Gastrointestinal System Disorders Q 306 - Gyan Darpan : Learning Portal
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Sunday 10 April 2022

Gastrointestinal System Disorders Q 306

A 40-year-old male client has been hospitalized with peptic ulcer disease. He is being treated with a histamine receptor antagonist (cimetidine), antacids, and diet. The nurse doing discharge planning will teach him that the action of cimetidine is to:
    A. Reduce gastric acid output.
    B. Protect the ulcer surface.
    C. Inhibit the production of hydrochloric acid (HCl).
    D. Inhibit vagus nerve stimulation.

Correct Answer: A. Reduce gastric acid output.

These drugs inhibit the action of histamine on the H2 receptors of parietal cells, thus reducing gastric acid output. The H2-receptor antagonist cimetidine competitively blocks histamine from stimulating the H2-receptors located on the gastric parietal cells (these cells are responsible for hydrochloric acid secretion and secretion of the intrinsic factor). The effect results in reducing the volume of gastric acid secretion from stimuli, including histamine, food, caffeine, and insulin.

Option B: Sucralfate exhibits its action by forming a protective layer, increasing bicarbonate production, exhibiting anti-peptic effects, promoting tissue growth, regeneration, and repair. Sucralfate is a medication used to treat duodenal ulcers, epithelial wounds, chemotherapy-induced mucositis, radiation proctitis, ulcers in Behcet disease, and burn wounds.
Option C: Ultimately, PPIs function to decrease acid secretion in the stomach. The proximal small bowel absorbs these drugs, and once in circulation, affects the parietal cells of the stomach. The parietal cells contain the H+/K+ ATPase enzyme, the proton pump, that PPIs block. This enzyme serves as the final step of acid secretion into the stomach.
Option D: Atropine is an antimuscarinic that works through competitive inhibition of postganglionic acetylcholine receptors and direct vagolytic action, which leads to parasympathetic inhibition of the acetylcholine receptors in smooth muscle. The end effect of increased parasympathetic inhibition allows for preexisting sympathetic stimulation to predominate, creating increased cardiac output and other associated antimuscarinic side effects as described herein.

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