The immediate metabolism of oxycodone in humans is as follows:
N-Demethylation to noroxycodone predominantly via CYP3A4
O-Demethylation to oxymorphone predominantly via CYP2D6
6-Ketoreduction to 6α- and 6β-oxycodol
N-Oxidation to oxycodone-N-oxideIn humans, N-demethylation of oxycodone to noroxycodone by CYP3A4 is the major metabolic pathway, accounting for 45% ± 21% of a dose of oxycodone, while O-demethylation of oxycodone into oxymorphone by CYP2D6 and 6-ketoreduction of oxycodone into 6-oxycodols represent relatively minor metabolic pathways, accounting for 11% ± 6% and 8% ± 6% of a dose of oxycodone, respectively.Several of the immediate metabolites of oxycodone are subsequently conjugated with glucuronic acid and excreted in the urine. 6α-Oxycodol and 6β-oxycodol are further metabolized by N-demethylation to nor-6α-oxycodol and nor-6β-oxycodol, respectively, and by N-oxidation to 6α-oxycodol-N-oxide and 6β-oxycodol-N-oxide (which can subsequently be glucuronidated as well). Oxymorphone is also further metabolized, as follows:
3-Glucuronidation to oxymorphone-3-glucuronide predominantly via UGT2B7
6-Ketoreduction to 6α-oxymorphol and 6β-oxymorphol
N-Demethylation to noroxymorphoneThe first pathway of the above three accounts for 40% of the metabolism of oxymorphone, making oxymorphone-3-glucuronide the main metabolite of oxymorphone, while the latter two pathways account for less than 10% of the metabolism of oxymorphone. After N-demethylation of oxymorphone, noroxymorphone is further glucuronidated to noroxymorphone-3-glucuronide.Because oxycodone is metabolized by the cytochrome P450 system in the liver, its pharmacokinetics can be influenced by genetic polymorphisms and drug interactions concerning this system, as well as by liver function. Some people are fast metabolizers of oxycodone, while others are slow metabolizers, resulting in polymorphism-dependent alterations in relative analgesia and toxicity.
Transverse vaginal septum: A transverse vaginal septum is another medical condition whereby an extra horizontal wall of tissue that has formed during embryological development creates a blockage in the vagina. Transverse vaginal septa are relatively rare anomalies, occurring in about 1 in 70,000 girls. The diagnosis can be made at various ages, from neonates presenting with hydrocolpos to young women presenting with primary amenorrhea and pelvic pain due to the development of hematocolpos. Often, women might have a normal hymeneal opening but this wall of tissue might be blocking the access to the vaginal canal. A small opening in the septum called the fenestration allows the menstrual blood to flow out of the vagina. However, it takes longer than the usual menstrual cycle. For the women who do not have a fenestration, blood will pool in the upper vagina and this would lead to serious abdominal pain. This also results in infertility. Treatment
As the causes for Hematocolpos are diverse, there are different surgical treatments which needs to be undertaken to cure it. Surgical interventions for congenital cervical atresia range from complete hysterectomy with canalization to conservative options, such as uterine cavity catheterization.For the women who have an imperforate hymen, a minor surgery is required incising the extra hymen membrane. It is generally treated surgically, with a hymenotomy or other surgery to remove any tissue that blocks the menstrual flow.