What is/are Oxycodone?
Oxycodone is a semi-synthetic opioid synthesized from poppy-derived thebaine. It is a narcotic analgesic generally indicated for relief of moderate to severe pain. It was developed in 1916 in Germany as one of several new semi-synthetic opioids in an attempt to improve on the existing opioids.
Oxycodone is available as single ingredient medication in immediate release and controlled release. Combination products formulated with non-narcotic ingredients such as NSAIDs and paracetamol are also available as immediate release formulation.
Oxycodone has been in clinical use since 1917. and it is used for managing moderate to moderately severe acute or chronic pain.It has been found to improve quality of life for those with many types of pain.
Controlled release oral tablet form is indicated for cancer and other chronic pains and intended to be taken every 12 hours. Immediate release forms are used more commonly for management of moderate pain. An Italian study concluded from investigating multiple studies that controlled release oxycodone is comparable to instant release oxycodone, morphine and hydromorphone in management of moderate to severe cancer pain. It indicated that side effect appears to be lesser than morphine and that it is a valid alternative to morphine and a first-line treatment for cancer pain.
In 2001, the European Association for Palliative Care recommended that oral oxycodone could be taken as a second-line alternative to oral morphine for cancer pain.
Oxycodone can be administered by parenteral or oral route.
Starting dose of 5–15 mg oral every 4 to 6 hours or 10 mg controlled release every 12 hours.
Maintenance dose of 10–30 mg every 4 hours or 20–640 mg controlled release form oxycodone per day for cancer pain with indication to use immediate release tablets as needed for break-through pain.
Common side effects include constipation, fatigue, dizziness, nausea, vomiting, dry mouth, anxiety, itching, and sweating.Less common side effects (experienced by less than 5% of patients) include loss of appetite, nervousness, abdominal pain, diarrhea, urine retention, dyspnea, and hiccups,
In high doses, overdoses, or in patients not tolerant to opiates, oxycodone can cause shallow breathing, bradycardia, cold-clammy skin, apnea, hypotension, miosis, circulatory collapse, respiratory arrest, and death.
Dependence, addiction and withdrawal
The risk of experiencing severe withdrawal symptoms is high if a patient has become physically dependent or addicted and discontinues oxycodone abruptly. Therefore, particularly in cases where the drug has been taken regularly over an extended period of time, use should be discontinued gradually rather than abruptly. People who use oxycodone in a recreational, hazardous, or harmful fashion (not as intended by the prescribing physician) are at even higher risk of severe withdrawal symptoms, as they tend to use higher-than-prescribed doses. The symptoms of oxycodone withdrawal are the same as for other opiate-based painkillers, and may include "anxiety, panic attack, nausea, insomnia, muscle pain, muscle weakness, fevers, and other flu-like symptoms".
Withdrawal symptoms have also been reported in newborns whose mothers had been either injecting or orally taking oxycodone during pregnancy.
Detection in biological fluids
Oxycodone and/or its major metabolites may be measured in blood or urine to monitor for clearance, abuse, confirm a diagnosis of poisoning, or assist in a medicolegal death investigation. Many commercial opiate screening tests cross-react appreciably with oxycodone and its metabolites, but chromatographic techniques can easily distinguish oxycodone from other opiates.
Mechanism of action
In 1997, a group of Australian researchers proposed (based on a study in rats) that oxycodone acts on κ-opioid receptors, unlike morphine, which acts upon μ-opioid receptors. Further research by this group indicated the drug appears to be a κ2b-opioid agonist. However, this conclusion has been disputed, primarily on the basis that oxycodone produces effects that are typical of μ-opioid agonists, mainly because oxycodone is metabolized in the liver to oxymorphone as a metabolite, which is a more potent opioid agonist with stronger/higher binding affinity to μ-opioid receptors compared to oxycodone.
In 2006, research by a Japanese group suggested the effect of oxycodone is mediated by different receptors in different situations. Specifically in diabetic mice, the κ-opioid receptor appears to be involved in the antinociceptive effects of oxycodone, while in nondiabetic mice, the μ1-opioid receptor seems to be primarily responsible for these effects.
This article uses material from the Wikipedia article Oxycodone, which is released under the Creative Commons Attribution-Share-Alike License 3.0.