Lecture 3: GI Elimination 1

Note: Lecture 1&2 were review Lecture 3: GI Elimination 1 Functions of the GI · Digestion of food into usable products · Elimination of waste products · Made of 2 sections: ① GI tract "alimentary canal" ↳ oral cavity to rectum ② Accessory Organs ↳ salivary glands, liver, gallbladder, pancreas Digestion Functions 1. Transport: peristalsis (stomach & intestines) ↳ too slow = increased reabsorption of water, food/drugs in GI long time, can lead to constipation or obstruction ↳ too fast = decreased absorption of nutrients/drugs/ water, decreased removal of waste product, i.e. diarrhea 2. Absorption: Villi in small intestine + water reabsorption in large intestine 3. Enzymes for digestion: HCl + stomach enzymes, bile, pancreatic juices Upper Gl: Stomach · Gastric Pits: indented depressions in the stomach, lined with mucous cells & specialized gastric cells · pH around 1.5-3.5 · Gastric glands have 3 types of cells: ① Parietal cells: Secrete 1-3 L of HCl (also secretes intrinsic factor for vitamin B12 absorption) ② Chief cells: secrete pepsinogen that gets activated into pepsin to break down proteins ③ Enteroendocrine cells: secrete gastrin · Parietal cells require stimuli to secrete HCl, activating H/K-ATPase "proton pump" 1. Gastrin: from G-cells (enteroendocrine cells) ↳ cholecystokinin receptors 2. Histamine: from endocrine cells Gastric Mucosal Protection (Alveoli) ↳ H2 receptors · Prostaglandin E2 stimulates mucous (foveolar) cells to secrete 3. Acetylcholine: from PSNS bicarbonate and mucous for protection from HCI and contents ↳ Ach receptors of the stomach ↳ this way stomach cells don't die when holding HCI · Small intestines have their own protection: Benefits of HCI: ↳ secretes alkaline pancreatic juice and bile to lower the PH to 7 · chemical digestion of food ↳ brush border enzymes help with nutrient absorption · destruction of pathogens (reduces numbers) · Nutrient absorption ↳ intrinsic factor synthesis for Vitamin B12 absorption ↳ ferrous iron converted to ferric iron for GI absorption - - - Reflux and GERD (Gastroesophageal Reflux Disease) · reflux of gastric contents into the esophagus "heartburn" ↳ if its persistent/chronic its likely GERD · Pathophysiology: ① Transient relaxations of esophageal sphincter, allows reflux ↳ can be due to diet, age, weight, pregnancy, stress etc. ② Delayed gastric emptying ↳ incompetent sphincter in congenital defects or syndromes · Clinical Presentation: ↳ pain (heartburn, chest pain) ↳ decreased appetite ↳ bleeding (low RBC's, hematemesis) ↳ complications include weight loss, reflux esophagitis, risk of esophageal cancer (Barretts esophagus) - - Treatment · avoid irritants ↳ eat smaller meals, lose weight etc. · surgery: fundoplication · decrease acidity: ① Antacids ↳ increase stomach PH for symptom relief only ↳ high drug interactions like ASA, can have many side effects ↳ drugs: · sodium bicarbonate (alka-seltzer, Eno) · aluminum hydroxide (Amphojel) · magnesium hydroxide (Milk of Magnesia) · aluminum h. & magnesium h. (Maalox, Diovol) · calcium carbonate (Tums, Caltrate) · calcium carbonate & magnesium h. (Rolaids) · pepto-bismol → very weak antacid, anti-diarrheal, antiinfective ② Proton Pump Inhibitors ↳ binds to H/K-ATPase enzymes to inhibit the proton pump and prevent HCl acid secretion ↳ more efficacious than antihistamines, but takes 1-2 days to reach therapeutic level ↳ drugs: omeprazole (Losec), Iansoprazole (Prevacib), Pantoprazole (Pantoloc) ③ H2 Receptor Antagonists (antihistamines) ↳ selective blockade (H2 specific) to decrease HCI ↳ drugs: ranitidine (Zantac), cimetidline (Tegamet), Famotidine (Pepcid) - - - -zole suffix Peptic Ulcer Disease (PUD) · failure of endogenous protection of mucosa causing mucosal inflammation and erosion of the stomach or duodenum ↳ duodenal ulcers 4x more common ↳ main cause of GI bleeds (chronic) · Clinical Presentation: ↳ severe pain, anorexia, bleeding (in emesis or stool), anemia · common causes: ↳ stress (decreased immune function) ↳ H-pylori infection (gram - bacteria) · present in 90% of duodenal and 75% of gastric ulcers · produces ammonia gas, can test through breath test or stool sample ↳ NSAID overuse (inhibition of COX-1 decreases prostaglandin secretion, making the gastric lining weaker) · Treatment: ↳ decrease acidity, treat infection if present, Stop NSAID use if required ↳ bugs and drugs - Peritonitis from Mucosal Perforation · inflammation of the peritoneum (lining of abdominal cavity) ↳ peritoneum lines all other organs so this waste etc. can affect other organs · MEDICAL EMERGENCY !!! · Clinical Presentation: ↳ evolves fast & life threatening, pain, fever, N&V, SNS symptoms Gastritis · inflammation of the gastric mucosa · can be caused by NSAID use or chemotherapy agents · chronic cause is likely an ongoing infection such as H. pylori ↳ ↑ risk of cancer ↳ ↑ risk of perforation · gastric mucosa cells often quickly multiply due to the chemicals of the stomach, so these agents can quickly cause the GI to become inflamed