**2.2 Pathophysiology**

Acute pancreatitis is due to an organ injury with a subsequent inflammatory response that may involve both adjacent and distant structures. The first pathogenetic event may be represented by an acinar cell injury (**Figure 1**) that produces pancreatic edema with the activation of the inflammatory pathway. The release of cytokines and chemokines leads to a systemic inflammatory response (SIRS) and to complications such as pancreatic necrosis, shock and distant organ failure.

Several hypotheses have been advanced explaining the mechanism of this acinar cell damage. The autodigestion model focused on a premature calcium-mediated intracellular trypsinogen activation in trypsin (**Figure 1**). Trypsin then activates digestive enzymes that mediate acinar cell injury. On the other hand, recent studies in animal models of AP highlight the pathogenetic role of colocalized zymogens and lysosomes, intra acinar activation of zymogens, nuclear factor-κb activation and inhibition of secretion [7].

**Figure 1.** *Pathophysiology of acute pancreatitis.*
