NURS 251
Pharmacology Module 7 COMPLETE STUDY GUIDE WITH
PROBLEM SET QUESTIONS AND
ANSWERS 2026 Portage Learning
THIS EXAM INCLUDES:
• NURS 251 Pharmacology Module 7 study guide
• Comprehensive module review
• Problem-set practice questions
• Answer guidance and explanations
• Clinical application and critical-thinking practice
• Portage Learning NURS 251 exam preparation
• 2026 updated study material
, NURS 251 Pharmacology Module 7 COMPLETE STUDY
GUIDE WITH PROBLEM SET QUESTIONS AND
ANSWERS 2025 Portage Learning
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.
Pharmacology Module 7 COMPLETE STUDY GUIDE WITH
PROBLEM SET QUESTIONS AND
ANSWERS 2026 Portage Learning
THIS EXAM INCLUDES:
• NURS 251 Pharmacology Module 7 study guide
• Comprehensive module review
• Problem-set practice questions
• Answer guidance and explanations
• Clinical application and critical-thinking practice
• Portage Learning NURS 251 exam preparation
• 2026 updated study material
, NURS 251 Pharmacology Module 7 COMPLETE STUDY
GUIDE WITH PROBLEM SET QUESTIONS AND
ANSWERS 2025 Portage Learning
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.
