Should a counselor remain value-objective about controversial issues presented by a client (such as abortion, suicide, adultery, drug use, domestic violence, child abuse, etc.)? Some counselors might argue that they should not express their values or criticize their clients for these behaviors, while others would say that expressing moral judgment is appropriate.
Consider the information above and chapter 3 of the textbook. Write a 1,000-1,250-word paper addressing the following:
Analyze the ethical implications of a counselor expressing their values to a client.
Identify actions a counselor might take when confronted with clients they find difficult to treat due to differences in values/beliefs regarding one or more of the following issues: abortion, suicide, adultery, drug use, domestic violence, child abuse
Identify factors that might lead a counselor to consider referring a client with any controversial issues to another counselor. Value Objectivity Paper
Describe steps a counselor should take if referral is not an option.
Be sure to use the ACA and NAADAC codes of ethics as guidelines when constructing your paper.
Plato argued powerfully in favor of the objectivity of values such as truth, good, and beauty. Objective values are those that lie outside of the individual and are not dependent upon her/his perception or belief. Some philosophers theorize that allvalues are relative to individuals or groups.
Are Values Subjective or Objective? … This is because objective facts are yoursubjective values. This means we make judgement or choices based on things that are there or being offered to us, therefore values are both subjective and objective.
Economists tend to speak of value as a subjective thing, whereas philosophers like to talk about values in the objective sense. Like rights, for example, are something that everybody has to have.
Objective Ethics refers to a view that a person’s action can always be seen as right or wrong, regardless of the situation or the consequences. It focuses on rules for governing what is considered to be morally right, wrong, or obligatory. … Objective Ethics is also known as moral absolutism or ethical absolutism. Value Objectivity Paper
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Week 8 discussion Discussion Prompt #1 Describe a clinical situation in which a registered nurse may encounter moral distress. Answer the AACN’s Four A’s found on page 84 in your Butts and Rich text to further explain the situation, and the possible mitigation strategies. Discussion Prompt #2 Describe different ways that social media use can violate ethical nursing practices. How can ethical social media use be beneficial to health care professionals and their patients?
Answer the AACN’s Four A’s found on page 84 in your Butts and Rich text to further explain the situation, and the possible mitigation strategiesAnswer the AACN’s Four A’s found on page 84 in your Butts and Rich text to further explain the situation, and the possible mitigation strategies“Human reasoning does not depend on our ability to cast answers at one another, but our
ability to find the sources of our disagreement” (Jameton, 1984, p.6). In providing healthcare
services, professionals often are faced with stressful situations and ethical dilemmas that can lead
to disagreements. Nurses come in contact with ethical dilemmas throughout their daily work due
to the paternalistic nature of the healthcare field, for example, a hospital’s policy to collect a
complete blood count specimen from all admitted patients regardless of need. This imposes a
costly and unnecessary risk for the patient. Nurses do not have the necessary resources to change
the practice due to their lack of authority (Jameton, 1984, p.6). “Doctors and nurses feel trapped
by the competing demands of administrators, insurance companies, lawyers, and patients’
families, and they are forced to compromise on what they believe is right for the patients”
(Theobald, 2013, p.5). Assignment: Moral Distress
These ethical situations experienced by healthcare workers were collectively termed
moral distress in 1984 by the philosophy professor, Andrew Jameton. When moral distress was
first coined by Jameton, it was defined as, “arising when one knows the right thing to do, but
institutional constraints make it nearly impossible to pursue the right course of action” (p.6).
Jameton taught many nursing students and saw the students’ morals were often being contested
when working in clinical settings. In his findings, he discovered many of his nursing students
were being morally challenged and thus were placed under significant moral distress. These
students were suffering before they even finished school and had to quickly learn to adapt to
their new profession (McCarthy & Gastmans, 2015, p. 132). Assignment: Moral Distress
https://superbnursingessays.com/wp-content/uploads/2022/01/LOGO-300x75.png00Naomi Nashttps://superbnursingessays.com/wp-content/uploads/2022/01/LOGO-300x75.pngNaomi Nas2022-06-08 08:58:332022-06-08 08:58:33Assignment: Moral Distress
Among the Resources in this module is the Rutherford (2008) article Standardized Nursing Language: What Does It Mean for Nursing Practice? In this article, the author recounts a visit to a local hospital to view the recent implementation of a new coding system.
During the visit, one of the nurses commented to her, “We document our care using standardized nursing languages but we don’t fully understand why we do” (Rutherford, 2008, para. 1).
How would you respond to a comment such as this one?
To Prepare:
Review the concepts of informatics as presented in the Resources, particularly Rutherford, M. (2008) Standardized Nursing Language: What Does It Mean for Nursing Practice? Standardized Nursing Terminology
Reflect on the role of a nurse leader as a knowledge worker.
Consider how knowledge may be informed by data that is collected/accessed.
The Assignment:
In a 2- to 3-page paper, address the following:
Explain how you would inform this nurse (and others) of the importance of standardized nursing terminologies.
Describe the benefits and challenges of implementing standardized nursing terminologies in nursing practice. Be specific and provide examples.
Be sure to support your paper with peer-reviewed research on standardized nursing terminologies that you consulted from the Walden Library.
Background: Nursing has always faced two significant challenges: (a) how to distinguish nursing’s contributions to patient care from those of medicine; and (b) how to incorporate descriptions of nursing care into the health record in a way that is commensurate with its importance to patients’ well-being.
As the development of the Electronic Health Record (EHR) and the Nationwide Health Information Network (NHIN), both of which rely on the EHR, accelerates, these issues become even more pressing.
Nursing’s contribution to patient care must be identified, and the optimum strategy to include parts of nursing care into the EHR must be determined. Standardized Nursing Terminology
Fortunately, the solution is already in place; it is found in the application of standardized nursing terminologies (SNTs).
The adoption of standardized terminology that reflect the uniqueness of nursing care is required to capture nursing’s independent contributions.
The professional languages used and understood within and between both professions are a major factor in distinguishing between the goals and practices of nursing and medicine.
The following are some of the advantages of using standardized nursing terminologies: (a) improved communication between nurses and other healthcare providers, (b) increased visibility of nursing interventions, (c) improved patient care, (d) improved data collection to evaluate nursing care outcomes, (e) greater adherence to standards of care, and (f) facilitation of nursing competency assessment. Standardized Nursing Terminology
Mr. Rogers is 2 days postoperative of a thoracotomy for removal of a malignant mass in his left chest. His pain is being managed via an epidural catheter with morphine (an opioid analgesic). As the nurse assumes care of Mr. Rogers, he is alert and fully oriented, and states that his current pain is 2 on a 1-to-10 scale. His vital signs are 37.8 – 92 – 12, 138/82. (Learning Objective 6)
What are benefits of epidural versus systemic administration of opioids?
b. The nurse monitors Mr. Rogers’ respiratory status and vital signs every 2 hours. What is the rationale for these frequent assessments?
c. The nurse monitors Mr. Rogers for what other complications of epidural analgesia?
d. Mr. Rogers complains of a severe headache. What should the nurse do?
e. Mr. Rogers’ epidural morphine and decreased mobility increase his chances of constipation. What interventions should be included in his plan of care to minimize constipation? QUESTION: Pain Management
Chapter 13, Fluid and Electrolytes: Balance and Disturbance
Mrs. Dean is 75-year-old woman admitted to the hospital for a small bowel obstruction. Her medical history includes hypertension. Mrs. Dean is NPO. She has a nasogastric (NG) tube to low continuous suction. She has an IV of 0.9% NS at 83 mL/hr. Current medications include furosemide 20 mg daily and hydromorphone 0.2 mg every 4 hours, as needed for pain. The morning electrolytes reveal serum potassium of 3.2 mEq/L. (Learning Objective 4)
a. What are possible causes of a low potassium level?
b. What action should the nurse take in relation to the serum potassium level?
c. What clinical manifestations might the nurse assess in Mrs. Dean? QUESTION: Pain Management
Question Description
Clinical inquiry is the practice of asking questions about clinical practice. To continuously improve patient care, all nurses should consistently use clinical inquiry to question why they are doing something the way they are doing it. Do they know why it is done this way, or is it just because we have always done it this way? Is it a common practice or a best practice?
In this Assignment, you will identify clinical areas of interest and inquiry and practice searching for research in support of maintaining or changing these practices. You will also analyze this research to compare research methodologies employed.
To Prepare:
Review the Resources and identify a clinical issue of interest that can form the basis of a clinical inquiry.
Based on the clinical issue of interest and using keywords related to the clinical issue of interest, search at least four different databases in the Walden Library to identify at least four relevant peer-reviewed articles related to your clinical issue of interest.
Review the results of your peer-reviewed research and reflect on the process of using an unfiltered database to search for peer-reviewed research. Discussion:Clinical Inquiry Research
Reflect on the types of research methodologies contained in the four relevant peer-reviewed articles you selected.
Part 1: An Introduction to Clinical Inquiry
Create a 4- to 5-slide PowerPoint presentation in which you do the following:
Identify and briefly describe your chosen clinical issue of interest.
Describe how you used keywords to search on your chosen clinical issue of interest.
Identify the four research databases that you used to conduct your search for the peer-reviewed articles you selected.
Provide APA citations of the four peer-reviewed articles you selected.
Part 2: Identifying Research Methodologies
After reading each of the four peer-reviewed articles you selected, use the Matrix Worksheet template to analyze the methodologies applied in each of the four peer-reviewed articles. Your analysis should include the following:
The full citation of each peer-reviewed article in APA format.
A brief (1-paragraph) statement explaining why you chose this peer-reviewed article and/or how it relates to your clinical issue of interest, including a brief explanation of the ethics of research related to your clinical issue of interest.
A brief (1-2 paragraph) description of the aims of the research of each peer-reviewed article.
A brief (1-2 paragraph) description of the research methodology used. Be sure to identify if the methodology used was qualitative, quantitative, or a mixed-methods approach. Be specific.
A brief (1- to 2-paragraph) description of the strengths of each of the research methodologies used, including reliability and validity of how the methodology was applied in each of the peer-reviewed articles you selected.
Question Description
Clinical inquiry is the practice of asking questions about clinical practice. To continuously improve patient care, all nurses should consistently use clinical inquiry to question why they are doing something the way they are doing it. Do they know why it is done this way, or is it just because we have always done it this way? Is it a common practice or a best practice?
In this Assignment, you will identify clinical areas of interest and inquiry and practice searching for research in support of maintaining or changing these practices. You will also analyze this research to compare research methodologies employed.
To Prepare:
Review the Resources and identify a clinical issue of interest that can form the basis of a clinical inquiry.
Based on the clinical issue of interest and using keywords related to the clinical issue of interest, search at least four different databases in the Walden Library to identify at least four relevant peer-reviewed articles related to your clinical issue of interest.
Review the results of your peer-reviewed research and reflect on the process of using an unfiltered database to search for peer-reviewed research. Discussion:Clinical Inquiry Research
Reflect on the types of research methodologies contained in the four relevant peer-reviewed articles you selected.
Part 1: An Introduction to Clinical Inquiry
Create a 4- to 5-slide PowerPoint presentation in which you do the following:
Identify and briefly describe your chosen clinical issue of interest.
Describe how you used keywords to search on your chosen clinical issue of interest.
Identify the four research databases that you used to conduct your search for the peer-reviewed articles you selected.
Provide APA citations of the four peer-reviewed articles you selected.
