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IC Tramadol?
- Thread starter JKurz1
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mikefear
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Tramadol (INN) (IPA: [ˈtræməˌdɒl]) is an atypical opioid which is a centrally acting analgesic, used for treating moderate to severe pain. It is a synthetic agent, unrelated to other opioids, and appears to have actions on the GABAergic, noradrenergic and serotonergic systems. Tramadol was developed by the German pharmaceutical company Grünenthal GmbH and marketed under the trade name Tramal. Grünenthal has also cross licensed the drug to many other pharmaceutical companies that market it under various names, some of which are listed below.
Tramadol is usually marketed as the hydrochloride salt (tramadol hydrochloride) and is available in both injectable (intravenous and/or intramuscular) and oral preparations (e.g. Zydol® in UK and Ultram® in US). It is also available in conjunction with paracetamol (acetaminophen) as Ultracet® or Tramacet®.
Dosages vary depending on the degree of pain experienced by the patient. Tramadol is approximately 10% as potent as morphine, when given by the IV/IM route. Oral doses range from 50–400 mg daily, with up to 600 mg daily when given IV/IM. The 'combination' pills each contain 37.5 mg of tramadol and 325 mg of paracetamol, with the recommended dose being one or two pills every four to six hours.
The mode of action of tramadol has yet to be fully elucidated, but it is believed to work through modulation of the GABAergic, noradrenergic and serotonergic systems. The contribution of non-opioid activity is demonstrated by the analgesic effects of tramadol not being fully antagonised by the μ-opioid receptor antagonist naloxone.
Tramadol is marketed as a racemic mixture with a weak affinity for the μ-opioid receptor (approximately 1/6000th that of morphine). The (+)-enantiomer is approximately four times more potent than the (-)-enantiomer in terms of μ-opioid receptor affinity and 5-HT reuptake, whereas the (-)-enantiomer is responsible for noradrenaline reuptake effects (Shipton, 2000). These actions appear to produce a synergistic analgesic effect, with (+)-tramadol exhibiting 10-fold higher analgesic activity than (-)-tramadol (Goeringer et al., 1997).
The serotonergic modulating properties of tramadol mean that it has the potential to interact with other serotonergic agents. There is an increased risk of serotonin syndrome when tramadol is taken in combination with serotonin reuptake inhibitors (e.g. SSRIs), since these agents not only potentiate the effect of 5-HT but also inhibit tramadol's metabolism.
It is suggested that tramadol could be effective for alleviating symptoms of depression and anxiety because of its action on GABAergic, noradrenergic and serotonergic systems. However, use of the drug for treatment of such disorders by a health professional is unlikely.
Tramadol may also be used to treat hypertension when other treatments have failed.
Tramadol undergoes hepatic metabolism via the cytochrome P450 isozyme CYP2D6, being O- and N-demethylated to 5 different metabolites. Of these, M1 is the most significant since it has 200 times the μ-affinity of (+)-tramadol, and furthermore has an elimination half-life of 9 hours compared to 6 hours for tramadol itself. In the 6% of the population who have slow CYP2D6 activity, there is therefore a slightly reduced analgesic effect. Phase II hepatic metabolism renders the metabolites water-soluble and they are renally excreted. Thus reduced doses may be used in renal and hepatic impairment.
The most commonly reported adverse drug reactions are nausea, vomiting and sweating. Drowsiness is reported, although it is less of an issue compared to other opioids. Respiratory depression, a common side effect of most opioids, is not clinically significant in normal doses. By itself, it does not decrease the seizure threshold, though it may do so if used in combination with SSRIs, tricyclic antidepressants, or in patients with epilepsy. A few seizures have been reported in humans receiving excessive single oral doses (700 mg) or large intravenous doses (300 mg).
Some controversy exists regarding the dependence liability of tramadol. Grünenthal has promoted it as an opioid with a low risk of dependence compared to traditional opioids, claiming little evidence of such dependence in clinical trials. They offer the theory that since the M1 metabolite is the principal agonist at μ-opioid receptors, the delayed agonist activity reduces dependence liability. The noradrenaline reuptake effects may also play a role in reducing dependence.
Despite these claims it is apparent, in community practice, that dependence to this agent does occur. This would be expected since analgesic and dependence effects are mediated by the same μ-opioid receptor. However, this dependence liability is considered relatively low by health authorities, such that tramadol is classified as a Schedule 4 Prescription Only Medicine in Australia, rather than as a Schedule 8 Controlled Drug like other opioids (Rossi, 2004). Similarly, tramadol is not currently scheduled by the U.S. DEA, unlike other opioid analgesics. Nevertheless, the Prescribing Information for Ultram warns that tramadol "may induce psychological and physical dependence of the morphine-type."
Tramadol is usually marketed as the hydrochloride salt (tramadol hydrochloride) and is available in both injectable (intravenous and/or intramuscular) and oral preparations (e.g. Zydol® in UK and Ultram® in US). It is also available in conjunction with paracetamol (acetaminophen) as Ultracet® or Tramacet®.
Dosages vary depending on the degree of pain experienced by the patient. Tramadol is approximately 10% as potent as morphine, when given by the IV/IM route. Oral doses range from 50–400 mg daily, with up to 600 mg daily when given IV/IM. The 'combination' pills each contain 37.5 mg of tramadol and 325 mg of paracetamol, with the recommended dose being one or two pills every four to six hours.
