In 1642, Johannes Wirsung of Padua first described the pancreatic duct and the concept of the pancreas as a secretory organ. In 1996, a gene for<unk>  chronic pancreatitis was mapped to chromosome 7.<unk>  may be classified on the basis of mode of inheritance into autosomal dominant, autosomal recessive and<unk>  with complex genetics.<unk>  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. The incidence of<unk>  is approximately 3.5–10 per 100,000 individuals in the USA. The median age at which the symptoms develop is 10 years. The symptoms of<unk>  usually develop in the first or second decade of life. Patients with<unk>  usually present with recurrent episodes of acute pancreatitis and may develop exocrine and endocrine insufficiency. If left untreated, patients with<unk>  may progress to develop pancreatitis, biliary or pancreatic ductal dilatation, jaundice, biliary obstruction, pancreatic duct stone or stricture, pancreatic pseudocysts, and pancreatic cancer. Mortality rate is found to be increased in patients who develop pancreatic cancer. There are no established criteria for the diagnosis of<unk>  but the diagnosis is usually made on the basis of clinical findings, a typical medical and family history, imaging methods, and pancreatic function tests. Pancreatic function tests include direct and indirect tests. Genetic testing is generally done for the following genes; PRSS1, CFTR, SPINK1 and CTRC. Contrast enhanced CT scan may be helpful in ruling out other diseases with similar presentation such as malignancy and pseudocysts. CT scan findings suggestive of chronic pancreatitis may include dilatation of the main pancreatic duct, calcifications, pancreatic gland enlargement, changes in pancreatic size, shape, and contour, and pancreatic pseudocysts. The goals of management for<unk>  include pain control, management of pancreatic insufficiency by pancreatic enzyme replacement and management of complications. Pain is managed in a stepwise approach of general recommendations, pancreatic enzyme replacement, analgesics and invasive procedures. General recommendations usually include smoking cessation, cessation of alcohol intake, small meals and hydration. Surgery is usually considered when pain management fails with medical and endoscopic therapies. The goals of surgery include effective pain relief, and to preserve long-term pancreatic function. Surgery for chronic pancreatitis tends to be divided into two areas - resectional and drainage procedures. Dilated pancreatic duct may be managed with lateral pancreaticojejunostomy (LPJ) and lateralpancreaticojejunostomy with localized pancreatic head resection. Nondilated pancreatic duct is usually managed with pancreaticoduodenectomy, duodenal-preserving pancreatic head resection (DPPHR), distal pancreatectomy (DP) and total pancreatectomy (TP).
Hereditary pancreatitis
Autoimmune pancreatitis
Chronic pancreatitis
Juvenile tropical pancreatitis syndrome
Primary sclerosing cholangitis
Chronic cholecystitis
Whipple's disease
Sialolithiasis