Describe the physiology and treatment of alkaline reflux Physiology Also known as biliary reflux Dysfunctional pyloric valve -> bile backflows from the duodenum into the stomach -> if LES is also weak -> moves into oesophagus -> irritation of the linings of the oesophagus and stomach -> inflammation -> esophagitis and gastritis. Clinical features: Upper abdominal pain Frequent heartburn Nausea Vomiting of bile Sour taste Results from mucosal injury by duodenal contents. Less likelihood of heartburn but a greater risk of regurgitation Complications: Barret’s oesophagus Increases the risk for oesophageal cancer. Diagnosis Upper GI Endoscopy: Inflammation Ulcers Ambulatory pH monitoring: Over 24 to 48 hours Detects acid and reflux episodes Oesophageal motility: Measures rhythmical muscle contractions of the oesophagus when swallowing. Helps assess the function of the LES. Bile acid testing: Collecting small contents though a tube and analysing them for bile acids. Barium swallow: Swallowing of a barium -> coats the linings of the digestive tract -> visible on AXR -> helps identify structural abnormalities and reflux. Treatment and Management LIFESTYLE MODIFICATIONS Dietary changes Dietary changes: avoid foods and beverages that trigger reflux e.g. fatty foods, chocolate, caffeine and alcohol. Eat smaller and more frequent meals. Weight management Helps to reduce pressure on the stomach and lowers the risk of reflux. Elevating the head of the bed Raising the head of the bed by about 6 to 8 inches -> helps prevent bile from flowing back into the oesophagus during sleep. MEDICATIONS Ursodeoxycholic acid: Hydrophilic bile. Altering bile composition: UDAC -> makes bile less hydrophobic and more hydrophilic -> reduces toxic potential -> minimises the damage bile causes to the stomach and oesophageal lining. Cytoprotective effects: UDCA -> stabilises the cell membrane against damaging the damaging effects of bile acids. Inhibits formation of mitochondrial pores and reduction of ER function -> prevents cell death. Anti-inflammatory properties: reduces inflammation in bile ducts and surrounding tissues -> alleviates symptoms and prevents further damage. Improving bile flow: UDCA-> promotion of bile acid secretion and other organic compounds -> improves bile flow and reduce bile stasis -> improve reflux. Sucralfate: Physical barrier -> forms a viscus, paste like substance that adheres to the mucosal lining of the stomach and the oesophagus -> protects the lining from erosive effects of bile acids, pepsin and stomach acids. Inhibition of pepsin -> directly inhibits pepsin activity -> decreases mucosal damage. Buffering action -> reacts with HCl in the stomach -> neutralisation. Cytoprotective effects -> enhances the production of prostaglandins and bicarbonate -> protects the mucosal lining and promotes healing. Bile acid sequestrants: Examples: cholestyramine, colestipol and colesevelam . These are resins. Binds to bile acids > prevents bile acids from being reabsorbed into the enterohepatic circulation. Reduction in bile acids pool -> reduce overall bile production. Liver compensates by converting more cholesterol into bile acids -> excreted Decreasing bile acid-induction irritation -> minimises irritation and inflammation. Improving symptoms. SURGICAL INTERVENTIONS Diversion surgery -> Roux-en-Y Gastric Bypass: Creates a new connection for bile drainage Diverts bile away from the stomach. I nvolves turning the stomach into a narrow tube and joining the small bowel to this portion of the stomach. Another join between two pieces of small bowel is performed further along the bowel to prevent a problem called bile reflux. Anti-reflux surgery -> Fundoplication: Strengthens the lower oesophageal sphincter -> prevents reflux.