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Exocrine Pancreas(2)胰腺外分泌(二)  

2011-01-25 11:10:55|  分类: 医学英语 |  标签: |举报 |字号 订阅

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Pancreas Divisum

Failure of the dorsal and ventral pancreatic duct systems to join during embryogenesis (see Fig. 55-2 ) is referred to as pancreas divisum. It results in a pancreas with divided drainage because the dorsal pancreas drains, through the duct of Santorini, to empty at the lesser papilla, whereas the ventral pancreas, composed of the head and uncinate process, drains through Vater's papilla. Pancreas divisum has been noted in as many as 11% of autopsy cases. The significance of pancreas divisum remains controversial.[1] Some have suggested that it may contribute to the development of pancreatitis by establishing a condition of relative outflow obstruction because the major fraction of pancreatic exocrine secretion is obliged to exit through the relatively small orifice of the lesser papilla. On the other hand, the presence of pancreas divisum and the development of pancreatitis are, in most patients, not related to each other in a cause-and-effect manner, and the corollary of this may also be true; that is, attempts to widen the orifice of the dorsal duct at the lesser papilla in patients with pancreas divisum and pancreatitis are unlikely to be of benefit.







Ectopic and Accessory Pancreas

Pancreatic tissue at ectopic sites is not unusual, and most ectopic pancreatic tissue is functional. The most common sites are in the walls of the stomach, duodenum, or ileum; in Meckel's diverticulum; or at the umbilicus. Less common sites include the colon, appendix, gallbladder, omentum, and mesentery. Islet tissue is frequently present when ectopic pancreas is located in the stomach and duodenum but not when it is present elsewhere. For the most part, ectopic pancreatic tissue is a submucosal, irregular nodule of firm, yellow tissue that may have a central umbilication. Pancreatic secretions often exit through this umbilication into the lumen of the stomach or intestine. Ulceration and, on occasion, bleeding can be associated with these lesions. They may also be associated with obstruction or be the lead point for intussusception. Resection or bypass is indicated in such cases.




Annular Pancreas

Annular pancreas refers to the presence of a band of normal pancreatic tissue that partially or completely encircles the second portion of the duodenum and extends into the head of the pancreas. It usually contains a duct that joins the main pancreatic duct. The basis for annular pancreas is uncertain. It may result from failure of normal clockwise rotation of the ventral pancreas, or it may result from expansion of ectopic pancreatic tissue in the duodenal wall. It presents with varying degrees of duodenal obstruction that, in children, is often associated with other congenital anomalies. It may be totally asymptomatic or present later in life with obstructive symptoms if pancreatitis develops in the annular segment. Treatment usually involves bypass, through duodenojejunostomy, rather than resection.




Developmental Pancreatic Cysts

Solitary (congenital, duplication, or dermoid) cysts of the pancreas are rare. In contrast, multiple pancreatic cysts, lined with cuboidal epithelium, are more common. They are frequently associated with polycystic disease of the liver or kidney, and they can be seen in up to half of patients with von Hippel-Lindau disease. Pancreatic cysts only rarely become symptomatic, and in general, no treatment is indicated.



胰腺的单发性囊肿(先天性重复或皮样囊肿)罕见。相比之下,胰腺多发性囊肿内衬立方上皮更常见。它们常常伴有肝或肾多囊性疾病,而且它们见于高达半数脑视网膜血管瘤病(von Hippel-Lindau disease)病人。胰腺囊肿仅罕见成为症状性的,因而一般不需要治疗。


About 2.5 liters of clear, colorless, bicarbonate-rich pancreatic juice, containing 6 to 20 g of protein, is secreted by the human pancreas each day. It plays a critical role in duodenal alkalinization and in food digestion.




Protein Secretion

With the possible exception of the lactating mammary gland, the exocrine pancreas synthesizes protein at a greater rate, per gram of tissue, than any other organ. More than 90% of that protein consists of digestive enzymes. Most of the digestive enzymes are synthesized and secreted by acinar cells as inactive proenzymes or zymogens that, in health, are activated only after they reach the duodenum where enterokinase activates trypsinogen and the trypsin catalyses the activation of the other zymogens. Some of the pancreatic digestive enzymes are synthesized and secreted in their active forms without the need for an activation step (e.g., amylase, lipase, ribonuclease). Acinar cells also synthesize proteins, including enzymes, that are not destined for secretion but, rather, are intended for use within the acinar cell itself. Examples of this latter group of proteins include the various structural proteins and lysosomal hydrolases.





Newly synthesized proteins are assembled within the cisternae of the rough endoplasmic reticulum and transported to the Golgi, where they are modified by glycosylation. Those destined for secretion pass through the Golgi stacks and are packaged within condensing vacuoles that evolve into zymogen granules as they migrate toward the luminal surface of the acinar cell. By a process involving membrane fusion and fission, the contents of the zymogen granules are then released into the acinar lumen.[2] Other proteins that are not destined for secretion are segregated away from the secretory pathway as they pass through the Golgi, and they are then targeted to their appropriate intracellular site.[


