Disorders of Motility Gastrointestinal Tract

Gastrointestinal Tract: Disorders of Motility
1.
The secretion of acid by the stomach is promoted by three phases. These, according to Huether and McCance (2017) are the cephalic phase, gastric phase, and the intestinal phase. As the authors further point out, while the cephalic phase is prompted by the smell, thought as well as taste of food, the gastric phase is prompted by stomach distention. The last phase, i.e. the intestinal phase, is prompted “by histamine and digested protein” (Huether and McCance, 2017, p. 888). It should be noted, from the onset, that in the words of Huether and McCance (2017), “gastric secretion is stimulated by the process of eating (gastric distention), by the actions of the hormone gastrin and paracrine pathways (e.g., histamine, ghrelin, somatostatin), and by the effects of the neurotransmitter acetylcholine and other chemicals (e.g., ethanol, coffee, protein)” (888).
A significant amount of gastric juices are secreted by the stomach. The said juices include, but they are not limited to, gastroferrin, intrinsic factor, enzymes, as well as acid and mucus (Huether and McCance, 2017). The main secretory units are the gastric glands in the stomach body and fundus. It is important to note that as Huether and McCance (2017) observe, the volume and flow rate determines the gastric juice composition. The secretion rate, on the other hand, is largely dependent on the time of day. In essence, as Huether and McCance (2017) further point out, a number of factors inhibit gastric secretion. These include pain, fear, rage, as well as tastes and unpleasant odor. While parasympathetic impulses are inhibited by sympathetic impulses discharge, hostility as well as aggression is associated with increased secretions – and may, as a matter of fact, contribute to certain kinds of gastric pathology.
It is important to note that gastric hydrochloric acid, as Huether and McCance (2017) observe, largely concerns itself with not only the dissolution of food fibers, but also functions as “a bactericide against swallowed microorganisms” (888). Pepsinogen is also converted to pepsin by gastric hydrochloric acid. According to Huether and McCance (2017), for acid to be produced by the parietal cells, chloride and hydrogen must be transported to the stomach lumen (from the parietal cells). In the words of the authors, “at a high rate of gastric secretion, bicarbonate moves into the plasma, producing an ‘alkaline tide’ in the venous blood, which also may result into a more alkaline urine” (Huether and McCance, 2017, p. 888). The vagus nerve is responsible for prompting the secretion of acid – with acetylcholine being released and gastrin secretion being stimulated. Histamine release is then stimulated by gastrin. It is the said histamine that prompts the secretion of acid via the activation of histamine receptors (Huether and McCance, 2017). According the authors, secretin and somatostatin inhibit the secretion of acid. It should be noted that a mucus coating protects the gastric mucosa from what the authors term as “the digestive actions of acid…” (Huether and McCance, 2017, p. 889).
It would be prudent to take into consideration the various changes that occur to gastric acid stimulation and production with GERD, PUD, and gastritis disorders. GERD is occasioned by the failure of the sphincter at the lower end of the esophagus to close properly. In the words of Huether and McCance (2017), “the lower esophageal sphincter (cardiac sphincter) prevents regurgitation from the stomach and caustic injury to the esophagus” (886). Thus, when the said sphincter fails to function as it should, the contents of the stomach are likely to leak into the esophagus. Next, when it comes to PUD, it is important to note that as has been pointed out elsewhere in this text, a layer of mucus coats the digestive tract so as to protect it from the digestive actions of acid. When this protective layer is etched away by the acid, then open sores sprout in the stomach lining. The etching away of the layer could be occasioned by certain pain relievers as well as by bacteria (H. pylori) (Fichna, 2016). Lastly, gastritis involves the erosion, irritation, or inflammation of the stomach lining. The disorder could be caused by a wide range of factors including NSAIDs, H. pylori, stress, or excessive intake of alcohol (Fichna, 2016).
2.
Several factors - including but not limited to genetics, gender, ethnicity, age, or behavior – could have an impact upon the pathophysiology of GERD, PUD, and gastritis.
GERD
In reference to GERD, it should be noted that “GERD and its complications are recognized as clustering within families, suggesting a genetic background for GERD phenotypes” (Bope and Kellerman, 2016, p. 46).
Diagnosis: I would recommend an upper endoscopy for the patient. In this case I would be seeking to detect esophagitis.
Treatment: I would prescribe lansoprazole (Prevacid) which is a proton pump inhibitor; and Baclofen to strengthen the cardiac sphincter.
PUD
Behaviors and lifestyles could put individuals at risk of PUD. Risk factors on this front are inclusive of excessive intake of alcohol which could essentially erode as well as irritate the stomach’s mucous lining (Bope and Kellerman, 2016).
Diagnosis: I would recommend an endoscopy so as to look for ulcers. A biopsy could be undertaken so as to test for H. pylori.
Treatment: to kill H. pylori (if detected), I would prescribe amoxicillin (Amoxil). To reduce acid production in the stomach, I would prescribe famotidine (Pepcid). I would recommend that the patient reduces their alcohol intake.
Gastritis
Like is the case with PUD, gastritis behaviors and lifestyles of individuals could put them at risk of gastritis. This is particularly the case with predisposition to stress and excessive intake of alcohol (Fichna, 2016).
Diagnosis: I would recommend an upper endoscopy to identify inflammation in stomach lining.
Treatment: I would recommend that the patient avoids alcohol and certain kinds of foods (such as spicy or hot foods). I would prescribe amoxicillin (Amoxil) if the disorder is occasioned by H. pylori. To reduce stomach acid, I would prescribe any H-2 blocker.
References
Bope, E.T. & Kellerman, R.D. (2016). Conn’s Current Therapy. New York, NY: Elsevier Health Sciences.
Fichna, J. (Ed.). (2016). Introduction to Gastrointestinal Diseases – Vol. 1. New York, NY: Springer.
Huether, S.E. & McCance, K.L. (2017). Understanding Pathophysiology (6th ed.). St. Louis, MO: Mosby.