Pharmacologic Options for the Treatment of Generalized Anxiety Disorder Example Solution

DSM V medical diagnosis of generalized anxiety disorder (GAD) is characterized by considerable dysfunction that affects a person’s everyday psychological, physical, and social functioning. Psychological, pharmaceutical, or a combination of these modalities may be used as GAD treatments (Carl et al., 2020). Due to the expense and resource limitations of psychological alternatives, pharmacologic treatment is frequently the first choice for doctors. The paper compares and contrasts the five pharmacologic treatments for GAD: Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin Norepinephrine Reuptake Inhibitors (SNRIs), Tricyclic Antidepressants (TCAs), and Monoamine Oxidase Inhibitors (MAOIs).

Pharmacokinetics and Pharmacodynamics Principles

SSRIs act by inhibiting the serotonin transporter on the presynaptic membrane; SNRIs inhibits both serotonin and norepinephrine transporters, while TCAs inhibit both serotonin and norepinephrine transporter, and muscarinic, histamine, and alpha-adrenergic receptors (Wyska, 2019). MAOIs block the action of monoamine oxidase, increasing the availability of monoamine neurotransmitters: norepinephrine, serotonin, and dopamine by limiting their breakdown.

Unlike antidepressant classes, SSRIs have little effect on other neurotransmitters, such as norepinephrine and dopamine. The liver’s cytochrome P-450 microsomal enzymes metabolize the four drug classes. They have a wide volume of distribution and are tightly bound to plasma proteins (Rosenthal & Burchum, 2020). The drugs are well absorbed orally and undergo extensive first-pass metabolism. Peak plasma level timing and half-lives vary from one drug class to another and between drugs in the same class. In 2 to 10 hours, peak plasma levels are reached for SSRIs, while MAOIs peak plasma concentrations are attained in 2–3 hours.

Safety, tolerability, and side-effect profiles of SSRIs and SNRIs are similar, except that venlafaxine and desvenlafaxine have been associated with a sustained rise in blood pressure. SSRIs and SNRIs mostly have similar side effects and are implicated in causing increased suicidal thoughts, serotonin syndrome, and increased risk of bleeding (Carl et al., 2020). Unlike TCAs, they do not have an affinity for other receptors such as adrenergic, muscarinic, and histamine; hence are better tolerated. The four drugs are implicated in the causation of serotonin syndrome. Therefore, serotonergic drugs should not be added to a patient’s regimen until 2 to 3 weeks after the stoppage of the drugs.

Pharmacokinetics and Pharmacodynamics Reflection

In my years of experience, dosing anxiolytics depends on the patient’s genetics, age, and comorbidities. Repeated tests showed that Serum antidepressant drug concentrations are typically over the suggested reference range in elderly patients compared to younger patients receiving the exact dosage. Secondly, due to the liver metabolism of the drugs, patients with liver diseases have been noted to have an increased incidence of toxicity. Therefore, anxiolytics doses in the old and patients with liver disease are slightly reduced. Women have been shown to have a worse safety profile, with adverse drug reactions being more common and severe in women than in men.

Factors Influencing Pharmacokinetics and Pharmacodynamics

Age, diet, gender, environment, pregnancy, body weight, the patient’s pathophysiology, genetics, and drug-drug or food-drug interactions all have an impact on pharmacokinetics. Pharmacodynamics of a drug may be impacted by physiological changes brought on by illness, genetic mutations, aging, or other medications (Rosenthal & Burchum, 2020). These alterations result from the diseases’ capacity to modify receptor binding, alter the quantity of binding proteins, or reduce receptor sensitivity. Regarding the genetic component, it is possible to estimate that around 25% of the total variability in medication response is genetic in nature.

Personalizing Plan of Care

Regulatory agencies add pharmacogenomics medicine labels into the summaries of product information to make it easier for medical practitioners to communicate genetic information to patients. Here, they indicate which genetic variant information is crucial to take into account when prescribing a treatment. Mandatory instructions, recommendations, and details concerning how pharmacogenomic variation should be taken into account regarding the indication or dose are all included on such drug labels; these details are believed to be helpful for individualized care plans (Slee et al., 2019). The Plan of care for the patient also entails frequent monitoring and reassessment.

Conclusion

SSRIs are the first-line drugs for the management of generalized anxiety disorder. They have the benefit of ease of dosing and having low overdose toxicity. The SSRIs are vastly favored over other antidepressant classes because of their greater tolerability and relatively benign safety profile. Since SSRIs do not seem to impact blood pressure or cardiac conduction in people with cardiac illness, they are not considered as concerning. Standard second lines include SNRIs and TCAs.

References

Carl, E., Witcraft, S. M., Kauffman, B. Y., Gillespie, E. M., Becker, E. S., Cuijpers, P., … & Powers, M. B. (2020). Psychological and pharmacological treatments for generalized anxiety disorder (GAD): a meta-analysis of randomized controlled trials. Cognitive Behaviour Therapy, 49(1), 1-21. https://doi.org/10.1080/16506073.2018.1560358

Rosenthal, L., & Burchum, J. (2020). Lehne’s pharmacotherapeutics for advanced practice nurses and physician assistants (2nd ed.). Saunders.

Slee, A., Nazareth, I., Bondaronek, P., Liu, Y., Cheng, Z., & Freemantle, N. (2019). Pharmacological treatments for generalised anxiety disorder: a systematic review and network meta-analysis. The Lancet, 393(10173), 768-777. https://doi.org/10.1016/S0140-6736(18)31793-8

Wyska, E. (2019). Pharmacokinetic considerations for current state-of-the-art antidepressants. Expert Opinion on Drug Metabolism & Toxicology, 15(10), 831-847. https://doi.org/10.1080/17425255.2019.1669560