By Domenic A. Ciraulo MD, Richard I. Shader, David J. Greenblatt MD, Wayne L. Creelman MD
Thoroughly up-to-date for its 3rd version, this instruction manual presents entire, present, and simply obtainable details on how psychotropic medicinal drugs have interaction with each other and with compounds used to regard non-psychiatric health conditions. The ebook is prepared for quick reference, contains various tables, and gives instructions for dealing with opposed effects.
The 3rd variation comprises an adversarial drug results desk within the appendix part, tables on receptor binding and dosing, and the newest info on medicines of abuse and chemical dependence. This variation additionally comprises drug-food interactions for every drug classification and interactions of psychotropic medicinal drugs with HIV medications.
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Extra info for Drug interactions in psychiatry
Almost all CYP3A substrates are metabolized by both isoforms. However, the catalytic activity for most substrates is higher with CYP3A4 (although exceptions to this general trend exist), making it a dominant contributor to net CYP3A activity in most individuals. Examples of drugs that are metabolized primarily by CYP3A span all therapeutic classes and include immunosuppressants such as cyclosporin A and tacrolimus; sedative-hypnotic agents such as midazolam and triazolam; antidepressants such as nefazodone and trazodone; anxiolytic agents such as alprazolam and buspirone; calcium channel blockers such as nifedipine, felodipine, and diltiazem; antiarrhythmic agents such as amiodarone, quinidine, and lidocaine; antiinfectives such as erythromycin, quinine, ritonavir, saquinavir, and amprenavir; antineoplastic agents such as etoposide, ifosfamide, tamoxifen, and vinblastine; synthetic opioids such as fentanyl, alfentanil, and sufentanil; and the nonsedating antihistaminic drugs terfenadine, loratadine, and astemizole.
Thus, a change in intrinsic clearance (as would occur in a metabolic drug interaction) results in a corresponding change in apparent oral clearance; this is reflected as a change in AUC following oral dosing, independent of the drug’s extraction ratio (unlike the situation with intravenous dosing, where exposure is not appreciably altered for highly extracted drugs). Although the effects of a change in intrinsic clearance on the apparent oral clearance (and thus, systemic AUC) of a drug are independent of extraction ratio, the effects on oral bioavailability and elimination half-life are not.
An empirical approach to diagnose the mechanism-based inhibition of CYP enzymes is to compare the potency of the inhibitor without and with preincubation with human liver microsomes in the presence of necessary cofactors for CYP activity. , the IC50 value is decreased) in the presence of preincubation. Equations 13 and 15 are not applicable when mechanism-based inactivation is observed and alternative mathematical models must be applied to account for the concentration- as well as time-dependent nature of the inhibition process.