Assignment: Decision Tree for Neurological and Musculoskeletal Disorders NURS 6521

Assignment: Decision Tree for Neurological and Musculoskeletal Disorders NURS 6521

Assignment: Decision Tree for Neurological and Musculoskeletal Disorders NURS 6521

The case study depicts a 43-year-old white male who presents with a complaint of pain. He uses a set of clutches when ambulating. The patient reports that he has been referred for psychiatric assessment by his family doctor since the doctor perceived that he had psychological pain (Laureate Education, 2016). The pain began seven years ago after sustaining a fall and landed on the right hip. Four years ago, it was revealed that the cartilage around the right hip joint had a 75% tear.  However, no surgeon was willing to perform a total hip replacement since they believed that there would be tissue repair over time (Laureate Education, 2016). He reports having severe cramping of the right extremity. A neurologist diagnosed  him with complex regional pain syndrome (CRPS). He states that he gets low moods at times but denies being depressed.  He had been prescribed with Hydrocone but used it in low doses due to drowsiness and constipation, and the drug does not manage pain effectively (Laureate Education, 2016). The mental status exam is unremarkable.

Decision Point One: Savella 12.5 mg orally once daily on Day 1, followed by 12.5 mg BD on Day 2 and 3, then 25 mg BD on days 4-7 and then 50 mg BD after that.

Reason: Savella is a serotonin-norepinephrine reuptake inhibitor that has NMDA antagonist activity, which brings analgesia at the nerve endings (Cording et al., 2015). It is indicated for fibromyalgia and thus effective for this client (Cording et al., 2015). I prescribed Savella to help in pain management and improve the overall mood.

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Expected Result: I anticipated that Savella would lower the degree of pain. However, it was expected that the client would experience adverse effects such as nausea, constipation, headache, hot flushes, and insomnia.

Expected Vs. Actual Results: The client returned to the clinic after for weeks without using crutches but with a bit of limping. He states that the pain has been more manageable. The pain is severe in the morning but improves throughout the day (Laureate Education, 2016). On a scale of 1-10, the client rates the pain at four and states that he gets to a point on most days where he does not need crutches. Nevertheless, he reported having increased sweating, sleeping difficulties, nausea, and palpitations (Laureate Education, 2016). His BP was 147/92, and the pulse at 110. He denied having suicidal ideations and was still future-oriented.

Decision Point 2: Continue with Savella but lower dose to 25 mg twice a day.

Reason: I selected this decision to lower the severity of the adverse effects of Savella, which include nausea, constipation, headache, hot flushes, and insomnia (Cording et al., 2015).

Expected Result: Reduction in the dose of Savella would help control the side effects but lower the degree of pain control.

Expected Vs. Actual Results: The client returned to the clinic in four weeks using crutches and rates his current pain at 7/10. He reports that his condition has declined since the previous month (Laureate Education, 2016). He states that he sleeps at night but frequently wakes up due to pain in the right leg and foot. The BP is at 124/87 and pulse at 87. He denies having palpitations and suicidal ideations but is discouraged by the slip in pain management and seems sad.

Decision Point 3: Change Savella to 25 mg in the morning and 50 mg at Bedtime.

I reduced the dosage in the morning since the pain is mostly under control and increased the dose at Bedtime when there is less control (Resmini et al., 2015).

Expected Result: By lowering the morning dose and increasing the bedtime dose, I expected that the client’s pain symptom would improve while at the same time controlling the side effects of Savella (Resmini et al., 2015).

Expected Vs. Actual Results: The client reported an improvement in the pain with a rate of 3/10 denied having any side effects from the drug.


Cording, M., Derry, S., Phillips, T., Moore, R. A., & Wiffen, P. J. (2015). Milnacipran for pain in fibromyalgia in adults. Cochrane Database of Systematic Reviews, (10).

Laureate Education. (2016). Case Study: A Caucasian man with hip pain. Baltimore, MD: Author.

