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lobelsteve

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Could make a mint on this. But it is my kids new middle school spirit shirts.

Members don't see this ad.
 
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Members don't see this ad :)
Does the standard model come saturated with cigarette smoke and stained with chocolate hazelnut coffee, or is that optional?
Comes with Mountain Dew and Marlboro lights.
 
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I thought today was "wear purple to show your support for Fibromyalgia" day. I wear purple every day so it worked out.
 
With hyphenated name on back
 
let's not forget the ...scooter..

You call it a "scooter"?

Around here we call it a "liquor-cycle."

(Pronounced "licker-sickle")
 
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You are all awful people. This is a serious problem with no objective evidence to support impairments or restrictions and limitations.

Supported meds: Lyrica, Cymbalta, Savella, Ultram, Flexeril, Skelaxin, Zanaflex, Robaxin, Baclofen, Naltrexone.

Unsupported meds: Opiates, Soma, NSAID, BZD, Steroids.
 
You are all awful people. This is a serious problem with no objective evidence to support impairments or restrictions and limitations.

Supported meds: Lyrica, Cymbalta, Savella, Ultram, Flexeril, Skelaxin, Zanaflex, Robaxin, Baclofen, Naltrexone.

Unsupported meds: Opiates, Soma, NSAID, BZD, Steroids.


Regarding Tramadol as not included with traditional opiates:

Drugs. 1997;53 Suppl 2:18-24.
[Pharmacology of tramadol].
[Article in French]
Dayer P1, Desmeules J, Collart L.
Author information

Abstract
(+/-)-Tramadol is a synthetic 4-phenyl-piperidine analogue of codeine. It is a central analgesic with a low affinity for opioid receptors. Its selectivity for mu receptors has recently been demonstrated, and the M1 metabolite of tramadol, produced by liver O-demethylation, shows a higher affinity for opioid receptors than the parent drug. The rate of production of this M1 derivative (O-demethyl tramadol), is influenced by a polymorphic isoenzyme of the debrisoquine-type, cytochrome P450 2D6 (CYP2D6). Nevertheless, this affinity for mu receptors of the CNS remains low, being 6000 times lower than that of morphine. Moreover, and in contrast to other opioids, the analgesic action of tramadol is only partially inhibited by the opioid antagonist naloxone, which suggests the existence of another mechanism of action. This was demonstrated by the discovery of a monoaminergic activity that inhibits noradrenaline (norepinephrine) and serotonin (5-hydroxytryptamine; 5-HT) reuptake, making a significant contribution to the analgesic action by blocking nociceptive impulses at the spinal level. (+/-)-Tramadol is a racemic mixture of 2 enantiomers, each one displaying differing affinities for various receptors. (+/-)-Tramadol is a selective agonist of mu receptors and preferentially inhibits serotonin reuptake, whereas (-)-tramadol mainly inhibits noradrenaline reuptake. The action of these 2 enantiomers is both complementary and synergistic and results in the analgesic effect of (+/-)-tramadol. After oral administration, tramadol demonstrates 68% bioavailability, with peak serum concentrations reached within 2 hours. The elimination kinetics can be described as 2-compartmental, with a half-life of 5.1 hours for tramadol and 9 hours for the M1 derivative after a single oral dose of 100mg. This explains the approximately 2-fold accumulation of the parent drug and its M1 derivative that is observed during multiple dose treatment with tramadol. The recommended daily dose of tramadol is between 50 and 100mg every 4 to 6 hours, with a maximum dose of 400 mg/day; the duration of the analgesic effect after a single oral dose of tramadol 100mg is about 6 hours. Adverse effects, and nausea in particular, are dose-dependent and therefore considerably more likely to appear if the loading dose is high. The reduction of this dose during the first days of treatment is an important factor in improving tolerability. Other adverse effects are generally similar to those of opioids, although they are usually less severe, and can include respiratory depression, dysphoria and constipation. Tramadol can be administered concomitantly with other analgesics, particularly those with peripheral action, while drugs that depress CNS function may enhance the sedative effect of tramadol. Tramadol should not be administered to patients receiving monoamine oxidase inhibitors, and administration with tricyclic antidepressant drugs should also be avoided. Tramadol has pharmacodynamic and pharmacokinetic properties that are highly unlikely to lead to dependence. This was confirmed by various controlled studies and postmarketing surveillance studies, which reported an extremely small number of patients developing tolerance or instances of tramadol abuse. Tramadol is a central acting analgesic which has been shown to be effective and well tolerated, and likely to be of value for treating several pain conditions (step II of the World Health Organization ladder) where treatment with strong opioids is not required.
 
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