what is oxycodone 30 mg ?
Oxycodone is used for managing moderate to severe acute or chronic pain when other treatments are not sufficient. It may improve quality of life in certain types of pain. It is unclear if use in chronic pain results in improved quality of life or ongoing pain relief.
Oxycodone is available as a controlled-release tablet, intended to be taken every 12 hours. A July 1996 study independent of Purdue Pharma, the drug's originator, found the controlled-release formulation had a variable duration of action ranging from 10 to 12 hours. A 2006 review found that controlled-release oxycodone is comparable to immediate-release oxycodone, morphine, and hydromorphone in management of moderate to severe cancer pain, with fewer side effects than morphine. The author concluded that the controlled-release form is a valid alternative to morphine and a first-line treatment for cancer pain. In 2014, the European Association for Palliative Care recommended oxycodone by mouth as a second-line alternative to morphine by mouth for cancer pain.
In the U.S., extended-release oxycodone is approved for use in children as young as eleven years old. The approved uses are for the relief of cancer pain, trauma pain, or pain due to major surgery, in children already treated with opioids, who can tolerate at least 20 mg per day of oxycodone; this provides an alternative to Duragesic (fentanyl), the only other extended-release opioid analgesic approved for children.
Most common side effects of oxycodone include reduced sensitivity to pain, delayed gastric emptying, euphoria, anxiolysis, feelings of relaxation, and respiratory depression Common side effects of oxycodone include constipation nausea vomiting somnolence dizziness , itching dry mouth and sweating Less common side effects (experienced by less than of patients) include loss of appetite, nervousness, abdominal pain, diarrhea, urinary retention, dyspnea, and hiccups. Most side effects generally become less intense over time, although issues related to constipation are likely to continue for the duration of use. Oxycodone in combination with naloxone in managed-release tablets, has been formulated to both deter abuse and reduce "opioid-induced constipation".
Oxycodone, a semi-synthetic opioid, is a highly selective full agonist of the μ-opioid receptor (MOR).[34][35] This is the main biological target of the endogenous opioid neuropeptide β-endorphin.[16] Oxycodone has low affinity for the δ-opioid receptor (DOR) and the κ-opioid receptor (KOR), where it is an agonist similarly.[34][35] After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by decreasing the amount of cAMP produced, closing calcium channels, and opening potassium channels.[56] Opioids like oxycodone are thought to produce their analgesic effects via activation of the MOR in the midbrain periaqueductal gray (PAG) and rostral ventromedial medulla (RVM). Conversely, they are thought to produce reward and addiction via activation of the MOR in the mesolimbic reward pathway, including in the ventral tegmental area, nucleus accumbens, and ventral pallidum.[58][59] Tolerance to the analgesic and rewarding effects of opioids is complex and occurs due to receptor-level tolerance (e.g., MOR downregulation), cellular-level tolerance (e.g., cAMP upregulation), and system-level tolerance (e.g., neural adaptation due to induction of ΔFosB expression).[60]
Taken orally, 20 mg of immediate-release oxycodone is considered to be equivalent in analgesic effect to 30 mg of morphine,while extended release oxycodone is considered to be twice as potent as oral morphine.
Similarly to most other opioids, oxycodone increases prolactin secretion, but its influence on testosterone levels is unknown. Unlike morphine, oxycodone lacks immunosuppressive activity (measured by natural killer cell activity and interleukin 2 production in vitro); the clinical relevance of this has not been clarified.
Active metabolites
A few of the metabolites of oxycodone have also been found to be active as MOR agonists, some of which notably have much higher affinity for (as well as higher efficacy at) the MOR in comparison.[64][65][66] Oxymorphone possesses 3- to 5-fold higher affinity for the MOR than does oxycodone,[8] while noroxycodone and noroxymorphone possess one-third of and 3-fold higher affinity for the MOR, respectively,[8][66] and MOR activation is 5- to 10-fold less with noroxycodone but 2-fold higher with noroxymorphone relative to oxycodone.Noroxycodone, noroxymorphone, and oxymorphone also have longer biological half-lives than oxycodone
Oxycodone is available as a controlled-release tablet, intended to be taken every 12 hours. A July 1996 study independent of Purdue Pharma, the drug's originator, found the controlled-release formulation had a variable duration of action ranging from 10 to 12 hours. A 2006 review found that controlled-release oxycodone is comparable to immediate-release oxycodone, morphine, and hydromorphone in management of moderate to severe cancer pain, with fewer side effects than morphine. The author concluded that the controlled-release form is a valid alternative to morphine and a first-line treatment for cancer pain. In 2014, the European Association for Palliative Care recommended oxycodone by mouth as a second-line alternative to morphine by mouth for cancer pain.
