Discussion: Foundational Neuroscience -NURS 6630

Discussion: Foundational Neuroscience -NURS 6630

A Sample Answer For the Assignment: Discussion: Foundational Neuroscience -NURS 6630

1. Explain the agonist-to-antagonist spectrum of action of psychopharmacologic agents, including how partial and inverse agonist functionality may impact the efficacy of psychopharmacologic treatments.

The agonist spectrum can be explained best as a scale from agonist to inverse agonist; with natural neurotransmitters being an agonist or drugs that stimulate the receptors for that action. Partial agonist follows the agonist because of drugs that stimulate the same receptors on a lower gradation of the spectrum (Stahl, 2021). The next level on the spectrum is the antagonist blocking the action of the agonist (Stahl, 2021).

The final function is the inverse agonist has two behaviors: (1) block the agonist, and (2) lower the level of activity below the starting point in absence of an agonist (Stahl, 2021). The best way to explain a partial agonist is to present a medication used in the treatment of depression. Vilazodone is a serotonin reuptake inhibitor, which causes a rise in serotonin at the synaptic cleft by preventing the re-uptake of serotonin at the presynaptic axon terminal (Comprodon & Roffman, 2016).

However, Vilazodone also signals the 5HT1A presynaptic receptors and causes a decrease in the production of serotonin acting as a partial agonist (Baumgartnera et al., 2020). The outcome of partial and inverse agonists can be a marked increase or decrease in the concentration of a drug from the inhibition or excitation of the drug’s receptors (Comprodon & Roffman, 2016).     

2. Compare and contrast the actions of g couple proteins and ion gated channels.

Two of the four methods of signal transduction involve neurotransmitters rather than hormones or neurotrophins (Stahl, 2021). G-coupled proteins and ion-gated channels are similar because they are stimulated by drugs that cause neurotransmitters to activate genes inside of the cell when a phosphate is added to the cAMP protein (Stahl, 2021).

Although they have similarities, the first, G-coupled proteins, cause a slow neuronal effect as a result of its action with cAMP and protein kinase A (Comprodon & Roffman, 2016). The second, ion-gated channels, cause a rapid neuronal effect on the membrane potential as a result of calcium and a kinase called CaMK (Comprodon & Roffman, 2016).

3. Explain how the role of epigenetics may contribute to pharmacologic action.

Epigenetics describes the heritable action of DNA when gene function changes from one generation to the next because of the influence of the external milieu (Comprodon & Roffman, 2016). DNA can be affected by experiences triggering phenotype modifications rather than genotype changes medications (Quevedo et al., 2022).

Stress, such as physical abuse in children, is positively correlated with the development of borderline personality disorder (Comprodon & Roffman, 2016; Quevedo et al., 2022). The downstream effect of neuroplasticity can result in changes at the genetic level resulting in DNA sequencing variations (Quevedo et al., 2022).

Once the chromatin’s structure is modified, the encoding of proteins may alter the original behavior of synaptic uptake of drugs causing changes of pharmacological action, such as enhanced or diminished responses to medications (Quevedo et al., 2022). The increased or decreased action at the receptor site may enhance or inhibit the action of a drug and cause an unexpected outcome.

4. Explain how this information may impact the way you prescribe medications to patients. Include a specific example of a situation or case with a patient in which the psychiatric mental health nurse practitioner must be aware of the medication’s action.

Epigenetic changes are crucial to understand when prescribing medications to patients who have suffered trauma (child abuse, substance misuse, malnutrition, etc.) resulting in DNA silencing or activation (Comprodon & Roffman, 2016). The stress response to physical, emotional, or sexual abuse can cause increased DNA methylation in various tissues in the body, namely blood, saliva, and brain tissue (Quevedo et al., 2022).

