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On oxycodone - Research Paper Example

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Oxycodone is basically an opioid-narcotic pain reliever, belonging to analgesic medication, and is synthesized from opium alkaloid thebaine (PubMed Health, 2012). Oxycodone is identified by brand names like OxyContin, OxyIR, Roxicodone, and Roxicodone. In terms of class and…
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Oxycodone Oxycodone Oxycodone is basically an opioid-narcotic pain reliever, belonging to analgesic medication, and is synthesized from opium alkaloid thebaine (PubMed Health, 2012). Oxycodone is identified by brand names like OxyContin, OxyIR, Roxicodone, and Roxicodone. In terms of class and category, Oxycodone is tagged as schedule II narcotic analgesic. It is a powerful narcotic pain-reliever, as well as being a cough suppressant just like morphine, or hydrocodone (National Institutes of Health, 2012). It is devised as sole ingredient compound mixed with acetaminophenl, or with ibuprofen and existing as generics. Oxycodone mechanism of action, entails stimulation of opioid-receptors inside an individual brain. Notably, it does not purge sensation of pain, but minimizes discomfort through increasing tolerance for pain. It also results in sedation plus respiratory depression (MedlinePlus, 2012).
(National Institutes of Health, 2012)
The key therapeutic intention of Oxycodone is to alleviate modest to relentless pain, and to enhance effectiveness of particular anesthesia drugs. It offers pain relief through binding to receptors located in spinal cord and brain, specifically the opiate receptors. Therefore, once the opiate receptors are blocked, it triggers discharge of dopamine from the brain (Portenoy & et al, 2007). Oxycodone is highly addictive, and can result in abuse plus dependency. Repeated use can result in the development of tolerance, and the prescribed dose will no longer be effective in creating intended results.
Unintended use mostly involves managing respiratory depression, by trying to experience a sense of euphoria, in addition to to holding back withdrawal symptoms, and as such, many of its abusers turn to heroin (Roth & etal, 2000). Users seek its euphoric, but relentless withdrawal effects together with its sedative property, since its high opioid content makes it to be absorbed over an extensive period. They then become mentally and physically reliant on it. The sensation sought by users, especially those with chronic disruptive pulmonary ailments and respiratory depression, involves decreasing their respiratory impel, and this simply results in apnea. It also causes severe hypotension, since it compromises the capacity to maintain blood pressure, while producing orthostatic hypotension (Riley & et al, 2008). Thus, vasodilatation generated by Oxycodone further diminishes cardiac output along with blood pressure.
Consequences of prolonged use include reduced levels of testosterone and enlargement of prostate. Other long term effects include disproportionate sweating, inflammation of arms and legs, central nervous system hyperactivity, in addition to chronic constipation (Kalso, 2005). It has traumatic psychological outcomes, and which impact the user memory, mood, plus cognition. This is because it affects brain chemicals, referred to as neurotransmitters, in addition to brain reward pathways. Oxycodone makes the brain to correlate its triggers and cues with pleasure. Thus, the brain chemistry is altered to fit dopamine levels, even as its sensitivity to pain increases. It also results in emotional problems, such as delusions effects and cognitive disruptions, thus, resulting in disorientation or confusion. Furthermore, it set off mood swings, panic attacks, long term sleep disorders and clinical depression (PubMed Health, 2012).
Oxycodone is classified as Schedule II and it is illegal to vend without DEA license or prescription. The FDA Unapproved Drugs Initiative has only approved certain drugs which contain Oxycodone (PubMed Health, 2012). Oxycodone functions by acting as a fragile agonist on mu, kappa, plus delta opioid-receptors in the CNS (Kalso, 2005). Thus, the binding of oxycodone opiate, excites the swap of GTP for GDP within G-protein complex, and it decreases the intracellular cAMP and adenylat-cyclase effectors, located on plasma-membrane inner, since it inhibits adenylate cyclase (Roth & et al, 2000). Consequently, release of nociceptive-neurotransmitters, like GABA, acetylcholine, as well as noradrenaline is inhibited. Furthermore, it inhibits discharge of vasopressin, insulin, and somatostatin. Oxycodone closes the N-type voltage-functioning calcium channels, while opening calcium-reliant inwardly. Hence, this in the end rectifies, mu plus delta receptor agonist, resulting in hyperpolarization, together with decreased neuronal excitability. It normally impacts mu-type opioid receptor in the brain and in vivo studies reveal it is an μ-opioid receptor agonist, that is why it creates analgesia effect, euphoria effect, and dependence (Riley & et al, 2008).
