Assignment:  Week 7 Discussion Alzheimer’s Dementia 

Assignment:  Week 7 Discussion Alzheimer’s Dementia 

Assignment:  Week 7 Discussion Alzheimer’s Dementia 

Week 7: Discussion
Activity Learning Outcomes
Through this discussion, the student will demonstrate the ability to:
1. Compares and contrasts the pathophysiology between Alzheimer\’s disease and frontotemporal dementia. (CO1)
2. Identifies the clinical findings from the case that supports a diagnosis of Alzheimer\’s disease. (CO3)
3. Explain one hypothesis that explains the development of Alzheimer\’s disease (CO3)
4. Discuss the patient\’s likely stage of Alzheimer\’s disease (CO4)

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Requirements
1. Read the case study below.
2. In your initial discussion post, answer the questions related to the case scenario and support your response with at least one evidence-based reference by Wed., 11:59 pm MT.
3. Provides a minimum of two responses weekly on separate days; e.g., replies to a post from a peer; AND faculty member’s question; OR two peers if no faculty question using appropriate resources, before Sun., 11:59 pm MT.
Case Scenario
A 76-year -old man is brought to the primary care office by his wife with concerns about his worsening memory. He is a retired lawyer who has recently been getting lost in the neighborhood where he has lived for 35 years. He was recently found wandering and has often been brought home by neighbors. When asked about this, he becomes angry and defensive and states that he was just trying to go to the store and get some bread.
His wife expressed concerns about his ability to make decisions as she came home two days ago to find that he allowed an unknown individual into the home to convince him to buy a home security system which they already have. He has also had trouble dressing himself and balancing his checkbook. At this point, she is considering hiring a day-time caregiver help him with dressing, meals and general supervision why she is at work.
Past Medical History: Gastroesophageal reflux (treated with diet); is negative for hypertension, hyperlipidemia, stroke or head injury or depression
Allergies: No known allergies
Medications: None
Family History
• Father deceased at age 78 of decline related to Alzheimer\’s disease
• Mother deceased at age 80 of natural causes 
• No siblings
Social History
• Denies smoking
• Denies alcohol or recreational drug use 
• Retired lawyer
• Hobby: Golf at least twice a week
Review of Systems
• Constitutional: Denies fatigue or insomnia
• HEENT: Denies nasal congestion, rhinorrhea or sore throat.  
• Chest: Denies dyspnea or coughing
• Heart: Denies chest pain, chest pressure or palpitations.
• Lymph: Denies lymph node swelling.
• Musculoskeletal: denies falls or loss of balance; denies joint point or swelling
General Physical Exam  
• Constitutional: Alert, angry but cooperative
• Vital Signs: BP-128/72, T-98.6 F, P-76, RR-20
• Wt. 178 lbs., Ht. 6\’0\”, BMI 24.1
HEENT
• Head normocephalic; Pupils equal and reactive to light bilaterally; EOM\’s intact
Neck/Lymph Nodes
• No abnormalities noted  
Lungs 
• Bilateral breath sounds clear throughout lung fields.
Heart 
• S1 and S2 regular rate and rhythm, no rubs or murmurs. 
Integumentary System 
• Warm, dry and intact. Nail beds pink without clubbing.  
Neurological
• Deep tendon reflexes (DTRs): 2/2; muscle tone and strength 5/5; no gait abnormalities; sensation intact bilaterally; no aphasia
Diagnostics
• Mini-Mental State Examination (MMSE): Baseline score 12 out of 30 (moderate dementia)
• MRI: hippocampal atrophy
• Based on the clinical presentation and diagnostic findings, the patient is diagnosed with Alzheimer\’s type dementia.
Discussion Questions
1. Compare and contrast the pathophysiology between Alzheimer\’s disease and frontotemporal dementia.
2. Identify the clinical findings from the case that supports a diagnosis of Alzheimer\’s disease.  
3. Explain one hypothesis that explains the development of Alzheimer\’s disease
4. Discuss the patient\’s likely stage of Alzheimer\’s disease.
Category Points % Description
Application of Course Knowledge 30 30% The student:
1. Compares and contrasts the pathophysiology betweenAlzheimer’s disease and frontotemporal dementia.
2. Identifies the clinical findings from the case that supports a diagnosis of Alzheimer’s disease.
3. Explains one hypothesis that explains the development of Alzheimer’s disease.
4. Discusses the patient’s likely stage of Alzheimer’s disease.
Support from Evidence-Based Practice 30 30% 1. Initial discussion post is supported with appropriate, scholarly sources; AND
2. Sources are published within the last 5 years (unless it is the most current CPG); AND
3. Reference list is provided and in-text citations match; AND
4. All answers are fully supported with an appropriate EBM argument.
Interactive Dialogue 30 30% In addition to providing a response to the initial post due by Wednesday, 11:59 p.m. MT, student provides a minimum of two responses weekly on separate days; e.g., replies to a post from a peer; AND faculty member’s question; OR two peers if no faculty question. A response to faculty could include a question posed to a student or the entire class or a faculty question directed towards another student. AND
• Evidence from appropriate scholarly sources are included; AND
• Reference list is provided and in-text citations match
90 90% Total CONTENT Points= 90 pts
DISCUSSION FORMAT
Category Points % Description
Organization 5 5% Organization:
1. Case study responses are presented in a logical format; AND
2. Responses are in sequence with the numbered questions; AND
3. The case study response is understandable and easy to follow; AND
4. All responses are relevant to the case topic.
Format 5 5% • Discussion post has minimal grammar, syntax, spelling, punctuation, or APA format errors.*
(*) APA style references and in text citations are required; however, there are no deductions for errors in indentation or spacing of references. All elements of the reference otherwise must be included.