Therefore, the PMHNP should be well versed in the biomechanics of a medication for appropriate and effective prescribing. One example is the higher reactivity of the HPA axis to adverse childhood experiences stimulating Corticotropin Releasing Hormone (CRH), which triggers the release of adrenocorticotropin hormone from the pituitary gland (Quevedo et al., 2022). A corticotropin releasing hormone antagonist may be ineffective if one’s mental health is severely affected by a history of abuse. Therefore, the PMHNP should consider an alternative medication to a CRH antagonist.

References

Baumgartnera, K., Doeringb, M., & Schwarz, E. (2020). Vilazodone poisoning: A systematic review. Clinical Toxicology, 58(5), 360–367.               https://doi.org/10.1080/15563650.2019.1691221

Links to an external site.

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.

Quevedo, Y., Booij, L., Herrera, L., Hernández, C., & Jiménez, J. P. (2022). Potential epigenetic mechanisms in psychotherapy: A pilot                study on DNA methylation and mentalization change in borderline personality disorder. Frontiers in Human Neuroscience.                              https://doi.org/10.3389/fnhum.2022.955005

As a psychiatric mental health nurse practitioner, it is essential for you to have a strong background in foundational neuroscience. In order to diagnose and treat clients, you must not only understand the pathophysiology of psychiatric disorders, but also how medications for these disorders impact the central nervous system.

These concepts of foundational neuroscience can be challenging to understand. Therefore, this Discussion is designed to encourage you to think through these concepts, develop a rationale for your thinking, and deepen your understanding by interacting with your colleagues.

Required Readings

Note: All Stahl resources can be accessed through the Walden Library using this link. This link will take you to a log-in page for the Walden Library. Once you log into the library, the Stahl website will appear.

Stahl, S. M. (2013). Stahl’s essential psychopharmacology: Neuroscientific basis and practical applications (4th ed.). New York, NY: Cambridge University Press *Preface, pp. ix–x

Note: To access the following chapters, click on the Essential Psychopharmacology, 4th ed tab on the Stahl Online website and select the appropriate chapter. Be sure to read all sections on the left navigation bar for each chapter.

Chapter 1, “Chemical Neurotransmission”

Chapter 2, “Transporters, Receptors, and Enzymes as Targets of Psychopharmacologic Drug Action”

Chapter 3, “Ion Channels as Targets of Psychopharmacologic Drug Action”

Document: Midterm Exam Study Guide (PDF)

Document: Final Exam Study Guide (PDF)

Required Media

Laureate Education (Producer). (2016i). Introduction to psychopharmacology [Video file]. Baltimore, MD: Author.

NURS 6630 – Psychopharmacologic Approaches to Treatment of Psychopathology Essay Week 1 Discussion: Foundational Neuroscience

Note: The approximate length of this media piece is 3 minutes.

Accessible player

Discussion: Foundational Neuroscience Optional Resources

Laureate Education (Producer). (2009). Pathopharmacology: Disorders of the nervous system: Exploring the human brain [Video file]. Baltimore, MD: Author.NURS 6630 – Psychopharmacologic Approaches to Treatment of Psychopathology Essay Assignment

Note: The approximate length of this media piece is 15 minutes.

Dr. Myslinski reviews the structure and function of the human brain. Using human brains, he examines and illustrates the development of the brain and areas impacted by disorders associated with the brain.

Accessible player

Laureate Education (Producer). (2012). Introduction to advanced pharmacology [Video file]. Baltimore, MD: Author.NURS 6630 – Psychopharmacologic Approaches to Treatment of Psychopathology Essay Assignment

Note: The approximate length of this media piece is 8 minutes.

In this media presentation, Dr. Terry Buttaro, associate professor of practice at Simmons School of Nursing and Health Sciences, discusses the importance of pharmacology for the advanced practice nurse.

Accessible player

To prepare for this Discussion:

Review this week’s Learning Resources.

Reflect on concepts of foundational neuroscience.

