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NURS 6630 University of Maryland Wk 2 Agonist to Antagonist Spectrum Response

NURS 6630 University of Maryland Wk 2 Agonist to Antagonist Spectrum Response

Question Description

Please repond to

Mackenzie Gray

Week 2 Discussion

COLLAPSE

Agonist-to-Antagonist Spectrum

An agonist is a drug that binds to and activates the receptor and yields a biological response (Salahudeen & Nishtala, 2017). Agonists allow the ion channels to be fully open, which enabling the drug to bind fully to the receptor site (Stahl, 2013). Agonists have an efficacy of one; therefore, these drugs are fully capable of producing a pharmacological response when bound to a receptor (Salahudeen & Nishtala, 2017).

An antagonist is a drug that binds to receptors and obstructs the agonist from the receptor site (Salahudeen & Nishtala, 2017). Antagonists can partially block agonists and reduce the agonist’s effects; however, antagonists may also completely block agonists if the concentration is high enough (Salahudeen & Nishtala, 2017). Antagonists have an efficacy of zero; therefore, these drugs are incapable of producing a pharmacological response (Salahudeen & Nishtala, 2017). Antagonists allow ions and receptors to be in their resting states (Stahl, 2013).

Partial and inverse agonists function in ways that can interfere with psychopharmacologic treatments. A partial agonist is a drug that can bind and activate the receptor, but it is unable to produce an adequate response (Salahudeen & Nishtala, 2017). Partial agonists have an efficacy range greater than zero but less than one (Salahudeen & Nishtala, 2017). An inverse agonist is an agonist that generates the opposite pharmacological response (Salahudeen & Nishtala, 2017).

G-Protein Coupled Receptors and Ion Gated Channels

G-protein coupled receptors (GPCRs) are essential proteins because cells use them to transmit extracellular stimuli into intracellular responses (Zhao et al., 2016). For example, GPCRs respond to hormones, neurotransmitters, and senses (Zhao et al., 2016). GCPR structure has seven transmembrane helices (Zhao et al., 2016). GPCRs are numerous and are the largest transmembrane receptor group in humans (Zhao et al., 2016). GCPRs bind to G proteins, which results in further signal pathways being activated (Zhao et al., 2016). GCPRs work slowly to relay messages due to the multi-step pathway to forward information (Camprodon & Roffman, 2016).

Ligand-gated ion channels have several long amino acid strands divided into smaller subunits around an ion channel (Stahl, 2013). The amino acid strands have receptor binding sites for various items, such as neurotransmitters, ions, and drugs (Stahl, 2013). Ligand-gated ion channels are often arranged in subunits consisting of five proteins, which are further divided into four transmembrane areas (Stahl, 2013). Ions flow through the channels rapidly compared to GPCRs (Camprodon & Roffman, 2016).

Epigenetics

Epigenetics is the study of how one’s environment or behaviors may alter their gene expression without changing the genetic code (Camprodon & Roffman, 2016). Research suggests that an individual’s epigenetic changes may influence their response to drugs, and provider awareness of epigenetic changes may be essential for therapeutic response to drugs (Schuebel et al., 2016). For example, if a patient experiences alteration to chromatin, they should be treated with a drug that affects the structure of chromatic, such as valproic acid (Camprodon & Roffman, 2016).

Prescribing Considerations

When prescribing medications, PMHNPs must be cognizant of a drug’s action and how individuals may metabolize the drug. For example, fluoxetine is metabolized by the cytochrome P450 2D6 (Eli Lilly and Company, 2006). Individuals who are deficient in this cytochrome may experience slower metabolization of fluoxetine, resulting in higher concentrations of fluoxetine (Eli Lilly and Company, 2006). These individuals may need a lower dose of fluoxetine to experience therapeutic effects (Eli Lilly and Company, 2006). Patients may experience mania if fluoxetine concentrations are too high (Eli Lilly and Company, 2006).

References

Camprodon, J. A., & Roffman, J. L. (2016). Psychiatric neuroscience: Incorporating pathophysiology into clinical case formulation. In T. A. Stern, M. Favo, T. E. Wilens, & J. F. Rosenbaum. (Eds.), Massachusetts General Hospital psychopharmacology and neurotherapeutics (pp. 1–19). Elsevier.

Eli Lilly and Company. (2006). Prozac [package insert]. Retrieved from https://www.accessdata.fda.gov/drugsatfda_docs/lab…

Salahudeen, M. S., & Nishtala, P. S. (2017). An overview of pharmacodynamic modelling, ligand-binding approach and its application in clinical practice. Saudi Pharmaceutical Journal: The Official Publication of the Saudi Pharmaceutical Society, 25(2), 165–175. https://doi.org/10.1016/j.jsps.2016.07.002

Schuebel, K., Gitik, M., Domschke, K., & Goldman, D. (2016). Making sense of epigenetics. The International Journal of Neuropsychopharmacology, 19(11), pyw058. https://doi.org/10.1093/ijnp/pyw058

Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). Cambridge University Press.

Zhao, J., Deng, Y., Jiang, Z., & Qing, H. (2016). G protein-coupled receptors (GPCRs) in Alzheimer’s Disease: A focus on BACE1 related GPCRs. Frontiers in Aging Neuroscience, 8, 58. https://doi.org/10.3389/fnagi.2016.00058

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