Chronic<unk>  is a progressive inflammatory process leading to irreversible structural damage to the pancreas resulting in exocrine and endocrine dysfunction. The pathogenesis is still unclear and multifactorial. Decreased bicarbonate secretion and intrapancreatic activation of digestive enzymes is thought to play an important role in the pathogenesis of chronic<unk> . Other factors that are thought to play an important role in the pathogenesis of chronic<unk>  may include intraductal plugging and obstruction, direct injury to pancreatic cells induced by toxins and toxic metabolites, antioxidants, ischemia, autoimmune disorders, the sentinal acute<unk>  event (SAPE), necrosis and fibrosis. Genes involved in the pathogenesis of chronic<unk>  include CFTR-cystic fibrosis gene mutation, SPINK-1 mutation, which encodes for trypsin inhibitor, PRSS-1 gene mutation linked to hereditary<unk> , claudin-2 (CLDN2), and carboxypeptidase A1 (CPA1) gene mutations. Associated conditions may include autoimmune conditions, primary biliary cirrhosis, primary sclerosing cholangitis, Sjögren syndrome, and renal tubular acidosis. Gross pathology may include enlarged or atrophic pancreas, cysts, calcifications, fibrosis and patchy focal necrosis. Microscopic histopathological analysis may show patchy focal disease characterized by a mononuclear infiltrate.
Chronic pancreatitis pathophysiology
Chronic cholecystitis pathophysiology
Hereditary pancreatitis pathophysiology
Pancreatic cancer pathophysiology
Ascending cholangitis pathophysiology
Sialolithiasis pathophysiology
Gallbladder cancer pathophysiology
Primary sclerosing cholangitis pathophysiology