GERD (Acid Reflux Disease)

Gastroesophageal reflux disease is a very prevalent health problem among adults. GERD can be defined as a condition that results from troublesome symptoms and complications caused by the gastric contents. Some of the symptoms that accompany the disease include Dysphagia, regurgitation, and heartburn. Although an extent of GERD plays a role in the natural antireflux mechanisms, there is a barrier between the stomach and the esophagus that prevents materials from coming up to the throat. Peristalsis also play an important role in clearing the esophagus in addition to saliva. Between the stomach and the esophagus is a valve like a feature referred to us Lower Esophageal Sphincter. The entire component in the anatomy that is involved in the natural anti-reflux mechanism includes the diaphragm, His angle, and Gubaroff valve. To understand the anatomy of GERD, the following are important: peristalsis, LES, and the Diaphragm (Kahrilas, 2008). 

Peristalsis 

In the entire reflux mechanism, the esophageal peristalsis plays a vital role. It is because peristalsis is the main determinant of the esophageal clearance. Severe GERD occurs when the esophageal peristalsis is defective. A symptom of that effect could be a mucosal damage. A weak or absent esophageal peristalsis may lead to GERD disease among individuals. Additionally, motor abnormalities that may occur in the esophagus may be a cause of GERD. Therefore GERD is a clinical manifestation of excessive reflux of gastric contents in the esophagus.it may present itself through symptoms like a chronic cough, Regurgitation and other laryngopharyngeal symptoms (Kahrilas, 2008). 

The fundamental abnormality that leads to GERD is the histopathological injury that results from the exposure of esophageal epithelium to gastric secretions. This occurs when the secretion of the gastric secretions exceeds the level of tolerance of the epithelium. The esophagogastric junction as a part of the esophagus has a function to prevent reflux of the gastric juice into the distal esophagus. A dysfunction in the mechanics of the esophagogastric junction may become an impediment to the reflux. As such, the high-pressure esophagogastric junction may fail to ensure proper isolation of the stomach from the esophagus allowing reflux of gastric acid into the esophagus. The contribution s to the dysfunction of the esophagogastric junction could be caused by a number of factors which shall form a part of the next discussion. They include the lower esophageal sphincter, the diaphragmatic pressure, and the architecture of muscles in the gastric cardia which influences the distal aspect of the esophagogastric junction (Kahrilas, 2008). 

The Lower Esophageal Sphincter (LES) 

Kahrilas, (2008) discusses: the lower esophageal sphincter is one of the contributors of the esophagogastric junction competence. It is a 3-4 cm of contracted muscles in the esophagogastric junction. The resting less tone often varies among individuals and would be approximately 10-30mm Hg in relation to the individual’s inter-gastric pressure. The migrating motor complex determines the fluctuations of LES based on the pressure. In an individual, the pressure fluctuates often fluctuates and can hit 80mm Hg. During sleep, the pressure in the LES increases while during the day, the pressure is lower. The smooth muscles and innervation have an important role in determining the behavior of the LES. Moreover, the few other factors affect the pressure in the LES. They include a myogenic factor, the pressure in the intra-abdomen, distention of gastric materials, hormones, peptides and other forms of medication. The LES depends on a neurological mechanism to maintain a forward and backward flow. Also, the distal aspect of the esophagogastric junction has a high vulnerability to disruption, especially by anatomical changes. The physiological assessments provide evidence that existence of high pressure in the esophagogastric junction, the distal is extended to the squamocolumnar junction. In the high-pressure zone, the lateral esophageal walls meet with the medial aspect of the stomach dome. Once anomalies happen due to fluctuations in the pressure at the LES which affects the movement as well as other disruptions due to anatomic changes, the susceptibility of an individual to GERD becomes high. When pressure in the LESS becomes lesser as result of strain or free reflux, GERD disease may occur. When the Hypotensive LESS is blown open coupled with increased pressure in the intra-abdomen; a strain induced reflux occurs which may lead to GERD. 