Resmini, G., Ratti, C., Canton, G., Murena, L., Moretti, A., & Iolascon, G. (2015). Treatment of complex regional pain syndrome. Clinical cases in mineral and bone metabolism: the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal Diseases12(Suppl 1), 26–30.


For your Assignment, your Instructor will assign you one of the decision tree interactive media pieces provided in the Resources. As you examine the patient case studies in this module’s Resources, consider how you might assess and treat patients presenting symptoms of neurological and musculoskeletal disorders.

assignment: decision tree for neurological and musculoskeletal disorders nurs 6521

Photo Credit: KATERYNA KON/SCIENCE PHOTO LIBRARY / Science Photo Library / Getty Images

To Prepare
  • Review the interactive media piece assigned by your Instructor.
  • Reflect on the patient’s symptoms and aspects of the disorder presented in the interactive media piece.
  • Consider how you might assess and treat patients presenting with the symptoms of the patient case study you were assigned.
  • You will be asked to make three decisions concerning the diagnosis and treatment for this patient. Reflect on potential co-morbid physical as well as patient factors that might impact the patient’s diagnosis and treatment.

Click here to ORDER NOW FOR AN ORIGINAL PAPER ASSIGNMENT:  Assignment: Decision Tree for Neurological and Musculoskeletal Disorders NURS 6521

By Day 7 of Week 8

Write a 1- to 2-page summary paper that addresses the following:

Briefly summarize the patient case study you were assigned, including each of the three decisions you took for the patient presented.

Based on the decisions you recommended for the patient case study, explain whether you believe the decisions provided were supported by the evidence-based literature. Be specific and provide examples. Be sure to support your response with evidence and references from outside resources.

What were you hoping to achieve with the decisions you recommended for the patient case study you were assigned? Support your response with evidence and references from outside resources.

Explain any difference between what you expected to achieve with each of the decisions and the results of the decision in the exercise. Describe whether they were different. Be specific and provide examples.

Assignment: Decision Tree for Neurological and Musculoskeletal Disorders

The case study is about a 76-year-old Iranian male accompanied to the office by his son after exhibiting odd behavior. The patient scored 18 out of 30 in the Mini-Mental State Exam. He is diagnosed with Major neurocognitive disorder secondary to Alzheimer’s disease. This paper provides a summary of the treatment decisions taken, what I was hoping to achieve, and compare the difference between the expected and actual results.

Decision One

In the first decision, I initiated the patient on Rivastigmine 1.5 mg PO BID with an increase to 3 mg orally BID in two weeks. The decision is supported by evidence-based literature since Rivastigmine is an irreversible inhibitor of acetylcholinesterase and its therapeutic effect includes improving cholinergic function. It improves cognitive symptoms by modifying acetylcholine transmitters (Khoury et al., 2018). Rivastigmine is indicated in treating mild to moderate AD dementia, as in the case of this patient. I hoped that initiating Rivastigmine would delay cognitive decline in the patient and enhance his performance of ADLs. I also hoped that Rivastigmine would improve the patient’s social behavior. The expected and actual outcomes were different since the patient still displayed odd social behaviors after four weeks of treatment. The MMSE score remained at 18, and the patient had deficits in registration, orientation, attention, recall, and calculation.

Decision Two

In decision two, I increased Rivastigmine to 4.5 mg orally BD. The dose was increased since the initial dose did not have a positive impact.  Khoury et al. (2018) explain that Rivastigmine should be gradually increased to allow the clinician to monitor adverse effects. The study further explains that Rivastigmine can take months to show improvement in neurocognitive symptoms, thus increasing the dose is important to show improvement over time. Therefore, the decision is based on evidence-based literature. I hoped that increasing the dose might result in a positive outcome in alleviating the patient’s cognitive and behavioral symptoms. The actual and expected outcomes were similar to some degree since the son reported that the father had started attending religious services with the family. However, the son reported that the father had not improved and was amused by serious things.

