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Biliary Dyskinesia

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Nuclear Hepatology

Abstract

Biliary dyskinesia consists primarily of two disease entities, sphincter of Oddi spasm (SOS) and cystic duct syndrome (CDS). These two entities are anatomically separate but physiologically related by an abnormal functional response to cholecystokinin. Sphincter of Oddi spasm is located within the sphincter at the distal end of the common bile duct, and cystic duct syndrome is confined mostly to the cystic duct of the gallbladder [1, 2]. In the literature, sphincter of Oddi spasm is also known by such names as papillary stenosis or bile duct dyskinesia, and cystic duct syndrome as chronic acalculous cholecystitis. Both the sphincter of Oddi and gallbladder contain receptors for cholecystokinin which is released endogenously into circulation from the intestinal mucosa upon entry of food into the duodenum [3, 4]. By binding to CCK-A type receptors, cholecystokinin normally stimulates the contraction of the gallbladder with simultaneous relaxation of the sphincter of Oddi. The cystic duct, which also contains CCK receptors, normally does not respond, because its serum threshold for contraction is set at a much higher level than the threshold for contraction of the fundus and body of the gallbladder [5]. Controversy over the existence of the entity of biliary dyskinesia prevailed for many years [6]. The availability of manometric studies has helped to understand the basic sphincter mechanism and the action of cholecystokinin on it in both health (Chap. 6) and disease, especially in patients with SOS (Table 10.1.1). A clear understanding of the bile secretion and flow mechanisms and the pathophysiologic changes associated with biliary dyskinesia are now complete due to the availability of quantitative cholescintigraphy and biliary manometry [7–9].

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© 2000 Springer-Verlag Berlin Heidelberg

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Krishnamurthy, G.T., Krishnamurthy, S. (2000). Biliary Dyskinesia. In: Nuclear Hepatology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-22654-4_10

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  • DOI: https://doi.org/10.1007/978-3-662-22654-4_10

  • Publisher Name: Springer, Berlin, Heidelberg

  • Print ISBN: 978-3-662-22656-8

  • Online ISBN: 978-3-662-22654-4

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