1 / 7100%
Gastrointestinal Tract: Disorders of Motility
Walden University
NURS 6501N-16, Advanced Pathophysiology
The gastrointestinal tract (GI) or the alimentary canal is made up of the mouth, the
esophagus, the stomach, the small intestine, the large intestine, the rectum and the anus. This
paper will describe the pathophysiology of gastric acid stimulation and production and also
explain the changes that occur to gastric acid stimulation and production with GERD, PUD, and
gastritis disorders. In this paper, this writer will also explain the impact of behavior as a factor in
the pathophysiology of GERD, PUD and gastritis disorders and also reflect on how to diagnose
and prescribe treatment for these disorders(Huether& McCance, 2017).
Pathophysiology of Gastric Acid Stimulation and Production
Huether& McCance (2017), states that gastric juice secretion is influenced by factors
known to facilitate the process of digestion through the following phases:(1)The cephalic phase -
Thought to be stimulated by the smell and taste of food. (2). The gastric phase - Stimulated by
the distention of the stomach. (3). The Intestinal phase - Stimulated by histamine and digested
proteins. The distention of the stomach brings about the secretion of gastric acid by the gastrin
hormone, the paracrine pathways such as the histamine, ghrelin, and the somatostatin. Other
factors that influence gastric acid secretion include effects of neurotransmitters acetylcholine and
other chemicals like coffee, ethanol, and proteins. The stomach is known to secretea vast volume
of gastric juices that includes the following: Mucus, acid, enzymes, hormones, intrinsic factor
and gastroferrin. Intestinal absorption of Vitamin B12 is dependent on the intrinsic factor which
is produced in the stomach while absorption of iron is facilitated by gastroferrin. The
composition of gastric juices depends on volume and flow rate but the rate and volume also
varies with the time of day and is known to be lowest in the morning and highest in the afternoon
and evening. Secretion of gastric juices can be hindered by somatostatin, unpleasant smells and
taste. It can also be inhibited by rage, fear or pain (Huether& McCance, 2017).
The major function of gastric acid is to dissolve food fibers, to act as a bactericide against
microorganisms in the stomach and to convert pepsinogen into pepsin. Gastric acid is produced
by the parietal cells and requires the transportation of hydrogen and chloride from the parietal
cells to the stomach lumen. The vagus nerve is known to stimulate secretion of gastric acid by
releasing acetylcholine which stimulates the secretion of gastrin. Gastrin is known to stimulate
the release of histamine into the gastric mucosa, which then stimulates secretion of acid due the
activation of histamine receptors on acid secretin parietal cells(Huether& McCance, 2017).
Gastric Acid Stimulation and Production changes with Gastric Disorders
Gastroesophageal reflux disease (GERD) starts from the reflux of gastric acid and pepsin
or bile salts from the stomach into the esophagus, thereby causing esophagitis. The severity of
resulting esophagitis depends on the acidity of the gastric contents and the length of time that the
esophageal mucosa was exposed to the refluxate. The refluxate causes mucosal injury and
inflammation of the esophageal which can cause redness, increased capillary permeability and
edema and even erosion (Huether& McCance, 2017).Gastric disorders like gastritis and peptic
ulcer disease (PUD) can cause injury and changes to the gastric lining. Injury to the protective
mucosal barrier is usually due to inhibition of prostaglandin which usually stimulates secretion
of mucous that protects the mucosa. Injury to the mucosal barrier causes inflammation,
reddening, edema, and damage of the mucosa due to erosion of the gastric lining. The destruction
of the mucosa leads to decreased secretion of intrinsic factor and also decreased gastric acid due
to loss of chief and parietal cells(Huether& McCance, 2017).
Diagnosis and Treatment
According to Huether& McCance (2017), diagnosis of GI disorders is based on family
medical history which should include information on smoking and alcohol consumption. The
advanced nurse practitioner (NP) should also gather additional information regarding clinical
manifestation including heartburn, episodes of nausea, vomiting, diarrhea or melena. Heartburn
may frequently be experienced as chest pain, so the NP must first rule out cardiac ischemia. The
NP should also conduct a physical examination including abdominal palpation for any distention,
tenderness or guarding. The NP may also order an esophageal endoscopy to determine the extent
of the disorder and check for any redness, bleeding, erosion, strictures and to also obtain a biopsy
(Huether& McCance, 2017, Anderson, 2010).
Pharmacological management includes avoiding aspirin and non-steroidal anti-
inflammatory drugs (NSAID) and use of over-the-counter antacids. The NP can also consider
ordering H2-blockers which work by reducing the amount of acid that the stomach produces or
proton pump inhibitors such as omeprazole. If the individual has H. pylori, then the NP should
consider antibiotics as part of the treatment. Other treatments would include prokinetics,
alginate-antacids(Huether& McCance, 2017, Anderson, 2010).
Behavior as a Risk Factor
Behaviors such as smoking, alcohol consumption, and obesity are known to contribute in
the development of GI disorders such as GERD, gastritis and PUD. The NP should therefore
consider educating the individual on the following lifestyle changes that can improve symptoms:
Working on losing weight for overweight individuals.Avoid smoking or drinking alcohol if they
do. Avoid eating chocolate, acidic, spicy and fatty foods, and drinking caffeinated drinks. Eating
smaller meals. Avoid laying down too soon after eating a meal. Elevate the head of bed when
sleeping. Sleeping on one’s the left side(Huether& McCance, 2017, Anderson, 2010).
GI disorders like GERD, PUD and gastritis can affect an individual’s quality of life
significantly. Treatment forthese disorders istherefore aimed at improving an individual’s quality
of life and to prevent more severe complications such as Barrett’s esophagus and esophageal
Anderson K. (2010). Gastroesophageal reflux disease...[corrected] [published errata appear in
RADIOL TECHNOL 2011 Jul-Aug;82(6):536].DRadiologic Technology,D81(3), 251–271.
Retrieved from https://ezp.waldenulibrary.org/login?url=https://search.ebscohost.com/
Hammer, G. G., & McPhee, S. (2014).DPathophysiology of disease: An introduction to clinical
medicine. (7th ed.) New York, NY: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017).DUnderstanding pathophysiology(6th ed.). St. Louis,
MO: Mosby.
Laureate Education, Inc. (Executive Producer). (2012c). The gastrointestinal system. Baltimore,
MD: Author.
Students also viewed