NURS 6630 Week 1 Short Answer Assessment
Walden University NURS 6630 Week 1 Short Answer Assessment– Step-By-Step Guide
This guide will demonstrate how to complete the Walden University NURS 6630 Week 1 Short Answer Assessment assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.
How to Research and Prepare for NURS 6630 Week 1 Short Answer Assessment
Whether one passes or fails an academic assignment such as the Walden University NURS 6630 Week 1 Short Answer Assessment depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.
After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.
How to Write the Introduction for NURS 6630 Week 1 Short Answer Assessment
The introduction for the Walden University NURS 6630 Week 1 Short Answer Assessment is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.
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How to Write the Body for NURS 6630 Week 1 Short Answer Assessment
After the introduction, move into the main part of the NURS 6630 Week 1 Short Answer Assessment assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.
Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.
How to Write the Conclusion for NURS 6630 Week 1 Short Answer Assessment
After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.
How to Format the References List for NURS 6630 Week 1 Short Answer Assessment
The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.
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Sample Answer for NURS 6630 Week 1 Short Answer Assessment
Major Depressive Disorder
Mood disorders are the most common mental health illnesses encountered by populations. Major Depressive Disorder (MDD) is a type of mood disorder characterized by sadness or depressed mood, which is persistent for two weeks. Other symptoms of MDD include loss of interest in everyday activities, loss/gain of appetite, loss/gain of weight, lack of energy, feelings of guilt, low concentration, sleep disturbances, and sometimes suicidal thoughts. in most cases, MDD co-occurs with substance use disorder. Substance use can be the cause of depression or a consequence of the illness, which results from the maladaptive need to cope with the negative impact of the depression (Alsheikh et al., 2020). The presence of substance use disorder complicates the treatment of the underlying depression. The purpose of this assignment is to demonstrate knowledge of pharmacological treatment for patients with multiple mental health conditions.
- Drug Therapy
The appropriate drug therapy for a patient with an alcoholism problem is Paroxetine, based on evidence for its effectiveness in treating social anxiety in patients with alcohol abuse problems (Gimeno et al., 2018). In general, alcohol use while taking antidepressants is not advisable because of the risk of drug-induced depression or exacerbating central nervous side effects such as drowsiness, confusion, and dizziness (Agabio et al., 2018). Some MDD drugs that are contraindicated with alcohol include Bupropion because of the risk of seizure and duloxetine due to the increased risk of liver damage. Finally, it takes 4 to 8 weeks for the remission of MDD symptoms.
- List 4 predictors of late-onset generalized anxiety disorder
- Childhood issues such as parental loss/separation/inadequate support
- History of parental mental illness
- Poverty
- Recent adverse life events (Welzel et al., 2021)
- List 4 potential neurobiology causes of psychotic major depression.
- Default Mode Network (DMN) functional connectivity
- Abnormalities in the subgenual cortex
- Decreased gamma-Aminobutyric acid neurotransmission (Croarkin, 2018)
- DMN hyperactivity
- Symptoms of an episode of major depression
- Feelings of sadness or hopelessness
- Irritability or anger outbursts
- Sleep disturbances
- Agitation or restlessness
- Lack of energy
- Trouble concentrating
- Feelings of worthlessness
- Drugs that precipitate insomnia
- Selective serotonin reuptake inhibitors example Zoloft (Xu et al., 2022)
- Anticonvulsants for example Topiramate
- Beta-agonists for example propranolol
Also Read:
Neurobiology and Medication Adherence Concepts
Assessing and Treating Vulnerable Populations for Depressive Disorders
Assessing and Treating Patients With Bipolar Disorder
Assessing and Treating Patients With Anxiety Disorders
Treatment for a Patient With a Common Condition
Study Guide for Medication Treatment Schizophrenia Spectrum and Other Psychosis Disorders
WEEK 8 Short Answer Assessment
Assessing and Treating Patients With Sleep Wake Disorders
Assessing and Treating Patients With ADHD
Psychopharmacologic Approaches to Treatment of Psychopathology
Assessing and Treating Patients With Impulsivity, Compulsivity, and Addiction
Conclusion
MDD is a mood-based disorder characterized by episodes of extreme sadness, loss of energy or interest in activities, sleep disturbances and other symptoms that often last for two weeks. When MDD occurs in a person with a history of alcohol abuse, treatment becomes challenging because mixing antidepressants with alcohol can cause more damage, for example, further induce depression. Therefore, it is important to evaluate the risk and benefits of the antidepressant for every patient and closely monitor them to determine tolerability. Some antidepressant drugs are contraindicated in people with alcohol use disorder, for example, duloxetine and Bupropion because they can cause serious side effects such as seizures. Finally, people with MDD undergo an episode of depression characterized by sadness, loss of energy, sleep disturbances, agitation, restlessness, issues with appetite, and trouble concentrating.
