1. exocrine 90%
1.1. excrete enzyme
1.2. ductal cells - secrete HCO3
1.2.1. HCO3 - neutralize HCL
1.2.2. alkaline secretion
1.2.3. raise pH of duodenal content (6 to 7)
1.2.3.1. In TBL : before HCO3 secreted, pH of duodenum 3 to 4 , inhibit stomach emptying until duodenum contents had been neutralized
1.3. acinar cells - sectete pancreatic enzyme
1.3.1. carbohydrate - amylase
1.3.1.1. hydrolyses starches, glycogen and carbs
1.3.1.1.1. except cellulose
1.3.2. protein - zymogen (inactive form)
1.3.2.1. trypsinogen to trypsin
1.3.2.2. chymotrypsinogen to chymotrypsin
1.3.2.3. procarboxypeptidase to carboxypeptidase
1.3.2.4. proelastase to elastase
1.3.3. why initially in inactive form? because it will digest each other. key: enzyme is protein
1.3.4. lipid - pancreatic lipase
1.3.4.1. hydrolyse neutral fat into fatty acids & monoglyceride
1.3.4.2. cholesterol esterase
1.3.4.2.1. hydrolyse cholesterol ester
1.3.4.3. phospholipase
1.3.4.3.1. splits FA from phospholipid
1.4. trypsin inhibitor
1.4.1. secreted by acinar cells
1.4.2. formed in cytoplasm of glandular cells
1.4.3. prevents activation of trypsin
1.5. phases
1.5.1. cephalic phase
1.5.1.1. intiated by smell, taste & conditioning
1.5.1.1.1. mediated by vagus nerve
1.5.2. gastric phase
1.5.2.1. initiated by distention of stomach
1.5.2.1.1. by vagus nerve
1.5.3. intestinal phase
1.5.3.1. accounts 80% of pancreatic secretion
1.5.3.1.1. stimulate both enzymatic & aqueous secretions
1.6. regulation
1.6.1. acetylcholine
1.6.1.1. stimulate pancreatic enzyme
1.6.2. CCK
1.6.2.1. stimulate pancreatic enzyme
1.6.3. secretin
1.6.3.1. stimulate bicarbonate
2. endocrine 2%
2.1. secrete hormone or chemical substances
2.2. alpha cells - glucagon
2.3. beta cells - insulin
3. clinical : pancreatitis
3.1. inflammation of pancreas
3.2. common causes
3.2.1. excess alcohol
3.2.2. gallstones
3.2.2.1. blockage at papilla of Vater
3.3. mechanism
3.3.1. gallstone -> blockage -> accumulation -> inflammation