Part 2: Identifying Research Methodologies
Discussion:Clinical Inquiry Research
After reading each of the four peer-reviewed articles you selected, use the Matrix Worksheet template to analyze the methodologies applied in each of the four peer-reviewed articles. Your analysis should include the following:
The full citation of each peer-reviewed article in APA format.
A brief (1-paragraph) statement explaining why you chose this peer-reviewed article and/or how it relates to your clinical issue of interest, including a brief explanation of the ethics of research related to your clinical issue of interest.
A brief (1-2 paragraph) description of the aims of the research of each peer-reviewed article.
A brief (1-2 paragraph) description of the research methodology used. Be sure to identify if the methodology used was qualitative, quantitative, or a mixed-methods approach. Be specific.
A brief (1- to 2-paragraph) description of the strengths of each of the research methodologies used, including reliability and validity of how the methodology was applied in each of the peer-reviewed articles you selected. Discussion:Clinical Inquiry Research
https://superbnursingessays.com/wp-content/uploads/2022/01/LOGO-300x75.png00Naomi Nashttps://superbnursingessays.com/wp-content/uploads/2022/01/LOGO-300x75.pngNaomi Nas2022-06-08 08:47:392022-06-08 08:47:39Discussion:Clinical Inquiry Research
The outstanding role that Psychiatric mental health nurse practitioners play in the management of psychiatric disorders cannot be underestimated. Undeniably, their knowledge regarding the pathophysiology of multifarious mental disorders need to be top notch. However, in addition to the pathophysiological knowhow, PMNHPs need to understand the various mechanisms of action of relevant medications and the manner in which they influence the central nervous system to stabilize the neurochemicals responsible for the existence of these conditions. Thus, PMNHPs require to have knowledge concerning the impact of psychopharmacological medications from their agnostic-to-antagonist spectrum of action. In addition, knowing about the roles of g-coupled proteins and ion gated channels in the entire process of managing mental health conditions becomes an important tool for these nurses. Further, other factors such as epigenetics also influence the pharmacologic action of drugs. As such, a collation of the above information may be fundamental in the prescription of medications to clients; hence, their analysis becomes important. NURS 6630 Discussion: Foundational Neuroscience
Agonist-To-Antagonist Spectrum of Action of Psychopharmacologic Agents
The prescription of psychopharmacological agents occurs based on the mechanisms of action of each molecule. Fundamentally, pharmacological actions of antipsychotics such as agonism and antagonism principally influences neurotransmitters or receptors. According to scholarship on the matter, agonists are referred to as the kinds of drugs or receptor ligands that bind to certain receptors in order to produce the desired therapeutic effect (Lee & Barron, 2017). Specifically, agonists bind to receptors and modulate the activation of the receptors in order to produce the requisite action. The modulation occurs when the agonists alter the conformation of the receptor in order to optimally open the ion channel as well as induce the maximum frequency of the receptors for binding purposes. As a consequence, a maximum downstream signal transduction that has the capacity to be mediated by a receptor occurs.
The above spectrum then moves to antagonists, which are utilized to stabilize the receptor to the resting phase. In other words, the antagonists are used to return ta receptor to its state when the agonists were not available. However, the resting state occasioned by the antagonists still has certain levels of ion flowing through the channel since the ion channel is not fully closed. Therefore, the agonist-to-antagonist spectrum of pharmacological agents entails agonists that open a receptor channel to maximal frequency and amount via antagonists that retain the resting state of a receptor, and lastly to inverse agonists that close and inactivate the receptor ion channel (Stahl, 2013). In between the antagonists and agonists are partial agonists that partially influences the receptor ion channels in comparison to the two. Further, antagonists have the potential to block everything within the agonist spectrum thus ensuring that the ion channel returns to its resting state. Thus, psychopharmacological agents assume this spectrum when addressing certain mental health conditions……………………………….. NURS 6630 Discussion: Foundational Neuroscience
NUR 6630 Week 1 Discussion: Foundational Neuroscience
In one’s role as a psychiatric mental health nurse practitioner, it becomes critically important that they possess knowledge in foundational neuroscience. The knowledge is particularly significant when it comes to the diagnosis and treatment of clients as it will
enable one to comprehend the pathophysiology of the various conditions in addition to the impact of psychotropic medications on the central nervous system. However, the theories involved in foundational neuroscience can become very difficult to understand. For this reason, the present Discussion: Foundational Neuroscience isformulated to encourage one to ruminate about the concepts, establish a rationale for their thinking as well as deepen their understanding by interaction with their colleagues.
Learning Objectives
Students will:
Compare the actions of g couple proteins to ion gated channels
Analyze the agonist-to-antagonist spectrum of action of psychopharmacologic agents
Analyze the impact of foundational neuroscience on the prescription of medications
Analyze the role of epigenetics in pharmacologic action
Learning Resources
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.
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) NURS 6630 Discussion: Foundational Neuroscience
Note: The approximate length of this media piece is 3 minutes.
Accessible player
Discussion: Foundational Neuroscience
The traditional receptor theory classified the pharmacological agents as agonists and antagonists. An agonist is a chemical substance that binds to the receptor to stabilize the receptor inactive conformation to produce a biological response. The agonist causes the action, whereas the antagonist blocks the effect of an agonist. The drugs that fix and stimulates the receptor are known as an agonist, and the drugs that fix but not stimulate the receptors are known as the agonist. The agonists have two main properties, which are affinity and efficacy. Affinity is the tendency of the medicine to bind with the target cells or receptor, and efficacy is the capability of the agonist to generate biological influence by affecting neurotransmitter function and influencing or activating the target receptor sites (Beaulieu and Gainetdinov, 2011). The same receptor type can be related to a different kind of drug-producing the same response despite being different in affinity and functionality. The antagonist has the affinity but not efficacy; hence they occupy the receptor and stops or reduce the agonists from producing the response. The intrinsic efficacy of the agonists is variable and is characterized as full or partial agonists. The partial agonists are the psychotropic drugs that influence the receptors to a smaller degree than the natural neurotransmitters (Stahl, 2013). For example, aripiprazole is partial agonist dopamine and is effective in treating Schizophrenia by acting as an antipsychotic. A partial agonist can produce either agonist or antagonist effects. When a partial agonist is utilized with the full agonist, a partial agonist produces an antagonist effect by competing with the full agonist (Berg & Clarke, 2018). For example, methadone is full opioid agonist while buprenorphine is a partial agonist in the absence of the methadone reducing craving and withdrawal. Buprenorphine has a strong affinity for opioid receptors as it acts as a partial antagonist and competes against morphine methadone to reduce its affinity. When Buprenorphine (partial agonist) and naloxone are given together, naloxone has inverse agonist effects that prevent abuse (Lutfy & Cowan, 2004). NURS 6630 Discussion: Foundational Neuroscience
Comparisons and contrast of the actions of g couple protein and ion gated channels
Ion channel receptors are an essential component of the nervous system that signals and directly converts a chemical neurotransmitter message to an electrical current. Protein-protein interactions with other ion channels regulate ionotropic receptors, G-protein coupled receptors, and intracellular proteins (Li, Wong & Lu, 2014). G-couple proteins have receptors that are structured with seven transmembrane regions. They span the membrane seven times, containing binding sites for neurotransmitters that enable targeting specific psychotropic drugs (Stahl, 2013). G-protein is responsible for maintaining the electrochemical gradient across the cell. Ion channels open and close in direct response to the binding of a chemical messenger like a neurotransmitter. Both ion-gated channels and G-couple protein are protein receptors embedded in the cell membranes that bind to a signaling molecule (Stahl, 2013). Membrane changes can cause an electrical current, resulting in a pulse of neurotransmitter and electrical signal or change of voltage across the targeted cell membrane, which will allow for rapid transmission of the signal synapse.
Role of epigenetics in the pharmacologic action
Epigenetics is the mechanism of gene control that can promote or suppress the expression of the genes without altering the genetic coding of an organism. In epigenetics, an explanation of the composition of all the cells in the body is similar to gene pairs, but differentiation in the elements of deleted or expressed genes is described. Neurotransmission, genes, drugs, or environment determines the type of genes which are expressed or inhibited and influence the memory, stress response, brain learning, mental disorders, and improvement of disorders through drugs or psychotherapy (Stahl, 2013). Epigenetics does not directly affect people’s psychiatric or mental health but affects the way medication works on the patient (Stefanski, & MacEwan, 2015).
Explanation of the impact on the prescription of medications to clients
As a health care provider, it is essential to know the drug actions and interactions and the importance of the concepts before prescribing the medication to clients. For example, for the treatment of benzodiazepine overdose, flumazenil is utilized. Flumazenil is a benzodiazepine antagonist. Transduction reduction occurs when an agonist is present, and the antagonist is given as channels get closed instead of maximal flow (Nutt, Stahl, Blier, Drago & Zohar, 2017). Therefore, it is essential to know the mechanism to prevent complications & to improve the clinical effect when utilizing multiple medications. In addition, patients who have developed a dependence on benzodiazepines may experience withdrawal symptoms such as seizures when administrated flumazenil (Nutt, Stahl, Blier, Drago & Zohar, 2017).
References
Beaulieu, J. M., and Gainetdinov, R. R. (2011). The physiology, signaling, and pharmacology of dopamine receptors. Pharmacology. Rev. 63, 182–217. Retrieved from doi: 10.1124/pr.110.002642.
Berg, K. A., & Clarke, W. P. (2018). Making Sense of Pharmacology: Inverse Agonism and Functional Selectivity. The international journal of Neuropsychopharmacology, 21(10), 962–977. https://doi.org/10.1093/ijnp/pyy071
Li, S., Wong, A. H., & Liu, F. (2014). Ligand-gated ion channel interacting proteins and their role in neuroprotection. Frontiers in cellular neuroscience, 8, 125. https://doi.org/10.3389/fncel.2014.00125
Lutfy, K., & Cowan, A. (2004). Buprenorphine: a unique drug with complex pharmacology. Current Neuropharmacology, 2(4), 395–402. https://doi.org/10.2174/1570159043359477
Nutt, D.S., Stahl, A.P, Blier, D., Drago, N.S., & Zohar. Key Concept in Psychopharmacology. Psychiatry 6(7), 263-267. Retrieved from https://doi.org/10.1016/j.mppsy.2007.05.002.
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
Stefanski, B., & MacEwan, D. J. (2015, June). Epigenetics and pharmacology. British Journal of Pharmacology, 172(11), 2701-2704.
SAMPLE 3
Discussion Post Week 1
When a drug binds to a receptor there are one of two paths it can take; these drugs either mimic the action of the regulatory molecules or they block the action of these regulatory molecules. An agonist is defined as a drug that mimics the body’s regulatory molecules. Partial agonists are drugs that can bind to the receptor but are not capable of producing the full effect of an agonist. These partial agonists produce responses that are moderately intrinsic. Any drug that has been classified as an antagonist will block the receptors so that they are unable to bind to the agonist (Rosenthal & Burchum, 2021). NURS 6630 Discussion: Foundational Neuroscience
One example of how a partial agonist may affect the overall efficacy of psychopharmacologic treatment would be the treatment of pain with the medication pentazocine, this medication alone could potentially offer some relief to the patient by binding to the receptors. If pentazocine is administered and the patient has already received the medication meperidine which is a full agonist, the pentazocine may alter the efficacy of the pentazocine by blocking some of the receptors; this partial agonist will not only be working as if it is an agonist but also appear to be working as an antagonist (Rosenthal & Burchum, 2021).
