(+)-트라마돌,염산염

Breast Feeding; Lactation; Milk, Human; Analgesics, Opioid; Narcotics

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Danger

H301 (57.8%): Toxic if swallowed [Danger Acute toxicity, oral]

P264, P270, P273, P301+P316, P301+P317, P321, P330, P391, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 135 reports by companies from 17 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Danger

H301 (41.5%): Toxic if swallowed [Danger Acute toxicity, oral]

Acute Tox. 3 (57.8%)

Acute Tox. 3 (41.5%)

In treating an overdose, primary attention should be given to maintaining adequate ventilation along with general supportive treatment. While naloxone will reverse some, but not all, symptoms caused by overdosage with ULTRAM, the risk of seizures is also increased with naloxone administration. (L1712)

Serious potential consequences of overdosage are respiratory depression, lethargy, coma, seizure, cardiac arrest and death. The respiratory depressant effects include carbon dioxide retention and secondary elevation of cerebrospinal fluid pressure, and may be markedly exaggerated in these patients (RxList, A308). Medical problems can include congested lungs, liver disease, tetanus, infection of the heart valves, skin abscesses, anemia and pneumonia. Death can occur from overdose.

Hepatic. The major metabolic pathways appear to be N- and O- demethylation and glucuronidation or sulfation in the liver. One metabolite (O-desmethyltramadol, denoted M1) is pharmacologically active in animal models. CYP3A4 and CYP2B6 facilitates the biotransformation of tramadol to N-desmethyl-tramadol. CYP2D6 facilitates the biotransformation of tramadol to O-desmethyl-tramadol. Racemic tramadol is rapidly and almost completely absorbed after oral administration. The mean absolute bioavailability of a 100 mg oral dose is approximately 75%.The mean peak plasma concentration of racemic tramadol and M1 occurs at two and three hours, respectively, after administration in healthy adults. Tramadol undergoes hepatic metabolism via the cytochrome P450 isozyme CYP2D6, being O- and N-demethylated to five different metabolites. Of these, M1 (O-Desmethyltramadol) is the most significant since it has 200 times the affinity of (+)-tramadol, and furthermore has an elimination half-life of nine hours, compared with six hours for tramadol itself. In the 6% of the population that have slow CYP2D6 activity, there is therefore a slightly reduced analgesic effect. Phase II hepatic metabolism renders the metabolites water-soluble, which are excreted by the kidneys. Thus, reduced doses may be used in renal and hepatic impairment (A308, L1160). Route of Elimination: Tramadol is eliminated primarily through metabolism by the liver and the metabolites are excreted primarily by the kidneys. Approximately 30% of the dose is excreted in the urine as unchanged drug, whereas 60% of the dose is excreted as metabolites. Half Life: Tramadol and its metabolites are excreted primarily in the urine with observed plasma half-lives of 6.3 and 7.4 hours for tramadol and M1, respectively.

TRAMADOL HCL

Full Opioid Agonists [MoA]; Opioid Agonist [EPC]

TRAMADOL HYDROCHLORIDE

Opioid Agonist [EPC]; Full Opioid Agonists [MoA]

TRAMADOL HCL ER

Opioid Agonist [EPC]; Full Opioid Agonists [MoA]

Compounds with activity like OPIATE ALKALOIDS, acting at OPIOID RECEPTORS. Properties include induction of ANALGESIA or NARCOSIS.

Agents that induce NARCOSIS. Narcotics include agents that cause somnolence or induced sleep (STUPOR); natural or synthetic derivatives of OPIUM or MORPHINE or any substance that has such effects. They are potent inducers of ANALGESIA and OPIOID-RELATED DISORDERS.