<unk>  pancreatitis is caused by genetic mutations in the regulatory regions present on trypsin. Mutations in PRSS1, SPINK1, CTRC, and CFTR gene result in weakening of defense mechanisms against pancreatitis. Defense mechanisms against pancreatitis include control of trypsin activity via prevention of premature activation of trypsinogen to trypsin and destruction, inhibition, or elimination of trypsin from the pancreas. Premature activation of digestive enzymes resulting in pancreatic injury, immune system activation, acute pancreatitis, and chronic pancreatitis.<unk>  pancreatitis may be associated with Shwachman-Diamond syndrome (SDS), Pearson marrow pancreas syndrome, CEL maturity-onset diabetes of the young (CEL-MODY) and Johanson-Blizzard syndrome. Gross examination may show enlarged or atrophic pancreas, cysts, calcifications and fibrosis. On microscopic histopathological analysis, non-invasive dysplastic intraductal lesions, called pancreatic intraepithelial neoplasia (PanIN), may be noticed.
Hereditary pancreatitis pathophysiology
Chronic pancreatitis pathophysiology
Chronic cholecystitis pathophysiology
Ascending cholangitis pathophysiology
Sialolithiasis pathophysiology
Diverticulosis pathophysiology
Gastrointestinal perforation pathophysiology
Spontaneous bacterial peritonitis pathophysiology