What is the pathophysiology of pancreatitis?

• A. Infection of the pancreas by bacteria.
• B. Autodigestion of the pancreas due to proteolytic enzymes.
• C. Autoimmune destruction of pancreatic beta cells.
• D. Ischemia of the pancreas due to arterial occlusion.

Answer: (B)

Pancreatitis mainly results from the pancreas digesting itself due to enzymes that become active inside the pancreatic tissue rather than in the gut. Normally, digestive enzymes are secreted as inactive zymogens and only activated in the small intestine; when injury or obstruction (such as from gallstones or alcohol-related acinar cell damage) causes premature activation, proteolytic enzymes like trypsin activate within the pancreas. This sets off a cascade that also activates lipase and other enzymes, leading to autodigestion of pancreatic parenchyma and surrounding fat (fat necrosis and saponification), inflammation, edema, and sometimes hemorrhage. The local injury triggers an inflammatory response that can spill over into the systemic circulation, producing broader illness. The other processes described—bacterial infection of the pancreas, autoimmune destruction of beta cells, or ischemia from arterial occlusion—do not describe the core mechanism of pancreatitis.