Oesophagus And Stomach - pediagenosis
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Tuesday, July 17, 2018

Oesophagus And Stomach

Oesophagus And Stomach
It is possible to swallow food and drink and for it to enter the stomach while standing on one’s head or experiencing zero gravity. A ring of skeletal muscle called the upper oesophageal sphincter usually closes the pharyngeal end of the oesophagus. During the oesophageal phase of swallowing, this sphincter is relaxed, allowing the bolus of food to pass through it. Immediately afterwards, the sphincter closes. Once in the oesophagus, the bolus is propelled the 25 cm (approximately) to the stomach by a process called peristalsis, a coordinated wave of relaxation in front of the bolus and contraction behind the bolus of the circular and longitudinal muscle layers of the oesophagus, forcing the food into the stomach in about 5 s. Before the bolus enters the stomach, it passes through another sphincter, the lower oesophageal sphincter, formed from a ring of smooth muscle which relaxes as the peristaltic wave reaches it. The swallowing centres in the medulla produce a sequence of events that lead to both efferent activity to somatic nerves (innervating skeletal muscle) and autonomic nerves (innervating smooth muscle). This sequence of events is influenced by afferent receptors in the oesophagus wall sending impulses back to the medulla. The sphincters and the peristaltic waves are principally controlled by activity in the vagus nerve and aided by a high degree of coordination of the activity within the enteric nerve plexuses within the tract itself.

Oesophagus And Stomach

Once the bolus of food passes through the lower oesophageal sphincter, it enters the stomach (Fig. 38a). The main functions of the stomach are to store food temporarily (as it can be ingested more rapidly than it can be digested) to chemically and mechanically digest food using acids, enzymes and movements, to regulate the release of the resulting chyme into the small intestine, and to secrete a substance called intrinsic factor which is essential for the absorption of vitamin B12. The stomach lies immediately below the diaphragm and, like the rest of the gastrointestinal tract, it has longitudinal and circular muscle layers and nerve plexuses in its walls; however, within the mucosa are specialized secretory cells that line the gastric glands or pits (Fig. 38b). When empty, the stomach has a volume of approximately 50 mL; however, when fully distended, its volume can be as much as 4 L. Proteins in the food are broken down into polypeptides in the stomach by enzymes called pepsins. These enzymes are produced in an inactive form called pepsinogens by the chief cells in the gastric mucosa, and are converted into active pepsins by the acid environment in the stomach (Fig. 38c). The acid in the stomach is hydrochloric acid and is produced by a specialized group of cells called parietal cells. The stomach can secrete as much as 2 L of acid per day, and the concentration of H+ ions in the stomach is estimated to be about 1 million times higher than that in the blood. This concentration of H+ ions requires a very efficient exchange of intracellular H+ for extracellular K+ using energy provided by the breakdown of adenosine triphosphate (ATP). This is achieved using a protein known as the proton pump or the H+–K+ ATPase protein (Fig. 38d).
The gastric mucosa does not digest itself because it is protected by an alkaline, mucin-rich fluid secreted by the gastric glands, which acts as a mucosal barrier by bathing the gastric epithelial cells. In addition, local mediators, such as prostaglandins, are released when the mucosa is irritated, and these increase the thickness of the mucous layer and stimulate the production of bicarbonate which neutralizes the acid.

Control of gastric secretions
Gastric secretions occur in basically three phases: cephalic, gastric and intestinal (Fig. 38e). The cephalic phase is brought about by the sight, smell, taste and mastication of food. At this stage, there is no food in the stomach and acid secretion is stimulated by the activation of the vagus and its actions on the enteric plexus. Postganglionic parasympathetic fibres in the myenteric plexus cause the release of acetylcholine (ACh) and stimulate the release of gastric juices from the gastric glands. Vagal stimulation also causes the release of a hormone called gastrin from cells in the antrum of the stomach called G-cells. Gastrin is secreted into the bloodstream and, when it reaches the gastric glands, it stimulates the release of acid and pepsinogens. Both vagal activity and gastrin also stimulate the release of histamine from mast cells, which, in turn, acts on parietal cells to produce more acid.
When food arrives in the stomach, it stimulates the gastric phase of secretion of acid, pepsinogen and mucus. The main stimuli for this phase are the distension of the stomach and the chemical composition of the food. Mechanoreceptors in the stomach wall are stretched and set up local myenteric reflexes and also longer vagovagal reflexes. Both cause the release of ACh which stimulates the release of gastrin, histamine and, in turn, acid, enzymes and mucus. Stimulation of the vagus also releases a specific peptide, gastrin-releasing peptide (GRP), which mainly acts directly on the G-cells to release gastrin. Whole proteins do not affect gastric secretions directly, but their break- down products, such as peptides and free amino acids, do so by directly stimulating gastrin secretion. A low pH (more acid) in the stomach inhibits gastrin secretion; therefore, when the stomach is empty or after food has entered it and acid has been secreted for some time, there is an inhibition of acid production. However, when food first enters the stomach, the pH rises (less acid) and this leads to a release of the inhibition and causes a maximum secretion of gastrin. Thus, gastric acid secretion is self-regulating.
The gastric phase normally lasts for about 3 h and the food in the stomach is converted into a sludge-like material called chyme. The chyme enters the first part of the small intestine, the duodenum, through the pyloric sphincter. The presence of chyme in the pyloric antrum distends it and causes antral contractions and opening of the sphincter. The rate at which the stomach empties depends on the volume in the antrum and the fall in the pH of the chyme, both leading to an increase in emptying. However, distension of the duodenum, the presence of fats and a decrease in pH in the duodenal lumen all cause an inhibition of gastric emptying. This mechanism leads to a precise supply of chyme to the intestines at a rate appropriate for it to be digested properly. (For a description of the intestinal phase of gastric secretion, see Chapter 39.)

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