Clinical Pancreatology for Practising Gastroenterologists by Juan Enrique Dominguez-Munoz

By Juan Enrique Dominguez-Munoz

So much sufferers being affected by pancreatic illnesses are controlled by way of basic internists, gastroenterologists and/or surgeons in non-specialized facilities. uncomplicated and scientific examine in pancreatology is consistently resulting in alterations within the administration of pancreatic illnesses, yet those advances are utilized to the scientific perform nearly solely in really expert facilities by way of really expert groups.The books and journals presently on hand are directed at pancreatologists and the knowledge doesn't achieve such a lot common clinicians and surgeons who deal with sufferers being affected by pancreatic illnesses. the purpose of this ebook is to supply practicing gastroenterologists and surgeons with transparent information about the prognosis and remedy of pancreatic illnesses.

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Thus, this review 14 focuses only on those areas which are currently believed to play an important role in the pathophysiology of pancreatitis. Pancreatic protein synthesis, transport, and secretion (Fig. 1) The pancreatic acinar cell is the most active proteinsynthesizing cell in the body and roughly 90% of newly synthesized proteins are digestive enzymes and digestive enzyme zymogens. These proteins are destined for secretion into the pancreatic ductal space and for discharge into the duodenum.

In the diet model of pancreatitis, this colocalization occurs because zymogen granules and lysosomes fuse by crinophagy. In the secretagogue models, colocalization is caused by both crinophagic fusion of zymogen granules with lysosomes and defective sorting of lysosomal hydrolases from digestive enzymes as they traverse the Golgi stacks. In vitro exposure of rat or mouse pancreatic acini with a supramaximally stimulating dose of cerulein leads to the colocalization of digestive enzyme zymogens with lysosomal hydrolases inside cytoplasmic vacuoles and this phenomenon is assumed to occur as a result of perturbed intracellular trafficking of these enzymes.

Some of the objections to the colocalization hypothesis include the following. 2 Mechanisms of colocalization. during normal intracellular trafficking. Thus, by itself, the colocalization phenomenon may not be of pathologic significance. 2 Similarly, since colocalization can be induced by various agents and interventions that do not, by themselves, cause either intracellular zymogen activation or pancreatitis, the colocalization phenomenon may not be of pathologic significance. 3 The extent of colocalization is not related to the severity of pancreatitis and, therefore, colocalization may not be of pathologic significance.

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