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Small intestine: general

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Abstract

The cardinal sign of small intestinal disease is diarrhoea, but this can also be caused by disease elsewhere. Conversely, diarrhoea is not always present, and there are many other signs of small intestinal dysfunction, although some are non-specific. This chapter describes the structure and function of the small intestine, and discusses pathophysiology and diagnostic approach.

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34.3 Functional anatomy of the small intestine. The small intestine is basically a tube with a serosal surface covered by visceral peritoneum and an inner absorptive and digestive surface, the mucosa. Beneath the outer serosa, longitudinal and circular muscle layers produce peristaltic and segmental contractions for propelling and mixing the luminal contents coordinated by the enteric nervous system. The submucosa is rich in blood and lymphatic vessels. The mucosa comprises the thin muscularis mucosa, the lamina propria and the columnar epithelium; it is thrown into folds and is covered by finger-like villi to increase the digestive and absorptive surface area. The luminal membrane of the enterocyte is thrown into processes called microvilli, which increase the luminal surface area. Tight junctions between enterocytes maintain epithelial integrity. Absorbed nutrients are passed from the enterocyte into the intercellular space for distribution to the body. Enterocytes, which are shed from the villus tip and are continually replaced through division of crypt cells, are the site of nutrient digestion and absorption. Goblet cells secrete protective mucus. Water-soluble nutrients pass into the rich capillary network of the lamina propria, and fat is passed as chylomicrons into the lacteals. Immunocytes in the lamina propria are involved in maintaining tolerance to luminal antigens. Drawn by S.J. Elmhurst BA Hons (www.livingart.org.uk) and reproduced with her permission.
Image of 34.5
34.5 Assimilation of folate and cobalamin. (a) Principles of folate absorption. Folic acid is a water-soluble vitamin that is plentiful in most commercial pet foods. However, dietary folic acid is present as folate polyglutamate, which cannot be readily absorbed. In the proximal small intestine, folate polyglutamate is converted by brush border folate deconjugase to folate monoglutamate, which is then absorbed by specific folate carriers located exclusively in the proximal small intestine. (b) Principles of cobalamin absorption. Cobalamin is also a water-soluble vitamin that is plentiful in most commercial dog and cat foods. Dietary cobalamin is bound to dietary protein and cannot be absorbed in this form. In the stomach, digestion of dietary protein is initiated by pepsin and hydrochloric acid, and cobalamin is released. Free cobalamin is immediately bound by R-proteins (haptocorrins) present in saliva and gastric secretions, thereby once again rendering the vitamin unabsorbable. In the small intestine, R-proteins are digested by pancreatic proteases and the liberated cobalamin is bound by intrinsic factor, of which approximately 90% is secreted by the pancreas in the dog, and 99% in the cat. Finally, cobalamin–intrinsic factor complexes are absorbed by specific receptors in the ileum. Note that a very small proportion of oral cobalamin is absorbed directly, and large daily doses can be used to supplement cobalamin deficiency.

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