Decision Three

In decision three, I increased Rivastigmine to 6 mg orally BD to improve the patient’s cognitive symptoms. Besides, the patient did not report any side effects with the drug, and thus increasing the dose was appropriate. Folch et al. (2018) assert that Rivastigmine should be increased to the maximum dose before changing or augmenting the treatment. I hoped that increasing the dose would improve the client’s social behavior to a greater degree, and the son would report an improvement in the father’s condition. Besides, I hoped that increasing the dose would improve the patient’s cognitive symptoms and the MMSE score. The expected and actual results were similar to some extent since the patient exhibited improved social interactions and engaged in family activities. Besides, the odd behaviors had decreased as the patient rarely got amused by serious things.


The patient was initiated with Rivastigmine 1.5 mg BD to improve the cognitive and behavioral symptoms. However, the initial dose did not achieve the desired effect, which resulted in increasing the dose to 4.5 BD. Increasing the dose led to some improvement in social interactions, but no cognitive improvement was noted. Rivastigmine was then increased to 6 mg BD to improve the cognitive and behavioral symptoms.




Folch, J., Busquets, O., Ettcheto, M., Sánchez-López, E., Castro-Torres, R. D., Verdaguer, E., Garcia, M. L., Olloquequi, J., Casadesús, G., Beas-Zarate, C., Pelegri, C., Vilaplana, J., Auladell, C., & Camins, A. (2018). Memantine for the Treatment of Dementia: A Review on its Current and Future Applications. Journal of Alzheimer’s disease: JAD62(3), 1223–1240.

Khoury, R., Rajamanickam, J., & Grossberg, G. T. (2018). An update on the safety of current therapies for Alzheimer’s disease: focus on rivastigmine. Therapeutic advances in drug safety9(3), 171–178.

You will submit this Assignment in Week 8.

Submission and Grading Information

To submit your completed Assignment for review and grading, do the following:

Please save your Assignment using the naming convention “WK8Assgn+last name+first initial.(extension)” as the name.

Click the Week 8 Assignment Rubric to review the Grading Criteria for the Assignment.

Click the Week 8 Assignment link. You will also be able to “View Rubric” for grading criteria from this area.

Next, from the Attach File area, click on the Browse My Computer button. Find the document you saved as “WK8Assgn+last name+first initial.(extension)” and click Open.

If applicable: From the Plagiarism Tools area, click the checkbox for I agree to submit my paper(s) to the Global Reference Database.

Click on the Submit button to complete your submission.

Grading Criteria

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Week 8 Assignment Rubric

Check Your Assignment Draft for Authenticity

To check your Assignment draft for authenticity:

Submit your Week 8 Assignment draft and review the originality report.

Submit Your Assignment by Day 7 of Week 8

To participate in this Assignment:

Week 8 Assignment



What’s Coming Up in Week 7?

assignment: decision tree for neurological and musculoskeletal disorders nurs 6521

Photo Credit: [BrianAJackson]/[iStock / Getty Images Plus]/Getty Images

Next week, you will continue working on your Assignment started in Week 6, and you will complete your Midterm Exam.

Next Week

Week 6: Neurologic and Musculoskeletal Disorders

Sabrina is a 26 year old female who has just been diagnosed with multiple sclerosis. She has scheduled an appointment for a follow up with her physician but has several questions about her diagnosis and is calling the Nurse Helpline for her hospital network. As she talks with the advanced practice nurse, she learns that her diagnosis also impacts her neurologic and musculoskeletal systems. Although multiple sclerosis is an autoimmune disorder, both the neurologic and musculoskeletal systems will be affected by adverse symptoms that Sabrina needs to be aware of and for which specific drug therapy plans and other treatment options need to be decided on.

As an advanced practice nurse, what types of drugs will best address potential neurologic and musculoskeletal symptoms Sabrina might experience?

