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• W2312477113 abstract "The patomechanism of OIBD comprises both peripheral and central mechanisms. The peripheral opioid effect on µ-opioid receptors in the gut wall plays the main role here [3]. High density of µ-opioid receptors was found in neurons of myenteric and submucosal plexus and immune cells in the lamina propria [4]. Opioid receptors (predominantly µ, also κ and δ) are located in the gut wall in the myenteric plexus and in the submucosal plexus. The former are responsible for GI motility and the latter for secretion. The µ-opioid receptors are activated in the wall of the stomach, small and large intestine by endogenous (enkephalins, endorphins and dynorphins) and exogenous (codeine, dihydrocodeine, hydrocodone, tramadol, morphine, oxycodone, hydromorphone, fentanyl, buprenorphine, methadone) opioids and modify GI function. Activation of µ-opioid receptors inhibits excitatory and inhibitory neural pathways within the enteric nervous system that coordinates motility. Inhibition of excitatory neural pathways depresses peristaltic contractions. The blockade of inhibitory neural pathways increases GI muscle activity, elevates resting muscle tone, spasm and non-propulsive motility patterns. These mechanisms are responsible for delayed gastric emptying and slowing the intestinal transit [5]. The central mechanism of opioid effects on GI tract was demonstrated as intracerebroventricular administration of morphine in rats inhibited gastrointestinal propulsion. This effect was reversed by intracerebroventricular administration of naloxone and vagotomy. Intrathecal administration of morphine reduced gastroduodenal motility and intramuscular morphine gave additional effects. Thus both central and peripheral opioid effects play a role in opioid GI effects [6]. Treatment of Opioid-Induced Bowel Dysfunction General measures comprise the meticulous assessment and applying prophylactic measures matched to patients’ general condition. Change of diet (increased food and fluid intake), more physical activity, sitting position during bowel movement and privacy during defecation process are recommended. Patients treated with opioids should be considered for prokinetic administration (metoclopramide, domperidone, itopryd) [7]. Reversible causes such as hypercalcemia should also be treated. Discontinuing or decreasing doses of drugs that may contribute to constipation development (such as tricyclics, neuroleptics, anticholinergics) should also be considered. Patients and families should be educated about the ways of prevention and treatment of OIBD. In majority of patients with OIBD laxatives need to be administered. The general recommendation is to combine oral administration of osmotic agents (usually lactulose or macrogol) which have an osmotic effect in the colon with stimulants activating neurons in the myenteric and submucosal plexus in colon and reducing absorption of water and electrolytes from the intraluminal contents: anthracenes (senna), polyphenolics (bisacodyl) or sodium picosulphate [8]. However, these drugs display limited efficacy in patients suffering" @default.
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• W2312477113 date "2012-01-01" @default.
• W2312477113 modified "2023-09-27" @default.
• W2312477113 title "Are we able to Manage Effectively Opioid-Induced Bowel Dysfunction?" @default.
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• W2312477113 doi "https://doi.org/10.4172/2161-0479.1000e113" @default.
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