Assignment:  Week 7 Discussion Alzheimer’s Dementia Sample

            Nurses and other care providers play vital roles in patient assessment, diagnosis, and management. They utilize clinical findings and additional studies, such as laboratory tests and imaging studies to provide more accurate diagnoses. Alzheimer’s disease and frontotemporal dementia are neurogenerative disorders with similar clinical manifestations but different pathophysiology. This essay focuses on a patient who presents with cognitive changes and is diagnosed with Alzheimer’s disease.

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Alzheimer’s Disease and Frontotemporal Dementia Pathophysiology

Alzheimer’s is a neurodegenerative disease with a complex etiology and whose brain changes are irreversible, a vital factor in the disease’s management. The condition stems from changes in the brain caused by cholinergic dysfunction, amyloid/tau toxicity, and oxidative stress/mitochondrial dysfunction (Thakur et al., 2018). These etiologies lead to the progressive deposition of beta-amyloid plaques and neurofibrillary tangles. These changes interfere with neuronal activity and conduction, leading to brain death in affected areas hence their characteristic brain lesions. The condition is progressive and begins with a decline in cognitive function, and the accumulation of toxic tau proteins causes brain atrophy and inflammation, leading to death.

Frontotemporal dementia is a neurodegenerative disease involving the anterior and temporal brain lobes. In contrast, Alzheimer’s disease begins in the entorhinal cortex and hippocampus and progresses to the cerebral cortex and many other brain regions in later stages. Khan and De Jesus (2022) note that the condition results from the formation of protein aggregates that cause neuronal degeneration. These proteins differ from Alzheimer’s and include DNA-binding protein TDP-43, microtubule-associated tau proteins, and tumor-associated protein fused in sarcoma. The location of the lesions is also different, and so are some of the clinical presentations depending on the affected areas (Goldman & Van Deerlin, 2018). Alzheimer’s disease also begins in individuals above 60 years, while frontotemporal dementia onset is in earlier years, between 40 and 70.

Clinical Findings from the Case That Supports a Diagnosis of Alzheimer’s Disease.  

An Alzheimer’s diagnosis is based on clinical findings, primarily clinical presentations. According to Thakur et al. (2018), patients with Alzheimer’s often present with progressive memory loss, forgetting the names of people and directions. The patient wandered after getting lost in a neighborhood he had lived in for 35 years, which is alarming. Alzheimer’s patients are also easily irritated and agitated, and these characteristics are often visible when they deny their presentations, as it is with the patient in this case study. The patient also has a positive history of Alzheimer’s disease. According to Cannon-Albright et al. (2019), individuals with a positive family history of Alzheimer’s have a 40-50% chance of getting the disease. The MRI scan reveals hippocampal atrophy, and the Mini-Mental Status Exam shows moderate dementia and clinical signs of Alzheimer’s disease.

