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Treating Generalized Anxiety Disorder using medications has been done using a variety of drug classes.  This includes SSRIs (selective serotonin reuptake inhibitors), SNRIs (serotonin-norepinephrine reuptake inhibitors), and benzodiazepines. 

SSRIs and SNRIs are considered first-line treatment for GAD, with paroxetine and escitalopram being approved SSRIs while venlafaxine and duloxetine are approved SNRIs.  SSRIs selectively block the reuptake of serotonin, which causes an increase in serotonin activity.  They have little effect on other neurotransmitters like dopamine and norepinephrine (Chu & Wadhwa 2022).  SSRIs are well absorbed orally, even with food, and widely distributed and highly bound to plasma proteins.  They are metabolized in the liver, primarily by CYP2D6 then excreted in the urine (Rosenthal & Burchum 2021).  SNRIs work by blocking the neuronal uptake of serotonin and norepinephrine with little effect on other neurotransmitters. Duloxetine is metabolized mainly by the hepatic enzyme P450 (Sansone & Sansone 2014).  

Benzodiazepines are the first-choice drug for the effects of acute anxiety.  They act as positive allosteric modulators on the GABA-a receptor.  GABA is the most common neurotransmitter in the nervous system, found in high concentrations in the cortex and limbic systems (Griffin et al 2014).  The benefit is that increasing the effect of GABA is that it is an inhibitory neurotransmitter and thus diminishes excitability to produce its intended effect.  Benzodiazepines aren’t recommended for long-term use, despite nearly 25% of individuals still being prescribed them after one year.  The risk of dependence, addiction, and withdrawal are complications of long-term use, and these medications need to be tapered off slowly to avoid adverse effects (Gerlach & Maust 2018).  Benzodiazepines are metabolized in the liver by P450 and excreted in the urine (Griffen et al 2013). 

Buspirone is another medication used for the treatment of GAD.  They differ from benzodiazepines in that they do not depress the central nervous system, do not have abuse potential, and can be as effective as benzos in the treatment of GAD.  Buspar has a strong affinity for serotonin 5HT1a receptors but describing how that affinity results in clinical outcomes is unknown.  It’s theorized that increase serotonin in the amygdala provides relief of symptoms (Wilson & Tripp 2022).  Buspar undergoes heavy first-pass metabolism, primarily by CYP3A4 and is excreted in urine and stool.  Buspar is generally used as a second-line medication if SSRIs are ineffective or not well tolerated (Wilson & Tripp 2022). 

These medications share some similarities in that SSRIs, SNRIs, and buspirone are prescribed for the management of GAD and not acute symptoms.  These medications can take upwards of four weeks to reach optimal results, whereas benzodiazepines being used for acute symptom management can yield results almost immediately.  Buspirone is only labeled for the treatment of short-term anxiety though patients have been monitored taking it for as long as a year without adverse side effects.  Buspirone does NOT bind to GABA receptors or benzodiazepines and thus cannot be used for the treatment of withdrawal. (Rosenthal & Burchum 2021). 

 

References

Chu A, Wadhwa R. Selective Serotonin Reuptake Inhibitors. [Updated 2022 May 8]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK554406/Links to an external site.

Gerlach, L., & Maust, D. (2018, September 18). 1 in 4 older adults prescribed a benzodiazepine goes on to risky long-term use, study finds. Institute for Healthcare Policy & Innovation. Retrieved from https://ihpi.umich.edu/news/1-4-older-adults-prescribed-benzodiazepine-goes-risky-long-term-use-study-finds

Griffin, C. E., 3rd, Kaye, A. M., Bueno, F. R., & Kaye, A. D. (2013). Benzodiazepine pharmacology and central nervous system-mediated effects. The Ochsner journal, 13(2), 214-223.

Rosenthal, L. D., & Burchum, J. R. (2021). Lehne’s pharmacotherapeutics for advanced practice nurses and physician assistants (2nd ed.) St. Louis, MO: Elsevier.

Sansone, R. A., & Sansone, L. A. (2014). Serotonin norepinephrine reuptake inhibitors: a pharmacological comparison. Innovations in clinical neuroscience, 11(3-4), 37-42.

Wilson TK, Tripp J. Buspirone. [Updated 2022 Sep 2]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK531477/

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