Secretion of protein from acinar cells is a regulated process. At rest, secretion occurs at a low or basal rate, but this rate can be markedly increased by secretory stimulation that, in the pancreas, is both hormonal and neural. Pancreatic acinar cells can express receptors for acetylcholine, cholecystokinin, secretin, and vasoactive intestinal peptide. Stimulation of secretion by either acetylcholine or cholecystokinin has been shown to involve activation of phospholipase C, generation of inositol triphosphate and diacyl glycerol, and a rise in intracellular ionized calcium levels that, by yet unidentified me-chanisms, up-regulates the rate of secretory protein discharge at the apical cell membrane. In contrast, secretin and vasoactive intestinal peptide activate adenylate cyclase, increase cellular levels of cyclic adenosine monophosphate (AMP), and activate protein kinase A. This also leads to protein secretion at the apical pole. Recent studies indicate that human acinar cells may not possess receptors for cholecystokinin and that, in humans, cholecystokinin stimulation of secretion is mediated by intrapancreatic nerves that express cholecystokinin receptors.[4]


Electrolyte Secretion

Although stimulation of acinar cells results in the secretion of a small amount of serum-like fluid, most of the fluid and electrolytes secreted from the pancreas arise from duct cells[5] ( Fig. 55-3 ). The earliest step in duct cell electrolyte secretion involves diffusion of circulating carbon dioxide into the duct cell, and that carbon dioxide is hydrated by carbonic anhydrase to yield carbonic acid. Subsequently, the carbonic acid dissociates into protons and bicarbonate ions. The protons diffuse out of the cell and are carried away in the circulation while the bicarbonate remains inside the cell. The fluid and electrolyte secretagogue secretin acts, through a cyclic AMP–mediated process, to stimulate chloride secretion, at the apical cell surface, through cystic fibrosis transmembrane regulator (chloride) channels. Then, through an apical chloride-bicarbonate exchanger, the actively secreted chloride is taken up again by the duct cell in exchange for bicarbonate. Taken together, the result of these events is the secretion of a bicarbonate-rich fluid into the duct and the discharge, into the circulation, of protons (see Fig. 55-3 ). In the absence of secretin stimulation, pancreatic juice has a more plasma-like composition because it is composed primarily of acinar cell secretions and there is little duct cell secretion of chloride to permit exchange with bicarbonate. With secretin stimulation, chloride secretion is increased, flow rates rise, and chloride-bicarbonate exchange results in juice that is rich in bicarbonate and poor in chloride.




Integrated Physiology

During the resting (interdigestive) phase of gastrointestinal function, pancreatic secretion is minimal and may be as low as 2% of that noted with maximal stimulation. The pancreatic response to a meal is a three-phase process that includes a cephalic phase, a gastric phase, and an intestinal phase. The cephalic phase, accounting for 10% to 15% of meal-stimulated pancreatic secretion, reflects the response to the sight, smell, or taste of food. It is believed to be almost exclusively mediated by peripherally released acetylcholine, which directly stimulates pancreatic secretion of enzymes and gastric secretion of acid. The acid indirectly stimulates pancreatic secretion of fluid and electrolytes by causing duodenal acidification and secretin release. The gastric phase of pancreatic secretion, accounting for 10% to 15% of meal-stimulated pancreatic secretion, reflects the response to gastric distention and the entry of food into the stomach. These events can cause release of gastrin and stimulate vagal afferents. By binding to cholecystokinin receptors, gastrin is itself a weak stimulant of pancreatic enzyme secretion. Vagal stimulation also increases enzyme secretion.

综合生理学(Integrated Physiology)



More important, however, gastrin and vagal stimulation cause gastric acid secretion, and this leads to duodenal acidification, release of secretin from the duodenum, and pancreatic secretion of fluid and electrolytes. The intestinal phase of pancreatic secretion reflects the response to food and gastric secretions entering the proximal intestine. Acidification of the duodenum and the presence of bile in the duodenum promote secretin release. In addition, in the duodenum and proximal small intestine, the presence of fat and protein, as well as their partial breakdown products, stimulates the release of cholecystokinin, and this cholecystokinin stimulates enzyme secretion from acinar cells. The intestinal phase of pancreatic secretion accounts for 70% to 75% of meal-stimulated pancreatic secretion.


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Luminal proteins, referred to as releasing factors, have been described that can also stimulate cholecystokinin and secretin release. The most well characterized are the releasing factors for cholecystokinin.[6] Two forms are known, one apparently synthesized by duodenal cells (cholecystokinin-releasing factor) and the other secreted by the pancreas (monitor peptide). Both forms are subject to degradation by trypsin. Thus, with high-protein meals that quench intraduodenal tryptic activity, the releasing factor remains intact, cholecystokinin release is increased, and pancreatic secretion is stimulated.





In contrast, when food is absent from the duodenum, the proteolytic activity that remains unquenched within the lumen degrades the releasing factor and, as a result, cholecystokinin release and pancreatic secretion are reduced. Some have argued that this feedback loop may, at least in part, explain the pain of chronic pancreatitis because, with pancreatic insufficiency, intraluminal proteolytic activity would be low and cholecystokinin release would increase. Based on this concept, some have advocated administration of exogenous pancreatic enzymes as a treatment for the chronic pain of pancreatitis. Presumably, administration of exogenous enzymes to such patients would result in degradation of the releasing factor and reduce pancreatic stimulation. However, evidence supporting a physiologic role for these releasing factors comes almost exclusively from experiments using rodents, and the actual existence of a physiologic feedback loop in humans has not been established.





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