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Intestine pathophysiology

Any event that leads to a significant increase in the amount of fluid retained in the stool may result in diarrhea. Large-stool diarrhea often signifies small intestinal involvement, whereas small-stool diarrhea usually originates in the colon. Diarrhea may be classified according to pathophysiologic... [Pg.312]

Cooper, E.S., Whyte-Alleng, C.A.M., Finzi-Smith, J.S. and McDonald, T.T. (1992) Intestinal nematode infections in children the pathophysiological price paid. Parasitology 104, S91-S103. [Pg.367]

Although it appears that severe IL-4-regulated enteropathy is not required for immune expulsion of T. spiralis, it is still possible that Th2 cytokines can act in a direct fashion to create an environment unfavourable for intestinal parasites. It remains to be shown directly whether these effects are sufficient to expel parasites. Indeed, there is considerable evidence to support a variety of pathophysiological effects of IL-4 and/or TNF on the gut. These effects may be mediated by factors including cytokines and mast-cell products (e.g. leukotrienes and 5-hydroxytryptamine). 7. spiralis infections result in increased fluid and mucus secretion into the lumen as well as increased intestinal propulsive activity and more rapid intestinal transit (Castro et al, 1979 Russell, 1986 Vermillion and Collins, 1988 Vermillion et al., 1991 Weisbrodt et al, 1994 Barbara et al, 1997). The increased contractility of radial and longitudinal muscle is greater in high-... [Pg.390]

Overall, in this chapter we have attempted to emphasize the need for more in vivo studies to be conducted to clarify the dynamic interplay between mechanisms of drug transport and metabolism in the human intestine under in vivo conditions. There is also a need to develop additional in vivo techniques for direct measurements of these processes in regions along the GI tract in humans, and to relate the findings to various physiological/pathophysiological conditions. This would clearly increase our knowledge of the mechanisms involved, and provide in vivo data to help develop and validate rapid and reliable in vitro intestinal models. [Pg.181]

Shneider, B. L. Intestinal bile acid transport biology, physiology, and pathophysiology. J. Pediatr. Gastroenterol. Nutr. 2001, 32, 407-417. [Pg.284]

Tabaqchali S The pathophysiological role of small intestinal bacterial flora. Scand J Gastroenterol Suppl 1970 6 139-163. [Pg.21]

Strocchi A, Levitt MD Intestinal gas, in Sleisenger MH, Fordtran JS (eds) Gastrointestinal Disease Pathophysiology, Diagnosis, Management, ed 5. Philadelphia, Saunders, 1993, pp 1035-1042. [Pg.114]

Irritable bowel syndrome (IBS) affects 10-22% of the general population (54) and results in high health care utilization (55). The pathophysiology is not clearly defined diet, psychological distress, infection, altered mucosal immunity, visceral hypersensitivity, intestinal dysmotility, and abnormal brain-gut interactions are potential mechanisms for this disorder (56). Treatment options vary and are generally selected based on the patient s primary symptom. [Pg.401]

Sha U, Walker WA Pathophysiology of intestinal food allergy. Adv Pediatr 2002 49 299-316. Faria A, Weiner H Oral tolerance Mechanisms and therapeutic applications. Adv Immunol 1999 73 153-264. [Pg.23]

Phillips, S.F., J.H. Pemberton, and R.G. Shorter. 1991. The large intestine Physiology, pathophysiology and disease. New York Raven Press. [Pg.28]

G. T. MacFarlane, and J. H. Cummings, The colonic flora, fermentation and large bowel digestion function, Chapter 4, The Large Intestine Physiology, Pathophysiology and Disease (S. F. Phillips, J. H. Pemberton, and R. G. Shorter, eds.), Raven Press, New York, 1991. [Pg.53]

Macfarlane GT, Gnminings JH. In Phillips SF, Pemberton JH, Shorter RG, eds. The Large Intestine Physiology, Pathophysiology, and Disease. New York, NY Raven Press 1991 51. [Pg.795]

Although the small, coated pancreatin preparations have been shown to be superior compared with unprotected pancreatin extracts, it should be noted that enzyme release requires several minutes after exposure to the intestinal milieu. This may further delay digestive action and shift the site of maximal absorption more distally this pathophysiological mechanism is exacerbated by accelerated gastrointestinal... [Pg.287]


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See also in sourсe #XX -- [ Pg.108 , Pg.113 ]




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