Pancreatitis, acute pathophysiology

F5. Frossard, J. L., Trypsin activation peptide (TAP) in acute pancreatitis From pathophysiology to clinical usefulness. JOP. J. Pancreas (Online) 2, 69-77 (2001). 

The authors report that cannabis is the most popular illicit drug in the world and heavy use may on rare occasions cause acute pancreatitis. The pathophysiologic mechanisms underlying illicit drug use and pancreatitis is not clearly established. Heavy cannabis use could tii er cannabinoid receptors located on pancreas and result in negative consequences. 

FIGURE 20-2. Algorithm for evaluation and treatment of acute pancreatitis. ERCP, endoscopic retrograde cholangiopancreatography. (From Berardi RR, Montgomery PA. Pancreatitis. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 726, with permission.)... 

The 19th century witnessed the beginning of studies on the pathophysiology of acute pancreatitis. In 1867 Kiine isolated an enzyme catalyzing the cleavage of peptide bonds, which was later termed trypsin (1877), and a few years later Heidenhain found trypsin in pancreatic cells in the form of inactive proenzyme. 

FIGURE 39-2. Pathophysiology of acute pancreatitis initiating and secondary events. PAF, platelet-activating factor TNF-a, tumor necrosis factor-a IL-1/J, interleukin-1 / IL-6, interleukin-6 IL-8, interleukin-8. 

Mayer J, Rau B, Gansauge F, et al. Inflammatory mediators in human acute pancreatitis Clinical and pathophysiological implications. Gut 2000 47 546-552. 

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