Pathophysiology

Although there are many distinct etiologies for acute pancreatitis, the specific mechanism that leads to the disease state remains unclear. The central pathophysiologic cause is believed to be the intracellular activation of digestive enzymes and subsequent autodigestion of the pancreas. l3 A number of factors (e.g., endotoxins, toxins, ischemia, infections, and anoxia) are believed to trigger the activation of proenzymes. Activated proteolytic enzymes, such as trypsin, then digest cellular membranes within the pancreas and cause edema, interstitial hemorrhage, vascular damage, coagulation, and cellular necrosis. 1 This noninfectious destruction of the pancreatic parenchyma rapidly causes a local inflammatory reaction that further contributes to the vascular dilatation, permeability, and edema.

The autodigestion theory replaces a previously held belief that the cause was primarily due to an anatomic "common channel" between the common bile duct and the pancreatic duct, in actuality a rare occurrence. Alternatively, it was proposed that obstruction at the ampulla of Vater was the primary initiating event in acute pancreatitis, but this does not produce pancreatitis in the experimental setting. Only by injecting bile, bacteria, and trypsin under pressure can pancreatitis be experimentally induced.2

Adult pancreatitis is distinguished from most other intraabdominal diseases by its propensity to cause remote systemic effects. It is believed that this represents an extension of the localized process into a generalized systemic inflammatory response. 4 This may lead to shock, adult respiratory distress syndrome (ARDS) and, eventually, multisystem organ failure. Recently, pancreatitis research has focused on the identification of systemic inflammatory mediators. A number of compounds has been implicated, including bradykinin, compliment, platelet-activating factor, nitrous oxide and, most recently, inflammatory cytokines. 4 Inflammatory mediators presently hold the most promise for the identification of better prognostic markers and potential therapies for acute pancreatitis. 5

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