Oxycodone is taken as oral dosage, or controlled-release tablets or parenteral dose, usually, 60%- 87% of oral dosage oxycodone reaches CNS compartment, compared to a parenteral dose (Portenoy & et al, 2007). Oxycodone has an elevated oral-bioavailability is owing to its low pre-systemic metabolism. Its absorption half-live is between 0.6-6.9 hours (Roth & et al, 2000). Its steady-state level of distribution is 2.6 L/kg to skeletal muscle, lungs, and the brain, and it is broken down inside the liver, before passing out of the body through the kidney into urine. Oxycodone is broadly metabolized through numerous metabolic pathways, so as to create noroxycodone, the oxymorphone plus noroxymorphone. Afterwards it is glucuronidated. CYP3A interceded Ndemethylation, toward noroxycodone is the prime metabolic trail of oxycodone (Portenoy & et al, 2007).
Oxycodone when used for a while makes the body to develop natural tolerance to it, and that is why in some people, it makes them to constantly increase the dose, so as to acquire similar effect. Thus, the increased tolerance easily results in dependence and this creates addiction. Physical dependence leads to withdrawal symptoms, with the most common side effect being, dizziness, loss of appetite, breathing difficulty, dry mouth and nausea (PubMed Health, 2012). Oxycodone tablets are contraindicated in patients having hypersensitivity toward opioid analgesic, especially those with considerable respiratory depression, or severe bronchial asthma and hypercarbia (MedlinePlus, 2012).
Standard therapeutic amount of Oxycodone can decrease respiratory push, leading to apnea. It also results in orthostatic hypotension when used in ambulatory patients. Its physiological effect is centered on CNS, and this decreases action of intestinal tract leading to constipation. Its respiratory distress symptoms comprises, complicatedness breathing, euphoria, nausea and dizziness. Others include itchy skin, vomiting, and general body weakness. Oxycodone toxic level is .05 mg/L, and it has no known adverse effect on fetus with the only probable side effect being potential for withdrawal, and respiratory depression of the baby after birth (Roth & et al, 2000). Pharmacological treatment guidelines involve using narcotic antagonists, such as naloxone, and nalmefene as antidotes. Thus, appropriate amount of naloxone hydrochloride and nalmefene should be done simultaneously, with focus being on respiratory resuscitation. Also, gastric emptying is helpful in eliminating unabsorbed oxycodone (Kalso, 2005).
Kalso, E. (2005). Oxycodone. J Pain Symptom Manage , 29 (5), S47-56.
MedlinePlus. (2012). Oxycodone . Retrieved December 4, 2012, from
National Institutes of Health. (2012). Oxycodone Hydrochloride - oxycodone hydrochloride capsule . Retrieved December 5, 2012, from
Portenoy, R., & et al. (2007). Long-term use of controlled-release oxycodone for noncancer pain: results of a 3-year registry study. Clin J Pain , 23 (4), 287-299.
PubMed Health. (2012). Oxycodone. Retrieved December 05, 2012, from
Riley, J., & et al. (2008). Oxycodone: a review of its use in the management of pain. Curr Med Res Opin , 24 (1), 175-192.
Roth, S. H., & et al. (2000). Around-the-clock, controlled-release oxycodone therapy for osteoarthritis-related pain: placebo-controlled trial and long-term evaluation. Arch Intern Med , 160 (6), 853-860. Read More
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