Pathophysiology

The pathophysiology of chronic pancreatitis remains poorly understood. 19 In contrast to acute pancreatitis, the pancreas is pathologically abnormal in chronic pancreatitis, both before and after exacerbation. In alcohol-induced disease, it is thought that either alcohol is directly toxic to acinar cells or induces pathologic changes in secretory function.20 The risk of alcohol-induced chronic pancreatitis is clearly related to the amount and duration of alcohol consumption. 17 Once established, the disease may progress despite abstinence, although the mortality rate is reduced. 1820 Chronic pancreatitis, regardless of the etiology, results in interstitial inflammation with duct obstruction and dilatation leading to parenchymal loss and fibrosis. This causes pain and eventual impairment of both exocrine and endocrine pancreatic functions, with endocrine impairment occurring later in the disease process. 19 Clinically significant malabsorption does not occur until more than 90 percent of glandular function is lost.17 The etiology of pain is likely multifactorial and may include parenchymal inflammation, pressure on acinar tissue or small ducts, perineural inflammation, and duodenal or common bile duct stenosis.20 It is controversial whether pain "burns out" as chronic pancreatitis progresses. 19

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