Why Does the Stomach Not Digest Itself - Essay Example

Physiology of the Stomach Name Institution The stomach is an extraordinary organ in the human body. It is among the few organs in the body that serve both an endocrine and exocrine function. It is in the stomach that digestion i.e. the breakdown of food into its individual components takes place, thus allowing for its further processing and absorption in the intestines. The stomach achieves this by secreting gastric acid and a mix of enzymes. It raises the question, “why does the stomach not digest itself?” In order to answer the issue, it is critical to analyze the anatomy, histology and physiology of the stomach as a body organ. Through, critical analysis of the anatomy, histology and physiology of the stomach can one deduce the basis of stomach functions. The factors affecting metabolism must also be looked into for a complete solution to be found. Gastro-duodenal physiology is an engine of secretory functions and their electrical, neural and hormonal controls (Armand et al. 1996). Conversely, the liquid mechanical capacities that hold and scatter particles, open substrate to catalysts, or renew the epithelial limit with supplements are minimally concentrated. Man (like most mammalian species) has a solitary stomach whose sections perform various functions both in parallel and succession. The stomach functions as a repository that holds minimal and high-thickness sustenance until this is changed into chyme. The stomach decreases the extent of strong particles and fat globules, and it matches the acidity/osmolality, caloric thickness and consistency of fluids. By expanding the surface territory on which digestive emissions connect with substrate, mechanical processing potentiates substance absorption. By controlling the arrival of supplements, the stomach helps fuel homeostasis. The stomach is a muscular appendage in the shape of the letter ‘J,' located directly below the diaphragm. In the gastrointestinal tract, it is a link between the oesophagus and the duodenum. Its position and size fluctuate regularly, with the movements of the diaphragm as it expands and contracts during respiration. The stomach is exceptionally distensible, and its volume can increase to hold up to about four litres. It empowers it to hold temporarily/store food while the process of digestion takes place. It is here where the processing of starch, proteins and triglycerides starts. Food entering the stomach has been, to some degree, mechanically broken down and diminished in size by mastication, and starch partially digested by the enzyme salivary amylase present in saliva. The stomach performs four essential tasks that aid in the early phases of assimilation and set up the ingested food for further processing in the small intestine of the digestive tract. To begin with, it serves as a temporary store, permitting a noticeably vast feast to be devoured rapidly and held in it for a relatively long period. The walls of the stomach are made of layers of elastic, smooth muscle allowing for it to increase or decrease its volume. The opening of the stomach is through the cardiac sphincter, located between it and the oesophagus. The sphincter stops the backflow of food. The pyloric sphincter at its duodenal end and its purpose is to regulate the evacuation of food from the stomach. It allows for the proper digestion of food by enzymes. Secondly, peristaltic contractions of the gastric smooth muscle blend and breakup food with gastric enzymes, bringing about liquefaction. It is vital for further digestion to take place in the small intestine (Schulze 2006). The liquefied mixture is identified as chyme, and it is gradually discharged into the duodenum then to the small intestine for further treatment. Thirdly, it is in the stomach that significant enzymatic action occurs, especially that of proteins. It secretes gastric juice which contains gastric acid that can eliminate microbes, pepsin to process proteins, intrinsic factor to ingest vitamin B12 and lipase to process lipids and triglycerides. The gastric epithelium known as gastric mucosa has a unique histology. It is because of this that the secretion of gastric juice is possible. The gastric mucosa is divided up into three distinct layers. As the exterior layer, the epithelial layer is composed of a stratum of simple columnar epithelial cells called surface mucous cells. The Lamina propria is the middle layer consisting of a layer of thin elastic connective tissue. The basal layer, Muscularis mucosa is made up of smooth muscle. The gastric mucosa has gastric glands formed by epithelial cells that have descended into the lamina propria. Gastric glands are made up of four main types of cells. The mucous neck cells secrete mucus and bicarbonate whose function is to act as a buffer between the lumen of the stomach and the epithelium. Thus, it is protecting the stomach lining. According to Sturdevant (1975), parietal or oxyntic cells produce intrinsic factor for vitamin B12 absorption and gastric acid (HCl) for breaking down of food. Chief cells secrete pepsinogen, the inert form of the enzyme pepsin for protein digestion and lipase for digestion of lipids. G cells: they secrete the hormone gastrin, which is perhaps the most significant secretion, controlling the bulk of the tasks of the stomach. These include the Stimulation of parietal and chief cells to secrete gastric acid and pepsinogen respectively. It also contracts lower oesophageal sphincter (cardiac sphincter), and so prevents backflow of food. Other effects include increasing gastric motility and peristalsis, and Relaxing of the pyloric sphincter to allow for the evacuation of the stomach. It also has D cells that secrete somatostatin; that inhibits gastric acid production, and enterochromaffin-like or mast cells that secrete histamine that increases