Gastroesophageal Reflux Disease

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Table of Contents

Description of Pathology
Normal Anatomy of the Major Body System Affected
Normal Physiology of the Major Body System Affected
Mechanism of Pathophysiology
Prevention
Treatment
Conclusion
References

Description of Pathology

Gastroesophageal reflux disease (GERD) is a medical condition characterized by a frequent flow of stomach acid back into the esophagus. The backwash is known as acid reflux or acid indigestion irritates the lining of the esophagus and can cause a number of physiological issues as well as general discomfort. While everyone experiences acid reflux periodically, GERD is identified at mild stages at least twice a week (Mayo Clinic, n.d.). During an episode of GERD, an individual may taste food and stomach acid at the back of the throat causing discomfort. One of the most recognizable symptoms of GERD is regular heartburn, resulting in a burning, painful sensation in the chest. Other symptoms that adults may experience include respiratory problems, vomiting, bad breath, and nausea (NIDDK, 2020).

While the condition is not critical, over time GERD may cause serious complications including esophagitis which is the inflammation of the esophagus and a risk for precancerous changes. An esophageal stricture is also possible, narrowing the esophagus, causing issues with swallowing. GERD may cause breathing stomach acid into the lungs leading to respiratory problems such as asthma or recurring pneumonia (Mayo Clinic, n.d.).

Overall, GERD is a prevalent condition, affecting approximately 20% of adults in Western countries on a mild basis, with a third of that population having damage to the esophagus (NIDDK, 2020). GERD is a condition which must be studied and understood by medical professionals due to its prevalence and hidden risks, and a detailed analysis of its pathophysiology will be presented in this report.

Normal Anatomy of the Major Body System Affected

The esophagus is a muscular tube which connects the pharynx to the stomach, acting as a channel for transporting food and is also meant to prevent reflux of gastroduodenal contents. It extends 18-26 cm within the posterior mediastinum to the lower esophageal sphincter (LES). The esophageal wall is different morphologically from the rest of the gastrointestinal tract because it has no serosa and consists of mucosa and other elements. The muscles are arranged into an inner circular and outer layers. The muscle portions are connected by the vagus nerve which controls peristalsis depending on physiologic conditions (Menesez & Herbella, 2017).

The anti-reflux barrier is a sophisticated anatomical structure which creates a high-pressure zone via a synergy between the lower esophageal sphincter (LES) and a crural diaphragm. The function of the barrier is supported by the structure of the gastroesophageal flap valve consisting of the pharyngoesophageal ligament and gastric sling fibers of the gastric cardia. These elements position the intrinsic LES within the extrinsic crural diaphragm so that they overlap and create an effective barrier. The LES consists of a short tonically contracted muscle at the distal end of the esophagus. The resting tone for healthy people ranges from 10 to 30 mmHG. Typically, this creates a strong barrier to offset gastroesophageal pressure gradient across the esophagogastric junction (EGJ) (Tack & Pandolfino, 2018).

Normal Physiology of the Major Body System Affected

The upper esophageal sphincter (UES), the LES, and the esophagus function in a coordinated manner to allow for swallowing. When food is ingested, the UES is opened and then closed, propelling the item through the esophageal body and the relaxed LES into the stomach, and the LES then closes to prevent movement back into the esophagus. There is a mechanical effect of peristalsis which cleans the esophagus, and a secondary peristalsis occurs without swallowing.

At rest, the UES and LES are tonically contracted. Contraction of LES is the function of the muscle, not neural intervention. Therefore, when inhibitory fibers are stimulated in response to secondary peristalsis, transient LES relaxation occurs (tLESR) for 10-60 seconds spontaneously, relaxsing the LES and crural diaphragm. tLESR is a vagally mediated reflex which is normal and is triggered by gastric distention (Menesez & Herbella, 2017).

Reflux occurs through 4 mechanisms: transient lower esophageal sphincter relations (tLESRs), low LES pressure, swallow associated LES relaxation, and straining periods with low LES pressure. Prevention mechanisms against reflux vary due to the physiologic circumstances and anatomy of the EGJ. As an example, the crural diagphragm controls increases in intra-abdominal pressure and straining, while basal LES pressure helps manage reflux during resutful recumbency. Larger fluctuations exceeding 80 mmHG may occur. LES pressure is affected by myogenic and neurogenic factors impacting intra-abdominal pressure such as gastric distention, hormones, food, and medications (Tack & Pandolfino, 2018).

Mechanism of Pathophysiology

The pathological mechanisms of GERD are a reflection of imbalance between symptom-eliciting factors and defensive mechanisms. Extent of symptoms and mucosal injury is dependent on frequency of reflux events, and duration of mucosal acidification. GERD develops when the reflux of noxious gastric juice occurs into the esophagus. Excessive reflux exposure is prevented via the function of an anti-reflux barrier which is impaired in the condition.

