An impoant triggering event in acute pancreatitis is activation of-
Pathophysiology of Aciute pancreatitis Acute pancreatitis occurs as a consequence of premature intracellular trypsinogen activation, releasing proteases that digest the pancreas and surrounding tissue. Triggers for this are many, including alcohol, gallstones and pancreatic duct obstruction . There is simultaneous activation of nuclear factor kappa B (NFkB), leading to mitochondrial dysfunction, autophagy and a 21 vigorous inflammatory response. The normal pancreas has only a poorly developed capsule, and adjacent structures, including the common bile duct, duodenum, splenic vein and transverse colon, are commonly involved in the inflammatory process. The severity of acute pancreatitis is dependent on the balance between the activity of released proteolytic enzymes and antiproteolytic factors. The latter comprise an intracellular pancreatic trypsin inhibitor protein and circulating b2-macroglobulin, a1-antitrypsin and C1-esterase inhibitors. . Acute pancreatitis is often self-limiting, but in some patients with severe disease, local complications, such as necrosis, pseudocyst or abscess, occur, as well as systemic complications that lead to multi-organ failure. Ref Davidson edition23rd pg 837
Pepsinogen
Prekallikrein
Trypsinogen
Lipase
G.I.T