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NURS 251 Pharmacology Module 7- Portage Learning $15.49   Add to cart

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NURS 251 Pharmacology Module 7- Portage Learning

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NURS 251 Pharmacology Module 7- Portage Learning//////NURS 251 Pharmacology Module 7- Portage Learning//////NURS 251 Pharmacology Module 7- Portage Learning//////NURS 251 Pharmacology Module 7- Portage Learning

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  • May 24, 2022
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  • 2022/2023
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NURS 251 Pharmacology Module 7

, Module 7
7.1 : Introduction to Gastroenterology

The organs of the upper gastrointestinal tract (mouth, pharynx, esophagus, stomach, and duodenum) work in
conjunction to first digest food and then absorb the nutrients obtained from the digested food. Both the stomach and
the upper part of the small intestines (duodenum) release hormones and enzymes that help in this process. When food
enters the body, the stomach is triggered to begin releasing gastric juices such as hydrochloric acid (HCl) and an enzyme
called pepsin.

HCl is released by parietal cells located in the stomach. Due to its acidic nature, HCl aids in the breakdown of food
entering the stomach.

Pepsin is the primary digestive enzyme found in the stomach. Pepsin is responsible for the catabolism (breaking down) of
proteins into polypeptides.

There are three major stimulators that affect the release of gastric juices: Acetylcholine (ACh), gastrin, and histamine.
First, the ingestion of food stimulates ACh to bind to its target receptors, stimulating the release of pepsin, gastrin,
histamine, and HCl from chief cells, G cells, enterochromaffin like (ECL) cells, and parietal cells respectively. Gastrin then
binds to its target receptors on ECL and parietal cells which stimulates the release of more histamine and more HCl. The
histamine then binds to the H2 receptors on the parietal cells which, in turn, increases the amount of HCl or gastric acid
released.




Figure 7.1 Stimulation of Gastric Juices. The figure above depicts the different cells involved in the release of the different gastric
juices. The process is started by ACH being released when food is ingested. The release of the initial gastrin and histamine go on to
stimulate the release of more histamine and HCL.

Peptic Ulcers and Gastrointestinal Esophageal Reflux Disease (GERD)
Peptic ulcers are defined as open sores in the mucous membranes of the mucosal lining of the stomach or duodenum.

Pathophysiology: The cause of peptic ulcers is not always the same. The majority of GI ulcers are caused by the
bacterium Helicobacter Pylori (H. Pylori). The bacterium is believed to enter the body through contaminated food or
water. Reacting to the bacteria, an inflammatory response is initiated, which is often associated with an increase in
stomach acid secretions.

The long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) is also closely related to the incidence of peptic
ulcers. NSAIDs block prostaglandins which play a role in inhibiting gastric acid secretion.

In both cases, the resulting increase in stomach acid secretions places a strain on the inner lining of the stomach until an
ulcer (break or tear) appears.

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