The gastrointestinal tract (GIT), is also known as the alimentary canal and together with the accessory organs such as the salivary glands, it makes up the digestive system, which is responsible for digestion of all food substances. The GIT is involved in a number of processes which include; food ingestion and propulsion, mechanical and chemical food digestion, food absorption, waste elimination and microbial protection. The tract consists of 6 organs, i.e. mouth, esophagus, stomach, large and small intestines, rectum and anus. In histological terms, there are four layers that make up the GIT; mucosa, sub-mucosa, muscularis and adventitia (Huether & McCance, 2017). Additionally, the tract consists of a number of nerves which are responsible for actions such as blood flow, secretion, mobility and sensation. The autonomic as well as the local nervous system control these nerves. Disorders of motility involve inability of the GI tract to control movement effectively. These disorders are caused by a number of aggressive factors that could be either indigenous or exogenous and they range from Gastrointestinal Reflux Disease (GERD) and Peptic Ulcer Disease (PUD), to gastritis (Sainani, 2016). This paper will discuss the normal pathophysiology of gastric acid stimulation and production, and the pathophysiology of GERD, PUB and gastritis, and also discuss how behavioral factors affect the respective pathophysiology and nurses` interventions during diagnosis and management of GERD, PUB and gastritis.
Normal Pathophysiology of Gastric Acid Stimulation and Production
The gastric mucosa consists of some specialized cells which secret substances such as gastrin, HCL, mucin, somatostatin pepsinogen and other intrinsic factors. Gastric hydrochloric acid, is the most important product secreted from the stomach. It has several functions which include; food fiber dissolution, protection of GIT against microorganisms and provision of a suitable medium where pepsinogen (inactive) can be converted to pepsin (Bortoli, 2013). For the pathophysiology of acid stimulation and production to be labelled normal, there needs to be an existing balance between gastric acid stimulation and secretion, and the mucosal defensive mechanism of the GIT. The parietal cells of the gastric glands produce the acid via water hydrolysis, and the process involves transportation of hydrogen and chloride into the stomach lumen from the parietal cells. An increase in the rate of gastric acid secretion, causes movement of bicarbonates to the plasma and as a result there may be production of an “alkaline tide”, which consequently results to production of alkalinized urine (Sainani, 2016). Under suitable conditions, the nerves in the stomach releases acetylcholine, which stimulates gastrin secretion. Histamine release from enterochromaffin cell is stimulated by gastrin. Binding and activation of Histamine-2 (H-2) receptors in the parietal cells stimulates acid secretion.
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The mechanism of acid production by the parietal cells involves expression of a primary transporter (H + K + ATPase pump) on the membranes of the parietal cells. Through active transport mechanisms, the pump exchanges H + ions for K + ions. Secretagogues bind to parietal cells and induce a change in the second messengers (Sung, 2014). This change regulates translocation and activation of the pump. Signals from the muscarinic transmitters as well as the gastric mucosa, stimulates the secretion of gastric acid. This ultimately leads to transport of cations by the pump in a phosphorylation and de-phosphorylation cycle of the transport protein. Activation of the KCL pathway leads to the pumping of hydronium ions across the parietal cells surface. In between meals, gastric acid production is usually low. However, there are usually three phases of gastric acid production during feeding. The cephalic phase which is stimulated by factors such as hypoglycemia, smell of food, taste, food chewing and swallowing; the gastric phase which is stimulated by distension and gastric content; and the intestinal phase which is stimulated by hormonal and nervous mechanisms (Bortoli, 2013).
The mucosa barrier, as well as abundant mucosal blood flow protects the GIT against the destructive actions of the acid and the pepsin. Prostaglandins protects the mucosal barrier by secretion of mucous and bicarbonates. In addition, they also inhibit acid production. Stimulation of the epithelial cells of the stomach by the cholinergic nervous system leads to secretion of mucous, which primarily protects the GIT against inflammation and irritation caused by acids and pepsin. There are several factors that can lead to the damage of the mucosal barrier, which consequently leads to ulceration and inflammation. These factors include: a bacteria known as Helicobacter pylori, NSAIDs, ethanol and ischemia. Alcohol and aspirin are some of the few substances that are usually absorbed in the stomach (Prakash Gyawali, 2017).
Changes in Gastric Acid Stimulation and Production with GERD
GERD is characterized by movement of harmful substances (reflux) such as gastric acid and pepsin from the stomach to the esophagus. This is usually as a result of poor food emptying, poor functioning of the valve and esophagus problems, the main cause being incompetent performance of anti-reflux barriers of the oesophagastric junction (Hammer & McPhee, 2014). Gastrointestinal Reflux (GER), is common particularly in infants. However, when this occurrence becomes common, i.e. occurring more than two times in two weeks, then it is characterized as GERD. Two main symptoms associated with GERD are heartburn and regurgitation (Bortoli, 2013).
Changes in Gastric Acid Stimulation and Production with PUD
According to Sung (2014), PUD is associated with stomach lesions. Increased acid secretion, mucosal damage and an imbalance between GIT protective mechanisms and the aggressive factors leads to Peptic Ulcer Disease (PUD).
