Gastric
acid is produced by the parietal cells present on the walls of the stomach. A
region called secretory canaliculus in these cells is known for its acidic
environment, and its pH is said to be 8. It is the site where gastric juice is
secreted into the lumen (Hammer & McPhee, 2014). This secretion of the acid
into the lumen is the result of messages coming from the neurocrine, hormonal
and paracrine inputs.
The G
cells in the pyloric mucosa of the stomach are responsible for producing
gastrin, which is the core hormonal trigger for the production of gastric acid.
A variety of inputs stimulates the parietal cells in order to secrete different
ions especially hydrogen ions. These ions flow into the gastric lumen and vary
in functions. It should be noticed that the core stimulus for the production
and secretion of gastric acid is Histamine 2 receptor. There is a point in
which the G cells release a significant quantity of gastrin in response, which
eventually binds to the CCK2 receptors (Parietal cells and ECL). The
combination of the parietal cells and gastrin leads to the discharge of
intracellular calcium. After this, the process of activating proton pump
begins.
A
significant number of changes take place during the production and stimulation
of gastric acid, as well as the development of PUD, GERD and different
gastritis diseases (Huether & McCance, 2017). For instance, when reflux of
acid from the stomach is released into the esophagus, the
Gastro-esophageal
reflux disease gets developed. Similarly, when the pressure of LES is lower
than the pressure of intragastric like LES hypotension, then GERD takes place.
It mostly occurs when the acidity content in the stomach is higher than the
normal range and when the sphincter is not performing its functions properly.
The
pathophysiology of PUD, GERD and gastritis are impacted because of the stomach
being swollen or inflamed, which is the result of increased gastric secretion
inside the body. This often leads to pylori infection and trauma (Hunt &
Yuan, 2011). The disorders can be diagnosed using traditional diagnosis methods
such as blood test and serum text. Treatments include the use of proton pump
inhibitors and H2-receptor blockers along with antacids. Some of the
alternating behavioral factors can assist in treating GERD, PUD, and gastritis.
People
with any of these diseases are encouraged to avoid smoking and drinking. In
addition, patients should be educated about lifestyle modifications (Talawah
& Woodward, 2013). Those who are obese must lose their weight as early as
possible, and for this purpose, they can join the weight loss programs
suggested by their healthcare experts. There is a strong need to treat GERD
before its too late and the patient develops peptic ulcer disease, with lesions
in their esophagus. Once the pathophysiology of the three diseases is
understood, it becomes easy for doctors to suggest drugs. NSAID drug is widely
being used to treat such complications, and behavioral factors need to be
understood so that the patient can be brought back to a healthy life. If it
does not happen, then they may lose their life within days or weeks, depending
on the severity level of the illness.
References
Hammer, G. D., &
McPhee, S. J. (2014). Pathophysiology of disease: An introduction to
clinical medicine. (7th ed.). China: McGraw-Hill Education.
Huether, S. E., & McCance, K.
L. (2017). Understanding pathophysiology (6th ed.). St. Louis,
MO: Mosby.
Hunt, R. H., & Yuan, Y.
(2011). Acid-NSAID/aspirin interaction in peptic ulcer disease. Digestive Diseases
(Basel, Switzerland), 29(5), 465-468. doi:10.1159/000332211
Mayo Clinic.
(n.d.). Peptic ulcer. Retrieved from http://www.mayoclinic.org/diseases-conditions/peptic-ulcer/home/ovc-20231363
Talawah, N. A., & Woodward,
S. (2013). Gastro-oesophageal reflux. Part 1: smoking and alcohol reduction. British
Journal Of Nursing, 22(3), 140-145.
University of Maryland Medical
Center. (n.d.). Gastritis. Retrieved
from http://www.umm.edu/health/medical/altmed/condition/gastritis