This week, you will evaluate patients for the treatment of neurologic and musculoskeletal disorders by focusing on specific patient case studies through a decision tree exercise. You will analyze the decisions you will make in the decision tree exercise and reflect on your experiences in proposing the recommended actions to address the health needs in the patient case study. Assignment: Decision Tree for Neurological and Musculoskeletal Disorders NURS 6521

Learning Objectives

Students will:

  • Evaluate patients for treatment of neurologic and musculoskeletal disorders
  • Analyze decisions made throughout the diagnosis and treatment of patients with neurologic and musculoskeletal disorders
  • Justify decisions made throughout the diagnosis and treatment of patients with neurologic and musculoskeletal disorders


Learning Resources

Required Readings (click to expand/reduce)

Rosenthal, L. D., & Burchum, J. R. (2021). Lehne’s pharmacotherapeutics for advanced practice nurses and physician assistants (2nd ed.) St. Louis, MO: Elsevier.

  • Chapter 11, “Basic Principles of Neuropharmacology” (pp. 67–71)
  • Chapter 12, “Physiology of the Peripheral Nervous System” (pp. 72–81)
  • Chapter 12, “Muscarinic Agonists and Cholinesterase Inhibitors” (pp. 82–89)
  • Chapter 14, “Muscarinic Antagonists” (pp. 90-98)
  • Chapter 15, “Adrenergic Agonists” (pp. 99–107)
  • Chapter 16, “Adrenergic Antagonists” (pp. 108–119)
  • Chapter 17, “Indirect-Acting Antiadrenergic Agents” (pp. 120–124)
  • Chapter 18, “Introduction to Central Nervous System Pharmacology” (pp. 125–126)
  • Chapter 19, “Drugs for Parkinson Disease” (pp. 127–142)
  • Chapter 20, “Drugs for Alzheimer Disease” (pp. 159–166)
  • Chapter 21, “Drugs for Seizure Disorders” (pp. 150–170)
  • Chapter 22, “Drugs for Muscle Spasm and Spasticity” (pp. 171–178)
  • Chapter 59, “Drug Therapy of Rheumatoid Arthritis” (pp. 513–527)
  • Chapter 60, “Drug Therapy of Gout” (pp. 528–536)
  • Chapter 61, “Drugs Affecting Calcium Levels and Bone Mineralization” (pp. 537–556)
Required Media (click to expand/reduce)

Laureate Education (Producer). (2019b). Alzheimer’s disease [Interactive media file]. Baltimore, MD: Author.

In this interactive media piece, you will engage in a set of decisions for prescribing and recommending pharmacotherapeutics to treat Alzheimer’s disease.

Laureate Education (Producer). (2019e). Complex regional pain disorder [Interactive media file]. Baltimore, MD: Author.

In this interactive media piece, you will engage in a set of decisions for prescribing and recommending pharmacotherapeutics to treat complex regional pain disorders.

Disorders of The Nervous System

Reflect on the comprehensive review of disorders of the nervous system and think about how you might recommend or prescribe pharmacotherapeutics to treat these disorders. (15m)