Two classes of postsynaptic receptors are G-protein coupled receptors and ion gated channels. Neurotransmitter receptors that are ligand-gated ion channels typically cause more rapid postsynaptic responses, G protein-coupled receptors mediate slower postsynaptic responses (Lodish et al, 2000).
As a provider, it is especially important to understand which medications our patients are prescribed and what each of these medications mechanism of action is if we unknowingly provide the patient with two medications that bind to the same receptors, we may in fact reduce the risk of properly treating our patient and causing the patient a great deal of pain or discomfort.
Epigenetics is the concept that genes may be altered without the alteration of the gene code and gene function maybe inherited (Stern et. al, 2016). Using epigenetics in pharmacology is beneficial as it allows us to create medications that can target many different receptor types and in turn provide more of a “global response” type of care (Stefanska & MacEwan, 2015). This type of epigenetic regulatory mechanism could potentially regulate large groups of genes, and this large group of genes maybe the underlying cause of a particular disease. By using epigenetics and a more global type of response we can treat diseases more effectively while if we were to target one single protein we may not be as successful in treating our patients.
References:
Rosenthal, L. D., & Burchum, J. R. (2021). Lehne’s pharmacotherapeutics for advanced
practice nurses and physician assistants (2nd ed.) St. Louis, MO: Elsevier.
Lodish, H., Berk, A., & Zibursky, S. L. (2000). Molecular cell biology 4th edition. W H Freeman
& Co.
Stern T.A, Favo, M., Wilens, T.E., & Rosenbaum, J. F. (2016). Massachusetts General Hospital Psychopharmacology and neurotherapeutics (pp. 1-19). Elsevier.
Stefanska, B., & MacEwan, D. J. (2015). Epigenetics and pharmacology. British journal of pharmacology, 172(11), 2701–2704. https://doi.org/10.1111/bph.13136
Optional Resources
Laureate Education (Producer). (2009). Pathopharmacology: Disorders of the nervous system: Exploring the human brain [Video file]. Baltimore, MD: Author.
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.
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.
Rubric Detail
Select Grid View or List View to change the rubric’s layout.
Name: NURS_6630_Week2_Discussion_Rubric
Response to the Discussion question is reflective with critical analysis and synthesis representative of knowledge gained from the course readings for the module and current credible sources.
40 (40%) – 44 (44%)
Thoroughly responds to the Discussion question(s).
Is reflective with critical analysis and synthesis representative of knowledge gained from the course readings for the module and current credible sources. NURS 6630 Discussion: Foundational Neuroscience
No less than 75% of post has exceptional depth and breadth.
Supported by at least three current credible sources.
35 (35%) – 39 (39%)
Responds to most of the Discussion question(s).
Is somewhat reflective with critical analysis and synthesis representative of knowledge gained from the course readings for the module.
50% of the post has exceptional depth and breadth.
Supported by at least three credible references.
31 (31%) – 34 (34%)
Responds to some of the Discussion question(s).
One to two criteria are not addressed or are superficially addressed.
Is somewhat lacking reflection and critical analysis and synthesis.
Somewhat represents knowledge gained from the course readings for the module.
Post is cited with fewer than two credible references.
0 (0%) – 30 (30%)
Does not respond to the Discussion question(s).
Lacks depth or superficially addresses criteria.
Lacks reflection and critical analysis and synthesis.
Does not represent knowledge gained from the course readings for the module.
Contains only one or no credible references.
Main Posting:
Writing
6 (6%) – 6 (6%)
Written clearly and concisely.
Contains no grammatical or spelling errors.
Adheres to current APA manual writing rules and style.
5 (5%) – 5 (5%)
Written concisely.
May contain one to two grammatical or spelling errors.
Adheres to current APA manual writing rules and style.
4 (4%) – 4 (4%)
Written somewhat concisely.
May contain more than two spelling or grammatical errors.
Contains some APA formatting errors.
0 (0%) – 3 (3%)
Not written clearly or concisely.
Contains more than two spelling or grammatical errors.
Does not adhere to current APA manual writing rules and style.
Main Posting:
Timely and full participation
9 (9%) – 10 (10%)
Meets requirements for timely, full, and active participation.
Posts main Discussion by due date.
8 (8%) – 8 (8%)
Posts main Discussion by due date.
Meets requirements for full participation.
7 (7%) – 7 (7%)
Posts main Discussion by due date.
0 (0%) – 6 (6%)
Does not meet requirements for full participation.
Does not post main Discussion by due date.
First Response:
Post to colleague’s main post that is reflective and justified with credible sources.
9 (9%) – 9 (9%)
Response exhibits critical thinking and application to practice settings.
Responds to questions posed by faculty.
The use of scholarly sources to support ideas demonstrates synthesis and understanding of learning objectives.
8 (8%) – 8 (8%)
Response has some depth and may exhibit critical thinking or application to practice setting.
7 (7%) – 7 (7%)
Response is on topic, may have some depth.
0 (0%) – 6 (6%)
Response may not be on topic, lacks depth.
First Response:
Writing
6 (6%) – 6 (6%)
Communication is professional and respectful to colleagues.
Response to faculty questions are fully answered, if posed.
Provides clear, concise opinions and ideas that are supported by two or more credible sources.
Response is effectively written in Standard, Edited English.
5 (5%) – 5 (5%)
Communication is mostly professional and respectful to colleagues.
Response to faculty questions are mostly answered, if posed.
Provides opinions and ideas that are supported by few credible sources.
Response is written in Standard, Edited English.
4 (4%) – 4 (4%)
Response posed in the Discussion may lack effective professional communication.
Response to faculty questions are somewhat answered, if posed.
Few or no credible sources are cited.
0 (0%) – 3 (3%)
Responses posted in the Discussion lack effective communication.
Response to faculty questions are missing.
No credible sources are cited.
First Response:
Timely and full participation
5 (5%) – 5 (5%)
Meets requirements for timely, full, and active participation.
Posts by due date.
4 (4%) – 4 (4%)
Meets requirements for full participation.
Posts by due date.
3 (3%) – 3 (3%)
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0 (0%) – 2 (2%)
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Second Response:
Post to colleague’s main post that is reflective and justified with credible sources.
9 (9%) – 9 (9%)
Response exhibits critical thinking and application to practice settings.
Responds to questions posed by faculty.
The use of scholarly sources to support ideas demonstrates synthesis and understanding of learning objectives.
8 (8%) – 8 (8%)
Response has some depth and may exhibit critical thinking or application to practice setting.
7 (7%) – 7 (7%)
Response is on topic, may have some depth.
0 (0%) – 6 (6%)
Response may not be on topic, lacks depth.
Second Response:
Writing
6 (6%) – 6 (6%)
Communication is professional and respectful to colleagues.
Response to faculty questions are fully answered, if posed.
Provides clear, concise opinions and ideas that are supported by two or more credible sources.
Response is effectively written in Standard, Edited English.
5 (5%) – 5 (5%)
Communication is mostly professional and respectful to colleagues.
Response to faculty questions are mostly answered, if posed.
Provides opinions and ideas that are supported by few credible sources.
Response is written in Standard, Edited English.
4 (4%) – 4 (4%)
Response posed in the Discussion may lack effective professional communication.
Response to faculty questions are somewhat answered, if posed.
Few or no credible sources are cited.
0 (0%) – 3 (3%)
Responses posted in the Discussion lack effective communication.
Response to faculty questions are missing.
No credible sources are cited.
Second Response:
Timely and full participation
5 (5%) – 5 (5%)
Meets requirements for timely, full, and active participation.
Posts by due date.
4 (4%) – 4 (4%)
Meets requirements for full participation.
Posts by due date.
3 (3%) – 3 (3%)
Posts by due date.
0 (0%) – 2 (2%)
Does not meet requirements for full participation.
Does not post by due date.
Total Points: 100
Name: NURS_6630_Week2_Discussion_Rubric
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
Ion channels as targets of psychopharmacological drug action
Many important psychopharmacological drugs target ion channels. The roles of ion channels as important regulators of synaptic neurotransmission were covered in Chapter 1. Here we discuss how targeting these molecular sites causes alterations in synaptic neurotransmission that are linked in turn to the therapeutic actions of various psychotropic drugs. Specifically, we cover ligand-gated ion channels and voltage-sensitive ion channels as targets of psychopharmacological drug action.
Ligand-gated ion channels as targets of psychopharmacological drug action
Ligand-gated ion channels, ionotropic receptors, and ion-channel-linked receptors: different terms for the same receptor/ion-channel complex
Ions normally cannot penetrate membranes because of their charge. In order to selectively control access of ions into and out of neurons, their membranes are decorated with all sorts of ion channels. The most important ion channels in psychopharmacology regulate calcium, sodium, chloride, and potassium. Many can be modified by various drugs, and this will be discussed throughout this chapter.
There are two major classes of ion channels, and each class has several names. One class of ion channels is opened by neurotransmitters and goes by the names ligand-gated ion channels, ionotropic receptors, and ion-channel-linked receptors. These channels and their associated receptors will be discussed next. The other major class of ion channel is opened by the charge or voltage across the membrane and is called either a voltage-sensitive or a voltage-gated ion channel; these will be discussed later in this chapter.
Ion channels that are opened and closed by actions of neurotransmitter ligands at receptors acting as gatekeepers are shown conceptually in Figure 3-1. When a neurotransmitter binds to a gatekeeper receptor on an ion channel, that neurotransmitter causes a conformational change in the receptor that opens the ion channel (Figure 3-1A). A neurotransmitter, drug, or hormone that binds to a receptor is sometimes called a ligand (literally, “tying”). Thus, ion channels linked to receptors that regulate their opening and closing are often called ligand-gated ion channels. Since these ion channels are also receptors, they are sometimes also called ionotropic receptors or ion-channel-linked receptors.
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Figure 3-1.Ligand-gated ion channel gatekeeper. This schematic shows a ligand-gated ion channel. In panel A, a receptor is serving as a molecular gatekeeper that acts on instruction from neurotransmission to open the channel and allow ions to travel into the cell. In panel B, the gatekeeper is keeping the channel closed so that ions cannot get into the cell. Ligand-gated ion channels are a type of receptor that forms an ion channel and are thus also called ion-channel-linked receptors or ionotropic receptors.
These terms will be used interchangeably with ligand-gated ion channels here.Numerous drugs act at many sites around such receptor/ion-channel complexes, leading to a wide variety of modifications of receptor/ion-channel actions. These modifications not only immediately alter the flow of ions through the channels, but with a delay can also change the downstream events that result from transduction of the signal that begins at these receptors. The downstream actions have been extensively discussed in Chapter 1 and include both activation and inactivation of phosphoproteins, shifting the activity of enzymes, the sensitivity of receptors, and the conductivity of ion channels. Other downstream actions include changes in gene expression and thus changes in which proteins are synthesized and which functions are amplified. Such functions can range from synaptogenesis, to receptor and enzyme synthesis, to communication with downstream neurons innervated by the neuron with the ionotropic receptor, and many more. The reader should have a good command of the function of signal transduction pathways described in Chapter 1 in order to understand how drugs acting at ligand-gated ion channels modify the signal transduction that arises from these receptors.