production of gastric acid. In addition mast cells also secrete bicarbonate and mucus, which lines and protect the gastric epithelium layer. The environment within the stomach is acidic, and maintaining this environment is critical to the functioning of the stomach. It is the function of the parietal cells to maintain the acidity levels. There are three stages in the regulation of gastric acid levels. The first is cephalic stage. Sight, smell, and taste of food sets off muscular reflexes that make the parasympathetic neurons discharge acetylcholine. It also results in the production and release of gastrin in the G cells. Acetylcholine and gastrin invigorate parietal cells to emit more gastric acid. Additionally, they cause the secretion of histamine by mast cells. Histamine acts in tandem to improve the impacts of acetylcholine and gastrin (Arnamd et al 1999). It also encourages the production of mucus and bicarbonate, which lines and protects the stomach lining from coming into direct contact with gastric acid and digestive enzymes. The result is an increase in volume mainly of gastric acid and increases the amount of buffer on the stomach lining. The gastric stage is second. Its purpose is to improve upon the secretion that began in the cephalic stage. It occurs when food reaches the stomach. Its purpose is the mixing, blending and breaking up of chyme, and also its acidification. Neural response is triggered by the stimulation of stretch receptors due to the filling of the stomach, and that of chemoreceptor’s as the acidity levels change, and hormonal response is due to the release of gastrin by G cells as a result of parasympathetic stimulation and the presence of protein (peptides and amino acids) in chyme (Armand et al 1996). Local factors such as histamine secretion by mast cells due to the filling of the stomach also aid in this. The result is an increase in the production of gastric acid and stomach enzymes, and also increases peristaltic waves (contractions) and gastric motility. This stage lasts three to four hours and begins with the ingestion of food, ending with its passage into the duodenum. The intestinal stage is quite long. Its function is to regulate the rate at which chyme flows into the duodenum. Here the neural mechanism is caused by the distension of the duodenum with the entry of chyme. The hormonal mechanism is triggered by the presence of acid, carbohydrates and lipids, which induces the release of cholecystokinin (CCK), gastric inhibitory polypeptide (GIP) and secretin (Sturdevant 1975). The presence of proteins and peptides also results in the release of gastrin. This, as a result, causes feedback inhibition on the production of gastric acid and pepsinogen resulting in a reduction of gastric motility. In the duodenum, Gastrin accelerates evacuation of the stomach by relaxing the pyloric sphincter. Cholesytokinin (CCK) triggers the secretion of pancreatic juices rich in enzymes and causes the gall blabber to contract; it releases bile which neutralises the gastric acid. Gastric inhibitory polypeptide (GIP) inhibits gastric secretions. Secretin also inhibits gastric secretions, while increasing the release of bicarbonate ions into pancreatic juices. In addition, it raises the rate of bile, intestinal secretion and mucus secretion. In conclusion, the answer to the question “why the stomach does not digest itself?” lies within the working of the stomach as a whole. Digestion within the stomach is mainly dependant the hormone gastrin and on gastric acid levels. The different regulatory mechanisms within the stomach, work in tandem to maintain these levels, thus preventing the stomach digesting itself. Ingestion of food stimulates production of gastric acid, but it also stimulates the production of mucus and bicarbonate by the mast cells, thus strengthening the buffer between the stomach contents and the gastric mucosa. Digestion enzymes are also not released in their active form. Pepsinogen turns into its active form pepsin on contact with gastric acid within the lumen of the stomach. This, as a result, prevents it from digesting the stomach lining from the inside. The gastric and intestinal stages work together to regulate the levels of gastric acid and enzymes secretion in the stomach. As food is passed from the stomach to the duodenum, its volume decreases, therefore, the amount of stimulus on its stretch receptors decreases, thus reducing overall neural response, there’s a reduction in release of acetylcholine, thus a reduction in stimulus on parietal cells and effect a reduction on gastric acid secretion as a whole. Reduction in protein and lipid levels within the stomach lumen itself reduces the secretion of pepsinogen and lipases from chief cells leading to an overall reduction of enzyme levels. At the same time, the release of cholecystokinin (CCK), gastric inhibitory polypeptide (GIP) and secretin, further reduces gastric secretions enabling the stomach to return the levels of gastric acid to the norm. References Armand, M., Pasquier, B., André, M., Borel, P., Senft, M., Peyrot, J., & Lairon, D. (1999). Digestion and absorption of 2 fat emulsions with different droplet sizes in the human digestive tract. The American journal of clinical nutrition, 70(6), 1096-1106. M. Armand , P. Borel , B. Pasquier , C. Dubois , M. Senft , M. Andre , J. Peyrot , J. Salducci ,  D. Lairon (1996). Physicochemical characteristics of emulsions during fat digestion in human stomach and duodenum. American Journal of Physiology-Gastrointestinal and Liver Physiology, 34(1), G172. Schulze, K. (2006). Imaging and modelling of digestion in the stomach and the duodenum. Neurogastroenterology & Motility, 18(3), 172-183. STURDEVANT, R. A. (1975). Effect of gastric alkalinization on lower esophageal sphincter pressure and serum gastrin. Gastroenterology, 68, 1137-1139. Read More