If tramadol is an SSRI, why would they prescribe it as a medication for citizens within chronic backache?

and then also put the same patient on a second SSRI and an SSI adjectives at once? Are the doctors chemically illiterate and can't see it's an OD of serotonin?
Answers:
Primarily, tramadol isn't an SSRI. It's an analgesic, and its primary modus operandi is to attach to mu-1 opioid receptors, just like morphine.
Actually it isn't a narcotic, and anyone who has have a drug seeking patient knows this, they get pissed when you prescribe them tramadol. It is a mu opioid receptor antagonist which make it an effect pain relieve for many people, however this doesn't necessarily build it a narcotic, that refers to psychotropic effects, not mechanism of action. After all, Immodium is an opiate. I don't see general public abusing that to get high.
It is not an SSRI. It does enjoy some serotonergic and noradrenergic effects, but these are relatively weak and keep it from being classified as an SNRI. Source(s): med student
Mechanism of action

The mode of action of tramadol has but to be fully understood, but it is believed to work through modulation of the noradrenergic and serotonergic systems in addition to its mild agonism of the μ-opioid receptor. The contribution of non-opioid commotion 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 tenancy affinity for the μ-opioid receptor (approximately 1/6000th that of morphine; Gutstein & Akil, 2006). 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, next to (+)-tramadol exhibiting 10-fold higher analgesic activity than (-)-tramadol (Goeringer et al., 1997).

The serotonergic modulating properties of tramadol mean that it have 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) or near use of a light box, since these agents not only potentiate the effect of 5-HT but also inhibit tramadol metabolism. Tramadol is also thought to have some NMDA-type antagonist effects which have given it a potential application in neuropathic pain states. Source(s): http://en.wikipedia.org/wiki/Tramadol
Tramadol (Ultracet) is not an SSRI. Tramadol is a narcotic medication for chronic pain. SSRIs are not narcotics (or even close) and are used to treat clinical depression. Source(s): I am a forensic psychopharmacologist, author of several text on drugs, the brain and behavior.
Tramadol is not an ssri. It act as a serotonin and norepinephrine reuptake inhibitor as well as an opiate agonist. So it causes a build up of serotonin and norepinephrine which help lift the pain treshold and psychological pain as well as it have an affinity for the opiate receptors which makes it a narcotic. So these two actions it performs brand it a good pain reliever.
I'd like know where on earth Google went to med school...

Tramadol is an opioid derivative analgesic. Source(s): PharmD candidate
It does appear to ignore the mechanism of action issue, and you angle a valid concern as to the issue of too much serotonin.

Hyperserotonin states promote heart valve damage, but most drug interactions are discovered after enough society have a problem and doctors then notice it.

There is a 45% placebo effect when it comes to misery evauation on any medication, and in the lab tramadol binds to narcotic mu receptors with 1/6000 as that of morphine, its active metabolites bind 2 to 4 times better but we are still chitchat something less than 1/1000th the potency of morphine. So it really does not make sense that it enjoys the popularity that it have.

see the following link regarding serotonin:

http://circ.ahajournals.org/cgi/content/… Source(s): Goodman and Gilman's Pharmacological Basis of Therapeutics, 11th edition, page 566

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