Disorders of the Nervous System©2019 Laureate Education, Inc.1Disorders of the Nervous SystemProgram Transcript[MUSIC PLAYING] NORBERT MYSLINSKI: In the year 2000, Alvin Toffler, who was the author of Future Shock back in the 1960s, was asked this question. What do you think is the most important question facing mankind in the new millennium? He answered by saying, “What does it mean to be human?” FEMALE SPEAKER: This week, Dr. Norbert Myslinski takes an in-depth look at the human brain and how it is affected by disorders of the nervous system. NORBERT MYSLINSKI: The most human part of the body is the brain. This is the human brain. It doesn’t look like very much. It’s only about three pounds, and it’s kind of wrinkled. But if you think about it, this is the product of 3 and 1/2 billion years of evolution. It is probably the most complicated machine, or organ, or article that we know of in the universe, and it is composed of a hundred billion neurons, a hundred billion neurons. And if you look at the supporting cells, the glia, there’s about a trillion. And if you look at one of the most important parts, the connections between all of these cells, the connections that are responsible for memory and for all of our activities, there’s about a quadrillion, a quadrillion with this individual brain. And I’m sure that through the centuries, through the millions of years of our existence on this planet, this brain has evolved, and this brain has had pathologies of different kinds, and changes of many kinds. Initially, we only had this part of the brain. The dinosaurs, for instance, had this basic brain. And this is the basic brain that controls our breathing, controls our respiration, controls our heart rate, controls of all the other autonomic or vegetative functions of the body. And so sometimes, we call this part of the brain the reptilian brain. It’s the vegetative part. And then as the brain evolved through the centuries, through the millennia, another big step in the evolution was the development of this part of the brain. That’s the limbic system. And the limbic system is responsible for emotion, the wagging of the tail of a dog, the purring of a cat. This big step occurred mainly with the mammals, and so we call this the mammalian brain or the emotional brain. And the next big step in the evolution of the brain was the cerebral cortex, this part. This is the flower of the human brain. That big step occurred with the


Disorders of the Nervous System©2019 Laureate Education, Inc.2development of the homo sapiens, and it involves cognition, and so we call this the human brain. And so we have this triune brain. It’s a brain that’s developed over the years through time in that order. But we see this development in that order everyday. We see it inside every woman who is pregnant, because every fetus who’s developing a brain develops it exactly the same way. We first have the vegetative reptilian brain. And then months later, we have the development of the limbic part of the brain. And then we have the development of the human or cognitive part of the brain. And the cognitive part of the brain continues developing after birth. It continues developing through childhood, through adulthood. And hopefully, it’ll continue until the day we die. So we have this development not only through the years, but also in utero. It’s very interesting that one of the major diseases that we have of the elderly is Alzheimer’s disease. Alzheimer’s disease is very dehumanizing because it attacks that part of the brain that is one of our main humanistic parts, and that is our memory. It attacks who we are, and it’s a progressive degenerative disease. And what’s interesting is that it destroys the brain in the reverse order of its development. And what happens first, there is a group of cells down here, nucleus of Meynert. And they have a neurotransmitter called acetylcholine. And it preferentially, this group of cells preferentially degenerates, and it has pathways to all different parts of the brain. But one of the parts is over here, the hippocampus, which has to do with memory, long-term memory. And so this is what happens first. And as it progresses, there are all these plaques and tangles, we call them, that develop and choke different cells of the brain. And it continues to increase through all parts of the brain until you get many different cognitive deficits. And after that, then it attacks the mammalian brain, the emotional part of the brain. After that, it attacks the reptilian brain, the vegetative brain, and then you lose your vital functions, and then you die about 10 to 12 years, usually, after first diagnosis. So you have this reversal. Now, it’s very interesting because a lot of people are afraid of losing their memory, of getting Alzheimer’s disease. And rightfully so, because as our population ages and more and more people are older, more and more people are going to get Alzheimer’s disease. There’s about 4 million in the United States right now. And if you are lucky enough to live to the age of 85, half— half of the people will have Alzheimer’s disease. So it’s going to be pretty prevalent, and it’s going to


