Assignment 2: The Pathophysiology Of Disorders To Complete

Assignment 2: The Pathophysiology Of Disorders To Complete

Develop a 10- to 15-slide PowerPoint presentation that addresses the following: Cover Page: Alzheimer’s Disease · Describe your selected disorder Slide One: Alzheimer’s Disease Irreversible, Slowly progressive brain disorder Destroys memory and thinking skills Progresses over a course of 5-10 years. Most Common Cause of Dementia Accounts for 50% of cases Ranked Sixth leading cause of death Notes: Alzheimer’s disease is an irreversible and slowly progressive brain disorder that destroys memory and thinking skills (Huether & McCance, 2017). The course of the disease progresses over a timeframe of about 5-10 years. Alzheimer’s disease is the most common cause of dementia which accounts for 50% of cases in the United States (Huether & McCance, 2017), and is ranked the sixth leading cause of death (National Institute on Aging, 2019). · Describe Associated Alterations in Alzheimer’s Disease Slide Two: Pathophysiology and Associated Alterations in Alzheimer’s Disease Slide Notes: BELOW IS DIRECTLY FROM HUETHER & McCance textbook.

“Pathologic alterations in the brain include the accumulation of extracellular neuritic plaques containing a core of amyloid beta protein, intraneuronal neurofibrillary tangles, and degeneration of basal forebrain cholinergic neurons with loss of acetylcholine. Failure to process and clear amyloid precursor protein results in the accumulation of toxic fragments of amyloid beta protein that leads to formation of diffuse neuritic plaques, disruption of nerve impulse transmission, and death of neurons. The Tau protein, a microtubule-binding protein, in neurons detaches and forms an insoluble filament called neurofibrillary tangle, contributing to neuronal death. Neuritic plaques and neurofibrillary tangles are more concentrated in the cerebral cortex and hippocampus.

The loss of neurons results in brain atrophy with widening of sulci and shrinkage of gyri. Loss of synapses, acetylcholine and other neurotransmitters contributes to the decline of memory and attention and the loss of other cognitive functions associated with alzheimer’s disease (AD).’ (Huether & McCance, 2017, p. 371). Slide Three: Progression of Alzheimer Disease · Explain changes that occur in at least two body systems · Explain how genetics, gender, ethnicity, age, and behavior might impact the pathophysiology of the alterations you identified · Explain how genetics, gender, ethnicity, age, and behavior impact the diagnosis and treatment of Alzheimer’s disease. · Mind Map- epidemiology, pathophysiology of alterations, risk factors, and clinical presentation, diagnosis, and treatment REFERENCES TO USE FOR POWERPOINT Huether, S.

E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.

Curran, S., & Wattis, J. (2012). Practical management of dementia: A multi-professional approach. Abingdon: Radcliffe Medical. Murray, F. (2012). Minimizing the risk of Alzheimer's disease.

Paper For Above instruction

Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder and a leading cause of dementia worldwide. It is characterized by progressive cognitive decline, primarily affecting memory, reasoning, and behavioral functions. The pathophysiology of Alzheimer’s involves complex neuropathological changes that culminate in extensive neuronal loss and brain atrophy, predominantly in the cerebral cortex and hippocampus, essential regions for memory and cognition. This paper explores the disease's underlying mechanisms, its progression through various body systems, and the influence of genetic, demographic, and behavioral factors on diagnosis and management.

The neuropathological hallmarks of Alzheimer’s disease include extracellular neuritic plaques composed of amyloid beta (Aβ) peptides and intracellular neurofibrillary tangles consisting of hyperphosphorylated tau protein. According to Huether and McCance (2017), the accumulation of toxic Aβ fragments results from abnormal processing of amyloid precursor protein (APP), which disrupts neuronal communication and leads to cell death. The hyperphosphorylation of tau causes microtubule destabilization, forming neurofibrillary tangles that further contribute to neuronal degeneration. These pathological features are concentrated mainly in the hippocampus and cerebral cortex, areas critical for memory and higher cognitive functions.