Assignment: Assessing and Treating Clients With Dementia

Click here to ORDER an A++ paper from our Verified MASTERS and DOCTORATE WRITERS: Discussion: Foundational Neuroscience -NURS 6630

The Alzheimer’s Association defines dementia as “a general term for a decline in mental ability severe enough to interfere with daily life” (Alzheimer’s Association, 2016). This term encompasses dozens of cognitive disorders of impaired memory formation, recall, and communication. The care and treatment of clients with dementia is dependent on multiple factors, including the stage of dementia, comorbidities, family support, and even the care setting.

In your role, as the psychiatric mental health nurse practitioner, you must be prepared to not only treat clients with these various cognitive disorders, but also the multiple behavioral issues that often accompany them. For this Assignment, as you examine the client case study in this week’s Learning Resources, consider how you might assess and treat clients presenting with dementia.

Reference: Alzheimer’s Association. (2016). What is dementia? Retrieved from http://www.alz.org/what-is-dementia.asp

To prepare for this Assignment:

· Review this week’s Learning Resources. Consider how to assess and treat clients requiring therapy for dementia.

The Assignment

Examine Case Study: An Elderly Iranian Man With Alzheimer’s Disease. You will be asked to make three decisions concerning the medication to prescribe to this client. Be sure to consider factors that might impact the client’s pharmacokinetic and pharmacodynamic processes. At each decision point stop to complete the following:

Introduction regarding disease state

High-level summary of patient case

Purpose of the essay statement

Decision #1

What options were listed?

Which decision did you select?

Why did you select this decision? Support your response with evidence and references to the Learning Resources.

Why didn’t you select the other two options?

What were you hoping to achieve by making this decision? Support your response with evidence and references to the Learning Resources.

Explain any difference between what you expected to achieve with Decision #1 and the results of the decision. Why were they different?

Decision #2

What options were listed?

What option did you choose?

Why did you select this decision? Support your response with evidence and references to the Learning Resources.

Why didn’t you select the other two options?

What were you hoping to achieve by making this decision? Support your response with evidence and references to the Learning Resources.

Explain any difference between what you expected to achieve with Decision #2 and the results of the decision. Why were they different?

Decision #3

What options were listed?

What option did you choose?

Why did you select this decision? Support your response with evidence and references to the Learning Resources.

Why didn’t you select the other two options?

What were you hoping to achieve by making this decision? Support your response with evidence and references to the Learning Resources.

Explain any difference between what you expected to achieve with Decision #3 and the results of the decision. Why were they different?

Also include how ethical considerations might impact your treatment plan and communication with clients.

Note : Support your rationale with a minimum of three academic resources. While you may use the course text to support your rationale, it will not count toward the resource requirement.

Note: To access this week’s required library resources, please click on the link to the Course Readings List, found in the Course Materials section of your Syllabus.

References

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

To access the following chapter, click on the Essential Psychopharmacology, 4th ed tab on the Stahl Online website and select the appropriate chapter. Be sure to read all sections on the left navigation bar for each chapter.

· Chapter 13, “Dementia and Its Treatment”

Stahl, S. M. (2014b). The prescriber’s guide (5th ed.). New York, NY: Cambridge University Press.

To access information on the following medications, click on The Prescriber’s Guide, 5th ed tab on the Stahl Online website and select the appropriate medication.

Review the following medications:

For insomnia

· donepezil

· galantamine

· memantine

· rivastigmine

Bui, Q. (2012). Antidepressants for agitation and psychosis in patients with dementia. American Family Physician, 85(1), 20–22. Retrieved from http://www.aafp.org/journals/afp.html

Note: Retrieved from from the Walden Library databases.

Meltzer, H. Y., Mills, R., Revell, S., Williams, H., Johnson, A., Bahr, D., & Friedman, J. H. (2010). Pimavanserin, a serotonin receptor inverse agonist for the treatment of Parkinson’s disease psychosis. Neuropsychopharmacology, 35, 881–891. Retrieved from http://www.nature.com/npp/journal/v35/n4/pdf/npp2009176a.pdf

Required Media

Laureate Education. (2016h). Case study: An elderly Iranian man with Alzheimer’s disease [Interactive media file]. Baltimore, MD: Author.