Disorders of the Nervous System©2019 Laureate Education, Inc.3increase in leaps and bounds as we get older, and it’s going to be a more and more important disease for the nursing profession and the health professionals. 65% of the dementias are of the Alzheimer’s type, but there are others that are not. And it’s important to be diagnosed, and to be examined, and tested, because if it’s a dementia not of Alzheimer’s, then it may be cured, even though Alzheimer’s itself is not curable, nowadays. Now, there’s another idea that I mentioned earlier, and that is that the human brain keeps on developing after we’re born until the day we die. And one of the reasons for that is because of the plasticity of the brain. That means the malleability. That means the changeability of the brain. The brain can adapt to challenges put to it, to experiences, to our needs, and our wants. It can keep changing. All of these connections, these quadrillion connections among the different parts of the brain do change, increase and decrease. As a matter of fact, the more we challenge the brain, the more we learn, the more we experience, the more connections you have, all right? If you take two animals and put one in insipid sort of adult environment and one in a rich environment and examine their brains at the end of their lives, the one in the rich environment has many more connections, many more synapses between the different— and that is the basis of memory. That is the basis of intelligence, not the number of your cells, not inside of your brain. It’s the number of synapses that we have, the number of engrams that we have withing the brain. So we have this plasticity, this growth developing. So your brain is continuously changing. Hopefully, the brain that you had before I started talking is not going to be the same brain as when I finish talking, OK? So it’s important not to traumatize the brain, and to protect it. And we’ve been giving many different protections for the brain. Unlike other organs and parts of the body, the brain has a skull to protect it. The brain has cerebral spinal fluid in it to protect it. The brain has a barrier between it and the blood that no other organ has. It’s called the blood-brain barrier to keep the toxins and bad materials of blood from getting into the brain. Before the golden age of pharmacology in the late ’50s, and they did everything they can, and they did a lot of experimentation with the brain. For instance, they were doing the frontal lobotomies that they thought would help individuals decrease agitation, as we know how terrible that was now. So they tried this stimulation of this pathway for people that are pathologically depressed, and there would be wires from there all the way down to a little box on their belt, and they’d press a button, and they feel good. And if you ask how


Disorders of the Nervous System©2019 Laureate Education, Inc.4they felt, they’d say, oh, I feel contentment, and joy, and so forth, and they feel good. But it didn’t last very long because that would destroy the pathway, and it would become refractory, and it wouldn’t work. And also, right after that, the pharmacology started, and the antipsychotic drugs came in, and so that was a lot less invasive, and a lot more effective. This dichotomy between the right and left sides of the brain is very important in understanding our perception of the world. I mentioned earlier that there are a quadrillion synapses within the brain, and this is the essential unit of memory, and it’s the essential unit of functioning of the brain. And when there is a disorder of the brain, more often than not, it has to do with the synapse. The synapse is that point of communication between two different neurons. And when you have this dysfunction or when the neuron itself dies, you have a decrease in a neurotransmitter. A neurotransmitter is a chemical that is essential for the communication. And so a lot of diseases are characterized and identified by the fact that they don’t have a certain neurotransmitter. There are many different types of neurotransmitters throughout the brain. An ideal way to study pathopharmacology is to look at a disease like Parkinson’s disease. Now, Parkinson’s disease was first analyzed back in the 1950s, when they looked at the brains of dead patients, and they did autopsies, and found that a small part of the basal ganglia called the nigostriatal pathway preferentially degenerates in these patients. And then the biochemists came along, and they analyzed the pathway, and they found that dopamine was the vital chemical, the neurotransmitter, within that pathway. And then the pharmacologists came along, and they said, you know what? I wonder if we can replace that dopamine, if we can alleviate some of the symptoms. And so they tried it. They gave dopamine. It didn’t work because it couldn’t cross the blood-brain barrier. But eventually, they gave a precursor that did cross the blood-brain barrier. And eventually, it did work, and it was called L-DOPA, and it was one of the big breakthroughs. And so patients with Parkinson’s disease then found out that their symptoms can be alleviated by taking this drug. And that’s because we replaced the neurotransmitter that is being depleted with an exogenous neurotransmitter of a similar type, and it alleviated the symptoms. If we look at Alzheimer’s disease, they thought that they could do the same thing. They looked at the Parkinson’s story, and they said, hey, if they can do it, we can


