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Motility disorders
Published in Michael JG Farthing, Anne B Ballinger, Drug Therapy for Gastrointestinal and Liver Diseases, 2019
The clinical picture of sphincter of Oddi dysfunction is incompletely understood, and limited by imprecise definition. Sphincter of Oddi dysfunction should be suspected in patients with biliary or pancreatic pain, with no demonstrable cause after conventional investigation. Hogan and Geenen have proposed a widely-accepted classification of sphincter of Oddi dysfunction, using clinical, biochemical and radiological criteria, known as the Milwaukee Biliary Group Classification126 (Table 7.5). A similar classification has been proposed for pancreatic pain.127
An update on the use of pharmacotherapy for opioid-induced bowel dysfunction
Published in Expert Opinion on Pharmacotherapy, 2023
Taraneh Mousavi, Shekoufeh Nikfar, Mohammad Abdollahi
After activating opioid receptors, either exogenously or through endogenous stimulators (e.g. endorphins, enkephalins, etc.), they are internalized and activate Gαi/o proteins, further inhibiting voltage-gated calcium channels, and hence, reducing neurotransmitters and cyclic adenosine monophosphate (cAMP) release. Opening inwardly rectifying potassium channels also leads to hyperpolarization and deactivation of postsynaptic neurons [3]. These intracellular mechanisms eventually alter the normal function of the GI tract [1,6,12], which can be categorized into alternating gut secretion, gut motility, and sphincter function in humans [14]. Human studies have demonstrated that opioid receptor agonists can reduce propulsive motility, extend GI transit time in different segments, decline gut secretion and increase muscle tone by suppressing inhibitory neuromuscular transmission and disrupting the balance between acetylcholine and nitric oxide/vasoactive intestinal peptide release [14–16]. Additionally, upon activation of κ and δ opioid receptors, excitatory cholinergic and non-cholinergic neuromuscular transmission is inhibited [13]. Opioids may also alter sphincter function, which can be either inductive or inhibitive. Although it has been shown that opioids can exert sphincter of Oddi dysfunction, their effect on the esophageal sphincter and anal sphincter is still a debate [14].
The postcholecystectomy syndrome in morbid obesity
Published in Baylor University Medical Center Proceedings, 2020
Cindy Ng, Michelle Ejimakor, Tove M. Goldson, Samuel N. Forjuoh
Cholelithiasis and/or choledocholithiasis are possible sequelae following gallbladder removal. Residual gallbladder from an incomplete cholecystectomy is a possible etiology, due to retained or regenerated stones.2,3,6 Symptoms may present as right upper quadrant abdominal pain or most commonly dyspepsia and may or may not include jaundice. This phenomenon can be referred to as postcholecystectomy syndrome, which occurs in 5% to 40% of patients, with onset ranging from 2 days to 40 years after a cholecystectomy.7–9 Gender-specific risk factors may contribute to the development of these symptoms.10 Biliary factors include choledocholithiasis, biliary stricture, and sphincter of Oddi dysfunction.5,6 Nonbiliary factors include pancreatic disorders, peptic ulcer, liver disease, irritable bowel syndrome, coronary artery disease, and gastroesophageal reflux.2,4
Indomethacin down-regulating HMGB1 and TNF-α to prevent pancreatitis after endoscopic retrograde cholangiopancreatography
Published in Scandinavian Journal of Gastroenterology, 2019
Lin Li, Miaomiao Liu, Tingting Zhang, Yuliang Jia, Yan Zhang, Heming Yuan, Guozheng Zhang, Chiyi He
Acute pancreatitis is a common and serious complication of endoscopic retrograde cholangiopancreatography (ERCP), it occurs in 1–10% of patients overall, but may approach 30% in high-risk patients [1–3], such as female gender, younger age, biliary sphincterotomy, precut papillotomy, suspected sphincter of oddi dysfunction, and previous ERCP-induced pancreatitis. Post-ERCP pancreatitis (PEP) accounts for substantial annual morbidity and occasional death which is diagnosed as new or worsening abdominal pain associated with at least a threefold increase in amylase range 24 h after the ERCP, and hospitalization for at least two nights [4]. However, hyperamylasemia is defined as serum amylase levels of more than three times the upper normal limit within 24 h after the ERCP which does not necessarily constitute pancreatitis [2].