Unit 6 Case Study 1
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 H. pylori colonization responses to increased gastrin, the increase in acid can contribute to the erosion of the mucosa and therefore ulcer formation. Studies in the varying occurrence of ulcers in third world countries despite high H. pylori colonization rates suggest dietary factors play a role in the pathogenesis of the disease. (Jenkins & Tortora pg. 826) D. Why does Zach’s G.I. tract need the substance that contributes to the formation of ulcers? How is this substance secreted by cells within the gastric pits? Zach’s G.I. tract needs the substance to assist in the breakdown of food for absorption. Epithelial cells extend into the lamina where they form secretory folds called gastric glands. Several of these glands open into the gastric pits and secretions from these glands flow into the pits. ((Jenkins & Tortora pg. 838-841)
E. If Zach’s only normal digestive enzymes come from his mouth, what substances will he be able to digest? If Zach’s only enzymes come from his mouth he will be able to digest starch because even though food is swallowed too quickly for all starches to be broken down in the mouth, salivary amylase in the swallowed food continues to act on the starches for about another hour and then the stomach acids inactivate it. And also dietary triglycerides because the enzyme secreted by lingual glands in tongue start to break these down but not active until the bolus reaches the stomach. (Jenkins & Tortora pg. 834)
F. What do you think the ultimate fate of Zach’s pancreas would be if the hepatopancreatic ampulla continued to be blocked? What do you think would happen to the liver and then eventually the rest of Zach’s body? Because of excessive pancreatic juice and bile Zach’s pancreas will not be able to function correctly. Because there is a blockage the secretions will continue to build causing further damage and inflammation. He will end up with extrahepatic jaundice, due to the blockage of bile drainage and he will...
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