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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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胰腺外分泌(二)

 

CONGENITAL ANOMALIES

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.

先天性异常

 

 

胰腺分裂

 

在胚胎发生期腹胰与背胰胰管系统未连接(见图55-2)被称为胰腺分裂。它引起胰腺分开引流,因为背胰通过副胰管引流,最后在副乳头排空,而腹胰,由胰头和钩突组成,通过Vater乳头引流。在尸检病例中胰腺分裂多达11%。胰腺分裂的意义仍有争议[1]。有些学者表明,通过确定相对流出梗阻的状态,胰腺分裂可能造成胰腺炎的发生,因为胰腺外分泌的主要部分不得不经副乳头相对小的口径排出。在另一方面,在大多数病人胰腺分裂和胰腺炎的产生彼此不存在因果关系,而且这个推论也可能是真实的;换句话说,在胰腺分裂和胰腺炎病人试图扩张副乳头外的背胰管口是不可能受益的。

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.

异位胰腺和副胰腺

 

在异常部位有胰腺组织不罕见,而且大多数异位胰腺组织是功能性的。最常见的部位是胃、十二指肠或回肠壁;美克尔憩室;脐部。少见部位包括结肠、阑尾、胆囊、网膜及肠系膜。当异位胰腺位于胃和十二指肠时常常含有胰岛组织,但当异位胰腺位于别处则不含。异位胰腺组织多半为粘膜下不规则坚硬结节状黄色组织,可能有中心脐样凹陷。胰腺分泌物常常通过这一脐样凹陷排入胃或肠腔。对引起溃疡和肠套叠这样的病例切除或旁路手术是有指征的。

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.

环状胰腺

 

环状胰腺指的是存在的正常胰腺组织束带部分或完全环绕十二指肠第二部,并延伸到胰头。它通常含有与主胰管汇合的胰管。环状胰腺的原因不清楚。它可能是由腹胰的正常顺时针旋转不成功引起,或它可能由位于十二指肠壁的异位胰腺组织膨胀引起。它表现为不同程度的十二指肠梗阻,而在儿童往往伴有其他先天性异常。它可能完全无症状,或如果在环状胰腺段发生胰腺炎在较晚年表现为梗阻症状。治疗通常涉及通过十二指肠空肠吻合术的旁路手术,而不是切除术。

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.

发育性胰腺囊肿

 

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。

PHYSIOLOGY

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.

生理学

 

成人胰腺每天分泌2.5升含有6-20g蛋白的透明无色富含碳酸氢盐的胰液。它在十二指肠碱化和在食物消化过程中起至关重要的作用。

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.

蛋白质分泌

 

可能除分泌乳汁的乳腺以外,胰腺外分泌比其他任何器官每克组织以更大的速率合成蛋白质。这些蛋白中超过90%由消化酶组成。大多数消化酶通过腺泡细胞合成和分泌,作为无活性的酶原在健康状态下只有在它们到达十二指肠后才被激活,在该处肠激酶激活胰蛋白酶原,然后胰蛋白酶催化其他酶原激活。胰腺有些消化酶被合成且以活性形式分泌,无需激活步骤(如淀粉酶、脂肪酶、核糖核酸酶)。腺泡细胞也合成蛋白,包括一些酶,它们并非注定分泌,可相当多的是为在腺泡细胞本身的应用而准备的。这后一组蛋白的例子包括许多不同的结构蛋白和溶酶体水解酶。

 

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.[

新合成的蛋白质在粗面内质网池内装配,并转运到高尔基体,在这里它们通过糖基化被修饰。这些注定通过高尔基体分泌的蛋白堆积,并在浓缩空泡内包装,当它们移往腺泡细胞腔表面时逐步发展为酶原颗粒。通过包括膜融合和分裂的过程,酶原颗粒的内容物释放到腺泡腔[2]。其他不必定分泌的蛋白当它们通过高尔基体时远离分泌通道被隔离,然后它们靶向恰当的细胞内部位[3]

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]

蛋白从腺泡细胞分泌是一个受调节的过程。在休息时,以低即基础速率分泌,但通过对胰腺激素和神经的分泌刺激这一速率能明显增加。胰腺腺泡细胞能表达乙酰胆碱、胆囊收缩素、分泌素和血管活性肠肽的受体。乙酰胆碱或胆囊收缩素对分泌的刺激已表明涉及磷脂酶C的激活、三磷酸肌醇和酰基甘油的产生以及细胞内离子钙水平的升高,后者通过什么机制不明,但能上调细胞膜顶端分泌性蛋白释放的速率。相比之下,分泌素和血管活性肠肽激活腺苷酸环化酶,增加细胞的环磷酸腺苷(AMP)的水平,并激活蛋白激酶A。这也导致在顶极的蛋白分泌。最近的研究表明,人腺泡细胞可能不具有胆囊收缩素受体,并表明人的胆囊收缩素对分泌的刺激是受胰内表达胆囊收缩素受体的神经介导的[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.

