EXMD 509 Lecture Notes - Lecture 3: Small Intestinal Bacterial Overgrowth, Gastric Outlet Obstruction, Iron-Deficiency Anemia

• School: McGill University
• Department: Experimental Medicine
• Course: EXMD 509
• Professor: Gary Wild

Document Summary

Stimulation via: gastrin (produced in antrum), ach (vagus nerve), histamine (mast cell) Presence of food in stomach 60% Food exiting stomach in form of chyme 10% Proton pump was first molecule cloned (of any medical significance) Mucous layer: produced by goblet cells. Epithelial cells: linked by tight junctions and form an important barrier against acid. Adequate blood flow: rich perfusion to the stomach to maintain its integrity. Peptic ulceration: pepsin is a proteolytic enzyme made my chief cells, stomach or duodenum. Oesophagitis: when ph of oes falls from 6 to 4, refluxing of gastric acid into the oes. Steatorrhea fat maldigestion: secondary to inactivation of lipase inactivation by acid, lipase is derived from the pancreas. If milieu is too acidic, lipase will not function correctly: no absorption of triglycerides eliminated in the stool, presence of fat droplets in or coating the stool. 200k to 400k ppl affected annually: probably an underestimation. Accounts for 10% of costs for digestive diseases.