Drug-induced modifications in signal transduction from ionotropic (sometimes called ionotrophic) receptors can have profound actions on psychiatric symptoms. About a fifth of psychotropic drugs currently utilized in clinical practice, including many drugs for the treatment of anxiety and insomnia such as the benzodiazepines, are known to act at these receptors. Because ionotropic receptors immediately change the flow of ions, drugs that act on these receptors can have an almost immediate effect, which is why many anxiolytics and hypnotics that act at these receptors may have immediate clinical onset. This is in contrast to the actions of many drugs at G-protein-linked receptors described in Chapter 2, some of which have clinical effects – such as antidepressant actions – that may occur with a delay necessitated by awaiting initiation of changes in cellular functions activated through the signal transduction cascade. Here we will describe how various drugs stimulate or block various molecular sites around the receptor/ion-channel complex. Throughout the textbook we will show how specific drugs acting at specific ionotropic receptors have specific actions on specific psychiatric disorders.
Ligand-gated ion channels: structure and function
Are ligand-gated ion channels receptors or ion channels? The answer is “yes” – ligand-gated ion channels are a type of receptor and they also form an ion channel. That is why they are called not only a channel (ligand-gated ion channel) but also a receptor (ionotropic receptor or ion-channel-linked receptor). These terms try to capture the dual function of these ion channels/receptors.
Ligand-gated ion channels comprise several long strings of amino acids assembled as subunits around an ion channel. Decorating these subunits are also multiple binding sites for everything from neurotransmitters to ions to drugs. That is, these complex proteins have several sites where some ions travel through a channel and others also bind to the channel; where one neurotransmitter or even two cotransmitters act at separate and distinct binding sites; where numerous allosteric modulators – i.e., natural substances or drugs that bind to a site different than where the neurotransmitter binds – increase or decrease the sensitivity of channel opening.
Pentameric subtypes
Many ligand-gated ion channels are assembled from five protein subunits; that is why they are called pentameric. The subunits for pentameric subtypes of ligand-gated ion channels each have four transmembrane regions (Figure 3-2A). These membrane proteins go in and out of the membrane four times (Figure 3-2A). When five copies of these subunits are selected (Figure 3-2B), they come together in space to form a fully functional pentameric receptor with the ion channel in the middle (Figure 3-2C). The receptor sites are in various locations on each of the subunits; some binding sites are in the channel, but many are present at different locations outside the channel. This pentameric structure is typical for GABAA receptors, nicotinic cholinergic receptors, serotonin 5HT3 receptors, and glycine receptors (Table 3-1). Drugs that act directly on pentameric ligand-gated ion channels are listed in Table 3-2.
If this structure were not complicated enough, pentameric ionotropic receptors actually have many different subtypes. Subtypes of pentameric ionotropic receptors are defined based upon which forms of each
Table 3-1 Pentameric ligand-gated ion channels
of the five subunits are chosen for assembly into a fully constituted receptor. That is, there are several subtypes for each of the four transmembrane subunits, making it possible to piece together several different constellations of fully constituted receptors. Although the natural neurotransmitter binds to every subtype of ionotropic receptor, some drugs used in clinical practice, and many more in clinical trials, are able to bind selectively to one or more of these subtypes, but not to others. This may have functional and clinical consequences. Specific receptor subtypes and the specific drugs that bind to them selectively are discussed in chapters that cover their specific clinical use.
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Figure 3-2.Ligand-gated ion channel structure. The four transmembrane regions of a single subunit of a pentameric ligand-gated ion channel form a cluster, as shown in panel A. An icon for this subunit is shown on the right in panel A. Five copies of the subunits come together in space (panel B) to form a functional ion channel in the middle (panel C). Pentameric ligand-gated ion channels have receptor binding sites located on all five subunits, both inside and outside the channel.
Table 3-2 Key ligand-gated ion channels directly targeted by psychotropic drugs
Ionotropic glutamate receptors have a different structure from the pentameric ionotropic receptors just discussed. The ligand-gated ion channels for glutamate comprise subunits that have three full transmembrane regions and a fourth re-entrant loop (Figure 3-3A), rather than four full transmembrane regions as shown in Figure 3-2A. When four copies of these subunits are selected (Figure 3-3B), they come together in space to form a fully functional ion channel in the middle with the four re-entrant loops lining the ion channel (Figure 3-3C). Thus, tetrameric subtypes of ion channels (Figure 3-3) are analogous to pentameric subtypes of ion channels (Figure 3-2), but have just four subunits rather than five. Receptor sites are in various locations on each of the subunits; some binding sites are in the channel, but many are present at different locations outside the channel.
This tetrameric structure is typical of the ionotropic glutamate receptors known as AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid) and NMDA (N-methyl-d-aspartate) subtypes (Table 3-3). Drugs that act directly at tetrameric ionotropic glutamate receptors are listed in Table 3-2. Receptor subtypes for glutamate according to the selective agonist acting at that receptor, as well as the specific molecular subunits that comprise that subtype, are listed in Table 3-3. Subtype-selective drugs for ionotropic glutamate receptors are under investigation but not currently used in clinical practice. NURS 6630 Discussion: Foundational Neuroscience
The agonist spectrum
The concept of an agonist spectrum for G-protein-linked receptors, discussed extensively in Chapter 2, can also be applied to ligand-gated ion channels (Figure 3-4). Thus, full agonists change the conformation of the receptor to open the ion channel the maximal amount and frequency allowed by that binding site (Figure 3-5). This then triggers the maximal amount of downstream signal transduction possible to be mediated by this binding site. The ion channel can open to an even greater extent (i.e., more frequently) than with a full agonist alone, but this requires the help of a second receptor site, that of a positive allosteric modulator, or PAM, as will be shown later.
Antagonists stabilize the receptor in the resting state, which is the same as the state of the receptor in the absence of agonist (Figure 3-6). Since there is no difference between the presence and absence of the antagonist, the antagonist is said to be neutral or silent. The resting state is not a fully closed ion channel, so there is some degree of ion flow through the channel even in the absence of agonist (Figure 3-6A) and even in the presence of antagonist (Figure 3-6B). This is due to occasional and infrequent opening of the channel even when an agonist is not present and even when an antagonist is present. This is called constitutive activity and is also discussed in Chapter 2 for G-protein-linked receptors. Antagonists
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Figure 3-3.Tetrameric ligand-gated ion channel structure. A single subunit of a tetrameric ligand-gated ion channel is shown to form a cluster in panel A, with an icon for this subunit shown on the right in panel A. Four copies of these subunits come together in space (panel B) to form a functional ion channel in the middle (panel C). Tetrameric ligand-gated ion channels have receptor binding sites located on all four subunits, both inside and outside the channel.
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Figure 3-4.Agonist spectrum. The agonist spectrum and its corresponding effects on the ion channel are shown here. This spectrum ranges from agonists (on the far left), which open the channel the maximal amount and frequency allowed by that binding site, through antagonists (middle of the spectrum), which retain the resting state with infrequent opening of the channel, to inverse agonists (on the far right), which put the ion channel into a closed and inactive state. Between agonists and antagonists are partial agonists, which increase the degree and frequency of ion-channel opening as compared to the resting state, but not as much as a full agonist. Antagonists can block anything in the agonist spectrum, returning the ion channel to the resting state in each instance.
of ion-channel-linked receptors reverse the action of agonists (Figure 3-7) and bring the receptor conformation back to the resting baseline state, but do not block any constitutive activity.Partial agonists produce a change in receptor conformation such that the ion channel opens to a greater extent and more frequently than in its resting state but less than in the presence of a full agonist (Figures 3-8 and 3-9). An antagonist reverses a partial agonist, just as it reverses a full agonist, returning the receptor to its resting state (Figure 3-10). Partial agonists thus produce ion flow and downstream signal transduction that is something more than the resting state in the absence of agonist, yet something less than a full agonist. Just as is the case for G-protein-linked receptors, how close this partial agonist is to a full agonist or to a silent antagonist on the agonist spectrum will determine the impact of a partial agonist on downstream signal transduction events.
The ideal therapeutic agent in some cases may need to have ion flow and signal transduction that is not too hot, yet not too cold, but just right, called the “Goldilocks” solution in Chapter 2, a concept that can apply here to ligand-gated ion channels as well. Such
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Figure 3-5.Actions of an agonist. In panel A, the ion channel is in its resting state, during which the channel opens infrequently (constitutive activity). In panel B, the agonist occupies its binding site on the ligand-gated ion channel, increasing the frequency at which the channel opens. This is represented as the red agonist turning the receptor red and opening the ion channel.
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Figure 3-6.Antagonists acting alone. In panel A, the ion channel is in its resting state, during which the channel opens infrequently. In panel B, the antagonist occupies the binding site normally occupied by the agonist on the ligand-gated ion channel. However, there is no consequence to this, and the ion channel does not affect the degree or frequency of opening of the channel compared to the resting state. This is represented as the yellow antagonist docking into the binding site and turning the receptor yellow but not affecting the state of the ion channel.
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Figure 3-7.Antagonist acting in presence of agonist. In panel A, the ion channel is bound by an agonist, which causes it to open at a greater frequency than in the resting state. This is represented as the red agonist turning the receptor red and opening the ion channel as it docks into its binding site. In panel B, the yellow antagonist prevails and shoves the red agonist off the binding site, reversing the agonist’s actions and restoring the resting state. Thus, the ion channel has returned to its status before the agonist acted.
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Figure 3-8.Actions of a partial agonist. In panel A, the ion channel is in its resting state and opens infrequently. In panel B, the partial agonist occupies its binding site on the ligand-gated ion channel and produces a conformational change such that the ion channel opens to a greater extent and at a greater frequency than in the resting state, though less than in the presence of a full agonist. This is depicted by the orange partial agonist turning the receptor orange and partially but not fully opening the ion channel.
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Figure 3-9.Net effect of partial agonist. Partial agonists act either as net agonists or as net antagonists, depending on the amount of agonist present. When full agonist is absent (on the far left), a partial agonist causes the channel to open more frequently as compared to the resting state and thus has a net agonist action (moving from left to right). However, in the presence of a full agonist (on the far right), a partial agonist decreases the frequency of channel opening in comparison to the full agonist and thus acts as a net antagonist (moving from right to left).
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Figure 3-10.Antagonist acting in presence of partial agonist. In panel A, a partial agonist occupies its binding site and causes the ion channel to open more frequently than in the resting state. This is represented as the orange partial agonist docking to its binding site, turning the receptor orange, and partially opening the ion channel. In panel B, the yellow antagonist prevails and shoves the orange partial agonist off the binding site, reversing the partial agonist’s actions. Thus the ion channel is returned to its resting state.
an ideal state may vary from one clinical situation to another, depending upon the balance between full agonism and silent antagonism that is desired. In cases where there is unstable neurotransmission throughout the brain, finding such a balance may stabilize receptor output somewhere between too much and too little downstream action. For this reason, partial agonists are also called “stabilizers,” since they have the theoretical capacity to find the stable solution between the extremes of too much full agonist action and no agonist action at all (Figure 3-9).Just as is the case for G-protein-linked receptors, partial agonists at ligand-gated ion channels can appear as net agonists, or as net antagonists, depending upon the amount of naturally occurring full agonist neurotransmitter that is present. Thus, when a full agonist neurotransmitter is absent, a partial agonist will be a net agonist (Figure 3-9). That is, from the resting state, a partial agonist initiates somewhat of an increase in the ion flow and downstream signal transduction cascade from the ion-channel-linked receptor. However, when full agonist neurotransmitter is present, the same partial agonist will become a net antagonist (Figure 3-9): it will decrease the level of full signal output to a lesser level, but not to zero. Thus, a partial agonist can simultaneously boost deficient neurotransmitter activity yet block excessive neurotransmitter activity, another reason that partial agonists are called stabilizers. An agonist and an antagonist in the same molecule acting at ligand-gated ion channels is quite an interesting new dimension to therapeutics. This concept has led to proposals that partial agonists could treat not only states that are theoretically deficient in full agonist, but also states that are theoretically in excess of full agonist. As mentioned in the discussion of G-protein-linked receptors in Chapter 2, a partial agonist at ligand-gated ion channels could also theoretically treat states that are mixtures of both excessive and deficient neurotransmitter activity. Partial agonists at ligand-gated ion channels are just beginning to enter use in clinical practice (Table 3-2), and several more are in clinical development.