If any of the 4 protective mechanisms described in the normal physiology are compromised, the harmful effects are increased along with number of reflux events and abnormal esophageal reflux exposure. The most common cause is LES dysfunction which occurs via mechanisms of transient relaxation, permanent relaxation, or a transient increase of intra-abdominal pressure which overwhelms the LES pressure capabilities.

In the context of diminished LES pressure, GERD occurs through strain-induced or free reflux. Strain-induced reflux results to a hypotensive LES being released due to abrupt increase in intra-abdominal pressure. This rarely occurs with LES pressure >10 mmHg or in patients without hiatus hernia. Meanwhile, free reflux is identified by a decrease in intra-esophageal Ph without change in pressure (Tack & Pandolfino, 2018).

The most frequent mechanism of tLESRs occurs during normal period of LES pressure, therefore independent of swallowing. tLESRs are characterized by diaphragmatic inhibition and persist for longer than typical LES relaxations during swallowing. The stimulus for tLESRs is a distention of the proximal stomach which stimulates the intraganglionic lamellar found at receptor ends of vagal afferents. The process is a complex mechanism of neurotransmitters and receptors which result in integrated motor response involve LES relaxation through reflex inhibitory actions and longitudinal muscle contraction which reduces EGJ obstruction and LES positioning, ultimately causing the GERD reflux (Tack & Pandolfino, 2018).

Delayed gastric emptying is another mechanism which leads to GERD. The delay leads to an increase in gastric contents which created added intragastric pressure that eventually collides with the LES. The LES is unable to withhold the pressure, resulting in acid reflux. Hiatal hernia is often mentioned in the context of GERD mechanisms, as it is a frequently encountered element in patients with symptomatic reflux but not a necessity. In hiatal hernia, the LES can migrate into the chest and lose the abdominal high-pressure zone. Furthermore, the diaphragmatic hiatus is potentially widened by a large hernia, disabling the crura function. Furthermore, gastric juice may be trapped in the hernial sac, and lead to reflux once the LES is relaxed (Tack & Pandolfino, 2018).

Prevention

Some of the underlying causes and risk factors of GERD come from lifestyle factors. Obesity is one of the primary due to excess belly fat which creates pressure on the stomach as well as the possibility of developing a hiatal hernia. Hormonal changes associated with obesity is also associated with GERD. Therefore, one of the primary prevention strategies is to maintain a healthy weight. Smoking is a causal factor as well since nicotine causes LES to relax unnecessarily. Eliminating smoking is a prevention strategy as well. For most individuals, changing food consumption habits is helpful to prevent mild GERD by eating smaller and more frequent meals, avoiding high fat or fried foods, and avoiding meals before bedtime or lying down (Mayo Clinic, n.d.).

Treatment

Most practitioners will recommend implementing lifestyle and dietary changes described above in cases of mild GERD. However, there are also treatments through medication, endoscopic therapy, and surgery. Medications such as antacids and histamine blockers which decrease acid levels and prokinetic agents which increase motility in the upper gastrointestinal tract are common prescriptions.

Transoral incisionless fundoplication (TIF or endoscopic therapy is a less invasive measure to a surgery and consists of using an endoscope to repair or recreate the valve which is the natural barrier to reflux. Finally, if none of the above work, surgery is an alternative which allows to strengthen the anti-reflux barrier through a procedure known as a Nissen fundoplication, providing permanent relief from reflux (John Hopkins Medicine, n.d.).

Conclusion

GERD is a common condition characterized by the release of acid reflux into the esophagus. This causes damage to the tissue and a number of side effects such as heartburn. An analysis of the anatomy and physiology shows that there is a natural barrier in the form of LES and crural diaphragm which are meant to prevent acid reflux. However, in a number of physiologic circumstances, the barriers are overwhelmed resulting in GERD. The condition is not serious and can be prevented and treated by lifestyle changes in most cases. However, pharmacological and surgical options exist which can regulate the acid reflux levels in the gastrointestinal tract.

References

John Hopkins Medicine. (n.d.). Gastroesophageal reflux disease (GERD) treatment. Web.

Mayo Clinic. (n.d.). Gastroesophageal reflux disease (GERD). Web.

Menezes, M. A., & Herbella, F. A. M. (2017). Pathophysiology of gastroesophageal reflux disease. World Journal of Surgery, 41, 1666-1671. Web.

National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). (2020). Acid reflux (GER & GERD) in adults. Web.

Tack, J., & Pandolfino, J. E. (2018). Pathophysiology of gastroesophageal reflux disease. Gastroenterology, 154(2), 277288. Web.

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