Pathophysiology of gastric acid stimulation and production

Select a patient factor from genetics, gender, ethnicity, age, or behavior. Consider how the
factor you selected might impact the pathophysiology of GERD, PUD, and gastritis. Reflect
on how you would diagnose and prescribe treatment of these disorders for a patient based
on this factor.
Write a 3 to 4-page paper that addresses the following: Describe the normal
pathophysiology of gastric acid stimulation and production. Explain the changes that occur
to gastric acid stimulation and production with GERD, PUD, and gastritis disorders.
Explain how the factor you selected might impact the pathophysiology of GERD, PUD, and
gastritis. Describe how you would diagnose and prescribe treatment of these disorders for a
patient based on the factor you selected.
Construct a mind map for gastritis. Include the epidemiology, pathophysiology, and
clinical presentation, as well as the diagnosis and treatment you explained in your paper.

Pathophysiology of gastric acid stimulation and production

The acid producing cells in the stomach that secret gastric acids are referred to as the
Gastric Parietal cells. These cells contain the secretory canaliculus where gastric acids are
produced into gastric lumen. The production of gastric acid in the gastric lumen occurs after the
response to messages received through neurocrine, hormonal, and paracrine messengers and
undergoes three phases that includes cephalic phase, gastric phase, and intestinal phase (Schubert
& Peura, 2008). The stimulation, production, regulation of gastric acid, and pepsin show that
there is a balance of chemo transmitters. These chemo transmitters are usually delivered to the
gastric mucosa through various pathways, which link both the inhibitory and stimulatory
mechanisms (Schubert & Peura, 2008).
On the other hand, the production, healing and defense mechanism against acid injury,
are regulated through overlapping neural, autocrine, paracrine and endocrine control pathways.
Though the acids are not important for life, the preservation of gastric acid production in the
vertebrate’s population shows an essential evolutionary advantage. The benefits of the acid in
this population are the facilitation of protein digestion and calcium, vitamin B12, and iron

PATHOPYSIOLOGY OF GASTRIC ACID 2
absorption. Gastric acid also suppresses the multiplication of bacteria and this help prevent
bacterial overgrowth in the small intestine and enteric infections (Lowry, Bhakta & Nag, 2011).
Changes that occur to gastric acid stimulation and production with GERD, PUD, and gastritis
disorders
GERD, commonly referred to as heartburn, is a common disorder caused by acid reflux
in the stomach. Human stomach naturally produces hydrochloric acid, which in turn signals
gastric gland to secret gastric acid that contains essential digestive enzymes used to breakdown
protein molecules for easier digestion (Lowry, Bhakta & Nag, 2011). Like other functions of the
body, too much or little acid can be produced. Many people will experiences acid reflux to the
esophagus when there is too much secretion of acid in the stomach causing irritation thus
resulting to a hurt burn. Gastric acid is one major factor that acts as a trigger to the symptoms of
GERD. Research done on the various factors that trigger GERD shows that providing advice
regarding dietary intolerance and lifestyle factors reduce the way gastric acid is produced in the
stomach (Adelman & Lewis, 2003).
With regard to Peptic Ulcer Disease (PUD), this disorder refers to the disturbance of
mucosal integrity in human stomach. This disturbance is caused by the local inflammation that
eventually leads to a properly defined mucosal defect. PUD can be either acute or chronic based
on the pathophysiology. They include those with excess acid secretion, those caused by anti-
inflammatory drugs, and ulcers of transferable etiology (Lowry, Bhakta & Nag, 2011). Massive
excretion of gastric acid is a major contributor to a person suffering from PUD. This happens to
people with increased parietal cells thus experiencing hypersecretion of gastric acid. Gastritis is
another disorder that is associated with gastric acid secretion. It is an irritation, erosion or
inflammation of the stomach lining and can occur gradually or suddenly. Factors that impede

PATHOPYSIOLOGY OF GASTRIC ACID 3
with mucosal defenses such as epidermal growth and secretion of excess insulin and gastric acid
influence disorders like gastritis. Any change of gastric secretion to a person having gastritis can
cause more collision in the stomach, which in turn causes abdominal pain (Schubert & Peura,
2008).
How gender affects the Pathophysiology of GERD, PUD, and gastritis
Despite the frequency of extensive research in the field of GERD, there is limited data
that address the features of GERD in men and women. In the recent past, research carried out to
establish features in women who tend to experience regurgitation, chest pain, and heartburn, has
showed small margin results with those in men. In summary, GERD is familiar in women, more
likely as regular in men, since women experience more severe and frequent symptoms of GERD
(Kahrilas, 2003).
PUD is more similar to GERD, as most women fall victim of this disorder more frequent
than men. This is because they secret less hormonal gastric acid because of other functions of the
body especially when they are pregnant, which they undertake, thus having less immune to
mucosa protection (Valle, 2012). On the other hand, gastritis is common in men than it is in
women. This is because men tend to use more alcohol than women do and this causes irritation
in the stomach. Women however tend to use drugs such as aspirin and other anti-inflammatory
drugs, which cause gastritis (Schubert, & Peura, 2008).
How to diagnose and prescribe treatment of these disorders
For the case of women, they should take precaution by undertaking screening for this
condition in a health center and this can safely manage the symptoms if they occur (Kahrilas,
2003). To diagnose PUD, both genders can take an acid-blocking medication for a diagnosis to
check whether PUD symptoms improve. In this case, if the ulcers are extensive, a change in an

PATHOPYSIOLOGY OF GASTRIC ACID 4
individual’s lifestyle, medication, or surgery can be options to treatment (Valle, 2012). Gastritis
diagnosis is mostly through a review of the family’s background, physical evaluation and a
doctor will sometimes recommend a blood test, stool test, or an upper endoscopy. Gastritis is
treated through intake of antacids to reduce stomach acids, antibiotics incase of pylori infection,
elimination of irritating foods and vitamin B12 shots if it caused by pernicious anemia (Schubert
& Peura, 2008)

Mind map for gastritis

Metabolic disorders
Drugs and chemicals
Auto-immune antibodies
against parietal cells
Helicobacter pylori is a
major factor in chronic
gastritis

Antacids
Surgical Ecision
Vitamin B12 shots
Symptom Management

TREATMENT

EPIDEMIOLOGY

Review of Family
background
Physical evaluation
Upper endoscopy
Blood test
Stool test

Anorexia
Epigastric pain
Nausea and vomiting
Vaugue abdominal
discomfort

GASTRITIS

CLINICAL
PRESENTA
TION

DIAGNOSIS

PATHOPYSIOLOGY OF GASTRIC ACID 5

References

Adelman, A. M., & Lewis, P. R. (2003). Gastritis, Esophagitis, and Peptic Ulcer Disease. In
Fundamentals of Family Medicine (pp. 288-303). Springer New York.
Kahrilas, P. J. (2003). GERD pathogenesis, pathophysiology, and clinical manifestations.
Cleveland Clinic journal of medicine, 70(Suppl 5), S4.
Lowry, A., Bhakta, K., & Nag, P. (2011). Gastroesophageal Reflux. New York: McGraw-Hill
Schubert, M. L., & Peura, D. A. (2008). Control of gastric acid secretion in health and disease.
Gastroenterology, 134(7), 1842-1860.
Valle, J. (2012). Peptic Ulcer Disease. In New York: McGraw-Hill.

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