Inverse agonists at ligand-gated ion channels are different from simple antagonists, and are neither neutral nor silent. Inverse agonists are explained in Chapter 2 in relation to G-protein-linked receptors. Inverse agonists at ligand-gated ion channels are thought to produce. NURS 6630 Discussion: Foundational Neuroscience
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Figure 3-11.Actions of an inverse agonist. In panel A, the ion channel is in its resting state and opens infrequently. In panel B, the inverse agonist occupies the binding site on the ligand-gated ion channel and causes it to close. This is the opposite of what an agonist does and is represented by the purple inverse agonist turning the receptor purple and closing the ion channel. Eventually, the inverse agonist stabilizes the ion channel in an inactive state, represented by the padlock on the channel itself.
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Figure 3-12.Antagonist acting in presence of inverse agonist. In panel A, the ion channel has been stabilized in an inactive form by the inverse agonist occupying its binding site on the ligand-gated ion channel. This is represented as the purple inverse agonist turning the receptor purple and closing and padlocking the ion channel. In panel B, the yellow antagonist prevails and shoves the purple inverse agonist off the binding site, returning the ion channel to its resting state. In this way, the antagonist’s effects on an inverse agonist’s actions are similar to its effects on an agonist’s actions; namely, it returns the ion channel to its resting state. However, in the presence of an inverse agonist, the antagonist increases the frequency of channel opening, whereas in the presence of an agonist, the antagonist decreases the frequency of channel opening. Thus an antagonist can reverse the actions of either an agonist or an inverse agonist despite the fact that it does nothing on its own.
a conformational change in these receptors that first closes the channel and then stabilizes it in an inactive form (Figure 3-11). Thus, this inactive conformation (Figure 3-11B) produces a functional reduction in ion flow and in consequent signal transduction compared to the resting state (Figure 3-11A) that is even less than that produced when there is either no agonist present or when a silent antagonist is present. Antagonists reverse
Figure 3-13.Inverse agonist actions reversed by antagonist. Antagonists cause conformational change in ligand-gated ion channels that stabilizes the receptors in the resting state (top left), the same state they are in when no agonist or inverse agonist is present (top right). Inverse agonists cause conformational change that closes the ion channel (bottom right). When an inverse agonist is bound over time, it may eventually stabilize the ion channel in an inactive conformation (bottom left). This stabilized conformation of an inactive ion channel can be quickly reversed by an antagonist, which restabilizes it in the resting state (top left).
this inactive state caused by inverse agonists, returning the channel to the resting state (Figure 3-12).In many ways, therefore, an inverse agonist does the opposite of an agonist. If an agonist increases signal transduction from baseline, an inverse agonist decreases it, even below baseline levels. Also, in contrast to antagonists, which stabilize the resting state, inverse agonists stabilize an inactivated state (Figures 3-11 and 3-13). It is not yet clear if the inactivated state of the inverse agonist can be distinguished clinically from the resting state of the silent antagonist at ionotropic receptors. In the meantime, inverse agonists remain an interesting pharmacological concept.
In summary, ion-channel-linked receptors act along an agonist spectrum, and drugs have been described that can produce conformational changes in these receptors to create any state from full agonist, to partial agonist, to silent antagonist, to inverse agonist (Figure 3-4). When one considers signal transduction along this spectrum, it is easy to understand why agents at each point along the agonist spectrum differ so much from each other, and why their clinical actions are so different.
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Figure 3-14.Five states of ligand-gated ion channels. Summarized here are five well-known states of ligand-gated ion channels. In the resting state, ligand-gated ion channels open infrequently, with consequent constitutive activity that may or may not lead to detectable signal transduction. In the open state, ligand-gated ion channels open to allow ion conductance through the channel, leading to signal transduction. In the closed state, ligand-gated ion channels are closed, allowing no ion flow to occur and thus reducing signal transduction to even less than is produced in the resting state. Channel desensitization is an adaptive state in which the receptor stops responding to agonist even if it is still bound. Channel inactivation is a state in which a closed ion channel over time becomes stabilized in an inactive conformation.
Different states of ligand-gated ion channels
There are even more states of ligand-gated ion channels than those determined by the agonist spectrum discussed above and shown in Figures 3-4 through 3-13. The states discussed so far are those that occur predominantly with acute administration of agents that work across the agonist spectrum. These range from the maximal opening of the ion channel caused by a full agonist to the maximal closing of the ion channel caused by an inverse agonist. Such changes in conformation caused by the acute action of agents across this spectrum are subject to change over time, because these receptors have the capacity to adapt, particularly when there is chronic or excessive exposure to such agents.
We have already discussed the resting state, the open state, and the closed state shown in Figure 3-14. The best-known adaptive states are those of desensitization and inactivation, also shown in Figure 3-14. We have also briefly discussed inactivation as a state that can be caused by acute administration of an inverse agonist, beginning with a rapid conformational change in the ion channel that first closes it, but over time stabilizes the channel in an inactive conformation that can be relatively quickly reversed by an antagonist, which then restabilizes the ion channel in the resting state (Figures 3-11 through 3-13).
Desensitization is yet another state of the ligand-gated ion channel shown in Figure 3-14. Ion-channel-linked receptor desensitization can be caused by prolonged exposure to agonists, and may be a way for receptors to protect themselves from overstimulation. An agonist acting at a ligand-gated ion channel first induces a change in receptor conformation that opens the channel, but the continuous presence of the agonist over time leads to another conformational change where the receptor essentially stops responding to the agonist even though the agonist is still present. This receptor is then considered to be desensitized (Figures 3-14 and 3-15). This state of desensitization can at first be reversed relatively quickly by removal of the agonist (Figure 3-15). However, if the agonist stays much longer, on the order of hours, then the receptor converts from a state of simple desensitization to one of inactivation (Figure 3-15). This state does not reverse simply upon removal of the agonist, since it also takes hours in the absence of agonist to revert to the resting state where the receptor is again sensitive to new exposure to agonist (Figure 3-15).
The state of inactivation may be best characterized for nicotinic cholinergic receptors, ligand-gated ion channels that are normally responsive to the endogenous neurotransmitter acetylcholine. Acetylcholine is quickly hydrolyzed by an abundance of the enzyme acetylcholinesterase, so it rarely gets the chance to desensitize and inactivate its nicotinic receptors. However, the drug nicotine is not hydrolyzed by acetylcholinesterase, and is famous for stimulating nicotinic cholinergic receptors so profoundly and so
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Figure 3-15.Opening, desensitizing, and inactivating by agonists. Agonists cause ligand-gated ion channels to open more frequently, increasing ion conductance in comparison to the resting state. Prolonged exposure to agonists can cause a ligand-gated ion channel to enter a desensitized state in which it no longer responds to the agonist even if it is still bound. Prompt removal of the agonist can reverse this state fairly quickly. However, if the agonist stays longer, it can cause a conformational change that leads to inactivation of the ion channel. This state is not immediately reversed when the agonist is removed.
enduringly that the receptors are not only rapidly desensitized, but enduringly inactivated, requiring hours in the absence of agonist to get back to the resting state. These transitions among various receptor states induced by agonists are shown in Figure 3-15. Desensitization of nicotinic receptors is discussed in further detail in Chapter 14.
Allosteric modulation: PAMs and NAMs
Ligand-gated ion channels are regulated by more than the neurotransmitter(s) that bind to them. That is, there are other molecules that are not neurotransmitters but that can bind to the receptor/ion-channel complex at different sites from where
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Figure 3-16.Positive allosteric modulators (PAMs). Allosteric modulators are ligands that bind to sites other than the neurotransmitter site on an ion-channel-linked receptor. Allosteric modulators have no activity of their own but rather enhance (positive allosteric modulators, or PAMs) or block (negative allosteric modulators, or NAMs) the actions of neurotransmitters. When a PAM binds to its site while an agonist is also bound, the channel opens more frequently than when only the agonist is bound, therefore allowing more ions into the cell.
neurotransmitter(s) bind. These sites are called allosteric (literally, “other site”) and ligands that bind there are called allosteric modulators. These ligands are modulators rather than neurotransmitters because they have little or no activity on their own in the absence of the neurotransmitter. Allosteric modulators thus only work in the presence of the neurotransmitter.There are two forms of allosteric modulators – those that boost what the neurotransmitter does and are thus called positive allosteric modulators (PAMs), and those that block what the neurotransmitter does and are thus called negative allosteric modulators (NAMs).
Specifically, when PAMs or NAMs bind to their allosteric sites while the neurotransmitter is not binding to its site, the PAM and the NAM do nothing. However, when a PAM binds to its allosteric site while the neurotransmitter is sitting at its site, the PAM causes conformational changes in the ligand-gated ion channel that open the channel even further and more frequently than happens with a full agonist by itself (Figure 3-16). That is why the PAM is called “positive.” Good examples of PAMs are benzodiazepines. These ligands boost the action of GABA at GABAA types of ligand-gated chloride ion channels. GABA binding to GABAA sites increases chloride ion flux by opening the ion channel, and benzodiazepines acting as agonists at benzodiazepine receptors elsewhere on the GABAA receptor complex cause the effect of GABA to be amplified in terms of chloride ion flux by opening the ion channel to a greater degree or more frequently. Clinically, this is exhibited as anxiolytic, hypnotic, anticonvulsant, amnestic, and muscle relaxant actions. In this example, benzodiazepines are acting as full agonists at the PAM site.
On the other hand, when a NAM binds to its allosteric site while the neurotransmitter resides at its agonist binding site, the NAM causes conformational
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Figure 3-17.Negative allosteric modulators (NAMs). Allosteric modulators are ligands that bind to sites other than the neurotransmitter site on an ion-channel-linked receptor. Allosteric modulators have no activity of their own but rather enhance (positive allosteric modulators, or PAMs) or block (negative allosteric modulators, or NAMs) the actions of neurotransmitters. When a NAM binds to its site while an agonist is also bound, the channel opens less frequently than when only the agonist is bound, therefore allowing fewer ions into the cell.
changes in the ligand-gated ion channel that block or reduce the actions that normally occur when the neurotransmitter acts alone (Figure 3-17). That is why the NAM is called “negative.” One example of a NAM is a benzodiazepine inverse agonist. Although these are only experimental, as expected, they have the opposite actions of benzodiazepine full agonists and thus diminish chloride conductance through the ion channel so much that they cause panic attacks, seizures, and some improvement in memory – the opposite clinical effects of a benzodiazepine full agonist. Thus, the same allosteric site can have either NAM or PAM actions, depending upon whether the ligand is a full agonist or an inverse agonist. NAMs for NMDA receptors include phencyclidine (PCP, also called “angel dust”) and its structurally related anesthetic agent ketamine. These agents bind to a site in the calcium channel, but can get into the channel to block it only when the channel is open. When either PCP or ketamine bind to their NAM site, they prevent glutamate/glycine cotransmission from opening the channel. NURS 6630 Discussion: Foundational Neuroscience
MHA 506 WEEK 3 BCG Growth-Share Matrix and GE/McKinsey Nine Cell Matrix
BCG Growth-Share Matrix and GE/McKinsey Nine Cell Matrix Assignment
The life cycle of any product or service is key in the development of a marketing strategy. As corporate goals or consumer interests change, so will products or services. External to an organization will also be the impact of technological advancements and regulatory changes on product and service development and life cycle.