BACKGROUND

Mr. Akkad is a 76 year old Iranian male who is brought to your office by his eldest son for “strange behavior.” Mr. Akkad was seen by his family physician who ruled out any organic basis for Mr. Akkad’s behavior. All laboratory and diagnostic imaging tests (including CT-scan of the head) were normal.

According to his son, he has been demonstrating some strange thoughts and behaviors for the past two years, but things seem to be getting worse. Per the client’s son, the family noticed that Mr. Akkad’s personality began to change a few years ago. He began to lose interest in religious activities with the family and became more “critical” of everyone. They also noticed that things he used to take seriously had become a source of “amusement” and “ridicule.”

Over the course of the past two years, the family has noticed that Mr. Akkad has been forgetting things. His son also reports that sometimes he has difficult “finding the right words” in a conversation and then will shift to an entirely different line of conversation.

SUBJECTIVE

During the clinical interview, Mr. Akkad is pleasant, cooperative and seems to enjoy speaking with you. You notice some confabulation during various aspects of memory testing, so the PMHNP performs a Mini-Mental State Exam. Mr. Akkad scores 18 out of 30 with primary deficits in orientation, registration, attention & calculation, and recall. The score suggests moderate dementia.

MENTAL STATUS EXAM

Mr. Akkad is 76 year old Iranian male who is cooperative with today’s clinical interview. His eye contact is poor. Speech is clear, coherent, but tangential at times. He makes no unusual motor movements and demonstrates no tic. Self-reported mood is euthymic. Affect however is restricted. He denies visual or auditory hallucinations.

No delusional or paranoid thought processes noted. He is alert and oriented to person, partially oriented to place, but is disoriented to time and event [he reports that he thought he was coming to lunch but “wound up here”- referring to your office, at which point he begins to laugh].

Insight and judgment are impaired. Impulse control is also impaired as evidenced by Mr. Akkad’s standing up during the clinical interview and walking towards the door. When the PMHNP asked where he was going, he stated that he did not know. Mr. Akkad denies suicidal or homicidal ideation.

Diagnosis: Major neurocognitive disorder due to Alzheimer’s disease (presumptive)

RESOURCES

§ Folstein, M. F., Folstein, S. E., & McHugh, P. R. (2002). Mini-Mental State Examination (MMSE). Lutz, FL: Psychological Assessment Resources.

Decision Point One

Select what the PMHNP should do:

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-red.pngBegin Exelon (rivastigmine) 1.5 mg orally BID with an increase to 3 mg orally BID in 2 weeks

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-blue.png Begin Aricept (donepezil) 5 mg orally at BEDTIME

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-yellow.png Begin Razadyne (galantamine) 4 mg orally BID

Decision Point One

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-blue.pngBegin Aricept (donepezil) 5 mg orally at BEDTIME

RESULTS OF DECISION POINT ONE

· Client returns to clinic in four weeks

· The client is accompanied by his son who reports that his father is “no better” from this medication

· He reports that his father is still disinterested in attending religious services/activities, and continues to exhibit disinhibited behaviors

· You continue to note confabulation and decide to administer the MMSE again. Mr. Akkad again scores 18 out of 30 with primary deficits in orientation, registration, attention & calculation, and recall

Decision Point Two

Select what the PMHNP should do next:

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-red.pngIncrease Aricept to 10 mg orally at BEDTIME

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-blue.pngDiscontinue Aricept and begin Razadyne (galantamine) extended release 24 mg orally daily

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-yellow.pngDiscontinue Aricept and begin Namenda (memantine) extended release, 28 mg orally daily

Decision Point Two https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-red.pngIncrease Aricept to 10 mg orally at BEDTIME

