The metabolism of analgesic agents involves enzyme-catalyzed changes in their chemical structure to increase water solubility and facilitate excretion from the body as a key step in terminating drug action.

Drug metabolism reactions are subdivided into:
Phase 1 “functionalization” reactions (e.g., oxidation, reduction, and hydrolysis catalyzed by the cytochrome P450 (CYP) superfamily of enzymes; and
Phase 2 metabolism to form water-soluble glucuronic acid, sulfate, and/or glutathione conjugates that are readily excreted via the kidney.

In some instances, metabolism may result in bioactivation to form analgesically active metabolites, such as the metabolism of morphine to morphine-6-glucuronide, the metabolism of codeine to morphine, or the metabolism of tramadol to its M1 metabolite.
Active metabolites may also contribute to adverse-event profiles, such as the metabolism of pethidine (meperidine), morphine, and hydromorphone to their neuroexcitatory metabolites, norpethidine, morphine-3-glucuronide, and hydromorphone-3-glucuronide, respectively.

See reference for more information.

Maree T. Smith. IASP: Pain: Clinical updates. Pharmacogenetics. November 2010 (Vol. 18, Issue 8).