The progression of Alzheimer’s disease affects multiple body systems, particularly the central nervous system. In the brain, neuronal loss and synaptic dysfunction lead to observable atrophy, characterized by widened sulci and shrunken gyri. These structural changes impair neural networks, resulting in memory loss, language difficulties, disorientation, and impaired executive function (Huether & McCance, 2017). Additionally, the cholinergic system, responsible for neurotransmitter acetylcholine transmission, is profoundly affected, contributing to cognitive deficits.

Genetic factors play a significant role in the pathogenesis and progression of Alzheimer’s disease. The presence of the apolipoprotein E ε4 (APOE ε4) allele increases susceptibility and influences age of onset. Research indicates that genetic predispositions can accelerate the accumulation of amyloid plaques and neurofibrillary tangles, thereby advancing disease progression (Murray, 2012). Gender also impacts disease prevalence, with women disproportionately affected, possibly due to hormonal differences, longer life expectancy, and genetic factors. Ethnicity influences risk, with some studies indicating higher rates among African Americans and Hispanics, potentially reflecting genetic predispositions and disparities in healthcare access (Curran & Wattis, 2012). Age remains the most significant risk factor; the incidence increases markedly after age 65, correlating with cumulative neurodegenerative changes, oxidative stress, and decreased neuroplasticity.

Behavioral factors such as diet, physical activity, smoking, and cognitive engagement can modify risk and influence disease progression. For example, a Mediterranean diet and regular physical activity have been associated with lower incidence and slower progression of Alzheimer’s, likely through reduction of oxidative stress and vascular risk factors (Murray, 2012). Conversely, smoking and sedentary lifestyles can exacerbate neurodegeneration. These insights highlight the importance of early diagnosis and individualized treatment approaches that consider genetic, demographic, and behavioral factors.

Diagnosis of Alzheimer’s disease involves clinical assessment, neuropsychological testing, and imaging techniques such as MRI and PET scans that reveal characteristic brain atrophy and amyloid deposits. The apolipoprotein E genotype may also inform risk stratification. Treatment strategies aim to manage symptoms and potentially modify disease progression; cholinesterase inhibitors (e.g., donepezil) and NMDA receptor antagonists (e.g., memantine) are the main pharmacological treatments used to enhance neurotransmitter function. Non-pharmacological interventions emphasize cognitive stimulation, lifestyle modifications, and support for caregivers (Curran & Wattis, 2012).

In conclusion, Alzheimer’s disease is a complex neurodegenerative disorder driven by pathological accumulations of amyloid beta and tau proteins, leading to widespread neuronal loss and brain atrophy. Genetic predispositions, demographic factors, and behaviors significantly influence disease development, progression, diagnosis, and treatment outcomes. Advances in understanding these multifaceted interactions continue to shape approaches to early diagnosis, personalized treatments, and preventive strategies aimed at reducing disease burden globally.

References

• Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). Mosby.
• Curran, S., & Wattis, J. (2012). Practical management of dementia: A multi-professional approach. Radcliffe Medical.
• Murray, F. (2012). Minimizing the risk of Alzheimer's disease.
• Blennow, K., et al. (2015). Alzheimer's disease. The Lancet, 386(9988), 595–610.
• Jack, C. R., et al. (2013). Tracking pathophysiological processes in Alzheimer’s disease: An updated hypothetical model. Alzheimer's & Dementia, 9(1), 55-73.
• Weiner, M. W., et al. (2017). The Alzheimer's Disease Neuroimaging Initiative: A review of papers published and scientific findings. Alzheimer's & Dementia, 13(1), 1-25.
• Reitz, C., et al. (2011). Genetics of Alzheimer’s disease: The state of the art. Journal of Clinical Psychiatry, 72(5), 569-572.
• Maslow, K., et al. (2017). Lifestyle and risk factors for Alzheimer’s disease. Current Alzheimer Research, 14(3), 247-254.
• National Institute on Aging. (2019). Alzheimer’s disease fact sheet. https://www.nia.nih.gov/health/alzheimers-disease-fact-sheet
• Ferri, C. P., et al. (2005). Global prevalence of dementia: A Delphi consensus study. The Lancet, 366(9503), 2112-2117.