The mode of action of tramadol has yet to be fully elucidated, but it is believed to work through modulation of the GABAergic, noradrenergic and serotonergic systems. The contribution of non-opioid activity is demonstrated by the analgesic effects of tramadol not being fully antagonised by the μ-opioid receptor antagonist naloxone.
Tramadol is marketed as a racemic mixture with a weak affinity for the μ-opioid receptor (approximately 1/6000th that of morphine). The (+)-enantiomer is approximately four times more potent than the (-)-enantiomer in terms of μ-opioid receptor affinity and 5-HT reuptake, whereas the (-)-enantiomer is responsible for noradrenaline reuptake effects (Shipton, 2000). These actions appear to produce a synergistic analgesic effect, with (+)-tramadol exhibiting 10-fold higher analgesic activity than (-)-tramadol (Goeringer et al., 1997).
The serotonergic modulating properties of tramadol mean that it has the potential to interact with other serotonergic agents. There is an increased risk of serotonin syndrome when tramadol is taken in combination with serotonin reuptake inhibitors (e.g. SSRIs), since these agents not only potentiate the effect of 5-HT but also inhibit tramadol's metabolism.
It is suggested that tramadol could be effective for alleviating symptoms of depression and anxiety because of its action on GABAergic, noradrenergic and serotonergic systems. However, use of the drug for treatment of such disorders by a health professional is unlikely.
Tramadol may also be used to treat hypertension when other treatments have failed.
Tramadol undergoes hepatic metabolism via the cytochrome P450 isozyme CYP2D6, being O- and N-demethylated to 5 different metabolites. Of these, M1 is the most significant since it has 200 times the μ-affinity of (+)-tramadol, and furthermore has an elimination half-life of 9 hours compared to 6 hours for tramadol itself. In the 6% of the population who have slow CYP2D6 activity, there is therefore a slightly reduced analgesic effect. Phase II hepatic metabolism renders the metabolites water-soluble and they are renally excreted. Thus reduced doses may be used in renal and hepatic impairment.
The most commonly reported adverse drug reactions are nausea, vomiting and sweating. Drowsiness is reported, although it is less of an issue compared to other opioids. Respiratory depression, a common side effect of most opioids, is not clinically significant in normal doses. By itself, it does not decrease the seizure threshold, though it may do so if used in combination with SSRIs, tricyclic antidepressants, or in patients with epilepsy. A few seizures have been reported in humans receiving excessive single oral doses (700 mg) or large intravenous doses (300 mg).
Some controversy exists regarding the dependence liability of tramadol. Grünenthal has promoted it as an opioid with a low risk of dependence compared to traditional opioids, claiming little evidence of such dependence in clinical trials. They offer the theory that since the M1 metabolite is the principal agonist at μ-opioid receptors, the delayed agonist activity reduces dependence liability. The noradrenaline reuptake effects may also play a role in reducing dependence.
Despite these claims it is apparent, in community practice, that dependence to this agent does occur. This would be expected since analgesic and dependence effects are mediated by the same μ-opioid receptor. However, this dependence liability is considered relatively low by health authorities, such that tramadol is classified as a Schedule 4 Prescription Only Medicine in Australia, rather than as a Schedule 8 Controlled Drug like other opioids (Rossi, 2004). Similarly, tramadol is not currently scheduled by the U.S. DEA, unlike other opioid analgesics. Nevertheless, the Prescribing Information for Ultram warns that tramadol "may induce psychological and physical dependence of the morphine-type."
Cauliflower Ear
New member
fuck pain killers...get that shit off the board...i hate them..they are the devil and they are all addictive
Um....sometimes people need painkillers for PAIN, not fun.....that seems to be his case. Temp pain reduction for a temp condition wont yield dependance in many cases (there is less dependance when actual physiological pain is present).
That said, it has some activity on the mu-opiate receptor, but doesnt have the typical opiate structure. It also has CNS effects as it acts as an SSRI. Dont take anti-depressant SSRIs with it.
Take it for your pain for a few days, then stop! No big deal. We give out pain meds in the hospital like candy, whenever a patient is in pain, the fear of addiction for legit pain is overstated......one of the big problems in hospitals is pain management or lack thereof.....we are taught that pain is a priority, so give them stuff if they need it.
That said, it has some activity on the mu-opiate receptor, but doesnt have the typical opiate structure. It also has CNS effects as it acts as an SSRI. Dont take anti-depressant SSRIs with it.
Take it for your pain for a few days, then stop! No big deal. We give out pain meds in the hospital like candy, whenever a patient is in pain, the fear of addiction for legit pain is overstated......one of the big problems in hospitals is pain management or lack thereof.....we are taught that pain is a priority, so give them stuff if they need it.
Cauliflower Ear
New member
bigrand said:
i understand..but i would rather them just smoke the chronic...that what I'm gonna do for the rest of my life after I'm done fighting...
Cauliflower Ear
New member
bigrand said:
i dont. thats why i said im goin to do it when im don fighting. I smoked a lot when i was younger...surfin all the time. I love it...but now that i am serious...finishing my bachlers, getting a job at this medical sales firm, and fighting 5-6 days a week, i dont smoke...but once ive made all my money and i retire from grappling...im gonna be the old dude ripping bong hits...in hawaii and surfin ed
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