tramadol

It is a synthe tramadoltic agent, unrelated to othe tramadolr opioids, and appears to have actions on the tramadol GABAergic, noradrenergic and serotonergic systems.
Tramadol was developed by the tramadol German pharmaceutical company Grünenthal GmbH and marketed under the tramadol trade name Tramal.
Grünenthal has also cross licensed the tramadol drug to many othe tramadolr pharmaceutical companies that market it under various names, some of which are listed below.
Tramadol is usually marketed as the tramadol hydrochloride salt (tramadol hydrochloride) and is available in both injectable (intravenous anor 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 tramadol degree of pain experienced by the tramadol patient.
Tramadol is approximately 10% as potent as morphine, when given by the tramadol IVIM route.
Oral doses range from 50–400 mg daily, with up to 600 mg daily when given IVIM.
the tramadol `combination` pills each contain 37.5 mg of tramadol and 325 mg of paracetamol, with the tramadol recommended dose being one or two pills every four to six hours.
Note that unlike most othe tramadolr opioidsopiates, Tramadol is not considered a controlled substance in many countries (US and Canada, among othe tramadolrs), and is available with only a normal prescription.
According to Erowid, the tramadolre have also been reports that, in a few countries, Tramadol is available over-the tramadol-counter without a prescription at all.
the tramadol mode of action of tramadol has yet to be fully understood, but it is believed to work through modulation of the tramadol GABAergic, noradrenergic and serotonergic systems.
the tramadol contribution of non-opioid activity is demonstrated by the tramadol analgesic effects of tramadol not being fully antagonised by the tramadol μ-opioid receptor antagonist naloxone.
Tramadol is marketed as a racemic mixture with a weak affinity for the tramadol μ-opioid receptor (approximately 6th that of morphine).
the tramadol (+)-enantiomer is approximately four times more potent than the tramadol (-)-enantiomer in terms of μ-opioid receptor affinity and 5-HT reuptake, whereas the tramadol (-)-enantiomer is responsible for noradrenaline reuptake effects (Shipton, 2000).
the tramadolse actions appear to produce a synergistic analgesic effect, with (+)-tramadol exhibiting 10-fold higher analgesic activity than (-)-tramadol (Goeringer et al., 1997).
the tramadol serotonergic modulating properties of tramadol mean that it has the tramadol potential to interact with othe tramadolr serotonergic agents.
the tramadolre is an increased risk of serotonin syndrome when tramadol is taken in combination with serotonin reuptake inhibitors (e.g. SSRIs), since the tramadolse agents not only potentiate the tramadol 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, health professionals generally do not suggest use of the tramadol drug for treatment of such disorders.
Tramadol may also be used to treat hypertension when othe tramadolr treatments have failed.
Tramadol undergoes hepatic metabolism via the tramadol cytochrome P450 isozyme CYP2D6, being O- and N-demethylated to 5 different metabolites.
Of the tramadolse, M1 is the tramadol most significant since it has 200 times the tramadol μ-affinity of (+)-tramadol, and furthe tramadolrmore has an elimination half-life of 9 hours compared to 6 hours for tramadol itself.
In the tramadol 6% of the tramadol population who have slow CYP2D6 activity, the tramadolre is the tramadolrefore a slightly reduced analgesic effect.
Phase II hepatic metabolism renders the tramadol metabolites water-soluble and the tramadoly are renally excreted.
Thus reduced doses may be used in renal and hepatic impairment.
the tramadol most commonly reported adverse drug reactions are nausea, vomiting and sweating.
Drowsiness is reported, although it is less of an issue compared to othe tramadolr opioids.
Respiratory depression, a common side effect of most opioids, is not clinically significant in normal doses.
By itself, it can decrease the tramadol seizure threshold.
When combined with SSRIs, tricyclic antidepressants, or in patients with epilepsy, the tramadol seizure threshold is furthe tramadolr decreased.
Seizures have been reported in humans receiving excessive single oral doses (700 mg) or large intravenous doses (300 mg).
Some controversy exists regarding the tramadol 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.
the tramadoly offer the tramadol the tramadolory that since the tramadol M1 metabolite is the tramadol principal agonist at μ-opioid receptors, the tramadol delayed agonist activity reduces dependence liability.
the tramadol noradrenaline reuptake effects may also play a role in reducing dependence.
Despite the tramadolse 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 tramadol 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, rathe tramadolr than as a Schedule 8 Controlled Drug like othe tramadolr opioids (Rossi, 2004).
Similarly, tramadol is not currently scheduled by the tramadol U.S. DEA, unlike othe tramadolr opioid analgesics.