References
Agabio, R., Trogu, E., & Pani, P. (2018). Antidepressants for the treatment of people with co‐occurring depression and alcohol dependence. Cochrane Database of Systematic Reviews, https://doi.org/10.1002/14651858.CD008581.pub2.
Alsheikh, A. M., Elemam, M., & El-bahnasawi, M. (2020). Treatment of Depression With Alcohol and Substance Dependence: A Systematic Review. Cureus , 12(10): e11168. doi:10.7759/cureus.11168.
Croarkin, P. (2018). Indexing the neurobiology of psychotic depression with resting state connectivity: Insights from the STOP-PD study. EBioMedicine, 37:32-33. https://doi.10.1016/j.ebiom.2018.10.010.
Gimeno, C., Dorado, M., Roncero, C., Szerman, N., Vega, P., Balanzá-Martínez, V., & Alvarez, F. (2018). Treatment of Comorbid Alcohol Dependence and Anxiety Disorder: Review of the Scientific Evidence and Recommendations for Treatment. Front Psychiatry, 8:173. https://doi.10.3389/fpsyt.2017.00173.
Welzel, F., Luppa, M., Pabst, A., Pentzek, M., Fuchs, A., Weeg, D., & Bickel, H. (2021). Incidence of Anxiety in Latest Life and Risk Factors. Results of the AgeCoDe/AgeQualiDe Study. Int J Environ Res Public Health, 18(23),12786. https://doi.10.3390/ijerph182312786.
Xu, G., Li, X., & Xu, C. (2022). Effect of insomnia in the major depressive disorder. BMC Neurology, 22, 341. https://doi.org/10.1186/s12883-022-02869-x.
Sample Answer 2 for NURS 6630 Week 1 Short Answer Assessment
Anatomy of the Neuron
Neurons are information messengers with three main parts namely the cell body, axon, and the dendrites (Kringelbach et al., 2020). The cell body is made up of a nucleus and cytoplasm and produces protein required to construct other parts of the neuron. The axon, on the other hand, extends from the cell body and carries signals away from the cell body while the dendrites carry signals toward the cell body and have numerous synapses to receive the signal from nearby neurons. Upon stimulation, neurons transmit an electrical impulse that passes through the dendrite, to the cell body, axon, axon terminal, and finally, the stimulus is passed (Kringelbach et al., 2020). At the axonal terminal, the axon releases neurotransmitters that depolarize neighboring cells through synapses and by binding to the membrane of the dendrite.
Subcortical Structures
Other structures within the brain are subcortical structures that act as information hubs for the nervous system. Their main role is to relay and modulate information circulating in different areas of the brain. They include the basal ganglia, limbic structures, pituitary gland, and the diencephalon (Malinowski, 2019).
The limbic systems play a great role in learning and memory addiction. The systems provide the anatomical substrate for emotions and motivated behaviors, including the circulatory for reward-related events and stress responses. Specifically, the hippocampus is used to mediate a cognitive/spatial form of memory. It controls learning and declarative memory which covers the memory of facts and events (Malinowski, 2019). The dorsal striatum also helps in memory by mediating the stimulus-response habit memory. Addiction on the other hand is linked to the limbic system through the orbitofrontal cortex and anterior cingulate gyrus (Malinowski, 2019).
In line with motor control, the nigra striatal region offers two anatomically and functionally distinct portions knowns as the substantia nigra pars compacta and the substantia nigra pars reticulata.