A Hypothesis that Explains the Development of Alzheimer’s Disease

The disease stems from changes in the brain caused by “cholinergic dysfunction, amyloid/tau toxicity, and oxidative stress/mitochondrial dysfunction, as mentioned earlier” (Thakur et al., 2018). In oxidative stress/mitochondrial dysfunction, the culprits are reactive oxygen and nitrogen species produced during normal and abnormal mitochondrial activities. The species are responsible for various signaling pathways (normal functions) and have destructive functions, destroying lipids, DNA, and cellular membrane structures (Thakur et al., 2018). The brain is the largest oxygen consumer and is more prone to oxidative stress than all other tissues. The brain is made of neurons made of fat cells, and reactive oxygen species lead to lipid peroxidation reaction, thus molecular apoptosis. Oxidative stress also promotes Aβ deposition, and tau hyperphosphorylation, leading to the loss of neurons and synapses, which are vital in Alzheimer’s development (Teixeira et al., 2019). Thakur et al. (2018) also note that a glutathione deficiency propagates neuronal injury.

Patient’s likely stage of Alzheimer’s disease.

Alzheimer’s disease is classified into three stages based on clinical findings. The states are “pre-clinical stage, Early-stage Alzheimer’s (mild), Middle-stage Alzheimer’s (moderate), and Late-stage Alzheimer’s (severe)” (Parnetti et al., 2019). The pre-clinical stage occurs when brain changes occur without any clinical manifestations. The early-stage Alzheimer stage is associated with independence, despite the memory loss manifestations. The symptoms may not be severe but are apparent to the doctor and family members who raise concerns. The next stage is Middle-stage Alzheimer’s (moderate): the patient in the case study is in this stage. The stage is characterized by marked changes in behavior and memory, accompanied by anger, frustration, irritability, agitation, and denial of the symptoms (Parnetti et al., 2019). The individual progressively loses the ability to perform daily activities and often needs help to achieve them. The patient’s wife expresses a need to employ a primary caregiver to cater to her husband’s needs while she is at work. The last stage is late-stage Alzheimers, characterized by extensive brain damage with marked behavioral, motor, and cognitive function changes. It is the final stage in which patients require round-the-clock observation and assistance.

Conclusion

            Alzheimer’s is a neurogenerative irreversible disorder that begins with marked cognitive changes such as memory loss. The disease differs from frontotemporal dementia based on the location of lesions (affected areas), proteins, and disease progression. Patients develop behavioral problems such as wandering and forgetting people and routes despite using such routes for long periods. The progressive degeneration leads to a self-care deficit and inability to perform activities of daily living, warranting assistance. Nurses should perform extensive assessments and utilize other clinical findings for definitive diagnosis and proper treatment.

References

Cannon-Albright, L. A., Foster, N. L., Schliep, K., Farnham, J. M., Teerlink, C. C., Kaddas, H., Tschanz, J., Corcoran, C., & Kauwe, J. S. (2019). Relative risk for Alzheimer’s disease based on complete family history. Neurology, 92(15), e1745-e1753. https://doi.org/10.1212/WNL.0000000000007231

Goldman, J. S., & Van Deerlin, V. M. (2018). Alzheimer’s disease and frontotemporal dementia: the current state of genetics and genetic testing since the advent of next-generation sequencing. Molecular Diagnosis & Therapy, 22(5), 505-513. https://doi.org/10.1007/s40291-018-0347-7

Khan, I., & De Jesus, O. (2022). Frontotemporal lobe dementia. In StatPearls [Internet]. StatPearls Publishing.

Parnetti, L., Chipi, E., Salvadori, N., D’Andrea, K., & Eusebi, P. (2019). Prevalence and risk of progression of pre-clinical Alzheimer’s disease stages: a systematic review and meta-analysis. Alzheimer’s Research & Therapy, 11(1), 1-13. https://doi.org/10.1186/s13195-018-0459-7

Teixeira, J. P., de Castro, A. A., Soares, F. V., da Cunha, E. F., & Ramalho, T. C. (2019). Future therapeutic perspectives into the Alzheimer’s disease targeting the oxidative stress hypothesis. Molecules, 24(23), 4410. https://doi.org/10.3390/molecules24234410

Thakur, A. K., Kamboj, P., Goswami, K., & Ahuja, K. (2018). Pathophysiology and management of Alzheimer’s disease: An overview. Journal of Analytical & Pharmaceutical Research, 7(1). https://doi.org/10.15406/japlr.2018.07.00230