Biliary dyskinesia is a disorder of some component of biliary part of the digestive system in which bile cannot physically move in the proper direction through the tubular biliary tract. It most commonly involves abnormal biliary tract peristalsis muscular coordination within the gallbladder in response to dietary stimulation of that organ to squirt the liquid bile through the common bile duct into the duodenum. Ineffective peristaltic contraction of that structure produces postprandial (after meals) right upper abdominal pain (cholecystodynia) and almost no other problem. When the dyskinesia is localized at the biliary outlet into the duodenum just as increased tonus of that outlet sphincter of Oddi, the backed-up bile can cause pancreatic injury with abdominal pain more toward the upper left side. In general, biliary dyskinesia is the disturbance in the coordination of peristaltic contraction of the biliary ducts, and/or reduction in the speed of emptying of the biliary tree into the duodenum. Mechanism
Normally, the downstream gallbladder stores and concentrates the bile which originates in liver hepatocyte cells and is released into the microscopic component of the biliary system by the liver. Through aggregating tubules of increasing diameter, the bile leaves the liver and reaches the upstream (proximal) component of the common bile duct. Apparently, the common bile duct beyond (distal to) the gallbladder tends to normally have a greater tone so that the bile backs up into the gallbladder. When bile enters the duodenum (the first part of the small intestine), it aids in digesting the fat within food leaving the stomach.
There is no specific antidote to barbiturate overdose; treatment is supportive, generally  including the administration of intravenous saline, naloxone, thiamine, glucose, sodium bicarbonate to alkalize the urine and increase rate of excretion, and activated charcoal via nasogastric tube.Acetaminophen exerts its toxicity through the production of a toxic metabolite that can cause liver damage at doses as low as four grams. Larger doses can precipitate acute liver failure, acute kidney injury, or gastrointestinal bleeding; death has been known to occur with ingestion of ten to fifteen grams. The specific antidote to acetaminophen overdose is N-acetylcysteine. Mechanism of action
Butalbital exerts a generalized depressant effect on the central nervous system and, in very high doses, has peripheral effects. Acetaminophen has analgesic and antipyretic effects mediated by a metabolite that acts at cannabinoid receptors. Caffeine is thought to produce constriction of cerebral blood vessels and serves to counteract the sedative effect of butalbital.Butalbital has a half-life of about 35 hours. Acetaminophen has a half-life of about 1.25 to 3 hours, but may be increased by liver damage and after an overdose. Caffeine has a half-life of about 2.5 to 4.5 hours. References
External links
"Acetaminophen mixture with butalbital". Drug Information Portal. U.S. National Library of Medicine. "Acetaminophen mixture with butalbital and caffeine". Drug Information Portal. U.S. National Library of Medicine.