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McGill University
PHGY 313
Russell Jones

Gastrinoma (Zollinger-Ellison syndrome) Symptoms: intermittent abdominal pain, steathorrea and diarrhea. Symptoms persisted with omeprazole so underwent a selective vagotomy of vagal nerves to stomach. Her basal acid secretion in response to pentagastrin was investigated and abnormal plasma gastrin levels were found. An endoscopy revealed hypertrophy of the gastric ruggae and ulceration in the 2nd stage duodenum. A CT scan showed a mass in her pancreas. Removal of the tumor (gastrinoma) cured her symptoms and gastrin levels. 1. Identify the mechanisms by which the increase in gastrin levels produced the symptoms in this patient and the mechanism of acid and pepsinogen secretion.  Gastrinoma tumours secrete excessive amounts of gastrin and pepsin into the portal blood stream. Only basal levels are affected.  Gastrin is released from G cells and stimulates acid release from oxyntic cells (both directly via CCK-B receptors and indirectly via ECL cells and histamine). The neural control is by the vagus nerve and sympathetic nerves.  To decrease acid secretion o D cells secrete somatostatin, a potent inhibitor of G cells and ECL activatedby CCK). o Other inhibitors include: CCK, secretin (activated by acid), GIP, VIP, prostoglandins  Pepsin release from chief cells: o Mainly by ACh release from vagus nerve o Gastrin stimulates H+ release which stimulates pepsinogen release (but also directly) o Excess gastrin overstimulates chief cells causing abnormally high pepsin levels 2. Why was hypertrophy of the gastric mucosa present? The excess acid in the stomach damages the mucosal barrier and the stomach can't keep up with replacing damaged cells and protecting itself. The pepsin also digest some of the mucosa when activated by acid. The mucosa hypertrophies to protect itself from this increase. 3. Why was ulceration present in the second stage duodenum? The chyme entering has a very low pH and high pepsin content. The damage occurs before the mixing of chyme with the alkaline secretions of the duodenum. The barrier here doesn't have the same protection as the stomach and ulcers are more common. 4. What is the explanation for the diarrhea and steathorrea? Diarrhea  Elevated gastrin concentrations cause massive secretions from all GI glands. The small intestine is overwhelmed with the hyperosmotic chyme and diarrhea occurs.  In the colon, the undigested nutrients ferment to further increase the hyperosmoticity and water goes down it's gradient into the lumen, further accentuating diarrhea.  Hypermotility occurs, decreasing transit time and increasing diarrhea. Steathorrea  Lipase requires a higher pH, and digestion is impaired in gastrinoma patients. Micelles don't form as well so the fat content in the feces increases.  Fat soluble nutrients are also impaired (ADEK vitamins) 5. What are the physiological consequences of excessive gastrin and acid production?  ADEK vitamins are required for night visi
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