Unit 6 Case Study 1 Zachary s Story
Zachary’s Story
Unit 6 Case Study 1
AP2630
Rhonda Carter
July 27, 2015
A. An ulcer starts by eroding the mucosa of the G.I. tract wall. What functions of digestion and/or reabsorption might be lost if this layer is no longer functional? What functions will be compromised if the ulcer eats through the submucosa and then the muscularis?
Absorption would not happen correctly some of the ingested and secreted may seep out of the lumen. This also could create a pathway of entry for pathogens if the ulcer ate through to the muscularis mucosa and also lose some control of defecation. (Jenkins & Tortora pg. 825,826)
B. If Zachary has a peptic ulcer affecting his stomach or duodenum, which components of the peritoneum will be affected?
If the ulcer eats a hole into the wall of the stomach, bacteria and partially digested food can spill through the opening into the peritoneum causing severe inflammation of the abdominopelvic cavity and the visceral peritoneum, which covers some other organs. (Jenkins & Tortora pg. 826)
C. How can Zach’s stomach contribute to the formation of ulcers in other parts of the G.I. tract? Which cells directly participant in ulcer formation, and how do they contribute to the creation of lesions in the G.I. tract wall?
Zachary’s stomach contributes to the formation of ulcers in other parts of the G.I. tract by the acids needed to breakdown food are excessive and cause the stomach to over work therefore causing surrounding parts to be over worked as well. If the stomach is always churning food the digestion processes is always on going. Parietal cells and gastric glands are directly related to the formation of ulcers. A major causing factor is chronic inflammation due to Helicobacter pylori that colonizes the mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis. Gastrin stimulates the production of gastric acid by parietal cells. In
Unit 6 Case Study 1
AP2630
Rhonda Carter
July 27, 2015
A. An ulcer starts by eroding the mucosa of the G.I. tract wall. What functions of digestion and/or reabsorption might be lost if this layer is no longer functional? What functions will be compromised if the ulcer eats through the submucosa and then the muscularis?
Absorption would not happen correctly some of the ingested and secreted may seep out of the lumen. This also could create a pathway of entry for pathogens if the ulcer ate through to the muscularis mucosa and also lose some control of defecation. (Jenkins & Tortora pg. 825,826)
B. If Zachary has a peptic ulcer affecting his stomach or duodenum, which components of the peritoneum will be affected?
If the ulcer eats a hole into the wall of the stomach, bacteria and partially digested food can spill through the opening into the peritoneum causing severe inflammation of the abdominopelvic cavity and the visceral peritoneum, which covers some other organs. (Jenkins & Tortora pg. 826)
C. How can Zach’s stomach contribute to the formation of ulcers in other parts of the G.I. tract? Which cells directly participant in ulcer formation, and how do they contribute to the creation of lesions in the G.I. tract wall?
Zachary’s stomach contributes to the formation of ulcers in other parts of the G.I. tract by the acids needed to breakdown food are excessive and cause the stomach to over work therefore causing surrounding parts to be over worked as well. If the stomach is always churning food the digestion processes is always on going. Parietal cells and gastric glands are directly related to the formation of ulcers. A major causing factor is chronic inflammation due to Helicobacter pylori that colonizes the mucosa. The immune system is unable to clear the infection, despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis. Gastrin stimulates the production of gastric acid by parietal cells. In
References: