pancreatitis, the development of chronic duodenitis is due to increased absorption of pancreatic enzymes; decrease in secretion of bicarbonates, which contributes to the acidification of duodenal contents and the action of aggressive factors of gastric juice; reduced resistance of the mucosa of the duodenum; in diseases of the lungs and cardiovascular system, the development of chronic duodenitis is promoted by hypoxia of the mucosa of the duodenum. In chronic renal failure, the development of chronic duodenitis is due to the release through the mucosa of the duodenum of toxic products of nitrogen metabolism.
In the development of chronic duodenitis in diseases of bile ducts, an important role is played by intestinal microflora. This factor plays a particularly important role in gastric Achilles. In these conditions, dysbiosis is easy to develop; proximal parts of the small intestine, including the 12-colon, populate the unusual for these departments bacterial flora.
Depending on the nature of morphological changes, duodenitis is surface, diffuse, atrophic and erosive.
With superficial duodenitis, dystrophic changes in the superficial epithelium (flattening and vacuolization of prismatic epithelium), stromal edema, lymphocytic and plasmocyte cellular infiltration are noted.
With diffuse chronic duodenitis, the changes described above are more pronounced. With superficial and diffuse duodenitis, hyperplasia and hypersecretion of the superficial epithelium are observed, an increase in the number of goblet cells, and an increase in their secretory function. These changes should be considered as compensatory-adaptive in response to the influence of aggressive factors that damage the mucosa of the duodenum.
With an atrophic chronic duodenitis, the mucous membrane is atrophied, thinned, the villi are flattened.
With erosive duodenitis, single or multiple erosions appear on the mucosa of the duodenum.
Depending on the extent of the inflammatory process in duodenum, duodenitis is diffuse (total) and local (limited), which includes duodenitis proximal (bulbit), papillitis (inflammation of the large papilla of the duodenum), distal duodenitis.
[