电解质分泌

 

虽然腺泡细胞的刺激能引起少量血清样液体的分泌,但胰腺分泌的大部分液体和电解质产生于导管细胞[5](图55-3)。在导管细胞中电解质分泌的最早步骤涉及循环二氧化碳弥散到导管细胞,而且二氧化碳被碳酸酐酶水化产生碳酸。随后,碳酸离解为质子和碳酸氢根离子。质子弥散到细胞外,并在循环运走,而此时碳酸氢根留在细胞内。在细胞表面顶端通过囊性纤维化跨膜调节剂(氯)通道,水电解质促分剂分泌素起作用,一个通过环磷酸腺苷(cAMP)介导的一个过程,刺激氯分泌。然后,通过顶端氯-碳酸氢根交换剂,主动分泌的氯再进入导管细胞交换碳酸氢根。这些活动合到一块的结果是富含碳酸氢根液体分泌到胰管,而质子释放入循环(见图55-3)。在没有分泌素刺激的情况下,胰液有更多血浆样成分,因为它主要由腺泡细胞分泌物组成的,而且几乎没有导管细胞分泌氯以交换碳酸氢根。用分泌素刺激,氯分泌增加,流量升高,氯-碳酸氢根交换引起胰液为富含碳酸氢根而缺少氯。

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)

 

在胃肠功能的休息期(消化间期),胰腺分泌是最少的,而且可能低达用最大刺激所观察到的分泌量的2%。胰腺对进餐的反应是三相过程,其包括头相、胃相和肠相。头相,占进餐刺激胰腺分泌的10%-15%,反映对食物视觉、嗅觉或味觉的反应。这被认为几乎完全由周围释放的乙酰胆碱介导的,它直接刺激胰腺酶的分泌和胃酸分泌。胃酸通过引起十二指肠酸化和分泌素释放间接刺激胰液分泌。胃相胰腺分泌占进餐刺激胰腺分泌的10%-15%,反映对胃膨胀和食物进入胃的反应。这些活动以引起胃泌素的释放,并刺激迷走神经的传入。通过与胆囊收缩素受体的结合,胃泌素本身是胰酶分泌的一弱刺激剂。迷走神经刺激也增加酶分泌。

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.

然而,更重要的是,胃泌素和迷走神经刺激引起胃酸分泌,而且这导致十二指肠酸化,分泌素从十二指肠释放,以及胰液及其电解质的分泌。肠相胰腺分泌反映的是对进入近侧小肠的食物和胃分泌物的反应。十二指肠酸化和十二指肠内胆汁有存在促进分泌素释放。此外,在十二指肠和近侧小肠内脂肪和蛋白质以及它们的降解产物的存在,刺激胆囊收缩素释放,而胆囊收缩素又刺激腺泡细胞酶分泌。肠相胰腺分泌占进食刺激胰腺分泌的70%-75%

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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.

 

反馈回路

 

被称为释放因子的腔内蛋白质已被发现也能刺激胆囊收缩素和分泌素释放。印象最深刻的特征是胆囊收缩素释放因子[6]。已知有两种,一种显然被十二指肠细胞合成的(胆囊收缩素释放因子),而另一种为胰腺所分泌(监测肽)。这两种胆囊收缩素释放因子都遭受胰蛋白酶的降解。因此,高蛋白餐能抑制十二指肠内胰蛋白酶活性,释放因子仍完好无损,胆囊收缩素释放增加,从而刺激胰腺分泌。

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.

相比之下,当十二指肠内缺乏食物,在肠腔内的蛋白水解活性仍不受抑制,从而降解胆囊收缩素释放因子,结果,胆囊收缩素释放和胰腺分泌减少。有些学者表明,这一反馈回路至少部分解释了慢性胰腺炎的疼痛,因为胰腺功能不全,肠腔内蛋白水解活性会降低,因而胆囊收缩素释放增加。基于这一概念,有些学者主张口服外源性胰酶作为胰腺炎慢性疼痛的一种治疗。对这种病人口服外源性胰酶很可能引起胆囊收缩素释放因子的降解,因而减少对胰腺的刺激。然而,支持这些释放因子的生理作用的证据几乎全部来自用啮齿类动物的实验,而且在人类生理性反馈回路的实际存在尚未确定。

 

 

 

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