Glial Cells
Other essential components in the central nervous system are the glial cells. They include the astrocytes whose role is to maintain the environment for neuronal signaling by controlling the level of neurotransmitters surrounding the synapses (Hirbec et al., 2020). Equally, oligodendrocytes wrap around the axons forming a protective layer called myelin sheath which enhances neuron signaling. The cells also include microglia, ependymal cells, and radial glial whose roles are clearing dead cells or removing harmful toxins, maintaining homeostasis, and regenerating neurons and other glial cells like astrocytes and oligodendrocytes respectively.
Neuron Communication
Neurons communicate with each other through synaptic transmission. A chemical synapse is registered at the axon terminal of the presynaptic neuron and the dendrite of the postsynaptic neuron (Malinowski, 2019). The dendrite picks up signals and passes the signals down to the axon, into the axon terminals, and into the synapses. The role of the chemical synapse is to transform the electrical signal in the presynaptic cell’s axon into a chemical signal and back into an electrical signal in the postsynaptic cell.
Neuroplasticity
Brain plasticity denotes the ability of the brain to reorganize itself and form new neural connections in response to extrinsic or intrinsic stimuli. Through axonal sprouting, the undamaged axons develop new nerve endings and reconnect neurons with severed or injured links (Mateos-Aparicio & Rodríguez-Moreno, 2019). For instance, undamaged brain sites of stroke patients rewire themselves to take over functions of the damaged brain sites. Similarly, the undamaged axons sprout nerve endings that connect with other undamaged nerve cells to form new neural pathways (Mateos-Aparicio & Rodríguez-Moreno, 2019). For example, exposing the brain to specific grammatical rules helps it process and develop language.
References
Hirbec, H., Déglon, N., Foo, L. C., Goshen, I., Grutzendler, J., Hangen, E., … & Escartin, C. (2020). Emerging technologies to study glial cells. Glia, 68(9), 1692-1728. https://doi.org/10.1002/glia.23780
Kringelbach, M. L., Cruzat, J., Cabral, J., Knudsen, G. M., Carhart-Harris, R., Whybrow, P. C., … & Deco, G. (2020). Dynamic coupling of whole-brain neuronal and neurotransmitter systems. Proceedings of the National Academy of Sciences, 117(17), 9566-9576. https://doi.org/10.1073/pnas.1921475117
Malinowski, M. N. (2019). Anatomy of the brain and brain stem. In Deer’s Treatment of Pain (pp. 49-59). Springer, Cham.
Mateos-Aparicio, P., & Rodríguez-Moreno, A. (2019). The impact of studying brain plasticity. Frontiers in cellular neuroscience, 13, 66. https://doi.org/10.3389/fncel.2019.00066
NURS 6630 Week 2 Psychopharmacology Scavenger Hunt Concept Map
Concept Map: Agonist Spectrum
Introduction
The agonist spectrum includes four types of agents: agonists, partial agonists, antagonists, and inverse agonists. Each of these agents interacts with specific receptors in the body, mediating distinct biological activities. Understanding these interactions and mechanisms is essential for applying medications appropriately in clinical practice.
Agonists
Definition: Agonists bind to receptors and activate them, producing a full biological response.
Characteristics:
- Full activation of the receptor.
- Maximum efficacy in eliciting a physiological response.
Mechanism:
- Agonists bind to the active site of the receptor, causing a conformational change that activates intracellular signaling pathways.
Example Medication:
- Oxycodone: An opioid agonist that targets the μ-opioid receptor, leading to analgesic effects by mimicking endogenous opioids like endorphins (Stein, 2016).
Partial Agonists
Definition: Partial agonists bind to receptors and produce a partial response, even when all receptors are occupied.
Characteristics:
- Partial activation of the receptor.
- Less than maximum efficacy compared to full agonists.
Mechanism:
- Partial agonists bind to the active site but induce a less efficient conformational change in the receptor, resulting in a submaximal response.
Example Medications:
- Aripiprazole: A partial agonist at dopamine D2 receptors, used in the treatment of schizophrenia and bipolar disorder. It stabilizes dopamine levels by partially activating these receptors (Shapiro et al., 2003).