Conduct an internet search for “BCG Growth-Share Matrix” and “GE/McKinsey Nine Cell Matrix” and learn how these tools are used to build strategic plans.
Write a 2- to 3-page paper that explains how BCG Growth-Share Matrices and GE/McKinsey Nine Cell Matrices are used in the health care industry to build strategic plans and how marketing can use them in the creation of marketing plans and communicating to their audience and service/product lines.
Cite at least 3 reputable references to support your assignment (e.g., trade or industry publications, government or agency websites, scholarly works, or other sources of similar quality).
Format your assignment according to APA guidelines.
Click the Assignment Files tab to submit your assignment. MHA 506 WEEK 3 BCG Growth-Share Matrix and GE/McKinsey Nine Cell Matrix
How to Invest in a Great Portfolio with GE-McKinsey
Business portfolio prioritization. Cell Matrix Assignment PaperDefinition
GE-McKinsey nine-box matrix
is a strategy tool that offers a systematic approach for the multi business corporation to prioritize its investments among its business units.
[1]
GE-McKinsey
is a framework that evaluates business portfolio, provides further strategic implications and helps to prioritize the investment needed for each business unit (BU).
[2]
Understanding the tool
In the business world, much like anywhere else, the problem of resource scarcity is affecting the decisions the companies make. With limited resources, but many opportunities of using them, the businesses need to choose how to use their cash best. The fight for investments takes place in every level of the company: between teams, functional departments, divisions or business units. The question of where and how much to invest is an ever going headache for those who allocate the resources.
How does this affect the diversified businesses? Multi business companies manage complex business portfolios, often, with as much as 50, 60 or 100 products and services. The products or business units differ in what they do, how well they perform or in their future prospects. This makes it very hard to make a decision in which products the company should invest. At least, it was hard until the BCG matrix and its improved version GE-McKinsey matrix came to help. These tools solved the problem by comparing the business units and assigning them to the groups that are worth investing in or the groups that should be harvested or divested.
In 1970s, General Electric was managing a huge and complex portfolio of unrelated products and was unsatisfied about the returns from its investments in the products. At the time, companies usually relied on projections of future cash flows, future market growth or some other future projections to make investment decisions, which was an unreliable method to allocate the resources. Therefore, GE consulted the McKinsey & Company and as a result the nine-box framework was designed. The nine-box matrix plots the BUs on its 9 cells that indicate whether the company should invest in a product, harvest/divest it or do a further research on the product and invest in it if there’re still some resources left. The BUs are evaluated on two axes: industry attractiveness and a competitive strength of a unit. MHA 506 WEEK 3 BCG Growth-Share Matrix and GE/McKinsey Nine Cell Matrix
Industry Attractiveness
Industry attractiveness indicates how hard or easy it will be for a company to compete in the market and earn profits. The more profitable the industry is the more attractive it becomes. When evaluating the industry attractiveness, analysts should look how an industry will change in the long run rather than in the near future, because the investments needed for the product usually require long lasting commitment. Cell Matrix Assignment Paper
Industry attractiveness consists of many factors that collectively determine the competition level in it. There’s no definite list of which factors should be included to determine industry attractiveness, but the following are the most common: [1]
Long run growth rate
Industry size
Industry profitability: entry barriers, exit barriers, supplier power, buyer power, threat of substitutes and available complements (use Porter’s Five Forces analysis to determine this)
Industry structure (use Structure-Conduct-Performance framework to determine this)
Product life cycle changes
Changes in demand
Trend of prices
Macro environment factors (use PEST or PESTEL for this)
Seasonality
Availability of labor
Market segmentation
Competitive strength of a business unit or a product
Along the X axis, the matrix measures how strong, in terms of competition, a particular business unit is against its rivals. In other words, managers try to determine whether a business unit has a sustainable competitive advantage (or at least temporary competitive advantage) or not. If the company has a sustainable competitive advantage, the next question is: “For how long it will be sustained?” Cell Matrix Assignment Paper
The following factors determine the competitive strength of a business unit:
Total market share
Market share growth compared to rivals
Brand strength (use brand value for this)
Profitability of the company
Customer loyalty
VRIO resources or capabilities (use VRIO framework to determine this)
Your business unit strength in meeting industry’s critical success factors (use Competitive Profile Matrix to determine this)
Strength of a value chain (use Value Chain Analysis and Benchmarking to determine this)
Level of product differentiation
Production flexibility
Advantages
Helps to prioritize the limited resources in order to achieve the best returns.
Managers become more aware of how their products or business units perform.
It’s more sophisticated business portfolio framework than the BCG matrix.
Identifies the strategic steps the company needs to make to improve the performance of its business portfolio.
Disadvantages
Requires a consultant or a highly experienced person to determine industry’s attractiveness and business unit strength as accurately as possible.
It is costly to conduct.
It doesn’t take into account the synergies that could exist between two or more business units.
Difference between GE McKinsey and BCG matrices
GE McKinsey matrix is a very similar portfolio evaluation framework to BCG matrix. Both matrices are used to analyze company’s product or business unit portfolio and facilitate the investment decisions.
The main differences:
Visual difference. BCG is only a four cell matrix, while GE McKinsey is a nine cell matrix. Nine cells provide better visual portrait of where business units stand in the matrix. It also separates the invest/grow cells from harvest/divest cells that are much closer to each other in the BCG matrix and may confuse others of what investment decisions to make.
Comprehensiveness. The reason why the GE McKinsey framework was developed is that BCG portfolio tool wasn’t sophisticated enough for the guys from General Electric. In BCG matrix, competitive strength of a business unit is equal to relative market share, which assumes that the larger the market share a business has the better it is positioned to compete in the market. This is true, but it’s too simplistic to assume that it’s the only factor affecting the competition in the market. The same is with industry attractiveness that is measured only as the market growth rate in BCG. It comes to no surprise that GE with its complex business portfolio needed something more comprehensive than that.
Using the tool
There are no established processes or models that managers could use when performing the analysis. Therefore, we designed the following steps to facilitate the process:
Step 1. Determine industry attractiveness of each business unit
Make a list of factors. The first thing you’ll need to do is to identify, which factors to include when measuring industry attractiveness. We’ve provided the list of the most common factors, but you should include the factors that are the most appropriate to your industries. MHA 506 WEEK 3 BCG Growth-Share Matrix and GE/McKinsey Nine Cell Matrix. Cell Matrix Assignment Paper
Assign weights. Weights indicate how important a factor is to industry’s attractiveness. A number from 0.01 (not important) to 1.0 (very important) should be assigned to each factor. The sum of all weights should equal to 1.0.
Rate the factors. The next thing you need to do is to rate each factor for each of your product or business unit. Choose the values between ‘1-5’ or ‘1-10’, where ‘1’ indicates the low industry attractiveness and ‘5’ or ‘10’ high industry attractiveness.
Calculate the total scores. Total score is the sum of all weighted scores for each business unit. Weighted scores are calculated by multiplying weights and ratings. Total scores allow comparing industry attractiveness for each business unit.
This is a tough task and one that usually requires involving a consultant who is an expert of the industries in question. The consultant will help you to determine the weights and to rate them properly so the analysis is as accurate as possible.
Step 2. Determine the competitive strength of each business unit
‘Step 2’ is the same as ‘Step 1’ only this time, instead of industry attractiveness, the competitive strength of a business unit is evaluated.
Make a list of factors. Choose the competitive strength factors from our list or add your own factors.
Assign weights. Weights indicate how important a factor is in achieving sustainable competitive advantage. A number from 0.01 (not important) to 1.0 (very important) should be assigned to each factor. The sum of all weights should equal to 1.0.
Rate the factors. Rate each factor for each of your product or business unit. Choose the values between ‘1-5’ or ‘1-10’, where ‘1’ indicates the weak strength and ‘5’ or ‘10’ powerful strength.
Calculate the total scores. See ‘Step 1’.
Step 3. Plot the business units on a matrix
With all the evaluations and scores in place, we can plot the business units on the matrix. Each business unit is represented as a circle. The size of the circle should correspond to the proportion of the business revenue generated by that business unit. For example, ‘Business unit 1’ generates 20% revenue and ‘Business unit 2’ generates 40% revenue for the company. The size of a circle for ‘Business unit 1’ will be half the size of a circle for ‘Business unit 2’.
Step 4. Analyze the information
There are different investment implications you should follow, depending on which boxes your business units have been plotted. There are 3 groups of boxes: investment/grow, selectivity/earnings and harvest/divest boxes. Each group of boxes indicates what you should do with your investments.
Invest/Grow box. Companies should invest into the business units that fall into these boxes as they promise the highest returns in the future. These business units will require a lot of cash because they’ll be operating in growing industries and will have to maintain or grow their market share. It is essential to provide as much resources as possible for BUs so there would be no constraints for them to grow. The investments should be provided for R&D, advertising, acquisitions and to increase the production capacity to meet the demand in the future.
Selectivity/Earnings box. You should invest into these BUs only if you have the money left over the investments in invest/grow business units group and if you believe that BUs will generate cash in the future. These business units are often considered last as there’s a lot of uncertainty with them. The general rule should be to invest in business units which operate in huge markets and there are not many dominant players in the market, so the investments would help to easily win larger market share.
Harvest/Divest box. The business units that are operating in unattractive industries, don’t have sustainable competitive advantages or are incapable of achieving it and are performing relatively poorly fall into harvest/divest boxes. What should companies do with these business units?
First, if the business unit generates surplus cash, companies should treat them the same as the business units that fall into ‘cash cows’ box in the BCG matrix. This means that the companies should invest into these business units just enough to keep them operating and collect all the cash generated by it. In other words, it’s worth to invest into such business as long as investments into it doesn’t exceed the cash generated from it. Cell Matrix Assignment Paper
Second, the business units that only make losses should be divested. If that’s impossible and there’s no way to turn the losses into profits, the company should liquidate the business unit.
Step 5. Identify the future direction of each business unit
The GE McKinsey matrix only provides the current picture of industry attractiveness and the competitive strength of a business unit and doesn’t consider how they may change in the future. Further analysis may reveal that investments into some of the business units can considerably improve their competitive positions or that the industry may experience major growth in the future. This affects the decisions we make about our investments into one or another business unit. MHA 506 WEEK 3 BCG Growth-Share Matrix and GE/McKinsey Nine Cell Matrix
For example, our previous evaluations show that the ‘Business Unit 1’ belongs to invest/grow box, but further analysis of an industry reveals that it’s going to shrink substantially in the near future. Therefore, in the near future, the business unit will be in harvest/divest group rather than invest/grow box. Would you still invest as much in ‘Business Unit 1’ as you would have invested initially? The answer is no and the matrix should take that into consideration.
How to do that? Well, the company should consult with the industry analysts to determine whether the industry attractiveness will grow, stay the same or decrease in the future. You should also discuss with your managers whether your business unit competitive strength will likely increase or decrease in the near future. When all the information is collected you should include it to your existing matrix, by adding the arrows to the circles. The arrows should point to the future position of a business unit. MHA 506 WEEK 3 BCG Growth-Share Matrix and GE/McKinsey Nine Cell Matrix
The following table shows how industry attractiveness and business unit competitive strength will change in 2 years.