RESULTS OF DECISION POINT TWO

· Client returns to clinic in four weeks

· Client’s son reports that the client is tolerating the medication well, but is still concerned that his father is no better

· He states that his father is attending religious services with the family, which the son and the rest of the family is happy about. He reports that his father is still easily amused by things he once found serious

Decision Point Three

Select what the PMHNP should do next:

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-red.pngContinue Aricept 10 mg orally at BEDTIME

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-blue.pngIncrease Aricept to 15 mg orally at BEDTIME x 6 weeks, then increase to 20 mg orally at BEDTIME

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-yellow.pngDiscontinue Aricept and begin Namenda 5 mg orally daily

Decision Point Three

https://mym.cdn.laureate-media.com/2dett4d/Walden/NURS/6630/10/mm/alzheimers_disease/img/pill-red.pngContinue Aricept 10 mg orally at BEDTIME

Guidance to Student

At this point, it would be prudent for the PMHNP to continue Aricept at 10 mg orally at bedtime. Recall that this medication can take several months before stabilization of deterioration is noted. At this point, the client is attending religious services with the family, which has made the family happy. Disinhibition may improve in a few weeks, or it may not improve at all. This is a counseling point that the PMHNP should review with the son.

There is no evidence that Aricept given at doses greater than 10 mg per day has any therapeutic benefit. It can, however, cause side effects. Increasing to 15 and 20 mg per day would not be appropriate.

There is nothing in the clinical presentation to suggest that the Aricept should be discontinued. Whereas it may be appropriate to add Namenda to the current drug profile, there is no need to discontinue Aricept. In fact, NMDA receptor antagonist therapy is often used with cholinesterase inhibitors in combination therapy to treat Alzheimer’s disease. The key to using both medications is slow titration upward toward therapeutic doses to minimize negative side effects.

Finally, it is important to note that changes in the MMSE should be evaluated over the course of months, not weeks. The absence of change in the MMSE after 4 weeks of treatment should not be a source of concern.

An agonist-to-antagonist spectrum of action of psycho pharmacologic agents, -is explained as when a chemical binds or connect to a receptor, the receptor activates, and a biological response is produced. When agonists activate receptors, like hormones, neurotransmitters, and other endogenous regulators that activate the receptors to which they bind (Golier, J. A., & Yehuda, R. (2018).

Antagonists have no effects on the receptor function, but it can block effectiveness and prevent receptor activation by endogenous molecules and drugs(Golier, J. A., & Yehuda, R. (2018).The antagonist can be a drug with an affinity to bind to a receptor but does not have any intrinsic activity.  The process is considered an example of a full agonist (Golier, J. A., & Yehuda, R. (2018).  

A partial agonist means that the molecules do not elicit a full response therefore does not obtain the maximum response from system even when they bind to the same number of receptors as an agonist (Golier, J. A., & Yehuda, R. (2018). When there is an agonist and a partial agonist working at the same time the partial agonist becomes an antagonist because they are both fighting for space on the same receptors (Frånberg, O et al)..

An antagonist refers to molecules that block agonist mediated responses. Inverse agonists are molecules that want to attach to the same receptors as agonists, but they produce an opposite response than the agonist on the target cell (Golier, J. A., & Yehuda, R. (2018).

Compare and contrast the actions of g couple proteins and ion gated channels.

G protein-coupled receptors (GPCRs) are a large family of cell surface receptors on the plasma membrane that transmit signals inside the cell through a type of protein called a G protein (Sunamita de Carvalho et al 2018).  G protein-coupled receptors serve many purposes in the body, and the disorder of GPCR signaling can cause disease.

G proteins bind with nucleotide guanosinetriphosphate (GTP) (Sunamita de Carvalho et al 2018). G protein divides into two portions (one called the α subunit, the other consisting of the β and γ subunits), which are released from the GPCR (Sunamita de Carvalho et al 2018). The subunits can interact with other