- Brexpiprazole: Another partial agonist at dopamine D2 receptors and serotonin 5-HT1A receptors, used for schizophrenia and major depressive disorder (Maeda et al., 2014).
Antagonists
Definition: Antagonists bind to receptors but do not activate them, blocking the action of agonists.
Characteristics:
- No activation of the receptor.
- Blocks agonist action, preventing a biological response.
Mechanism:
- Antagonists occupy the active site or an allosteric site on the receptor without triggering the intracellular signaling pathways, thereby blocking agonist binding.
Example Medications:
- Naloxone: An opioid antagonist that binds to μ-opioid receptors with high affinity, reversing the effects of opioid overdose by displacing opioid agonists from the receptor (Jordan et al., 2024).
- Haloperidol: An antagonist of dopamine D2 receptors, used to treat psychotic disorders by blocking dopamine activity (Seeman, 2002).
- Risperidone: An antagonist at both dopamine D2 and serotonin 5-HT2A receptors, used for schizophrenia and bipolar disorder (Siafis et al., 2018).
Inverse Agonists
Definition: Inverse agonists bind to the same receptor as agonists but induce the opposite effect, reducing basal activity of the receptor.
Characteristics:
- Decreases receptor activity below basal levels.
- Produces opposite effects to those of agonists.
Mechanism:
- Inverse agonists stabilize the receptor in its inactive form, decreasing constitutive activity and reducing downstream signaling.
Example Medications:
- Pimavanserin: An inverse agonist at serotonin 5-HT2A receptors, used to treat Parkinson’s disease psychosis by reducing excessive serotonin signaling (Meltzer et al., 2009).
Application of Medications to Agonist Spectrum
- Oxycodone: Agonist
- Brexpiprazole: Partial Agonist
- Aripiprazole: Partial Agonist
- Naloxone: Antagonist
- Haloperidol: Antagonist
- Risperidone: Antagonist
- Pimavanserin: Inverse Agonist
Concept Map Design
The concept map visually represents the agonist spectrum with distinct branches for each agonist type. Each branch includes the definition, characteristics, mechanism of action, and examples of medications.
Conclusion
The concept map provides a comprehensive overview of the four agonist types, their mechanisms, and examples of relevant medications. Understanding these distinctions is crucial for effective pharmacological intervention and patient care.
References
Jordan, M. R., Patel, P., & Morrisonponce, D. (2024, May 5). Naloxone. StatPearls – NCBI Bookshelf. https://www.ncbi.nlm.nih.gov/books/NBK441910/
Siafis, S., Tzachanis, D., Samara, M., & Papazisis, G. (2018). Antipsychotic Drugs: From Receptor-binding Profiles to Metabolic Side Effects. Current Neuropharmacology, 16(8), 1210–1223. https://doi.org/10.2174/1570159×15666170630163616
Maeda, K., Sugino, H., Akazawa, H., Amada, N., Shimada, J., Futamura, T., … & Kikuchi, T. (2014). Brexpiprazole I: In vitro and in
vivo characterization of a novel serotonin-dopamine activity modulator. Journal of Pharmacology and Experimental
Therapeutics, 350(3), 589-604.
Seeman, P. (2002). Atypical antipsychotics: Mechanism of action. Canadian Journal of Psychiatry, 47(1), 27-38.
Shapiro, D. A., Renock, S., Arrington, E., Chiodo, L. A., Liu, L. X., Sibley, D. R., … & Roth, B. L. (2003). Aripiprazole, a novel
atypical antipsychotic drug with a unique and robust pharmacology. Neuropsychopharmacology, 28(8), 1400-1411.
Stein, C. (2016). Opioid receptors. Annual Review of Medicine, 67, 433-451.
Meltzer, H. Y., Mills, R., Revell, S., Williams, H., Johnson, A., Bahr, D., & Friedman, J. H. (2009). Pimavanserin, a Serotonin2A Receptor Inverse Agonist, for the Treatment of Parkinson’s Disease Psychosis. Neuropsychopharmacology, 35(4), 881–892. https://doi.org/10.1038/npp.2009.176