Step 6. Prioritize your investments
The last step is to decide where and how to invest the company’s money. While the matrix makes it easier by evaluating the business units and identifying the best ones to invest in, it still doesn’t answer some very important questions:
Is it really worth investing into some business units?
How much exactly to invest in?
Where to invest into business units (more to R&D, marketing, value chain?) to improve their performance?
Doing the GE McKinsey matrix and answering all the questions takes time, effort and money, but it’s still one of the most important product portfolio management tools that significantly facilitate investment decisions. Cell Matrix Assignment Paper
https://superbnursingessays.com/wp-content/uploads/2022/01/LOGO-300x75.png00Naomi Nashttps://superbnursingessays.com/wp-content/uploads/2022/01/LOGO-300x75.pngNaomi Nas2022-06-08 08:40:112022-06-08 08:40:11Cell Matrix Assignment Paper
(1 pts.) Sandy is interested in sexual activity and does become sexually aroused. However, despite sexual stimulation, she cannot achieve orgasm. Sandy might have which sexual dysfunction?
A) female orgasmic disorder
B) vaginismus
C) dysorgasmia
D) hypoactive sexual desire disorder
# 1.15
(1 pts.) Karen and Mark are being treated for a sexual dysfunction and their therapist is urging them to take turns stimulating each in nonsexual ways for a few weeks. Their therapist is using which of the following methods?
A) the squeeze technique
B) the start-stop procedure
C) systematic resensitization
D) sensate focus
# 1.16
(1 pts.) Clark has recently become interested in being spanked before engaging in intercourse. He can become sexually aroused if he is not spanked but enjoys this as a sort of passing fancy. How might you describe dark’s condition? Assignment: Sexual stimulatio
D) He does not necessarily have a sexual disorder.
# 1.17
(1 pts.) Bob has intense recurrent fantasies in which he is walking along the beach and a woman approaches. As she gets near, he unbuttons his pants and exposes his genitals to her. At that instant, she falls madly in love with him and they make love in the sand. Bob occasionally acts out these fantasies, and might be given the diagnosis of
A) sexual sadism.
B) exhibitionism.
C) transvestic fetishism.
D) frotteurism.
# 1.18
(1 pts.) A woman is erotically obsessed with men’s ankles to the point of exclusion of all other erotic stimuli. This woman’s desires are illustrative of
A) partialism.
B) sadism.
C) frotteurism.
D) voyeurism.
# 1.19
(1 pts.) Jeff has a compulsive desire to wear women’s clothes. He is able to achieve sexual arousal only when he cross-dresses. Jeff might be given the diagnosis of
A) sexual sadism.
B) voyeurism.
C) fetishism.
D) transvestic fetishism.
# 1.20
(1 pts.) In the 70s, Dr. Richard Raskin underwent a radical surgery in which his assigned sex was changed. He is now known as a woman named Renee Richards. Prior to the surgery Dr. Raskin might have been diagnosed as having
A) sexual aversion disorder.
B) gender identity disorder.
C) transvestic fetishism.
D) male erectile disorder.
# 1.21
(1 pts.) John gets nauseous when he thinks about having sexual intercourse and he actively avoids the sexual advances of others. John might be diagnosed as having
A) male erectile disorder.
B) sexual aversion disorder.
C) dyspareunia.
D) inhibited male orgasm disorder.
# 1.22
(1 pts.) Joseph experiences such intense and recurrent genital pain during sexual intercourse that even the thought of having sex is unbearable. Joseph might have
A) erectile disorder.
B) vaginismus.
C) dyspareunia.
D) inhibited male orgasm.
# 1.23
(1 pts.) Based on this information in the case report in the textbook, what assessment information might have led Dr. Tobin to conclude that Shaun Boyden was abused as a child? Assignment: Sexual stimulation
A) His Rorschach responses indicated a great deal of impulsivity.
B) Shaun’s verbal IQ was somewhat higher than his performance IQ.
C) Shaun’s score on one of the MMPI lie scales indicated his responses were guarded.
D) His TAT stories contained themes of victimization.
https://superbnursingessays.com/wp-content/uploads/2022/01/LOGO-300x75.png00Naomi Nashttps://superbnursingessays.com/wp-content/uploads/2022/01/LOGO-300x75.pngNaomi Nas2022-06-08 08:34:022022-06-08 08:34:02Assignment: Sexual stimulation
A patient recovering from shingles presents with tenderness and sensitivity to the upper back. He states it is bothersome to put a shirt on most days. This patient has end stage renal disease (ESRD) and is scheduled to have hemodialysis tomorrow but states that he does not know how he can lie in a recliner for 3 hours feeling this uncomfortable. What will be the PMHNP’s priority?
a) order herpes simplex virus (HSV) antibody testing
b) Order a blood urea nitrogen (BUN) and creatinine STAT
c) Prescribe lidocaine 5%
d) Prescribe hydromorphone (dilaudid) 2mg
Question 21
The PMHNP prescribed a patient lamotrigine (Lamictal), 25 mg by mouth daily, for nerve pain 6 months ago. The patient suddenly presents to the office with the complaint that the medication is no longer working and complains of increased pain. What action will the PMHNP most likely take?
a) Increase the dose of lamotrigine (Lamictal) to 25mg twice daily
b) Ask if the pt has been taking the medication as prescribed
c) Order gabapentin, 100mg TID because lamotrigine is no longer working for this patient
d) Order a CBC to assess for an infection
Question 22
An elderly woman with a hx of alzheimer’s disease, coronary artery disease, and myocardial infarction had a fall at home 3 months ago that resulted in her receiving an open reduction internal fixation. While assessing this patient, the pmhnp is made aware that the patient continues to experience mild to moderate pain. What is the pmhnp most likely to do? Assignment: PMHNP’s priority
a) order an X-ray because it is possible that she dislocated her hip
b) order ibuprofen because she mayneed long term treatment and chronic pain is not uncommon
c) Order naproxen because she may havarthritis and chronic pain is not uncommon
d) Order morphine and physical therapy
Question 23
The PMHNP is assessing a 49-year-old male with a history of depression, post-traumatic stress disorder (PTSD), alcoholism with malnutrition, diabetes mellitus type 2, and hypertension. His physical assessment is unremarkable with the exception of peripheral edema bilaterally to his lower extremities and a chief complaint of pain with numbness and tingling to each leg 5/10. The PMHNP starts this patient on a low dose of doxepin (Sinequan). What is the next action that must be taken by the PMHNP?
a) Orders liver function tests
b) Educate the patient on avoiding grapefruits when taking this medication
c) Encourage this patient to keep fluids to 1500ml/day until the swelling subside
The PMHNP is evaluating a 30-year-old female patient who states that she notices pain and a drastic change in mood before the start of her menstrual cycle. The patient states that she has tried diet and lifestyle changes but nothing has worked. What will the PMHNP most likely do?
a) Prescribe estrin FE 24 birth control
b) Prescribe Ibuprofen 800mg every 8 hours as needed for pain
c) Prescribe desvenlafaxine (Pristiq) 50mg daily
d) Prescribe Risperdal 2mg TID
Question 25
A patient with chronic back pain has been prescribed a serotonin-norepinephrine reuptake inhibitor (SNRI). How does the PMHNP describe the action of SNRIs on the inhibition of pain to the patient?
a) “the SNRI can increase noradrenergic neurotransmission in the descending spinal pathway to the dorsal horn”
b) “the SNRI can decrease noradrenergic neurotransmission in the descending spinal pathway to the dorsal horn”
c) “the SNRI can reduce brain atrophy by slowing the gray matter loss in the dorsolateral prefrontal cortex”
d) “the SNRI can increase neurotransmission to descending neurons”
Question 26
A patient with fibromyalgia and major depression needs to be treated for symptoms of pain. Which is the PMHNP most likely to prescribe for this patient? Assignment: PMHNP’s priority
a) Venlafaxine (Effexor)
b) Duloxetine (Cymbalta)
c) Clozapine (Clozaril)
d) Phenytoin (Dilantin)
Question 27
The PMHNP prescribes gabapentin (Neurontin) for a patient’s chronic pain. How does the PMHNP anticipate the drug to work?
a) It will bind to the alpha-2-delta ligand subunit of voltage-sensitive calcium channels
b) It will induce synaptic changes, including sprouting
c) It will act on the presynaptic neuron to trigger sodium influx
d) It will Inhibit activity of dorsal horn neurons to suppress body input from reaching the brain
Question 28
Mrs. Rosen is a 49-year-old patient who is experiencing fibro-fog. What does the PMHNP prescribe for Mrs. Rosen to improve this condition?
a) Venlafaxine (Effexor)
b) Armodafinil (Nuvigil)
c) Bupropion (Wellbutrin)
d) All of the above
Question 29
The PMHNP is caring for a patient with fibromyalgia. Which second-line treatment does the PMHNP select that may be effective for managing this patient’s pain?
a) Methylphenidate (Ritalin)
b) Viloxazine (Vivalan)
c) Imipramine (Tofranil)
d) Bupropion (Wellbutrin)
Question 30
The PMHNP is attempting to treat a patient’s chronic pain by having the agent bind the open channel conformation of VSCCs to block those channels with a “use-dependent” form of inhibition. Which agent will the PMHNP most likely select?
a) Pregabalin (Lyrica)
b) Duloxetine (Cymbalta)
c) Modafinil (Provigil)
d) Atomoxetine (Strattera)
Question 31
A patient with irritable bowel syndrome reports chronic stomach pain. The PMHNP wants to prescribe the patient an agent that will cause irrelevant nociceptive inputs from the pain to be ignored and no longer perceived as painful. Which drug will the PMHNP prescribe?
a) Pregabalin (Lyrica)
b) Gabapentin (Neurontin)
c) Duloxetine (Cymbalta)
d) B and C
Question 32
The PMHNP wants to use a symptom-based approach to treating a patient with fibromyalgia. How does the PMHNP go about treating this patient? Assignment: PMHNP’s priority
a) Prescribing the patient an agent that ignores the painful symptoms by initiating a reaction known as “fibro-fog”
b) Targeting the patient’s symptoms with anticonvulsants that inhibits gray matter loss in the dorsolateral prefrontal cortex
c) Mzatching the patient’s symptoms with the malfunctioning brain circuits and neurotransimitters that might mediate those symptoms
d) None of the above
Question 33
The PMHNP is working with the student to care for a patient with diabetic peripheral neuropathic pain. The student asks the PMHNP why SSRIs are not consistently useful in treating this particular patient’s pain. What is the best response by the PMHNP?
a) “SSRIs only increase norepinephrine levels”
b) “SSRIs only increase serotonin levels”
c) “SSRIs only increase serotonin and norepinephrine levels”
d) “SSRIs do not increase serotonin or norepinephrine levels”
A patient with gambling disorder and no other psychiatric comorbidities is being treated with pharmacological agents. Which drug is the PMHNP most likely to prescribe?
a) Antipsychotics
b) Lithium
c) SSRI
d) Naltrexone
Question 35
Kevin is an adolescent who has been diagnosed with kleptomania. His parents are interested in seeking pharmacological treatment. What does the PMHNP tell the parents regarding his treatment options?
a) “Naltrexone may be an appropriate option to discuss”
b) “there are many medicine options that treat Kleptomania”
c) “Kevin may need to be prescribed antipsychotics to treat this illness”
d) “Lithium has proven effective for treating kleptomania”
Question 36
Which statement best describes a pharmacological approach to treating patients for impulsive aggression?