The Angle of His 

The angle of His is the point at which the esophagus meets the stomach. The angle of His is made up of the fibers of collar sling and some circular muscles around the Gastro-Esophageal Junction. It serves to create a valve alongside the LES. As a valve, it prevents the reflux of the gastric contents like gastric acid, enzymes as well as the duodenal bile from getting back into the esophagus. In most cases, the angle is usually underdeveloped, and the esophagus joins the stomach at a vertical angle joint. Consequently, regurgitation ends up occurring to push up the stomach contents into the esophagus. In small children, the angle of His is less developed and is often a reason for Pediatric GERD. However, the turn of the angle becomes acuter as a child grows to subside the regurgitation. The angle of His should have an acute turn to enable a greater force to move down the food around its sharp bend. However, the process may cause excitation in an individual’s LES failure resulting into Dysphoria. Consequently, the stomach contents shall be able to slow back into the esophagus resulting in GERD. Noteworthy is that the degree of turn of the His angle is an important contributor to the GERD. Any dysfunction or disorder in the angle of His exacerbates the GERD (Kahrilas, 2008). 

Figure 1: The angle of His 

The Diaphragm Sphincter and Pressure Hernia 

Kahrilas, (2008) explains: the enlargement of EGJ pressure observed among a vast number of activities connected with transient increments in intra-abdominal pressure is owing to the withdrawal of the crura Diaphragm. With a rest hernia, crural diaphragm capacity is possibly traded off both by its hub displacement and conceivably by atrophy resulting from dilatation of the pressure. Physiological and anatomical factors span of a rest hernia appears to have the most noteworthy relationship with the high likelihood of strain-prompted reflux. The ramifications of this perception are that patients with break hernia display dynamic hindrance of the diaphragmatic segment of EGJ capacity corresponding to the degree of pivotal herniation. Another impact that a hiatus hernia applies on the counter reflux obstruction is to decrease the intraluminal pressure inside the EGJ. Significant tests reveal that recreating the impact of a hiatus hernia by separating the phrenoesophageal tendon lessen the LES pressure. Similarly, manometric studies in people utilizing a topographic representation of the EGJ high-pressure zone of rest hernia patients reveal unmistakable inherent sphincter and Hiatal waterway pressure segments, each of which was of lower size than the EGJ pressure of a comparator gathering of ordinary controls. Be that as it may, reenacting diminishment of a hernia by repositioning the natural sphincter back inside the Hiatal waterway and numerically summing superimposed pressures brought about figured EGJ pressures that have all intents and purposes indistinct from those of the control subjects. Alongside past examinations, this information additionally exhibits that a hiatus hernia decreased the length of the EGJ high-pressure zone. This is likely the consequence of interruption of the EGJ section distal to the SCJ owing to the restricting sling and fasten strands of the gastric cardia. It is additionally the reasonable clarification for the clinical connection set up in a significant number of surgical distributions that EGJ skill is contrarily identified with manometrically characterized EGJ erring from Erosive Esophagitis. 

GERD and Mucosal Damage 

With continued Gastroesophageal Reflux, the esophagus is exposed to gastric acids which cause it to be eroded. Up to 50% of GERD patients are often suffering from Erosive Esophagitis (Kahrilas, 2008). Both erosive and non-erosive GERD are stages of Gastroesophageal Diseases. In such cases, the individual may experience mucosal inflammation. Esophagitis may also lead to further altering of the peristalsis process. However, immediate therapy for GERD would easily ameliorate the Esophageal Peristalsis. GERD does play a huge role in the refluxate. Both gastric, as well as duodenal contents, can reflux into the esophagus including nearby organs. Gastric Hydrochloric Acid is very harmful to the Oesophagus and can lead to its corrosion. Gastro-esophageal refluxate usually is composed of other agents that are noxious like pepsin (Kahrilas, 2008). A common component of the refluxate often referred to as bile reflux is consisting of both bile and salt including other pancreatic salts cause injury to an individual’s esophagus by corroding the mucosal layer. The pattern of exposure of the esophagus to the refluxate and the volume of the refluxate determine the level of corrosion that takes place. The reflux events can be perceived by the individual when there is the great proximal extent of the refluxate as well as high volumes of the same. 

In conclusion, the anatomy of GERD constitutes majorly the peristalsis which occurs in the esophagus, the His angle competence, the Lower Esophageal Sphincter and the diaphragm whose dysfunctions may result in the occurrence of GERD. 

Reference 

Kahrilas, P. J. (2008). Gastroesophageal reflux disease.    New England Journal of Medicine ,    359 (16), 1700-1707.