Disorders of the Nervous System©2019 Laureate Education, Inc.5do it with Alzheimer’s. Because in Alzheimer’s, we also have a small pathway that degenerates, but that has acetylcholine as its neurotransmitter. So they tried to give a drug to exacerbate the acetylcholine in the brain, and it did not work. Then they tried some other drugs, but it seemed to work, but they had a big side effect of liver toxicity. And so they put that drug aside. And so they kept studying, and studying, and studying. So by 10, 20, 30 years later, they bring that drug out again which had the big liver toxicity. They were able to find a way to minimize the liver toxicity, and they found that it does work in some Alzheimer’s patients. and that this drug is Aricept. It was the first drugs used to treat Alzheimer’s disease. So that’s one way in which pharmacology can be used to alleviate the symptoms of neurodegenerative disorders. You have similar ideas with Huntington’s chora, Huntington’s disease. You have a similar situation with epilepsy in the sense that you’re not really replacing something, but you’re exacerbating the pathway that can actively inhibit these epileptic foci that I talked about before from spontaneously discharging, and causing that epileptic seizure. So you can give drugs to exacerbate certain pathways, stimulate certain pathways, just like drugs [INAUDIBLE] stimulate the positive reinforcement area, and make us feel good. Now, you can have drugs that can stimulate other pathways in the brain pharmacologically so that you can alleviate symptoms, inhibit certain things, stimulate certain things, and so forth. Now, besides chemically doing it, some of the more recent therapies are going back 50 years, and they’re trying to electrically stimulate certain parts of the brain. Yeah, you have certain therapies now based on new technological developments where you have, for instance, deep brain stimulation, where they actually take an electrode, and stimulate, and implant it in the brain semi-permanently so that if you stimulate it, then you can alleviate the movements of somebody with Parkinson’s disease, and they can control their movements, and they have an actual electrode in there being stimulated in a certain part of the brain. So you can do it physically as well as chemically. Sometimes, you surgically can remove a certain part of the brain to alleviate symptoms, like in Parkinson’s disease. So there’s a lot of avenues of approach that we can use to treat the brain, whether surgically or pharmacologically.

The case study concerns a 43-year-old man with a history of chronic pain for several years after sustaining a fall and now ambulates with crutches. He has been referred for a psychiatric evaluation by his family physician after suspecting his pain is psychological, and he has been exaggerating the pain to get a narcotic prescription to get high. He complains of cooling and intense cramping in the right leg. He has been diagnosed with complex regional pain syndrome (CRPS). The purpose of this paper is to explain the interventions for each decision and if they are backed by evidence-based literature.

Decisions Recommended For the Patient Case Study

The first decision was to start Amitriptyline 25 mg PO QHS and increase it by 25 mg every week to a maximum of 200 mg daily. The decision is supported by the study by Shim et al. (2019), which found that Amitriptyline is an effective evidence-based treatment for neuropathic pain disorder and peripheral diabetic neuropathic pain. In decision two, I maintained Amitriptyline and increased the dose to 125 mg with a maximum target of 200 mg. The patient was to take the medication an hour earlier than usual. Increasing the dose is supported by the article by Eldufani et al. (2020), which recommends slow titration of the Amitriptyline dose if a patient exhibits a positive response to the initial dose. It also recommends taking the bedtime dose an hour earlier to minimize morning sleepiness.

In decision three, I continued Amitriptyline at 125 mg and referred the patient to a life coach for counseling on nutrition and exercise. Weight gain is a documented side effect of Amitriptyline. Brueckle (2020) backs this intervention by asserting that patients on medications associated with weight gain should be counseled on lifestyle modification in diet and exercise for a healthy weight.

What I Was Hoping To Achieve With the Decisions I Recommended For the Patient Case Study

By initiating the patient on Amitriptyline, I hoped it would help improve the client’s mood swings, alleviate pain to 4/10, and ambulate without crutches within four weeks. Komoly (2019) established that Amitriptyline helps alleviate pain and autonomic and motor symptoms in CRPS cases. I hoped that increasing Amitriptyline to 125 mg would alleviate the limb to 3/10, and taking the drug an hour earlier would prevent morning sleepiness. Taking the medication an hour earlier decreases morning sleepiness (Rosenthal & Burchum, 2021). In decision three, I hoped that referring the client for lifestyle modification counseling would guide him in practicing a healthy lifestyle in dietary and physical exercise habits that would prevent unhealthy weight gain. Aguilar-Latorre et al. (2022) recommend counseling on lifestyle modification to enable patients on TCAs to manage their weight and avoid being overweight/obese.

