Below is a discussion post by a

Below is a discussion post by a colleague. I need assistance by responding to the post by suggesting additional factors that might have interfered with the pharmacokinetic and pharmacodynamic processes of the patients diagnosed with GAD. In addition, suggest different treatment options I would suggest treating a patient with the topic of discussion. COLLEAGUE POST: Comparing and Contrasting Pharmacologic Options for the Treatment of Generalized Anxiety Disorder Anxiety disorders are considered the most common mental disorders. These disorders can increase the risk for comorbid mood and substance use disorders, significantly contributing to the global disease burden (Garakani et al., 2020). For this reason, in people diagnosed with anxiety disorders like GAD, anxiolytics are the most prescribed psychoactive drugs. Pharmacokinetics and Pharmacodynamics of Anxiolytic Medications Used to Treat GAD The FDA-approved anxiolytic medications used to treat GAD are benzodiazepines, Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs), and Buspirone (Garakani et al., 2020). Benzodiazepines are allosteric modulators of the GABA A receptor. In addition to these central receptors, there are peripheral receptors. Benzodiazepines cause a down-regulation of GABA A receptors, and at the central level, benzodiazepines mainly bind to the nanomolar BZ2 site (Chen et al., 2017). These medications are well-individualized in their chemical structure and possess homogeneous pharmacological properties. Benzodiazepines are weak acids of variable constant dissociation with high lipophilicity, which allows rapid passage through the membranes. Almost all benzodiazepines are insoluble in water; therefore, organic solutions are necessary for parenterally administrable forms (Chen et al., 2017). The antidepressants SSRIs and SNRIs are also used as anxiolytic drugs. SSRIs and SNRIs have a similar antianxiety effect. According to Garakani et al. (2020), these medications work on synapses where the serotonin activates 5-HT heteroreceptors on other serotonergic neurons. These heteroreceptors inhibit serotonin release at synapses related to anxiety. SSRIs are metabolized in the liver by cytochrome P-450 mixed function oxidase (MFO) microsomal enzymes (Garakani et al., 2020). They are highly bound to plasma proteins and have a large volume of distribution. Peak plasma levels are reached in 2 to 10 hours. Also, SNRIs are primarily metabolized by the liver by the cytochrome P450 CYP2D6 enzyme and have a large volume of distribution. However, their onset, peak, and duration of action are highly variable and depend on the formulation (Garakani et al., 2020). On the other hand, Buspirone binds to 5-HT1A receptors and antagonizes dopamine receptors preferentially presynaptic sites (Garakani et al., 2020). Buspirone is almost wholly absorbed orally and has a significant first-pass effect. The plasma peak is reached in less than one hour for a 10 mg dose. It is 95% bound to plasma proteins (Garakani et al., 2020). The metabolism of Buspirone is characterized by hydroxylation and oxidative degradation that lead to the formation of metabolites with little or no activity. The elimination of Buspirone is made by the urinary and biliary routes. The apparent elimination half-life is, on average, 2 to 4 hours. Repeated administrations demonstrate a linear relationship between plasma concentrations with the administered dose (Garakani et al., 2020). Similarities and Differences between the Treatment options SSRIs’ efficacy is comparable to benzodiazepines, with fewer adverse effects. However, their chronic use does not result in the development of dependence (Strawn et al., 2018). Although SSRIs run the risk of antidepressant discontinuation syndrome, this is mild when compared to the withdrawal effects seen in benzodiazepines (Strawn et al., 2018). On the other hand, compared with benzodiazepines, Buspirone has a low inhibitory effect on motor activity and is neither an anticonvulsant nor a muscle relaxant (Strawn et al., 2018).

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