People are cautioned to seek immediate medical care if symptoms such as irregular heartbeat/palpitations, shortness of breath, dizziness, or fainting occur while taking ondansetron. Overdose
No specific treatment is available for ondansetron overdose; people are managed with supportive measures. An antidote to ondansetron is not known. Pharmacology
Pharmacodynamics
Ondansetron is a highly selective serotonin 5-HT3 receptor antagonist, with low affinity for dopamine receptors. The 5-HT3 receptors are present both peripherally on vagal nerve terminals and centrally in the chemoreceptor trigger zone of the area postrema in the medulla. Serotonin is released by the enterochromaffin cells of the small intestine in response to chemotherapeutic agents and may stimulate vagal afferents (via 5-HT3 receptors) to initiate the vomiting reflex. It is thought that ondansetrons antiemetic action is mediated mostly via antagonism of vagal afferents with a minor contribution from antagonism of central receptors. Pharmacokinetics
Ondansetron may have a degree of peripheral selectivity due to binding to P-glycoprotein and efflux out of the brain at the blood–brain barrier. History
Ondansetron (marketed under the brand name Zofran) was developed in the mid-1980s by GlaxoSmithKline in London. It was granted US patent protection in September 1987, received a use patent June 1988, and was approved by the US FDA in January 1991. It was granted another divisional patent in November 1996. Finally, owing to GlaxoSmithKlines research on pediatric use, ondansetrons patent protection was extended until December 2006.
Stored triglycerides in the adipocytes are released and split by pancreatic lipases into fatty acids and glycerol molecules. The resultant fatty acids react with extracellular calcium to make calcium soaps (i.e. fatty acid salts) that give fat necrosis its characteristic chalky-white appearance. Fat necrosis is an example of dystrophic calcification because the calcification occurs at normal serum calcium levels.Besides pancreatitis, fat necrosis is also associated with conditions such as pancreatic carcinoma and pancreatic trauma. Although the peripancreatic region is the most commonly affected site in pancreatic disease (due to direct contact with enzymes), associated fat necrosis can occur around the body in subcutaneous tissue, hand and foot joints, and bone marrow. These extrapancreatic complications are known as pancreatic panniculitis.Beyond saponification and calcification, fat necrosis concludes with fibrosis and the formation of grey-yellow scar tissue. It is also possible for calcification to occur around the edges of a fatty necrotic lesion, enclosing the fat in a cyst. These "oil cysts" may persist for months to years without undergoing fibrosis. This is often the case in breast fat necrosis, where the underlying oil cysts can be visualised using sonography, X-Ray, CT, or MRI. Diagnosis
Although fat necrosis can be diagnosed through a routine checkup with a physician, called a physical, a patient can also perform a physical checkup on themselves. For additional diagnosis, a physician would request one or more of the following scans or tests.