Discussion Week 8 _ NURS 6521

Instructions:

Read a selection of your colleagues’ responses and respond to  your colleagues 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 you would suggest to treat a patient with the topic of discussion.

**minimum of three (3) scholarly references are required for each reply cited within the body of the reply & at the end**

Reply # 2

Chioma murphy 

Top of Form

My experience, and observations from the last 5 years and how pharmacokinetic and pharmacodynamic factors altered my patient’s response to a drug

Three years ago, I had a patient who was diagnosed with Generalized Anxiety Disorder (GAD) and was prescribed alprazolam (Xanax) a Benzodiazepines to manage his GAD. In the course of my discussion with this patient I found out that he never disclosed to his health provider, the actual amount of alcoholic drinks he consumed on a daily bases. The patient had lied to his health provider that he consumed about three to four beers a week. Whereas he actually drank up to 12 cans of beer in a night. He also received multiple prescriptions for alprazolam because he went to his health provider giving account of misplaced prescriptions and insisted on repeat prescriptions. 

The patient was received and admitted in a comatose state because he continued his regular drinking habit, after taking his prescribed alprazolam. According to the patient, on that evening of the incidence, he became very light headed, and dropped to the floor after concurrent consumption of alcoholic beverages and alprazolam. Patient was lucky because his neighbor walked in on him, and found him lying in a pool of his own blood, and then called 911.

How my patient’s behavior influenced the his pharmacokinetic and pharmacodynamic processes

Benzodiazepines are first-choice drugs for anxiety disorders because they produce immediate effects (Rosenthal, L. D., & Burchum, J. R., 2018). Benzodiazepines act by potentiating the inhibitory actives of the gamma-aminobutyric acid (GABA) neurotransmitter receptor binding at the interface of the GABA-A receptor (Kang,  M, et al., 2021). This action causes an increase of influx of chloride ions through the GABA ion channels, postsynaptic hyperpolarization, and ultimately decreasing the possibility of generating an action potential (Kang,  M, et al., 2021).

Benzodiazepines taken in therapeutic or toxic doses rarely causes a significant respiratory depression. Compared to other barbiturates, benzodiazepines have low incidence of respiratory depression because there are few binding sites in the brainstem where the respiratory center is located (Kang,  M, et al., 2021). The most common cause of respiratory depression with benzodiazepine is toxicity involving coingestants, the leading substance being ethanol usually in the form of alcohol (Kang,  M, et al., 2021). Alcohol ingestion in high levels has strong affinity with the GABA receptors  (LaHood, A. J, et al., 2021). The alcohol will primarily act on the central nervous system by enhancing the binding of GABA (a primary inhibitory neurotransmitter of the CNS), allowing influx of chloride to the cell, inhibiting cellular excitability which results in cognitive dysfunction, sedation, and decreased coordination (LaHood, A. J, et al., 2021).

Benzodiazepines and alcohol used concurrently, produced a synergistic effect that intensified their sedative effects, and led to CNS depression with normal vital signs in my patient, a classic presentation of an isolated benzodiazepine toxicity (Kang,  M, et al., 2021).

Personalized plan of care considering patient’s behavior, pharmacokinetic and pharmacodynamic processes and patient history with GAD

The typical treatment plan for acute benzodiazepine toxicity is supportive care, which may necessitate endotracheal intubation for airway management, ECG, and CT without contrast especially since the patient fell down (Kang,  M, et al., 2021). Urine test may not be so useful in identifying some benzodiazepines especially in the absence of recent exposure to the drugs. However, for this patient, a personalized planned of care shall include: Screening for alcohol use disorder (LaHood, A. J, et al., 2021), psychological counseling and appropriate deaddiction therapy (Kang,  M, et al., 2021), and based on history of alcoholism another drug approved by the U.S. Food and Drug Administration (FDA) for treatment of GAD should be considered. For example, the patient’s drugs should be switched from alprazolam to Buspirone. 

Buspirone should be initiated 2 to 4 weeks starting to tapper patient of benzodiazepine because of pharmacokinetics of benzodiazepine (Rosenthal, L. D., & Burchum, J. R., 2018). After oral administration of  benzodiazepine, it is quickly consumed by the gastrointestinal tract (Pathak, S., et al 2020). Alprazolam is fast acting and considered a little acting high-effectiveness benzodiazepine with a half existence of 6–27 (Pathak, S., et al 2020). A problem that may be encountered with alprazolam is the beginning of a rebound of uneasiness related to withdrawal and because alprazolam has a short end half-existence (Pathak, S., et al 2020). 

Buspirone, on the other hand, begins to develop anxiolytic effects slowly (within a week), and reached optimal effectiveness in several more weeks (Rosenthal, L. D., & Burchum, J. R., 2018). Buspirone is another drug approved for GAD (Rosenthal, L. D., & Burchum, J. R., 2018). It does not have potential for abuse, it does not enhance CNS depression and it is drugs suitable for patients known to abuse drugs or alcohol (Rosenthal, L. D., & Burchum, J. R., 2018). Buspirone binds with does not bind to the receptors for GABA that benzodiazepines binds (Rosenthal, L. D., & Burchum, J. R., 2018). Buspirone has high affinity to serotoninreceptors and low affinity to dopamine receptors (Rosenthal, L. D., & Burchum, J. R., 2018).

Past year alcohol use and drug or alcohol dependence has been associated with 

odds of benzodiazepine misuse (Hirschtritt, M. E., et al., 2019). A suitable plan of care for this patient should therefore include switching the patient to buspirone because, buspiron has the same effect as benzodiazepine, buspiron does not intensify CNS depression, buspiron has no potential for abuse, and buspiron is suitable for known drug abusers (Rosenthal, L. D., & Burchum, J. R., 2018). However, buspirone should be initiated 2 to 4 weeks and benzodiazepines should be tapered gradually to minimize withdrawal symptoms because anxiolytic effects of buspirone, gradually develops (Rosenthal, L. D., & Burchum, J. R., 2018).

References

Hirschtritt, M. E., Palzes, V. A., Kline-simon, A. H., Kroenke, K., Campbell, C. I., Sterling, S. A., (2019). Benzodiazepine and Unhealthy Alcohol Use Among Adult Outpatients. The American Journal of Managed Care 25(12). https://www.ajmc.com/view/benzodiazepine-and-unhealthy-alcohol-use-among-adult-outpatients

Kang, M., Galuska, M. A., Ghassemzadeh, S., (2021). Benzodiazepine Toxicity. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK482238/

LaHood, A. J., Kok, S. J., (2021). Ethanol Toxicity. StatPearls Publishing. https://www.ncbi.nlm.nih.gov/books/NBK557381/

Pathak, S., Gupta, G., Gilhotra, R. M., (2020). A Review on Benzodiazepine Pharmacology and Central Nervous System-Mediated Effects. SGVU Journal of Pharmaceutical Research & Education. http://www.gyanvihar.org/researchjournals/

Rosenthal, L. D., & Burchum, J. R. (2018). Lehne’s pharmacotherapeutics for advanced practice nurses and physician assistants. St. Louis, MO: Elsevier