Changes in Gastric Acid Stimulation and Production with Gastritis
Gastritis is a condition resulting from damage of the stomach lining. Bacterial infection with H. pylori is the major cause of gastritis where the infection leads to inflammation of the stomach lining. Inflammation of the stomach lining leads to reduced gastric acid production (Prakash Gyawali, 2017).
How Behavior Impacts the Pathophysiology of GERD
Studies reveal that certain eating habits, for instance eating quickly and irregularly, eating heavy or big meals, eating just before sleep may facilitate the development of symptoms of GERD. With these kind of feeding habits, especially feeding on big meals, studies have shown have agreed with the biomechanical theory, according to which, excessive stretching of muscular walls due to presence of big meals and accumulation of air in the fundus of the stomach while feeding results in the weakening of the mechanisms for regulation of the lower oesophageal sphincter ( Jarosz and Taraszewska, 2014). Smoking behaviors, especially tobacco smoking has also been shown to play a role in development of GERD. Studies have shown that cigarettes smoking tends to lower the Lower esophageal sphincter pressure (LES) pressure and reduce the secretion levels of salivary bicarbonate, and the has the overall effect of the reduction of the physiological neutralizing effect of saliva on intraesophageal acid and prolonged acid clearance (Festi et al., 2009).
How Behavior Impacts the Pathophysiology of PUD
Behaviors such as cigarette smoking have been shown to be risk factors for the development of PUD. According to previous studies, smoking leads to a weakening of the protective mechanisms of the gastric mucosa by inhibiting the renewal of epithelial cells in the GI tract, reduction in the level of growth factor (EGF), which in turn inhibits mucosal cell proliferation, elevates the production of gastric acid and decreasing the secretion levels of bicarbonate anions, induces pyloric incompetence and elevates biliary reflux, thus causing the bile salts to destroy the gastric mucosa. Coffee consumption has also been associated with the development of PUD symptoms. As stated in previous studies, caffeine tends to induce gastric acid secretion through its action as a phosphodiesterase inhibitor and causing an increase in cyclic AMP. Consumption of alcoholic beverages also raises the chances of development of PUD associated symptoms. This is because alcohol significantly increases the secretion as well as the release of gastric acid. Alcohol may also induce mucosal injury, which leads to a decreased prostaglandin formation leading to development of PUD (Lee et al., 2017).
How Behavior Impacts the Pathophysiology of Gastritis
Alcohol abuse behaviors have been shown to contribute significantly to the development of gastritis. The gastrointestinal system takes part in the absorption and metabolism of alcohol, and is a crucial target for alcohol-induced pathophysiology like gastric dysmotility. Studies have shown that alcohol concentrations of over 10% tend to interfere with the gastric mucosa barrier and increase the permeability of the mucosa. Wine and beer (beverages with low alcohol content) tend to stimulate secretion of gastric acid, gastrin release and elevate gastric emptying. These effects may bear little to no effect after isolated episodes of alcohol intake. Nonetheless, the direct consequence of repeated intake of high level alcohol content on the gastric mucosa may facilitate the development of chronic gastritis (Molina, 2014).
Diagnosis and Treatment Prescription of GERD, PUD and Gastritis
Proper diagnosis for these disorders lies with the ability of a nurse to establish and examine a patient’s history and background in relation to their health behaviors. While putting the behavioral factors into consideration, it is the responsibility of the nurse to acquire a patient’s information by asking appropriate questions. For instance, a line of questioning directed towards the family where a nurse enquires about eating behaviors of the patient. Specifically, the nurse is required to inquire about the types and size of food ingested, as well as the pattern of ingestion with a special focus on the eating and sleeping behavior. Additionally the nurse can inquire on the smoking and alcohol use behaviors exhibited by the patient. With regard to previous studies which claim that different behavioral factors are associated with the development of symptoms associated with GERD, PUG and gastritis inflammation of GIT, various behaviors mentioned above can be used to establish whether an individual is at risk of development of GERD, PUB and gastritis (Sainani, 2016). Upper endoscopy, blood tests and stool tests are the major diagnostic procedures that can be used to rule out GERD, PUD and Gastritis (Vaezi & Richter, 2018).
While prescribing essential treatment for these disorders, consideration of the best multidrug therapy that can alleviate the symptoms associated with the disorders is paramount. Proton Pump Inhibitors are the newest group of drugs that have showed great effectivity in treatment. In addition, H-2 blockers have also been used effectively since they prevent interaction of histamine with its receptors, which as it has been mentioned above is involved in acid secretion (Sung, 2014). It is therefore critical for a nurse to have adequate knowledge regarding disorders of gastrointestinal motility since this will ensure correct diagnosis and hence effective treatment.
Conclusion
Though there are numerous studies that have been conducted in relation to how different dietary behaviors influence acid stimulation and secretion, the role that these behavioral factors play in the development of GERD, PUD and Gastritis is yet to be completely elucidated. However, more studies with regards to association of GERD and feeding behaviors s have been carried. Studies on the relationship of PUD and Gastritis with patient behaviors on the other hand are still limited. With the prevalence of motility of disorders of GIT increasing with time, there is need for extensive research on the area, as this can ultimately help improve treatment of the disorders.
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