Gastrointestinal Tract: Disorders of Motility
Gastrointestinal diseases involve various but overlapping mechanisms of pathology. These mechanisms are often associated with acid secretion, poor defence of the mucosal lining or reflux of the acid. This paper seeks to explore the interrelationship between gastric acid with GERD, PUD, and gastritis. In achieving this, the paper evaluates stimulation and secretion of gastric acid and how these aspects vary in the presence of the gastrointestinal diseases. The paper also assesses how behaviour affects the pathophysiology of the diseases in consideration and how treatment can be administered in such instances.
Inhibitory and stimulatory neurohormonal mechanisms are responsible for the secretion of gastric acid in the upper gastrointestinal tract. The hormones involved in the secretion of the acid are histamine and gastric while the vagus nerve is the neuronal effector (Silva, & de Sousa, 2011, p.4). Food ingestion stimulates gastric secretion and occurs in three phases each with a different activator. These phases include cephalic, intestinal and gastric phases.
The cephalic phase involves the central nervous system. This phase is activated by a conditional reflex of such as smell or thought of food that results in the release of acetylcholine neurotransmitter (ACh) and gastrin-releasing peptide. ACh stimulates secretion of gastric acid from the parietal cells while gastrin-releasing peptide cause indirect stimulation of the parietal cells. Gastrin-releasing peptide stimulates gastrin secretion by G cells. Lawrence (2013, p.247) explain that gastric phase is activated by the entrance of food into the stomach. Food in the stomach stimulates stretch receptors that activate intragastric parasympathetic reflex pathways. These pathways stimulate gastrin secretion. The secreted gastric cause either direct secretion of acid through CCK8 receptor activation or indirectly via enterochromaffin cells.
Stimulation of gastric acid in the intestinal phase occurs upon the arrival of digestion products in the small intestines. These products cause elevated levels of serum peptides such as enterooxyntin that stimulate gastric secretion (Lawrence, 2013, p.247). The process of gastric acid secretion may be affected by the presence of gastrointestinal disorders. GERD and PUD have no effect on the stimulation or secretion of gastric acid (Qadeer & Falk, 2010). Aditi and Graham (2012) explain that gastric ulcers is associated with a normal or decreased gastric acid stimulation and secretion.
Pathophysiology of gastrointestinal disorders may be affected by behaviour (Clarke, 2015b). An individual’s behaviour determines their psychological states such as in aspects of stress, anger and sadness. Psychological state, on the other hand, affects the physiology of the gut (Konturek P., Brzozowski & Konturek S.,2011). The existence of these states cause gastrointestinal motility alterations, changes in gastrointestinal secretions and increase visceral perceptions. Diagnosis of GERD can be made using proton pump inhibitor empirical trials while endoscopy could be done for peptic ulcers and gastritis (Qadeer & Falk, 2010). In the case of psychologically induced gastrointestinal disorder, behavioural therapy, stress management or dynamic psychotherapy may be used depending on the specific case as adjunctive therapies to medical administration (Clarke, 2015a; Silva & de Sousa, 2011, pp.17-18). For instance, histamine-2 receptor antagonists such as cimetidine could be administered alongside stress management in case of GERD or PUD. Sucralfate could be used for gastritis to achieve prophylaxis while psychotherapy would help to alleviate stress level.
Gastric acid secretion has been shown to be regulated by inhibitory and stimulatory neurohormonal mechanisms. Acid secretion has been shown to occur in three phases either by a direct or indirect process. GERD and PUD do not have any effect on the secretion and stimulation of gastric acid but rather affect defence on the mucosal lining. Behaviour affects the pathophysiology of gastrointestinal diseases primarily through its psychological effects such as stress and their treatment ought to consider it. Treatment in the presence of behavioural factor requires prevention of prophylaxis. Therefore, a pharmacological treatment should be used alongside a behaviour management plan.
Mind Gap for Stress-induced gastritis
| Gastritis |
| Epidemiology (in the U.S)
· Overt bleeding in 6% · Clinically significant hemorrhage in 2-3% · 52-100% with intraepithelial hemorrhage
|
| Diagnosis
· Endoscopy · Hematocrit |
| Clinical presentation
· Melena · Vomiting and nausea · Hematemesis |
| Pathophysiology
· Gastric acid secretion alteration · Mucosal blood flow reduction · Altered gastric motility
|
| Treatment
· Psychotherapy · Pharmacotherapy through the use of sucralfate
|
References
Aditi, A., & Graham, D. Y. (2012). Vitamin C, gastritis, and gastric disease: a historical review and update. Digestive diseases and sciences, 57(10), 2504-2515.
Clarke, R. C. (2015a). Stress-Induced Gastritis Treatment & Management. Medscape. Retrieved from http://emedicine.medscape.com/article/176319-treatment
Clarke, R. C. (2015b). Stress-Induced Gastritis. Medscape. Retrived from http://emedicine.medscape.com/article/176319-overview
Konturek, P. C., Brzozowski, T., & Konturek, S. J. (2011). Stress and the gut: pathophysiology, clinical consequences, diagnostic approach and treatment options. J Physiol Pharmacol, 62(6), 591-599.
Lawrence, P. F. (2013). Essentials of general surgery. Philadelphia, PA: Wolters Kluwer Health/Lippincott Williams & Wilkins.
Qadeer, M.A. and Falk, G.W. (2010). Acid Peptic Disorders. ClevelandClinicmeded. Retrieved from http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/gastroenterology/acid-peptic-disorders/
Silva, M. I. G., & de Sousa, F. C. F. (2011). Gastric ulcer etiology. Peptic ulcer disease, 1.
