Dyspepsia pathophysiology
|
Dyspepsia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Dyspepsia pathophysiology On the Web |
|
American Roentgen Ray Society Images of Dyspepsia pathophysiology |
|
Risk calculators and risk factors for Dyspepsia pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Physiology of Digestion
- In humans, digestion begins in the mouth where food is chewed.
- Salivary amylase aids in the chemical breakdown of polysaccharides such as starch into disaccharides such as maltose.
- The chewed food is pushed down the esophagus to the stomach through peristaltic contraction of these muscles.
- Food enters the stomach where it is further broken apart and thoroughly mixed with gastric acid, pepsin and other digestive enzymes to break down proteins.
- After consumption of food, digestive "tonic" and peristaltic contractions begin, which helps break down the food and move it through. Gastric emptying is the release of food from the stomach into the duodenum.
- Gastric emptying has attracted medical interest as rapid gastric emptying is related to obesity and delayed gastric emptying syndrome is associated with diabetes mellitus, aging, and gastroesophageal reflux.
- After being processed in the stomach, food is passed to the small intestine. The majority of digestion and absorption occurs here after the milky chyme enters the duodenum. Here it is further mixed with three different liquids:
- Bile which is produced by the liver and stored in the gallbladder emulsifies fats and neutralizes the chyme.
- Pancreatic juice made by the pancreas. It secrete enzymes such as pancreatic amylase, pancreatic lipase, and trypsinogen.
- Intestinal juice secreted by the intestinal glands in the small intestine. It contains enzymes such as enteropeptidase, erepsin, trypsin, chymotrypsin, maltase, lactase and sucrase.
Pathophysiology of Functional Dyspepsia
- The symptoms of functional dyspepsia are directly caused by two major physiological abnormalities
- Abnormal gastric motility
- Visceral hypersensitivity
- These mechanisms occur in patients who have acquired excessive responsiveness to stress as a result of the environment during early life, genetic abnormalities, residual inflammation after gastrointestinal infections, or other causes, with the process modified by factors including psychophysiological abnormalities, abnormal secretion of gastric acid, Helicobacter pylori infection, diet, and lifestyle.
- If the basis of this model of FD pathogenesis is excessive responsiveness of gastrointestinal function to stress and external stimuli, psychosomatic approaches to alter stress perception could be important treatment options.[1]