In the U.S., extended-release oxycodone is approved for use in children as young as eleven years old. The approved uses are for the relief of cancer pain, trauma pain, or pain due to major surgery, in children already treated with opioids, who can tolerate at least 20 mg per day of oxycodone; this provides an alternative to Duragesic (fentanyl), the only other extended-release opioid analgesic approved for children.
Most common side effects of oxycodone include reduced sensitivity to pain, delayed gastric emptying, euphoria, anxiolysis, feelings of relaxation, and respiratory depression Common side effects of oxycodone include constipation nausea vomiting somnolence dizziness , itching dry mouth and sweating Less common side effects (experienced by less than of patients) include loss of appetite, nervousness, abdominal pain, diarrhea, urinary retention, dyspnea, and hiccups. Most side effects generally become less intense over time, although issues related to constipation are likely to continue for the duration of use. Oxycodone in combination with naloxone in managed-release tablets, has been formulated to both deter abuse and reduce "opioid-induced constipation".
Oxycodone, a semi-synthetic opioid, is a highly selective full agonist of the μ-opioid receptor (MOR).[34][35] This is the main biological target of the endogenous opioid neuropeptide β-endorphin.[16] Oxycodone has low affinity for the δ-opioid receptor (DOR) and the κ-opioid receptor (KOR), where it is an agonist similarly.[34][35] After oxycodone binds to the MOR, a G protein-complex is released, which inhibits the release of neurotransmitters by the cell by decreasing the amount of cAMP produced, closing calcium channels, and opening potassium channels.[56] Opioids like oxycodone are thought to produce their analgesic effects via activation of the MOR in the midbrain periaqueductal gray (PAG) and rostral ventromedial medulla (RVM). Conversely, they are thought to produce reward and addiction via activation of the MOR in the mesolimbic reward pathway, including in the ventral tegmental area, nucleus accumbens, and ventral pallidum.[58][59] Tolerance to the analgesic and rewarding effects of opioids is complex and occurs due to receptor-level tolerance (e.g., MOR downregulation), cellular-level tolerance (e.g., cAMP upregulation), and system-level tolerance (e.g., neural adaptation due to induction of ΔFosB expression).[60]
Taken orally, 20 mg of immediate-release oxycodone is considered to be equivalent in analgesic effect to 30 mg of morphine,while extended release oxycodone is considered to be twice as potent as oral morphine.
Similarly to most other opioids, oxycodone increases prolactin secretion, but its influence on testosterone levels is unknown. Unlike morphine, oxycodone lacks immunosuppressive activity (measured by natural killer cell activity and interleukin 2 production in vitro); the clinical relevance of this has not been clarified.
Active metabolites
A few of the metabolites of oxycodone have also been found to be active as MOR agonists, some of which notably have much higher affinity for (as well as higher efficacy at) the MOR in comparison.[64][65][66] Oxymorphone possesses 3- to 5-fold higher affinity for the MOR than does oxycodone,[8] while noroxycodone and noroxymorphone possess one-third of and 3-fold higher affinity for the MOR, respectively,[8][66] and MOR activation is 5- to 10-fold less with noroxycodone but 2-fold higher with noroxymorphone relative to oxycodone.Noroxycodone, noroxymorphone, and oxymorphone also have longer biological half-lives than oxycodone
However, despite the greater in vitro activity of some of its metabolites, it has been determined that oxycodone itself is responsible for 83.0% and 94.8% of its analgesic effect following oral and intravenous administration, respectively.[65] Oxymorphone plays only a minor role, being responsible for 15.8% and 4.5% of the analgesic effect of oxycodone after oral and intravenous administration, respectively.[65] Although the CYP2D6 genotype and the route of administration result in differential rates of oxymorphone formation, the unchanged parent compound remains the major contributor to the overall analgesic effect of oxycodone.[65] In contrast to oxycodone and oxymorphone, noroxycodone and noroxymorphone, while also potent MOR agonists, poorly cross the blood–brain barrier into the central nervous system, and for this reason are only minimally analgesic in comparison