Difference between What You Expected To Achieve With Each of the Decisions and the Results of the Decision in the Exercise

In the first decision, the pain decreased to a 6/10, and the patient ambulated without crutches. The pain severity was not as anticipated, probably because of the low Amitriptyline dose and duration it takes to have maximum effect. In the second decision, the patient’s pain was reduced to 4/10, comparable to the expected outcome of a pain severity of 3/10.


The PMHNP started the patient on an initial dose of Amitriptyline of 25 mg QHS, which was to be increased by 25 mg weekly to 200 mg. The drug led to a positive response and was increased to 125 mg QHS to improve the patient’s pain. The medication led to weight gain, and the PMHNP referred the client to a life coach for counseling on a healthy lifestyle.



Aguilar-Latorre, A., Pérez Algorta, G., Navarro-Guzmán, C., Serrano-Ripoll, M. J., & Oliván-Blázquez, B. (2022). Effectiveness of a lifestyle modification programme in the treatment of depression symptoms in primary care. Frontiers in medicine9, 954644.

Brueckle, M. S., Thomas, E. T., Seide, S. E., Pilz, M., Gonzalez-Gonzalez, A. I., Nguyen, T. S., … & Muth, C. (2020). Adverse drug reactions associated with Amitriptyline—protocol for a systematic multiple-indication review and meta-analysis. Systematic reviews9(1), 1-8.

Eldufani, J., Elahmer, N., & Blaise, G. (2020). A medical mystery of complex regional pain syndrome. Heliyon6(2), e03329.

Komoly, S. (2019). Treatment of complex regional pain syndrome with Amitriptyline. Ideggyogyaszati szemle72(7-8), 279-281.

Rosenthal, L. D., & Burchum, J. R. (2021). Lehne’s pharmacotherapeutics for advanced practice nurses and physician assistants (2nd ed.) St. Louis, MO: Elsevier.

Shim, H., Rose, J., Halle, S., & Shekane, P. (2019). Complex regional pain syndrome: a narrative review for the practicing clinician. British Journal of Anaesthesia123(2), e424–e433.

I absolutely loved your response, and I found it not only incredibly informative, but succinct as well. In short, I greatly appreciate the plethora of tests you recommended for the sake of maximizing the certainty under which one might offer the patient a diagnosis. As you mentioned, not only does this “help guide the differential diagnoses with physical exam findings”; however, it also “saves the patient money”. Another thing I appreciated was your focus on trying to find a possible connection between the two ankles and their respective pains (this, I saw as evidenced chiefly through your proposed physical examination assessing and comparing the movement, tenderness, range of motion, pain, etc. of the patient’s ankles). You ask many questions at the beginning of your response, and I also want to voice how much I appreciate that as well. It is important to delve deeply and patiently into treating a patient, and if not much information is given (as was the case here), this habit of intense inquiry will serve you – and your patients – very well. Las, I would like to note how you wrote that each ankle injury assessment can be conducted fluently and swiftly, as this is also important in healthcare. Oftentimes, practitioners and patients don’t have copious amounts of time to spend on an issue, and timeliness is important. For these reasons, once again, I absolutely loved this response!

Ball, J., Dains, J. E., Flynn, J. A., Solomon, B. S., & Stewart, R. W. (2019). Seidel’s guide to physical examination: An interprofessional approach (9th ed.). Elsevier.

Larkins, L. W., Baker, R. T., & Baker, J. G. (2020). Physical examination of the ankle: A review of the original orthopedic special test description and scientific validity of common tests for ankle examination. Archives of rehabilitation research and clinical translation, 2(3), 100072. to an external site.

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