Classification<unk>  is a synthetic opioid in the phenylpiperidine family, which includes sufentanil, alfentanil, remifentanil, and carfentanil. Structure-activity The structures of opioids share many similarities. Whereas opioids like codeine, hydrocodone, oxycodone, and hydromorphone are synthesized by simple modifications of morphine,<unk>  and its relatives are synthesized by modifications of meperidine. Meperidine is a fully synthetic opioid, and other members of the phenylpiperidine family like alfentanil and sufentanil are complex versions of this structure. Like other opioids,<unk>  is a weak base that is highly lipid-soluble, protein-bound, and protonated at physiological pH. All of these factors allow it to rapidly cross cellular membranes, contributing to its quick effect in the body and the central nervous system. Mechanism of action<unk>  at opioid receptors Affinities, Ratio MOR:DOR:KOR 0.39 nM >1,000 nM 255 nM 1:>2564:654<unk> , like other opioids, acts on opioid receptors. These receptors are G-protein-coupled receptors, which contain seven transmembrane portions, intracellular loops, extracellular loops, intracellular C-terminus, and extracellular N-terminus. The extracellular N-terminus is important in differentiating different types of binding substrates. When<unk>  binds, downstream signaling leads to the inhibitory effects, such as decreased cAMP production, decreased calcium ion influx, and increased potassium efflux. This inhibits the ascending pathways in the central nervous system to increase pain threshold by changing the perception of pain; this is mediated by decreasing propagation of nociceptive signals, resulting in analgesic effects. As a μ-receptor agonist,<unk>  binds 50 to 100 times more potently than morphine. It can also bind to the delta and kappa opioid receptors but with a lower affinity. It has high lipid solubility, allowing it to more easily penetrate the central nervous system. It attenuates "second pain" with primary effects on slow-conducting, unmyelintated C-fibers and is less effective on neuropathic pain and "first pain" signals through small, myelinated A-fibers.<unk>  can produce the following clinical effects strongly, through μ-receptor agonism. * Supraspinal analgesia (μ1) * Respiratory depression (μ2) * Physical dependence * Muscle rigidity It produces sedation and spinal analgesia through Κ-receptor agonism. Therapeutic effects * Pain relief: Primarily,<unk>  provides the relief of pain by acting on the brain and spinal μ-receptors. * Sedation:<unk>  produces sleep and drowsiness, as the dosage is increased, and can produce the δ-waves often seen in natural sleep on electroencephalogram. * Suppression of the cough reflex:<unk>  can decrease the struggle against an endotracheal tube and excessive coughing by decreasing the cough reflex, becoming useful when intubating people who are awake and have compromised airways. After receiving a bolus dose of<unk> , people can also experience paradoxical coughing, which is a phenomenon that is not well understood. Detection in biological fluids<unk>  may be measured in blood or urine to monitor for abuse, confirm a diagnosis of poisoning, or assist in a medicolegal death investigation. Commercially available immunoassays are often used as initial screening tests, but chromatographic techniques are generally used for confirmation and quantitation. The Marquis Color test may also be used to detect the presence of<unk> . Using formaldehyde and sulfuric acid, the solution will turn purple when introduced to opium drugs. Blood or plasma<unk>  concentrations are expected to be in a range of 0.3–3.0 μg/L in persons using the medication therapeutically, 1–10 μg/L in intoxicated people, and 3–300 μg/L in victims of acute overdosage. Paper spray-mass spectrometry (PS-MS) may be useful for initial testing of samples.
Fentanyl
Remifentanil
Ketamine
Alfentanil
Propofol
Etomidate
Sevoflurane
Methoxyflurane