a) Anticonvulsant mood stabilizers can eradicate limbic irritability
b) Atypical antipsychotics can increase subcortical dopaminergic stimulation
c) Stimulants can be used to decrease frontal inhibition
d) Opioid antagonists can be used to reduce drive
Question 37
A patient with hypersexual disorder is being assessed for possible pharmacologic treatment. Why does the PMHNP prescribe an antiandrogen for this patient?
a) It will prevent feelings of euphoria
b) It will amplify impulse control
c) It will block testosterone
d) It will redirect the patient to think about other things
Question 38
Mrs. Kenner is concerned that her teenage daughter spends too much time on the Internet. She inquires about possible treatments for her daughter’s addiction. Which response by the PMHNP demonstrates understanding of pharmacologic approaches for compulsive disorders?
a) “Compulsive internet use can be treated similarly to how we treat people with substance use disorders”
b) “internet addiction is treated with drugs that help block the tension/arousal state your daughter experiences”
c) “When it comes to internet addiction, we prefer to treat patients with pharmaceuticals rather than psychosocial methods”
d) “there are no evidence-based treatments for internet addiction, but there are behavioral therapies your daughter can try”
Question 39
Mr. Peterson is meeting with the PMHNP to discuss healthier dietary habits. With a BMI of 33, Mr. Peterson is obese and needs to modify his food intake. “Sometimes I think I’m addicted to food the way some people are addicted to drugs”, he says. Which statement best describes the neurobiological parallels between food and drug addiction?
a) There is decreased activation of the prefrontal cortex
b) There is increased sensation of the reactive reward system
c) There is reduced activation of regions that process palatability
d) There are amplified reward circuits that activate upon consumption
Question 40
The PMHNP is caring for a patient who reports excessive arousal at nighttime. What could the PMHNP use for a time-limited duration to shift the patient’s brain from a hyperactive state to a sleep state?
a) Histamine 2 receptor antagonist
b) Benzodiazepines
c) Stimulants
d) Caffeine
Question 41
The PMHNP is caring for a patient who experiences too much overstimulation and anxiety during daytime hours. The patient agrees to a pharmacological treatment but states, “I don’t want to feel sedated or drowsy from the medicine.” Which decision made by the PMHNP demonstrates proper knowledge of this patient’s symptoms and appropriate treatment options?
a) Avoiding prescribing the patient a drug that blocks H1 receptors
b) Prescribing the patient a drug that acts on H2 receptors
c) Stopping the patient from taking medicine that unblocks H1 receptors
Use Appendix A of Your Textbook as a Guide. You may also refer to the following websites for this lab and any that follow: http://www.eskeletons.org/,http://
humanorigins.si.edu/evidence/3d-collection, and https://human.biodigital.com/ (for this website you will need to create an account but it is free!)
Lab Objectives:
• Apply positional terminology to describe the relationships of osteological features
• Identify and label the largest bones and features of the human skull and skeleton
• Identify the human dental formula and different tooth types
• Examine the functional implications of different skeletal regions
• Understand the dynamic biology of the human skeleton over an individual’s lifespan
Purpose: To provide an introduction to basic osteological knowledge. Assignment: Human Osteology
Osteology is the detailed study of bones and teeth. It should come as no surprise that for many centuries people have been heavily invested in studying human anatomy for its medical applications. The fundamentals of human anatomy were understood by most ancient civilizations, and the study of anatomy in Western universities – even through the Middle Ages – was founded on the antique writings of the Greek physician Aelius Galenus (“Galen”) from the late 100’s A.D. Ironically, the laws of the Roman Empire that Galen served forbade the dissection of human beings, and therefore his anatomical descriptions were based not on the direct study of humans, but rather the comparative study of animals such as pigs and primates. It wasn’t until the Renaissance that intellectual curiosity in the human body was reborn and the study of human anatomy was pursued again in earnest. Principal among these anatomists were figures such as Henry Gray (of “Gray’s Anatomy”) and Georges Cuvier, who pushed the study of comparative anatomy to new limits and founded the field of paleontology.
While the skeleton plays an obvious role as the support system for the rest of the body—making movement possible, and protecting vital organs like the heart, lungs, and brain—a new understanding is emerging of bones as an important, dynamic organ of the body. Your bones achieve their shape thanks to the influence of the muscles, blood vessels, and nerves that surround them, but continue to change throughout life in response to activity, nutrition, and disease. In addition to vital metabolic and physiological functions, bones produce a hormone (an important messaging molecule in the body) named osteocalcin that plays a vital role in your body’s ability to maintain healthy blood sugar, regulate testosterone levels, and stave off depression.
Despite its deep roots in the study of anatomy, human osteology, especially in terms of variation and development, is still the subject of much new research utilizing state-of-the-art methods. Bone histology, laser scanning, computed tomography, and strain analyses are just some of the newest techniques used at both the micro and macro scale to examine the properties of human bone from every angle. Using such powerful methods, biological anthropologists are able to answer questions about human identity, ancestry, lifestyle, development, and evolution from studying bones alone
Observe the articulated human and macaque skeletons, both in anatomical position, to answer the following questions. The definitions of these terms always have the same meaning, but the direction they point in will change based on an animal’s normal posture. For instance, think about how you, a biped, normally stand vs. a quadruped, like a dog (or a horse, or a baboon). Assignment: Human Osteology
!
Anatomical Plane Definitions:
• Coronal Plane:
Divides the body into anterior and posterior halves.
• Sagittal Plane:
Divides the body into left and right halves.
• Transverse Plane:
Divides the body into superior and inferior halves
Use the definitions on page 2 of this lab to answer the following questions about the articulated human and macaque skeletons: (1 pt)
! \
A is ______________________ or ______________________ to B on the human skeleton.
C is ______________________ or ______________________ to D on the macaque skeleton.
F is ______________________ to G on both the macaque and human skeleton.
The blue line runs along the ________________________ plane of the human skeleton.
STATION 2: Skull
The skull plays an important role in understanding evolutionary history. (1.25 pts)
( Photo credit: eskeletons.org )
!
Name the three sutures marked with #s. Name the three bones marked with letters.
1. _______________________________ A. _______________________________
2. _______________________________ B. _______________________________ 3. _______________________________ C. _______________________________
4. Which two bones make up the zygomatic arch?
STATION 3: Dentition
Because teeth preserve well in the fossil/archaeological record, they are often used in constructing phylogenetic relationships among living and extinct organisms. (1.25 pts) Examine the following pictures and answer the following questions.!
1. What are the four human tooth types?
2. What is the human dental formula? Please write out in the standard order.
3. Name the bone that holds the upper teeth and the bone that holds the lower teeth.
STATION 4: Vertebral Column
Examine the vertebral column. There are 24 movable vertebrae – 7 cervical, 12 thoracic, and 5 lumbar. The sacrum and coccyx are fused vertebrae and form part of the bony pelvis. (0.5 pt) Watch this video: https://www.youtube.com/watch?v=9kweC-1XCoY.
!
1. The vertebrae bear body weight, anchor ligaments and muscles, and protect the spinal cord. What is the name of the repeating structure that separates each unfused vertebra?
2. Which group of vertebrae articulates with the ribs?
STATION 5: Pelvis
The human pelvis protects and supports abdominal organs, while anchoring muscles of the abdomen and lower limb. It is an area that provides critical information on locomotion patterns and sex determination. (1 pt)
1. Which three bones fuse to form the os coxa? Underline the bone on which you sit.
2. Just observe the ball-and-socket hip joint. Notice how the femoral head articulates with the acetabulum in this video (https://www.youtube.com/watch?v=gQnMPHoDGEc). You will see how this joint looks different from the shoulder joint in Station 6. (No written response is required here.) Assignment: Human Osteology
STATION 6: Upper limb
Observe the provided specimen and the articulated skeleton near this station when answering these questions. (1.5 pts)
!
1. Which bone of the lower arm is on the same side as your pinkie? _________________ 2. Which bone of the lower arm is on the same side as your thumb? _________________
3. A) List the two bones that, along with the humerus, form the shoulder joint.
B) Name the two features of the distal humerus that articulate with the radius and ulna at the elbow joint.
4. Compare the shoulder joint (https://www.youtube.com/watch?v=5pjk_yW-JsU) to the hip joint in Station 5.
STATION 7: Hands & Feet
Compare the articulated hand (http://www.eskeletons.org/boneviewer/nid/12537/region/hands/ bone/Articulated%20hand) and foot (http://www.eskeletons.org/boneviewer/nid/12537/region/ feet/bone/Articulated%20foot) . The rays or digits are numbered one through five beginning with the thumb or big toe. (0.5 pt)
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1. What are some of the differences you observe between the hand and the foot? How can these differences be attributed to function?
Reading Assignment: Ruff CB (2006) Gracilization of the modern human skeleton. American Scientist 94(6): 508-514. (2 pts)
Do not copy from the text without proper quotation marks and attribution.
1. Define the following terms as they apply to skeletal material. Be sure your definitions make sense in an osteological context:
a. Robust:
b. Gracile:
2. Describe how bone properties change during the normal aging process throughout a modern human lifespan. (You can draw a diagram illustrating this if you wish, but if you do its meaning must be clear to receive credit.) Note that there are two phases to describe: 1) bone growth as the individual grows to maturity, and 2) bone degeneration in old age.
3. What cultural explanations have been used to account for the gracilization of the human skeleton during our recent evolution?
After Lab Activity: (1 pt)
Use Appendix A of your text and the following terms list to label the skeleton. Assignment: Human Osteology
Sternum
Frontal
Parietal
Mandible
Metatarsals
Clavicle
Scapula
Humerus
Patella
Tibia
Ulna
Fibula
Metacarpals
Os Coxa (also innominate bone)
Femur
Carpals
Tarsals
Radius
Vertebra
Phalanges (use this term twice)
https://superbnursingessays.com/wp-content/uploads/2022/01/LOGO-300x75.png00Naomi Nashttps://superbnursingessays.com/wp-content/uploads/2022/01/LOGO-300x75.pngNaomi Nas2022-06-08 08:28:202022-06-08 08:28:20Assignment: Human Osteology
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In 1970s, General Electric was managing a huge and complex portfolio of unrelated products and was unsatisfied about the returns from its investments in the products. At the time, companies usually relied on projections of future cash flows, future market growth or some other future projections to make investment decisions, which was an unreliable method to allocate the resources. Therefore, GE consulted the McKinsey & Company and as a result the nine-box framework was designed. The nine-box matrix plots the BUs on its 9 cells that indicate whether the company should invest in a product, harvest/divest it or do a further research on the product and invest in it if there’re still some resources left. The BUs are evaluated on two axes: industry attractiveness and a competitive strength of a unit. MHA 506 WEEK 3 BCG Growth-Share Matrix and GE/McKinsey Nine Cell Matrix
With all the evaluations and scores in place, we can plot the business units on the matrix. Each business unit is represented as a circle. The size of the circle should correspond to the proportion of the business revenue generated by that business unit. For example, ‘Business unit 1’ generates 20% revenue and ‘Business unit 2’ generates 40% revenue for the company. The size of a circle for ‘Business unit 1’ will be half the size of a circle for ‘Business unit 2’.
There are different investment implications you should follow, depending on which boxes your business units have been plotted. There are 3 groups of boxes: investment/grow, selectivity/earnings and harvest/divest boxes. Each group of boxes indicates what you should do with your investments.
