NURS 6501N - Week 10 assignment. Questions and Answers

NURS 6501N - Week 10 assignment. Questions and Answers Alzheimer’s disease (AD) is the most common cause of dementia associated with a progressive neurodegenerative disorder. A prevalence of 44 million people throughout the world in 2015, and this figure is estimated to double by 2050 (Mendiola-Precoma et. al, 2016) • Alzheimer’s disease (AD) is an age-related, progressive, and irreversible neurodegenerative disorder characterized by cognitive and memory impairment (Mendiola-Precoma et. al, 2016). • Runs over 5-10 years, typically beginning with a learning impairment and recent memory loss. A frontal lobe gait imbalance appears. Steps are short, and shuffled, difficulty turning. High risk for falling backward (Hammer & McPhee, 2012). • Later in the disease, social graces are lost. Paranoia, hallucinations, and delusions may occur. Terminal patients are bedridden, mute and incontinent (Hammer & McPhee, 2012) Introduction: • Etiology: Unknown • Amyloid PlaquesAmyloid plaques and neurofibrillary tangles are classic neuropathological signs of AD. Plaques mostly consist of protein fragment beta-amyloid which is produced by amyloid precursor protein (Alzheimer Association, 2017). • Tangles consist of tau, a protein normally involved in maintaining nerve cells. Excessive phosphorylation appears to contribute to tangling and prevents protein from carrying out its normal function (Alzheimer Association, 2017). • Cellular Damage:Damage to cellular structures by toxins or free radicals is also characterized with the pathology of AD. Brain inflammation is typical Alzheimer’s Association, 2017). • Etiology: Unknown • Amyloid PlaquesAmyloid plaques and neurofibrillary tangles are classic neuropathological signs of AD. Plaques mostly consist of protein fragment beta-amyloid which is produced by amyloid precursor protein (Alzheimer Association, 2017). • Tangles consist of tau, a protein normally involved in maintaining nerve cells. Excessive phosphorylation appears to contribute to tangling and prevents protein from carrying out its normal function (Alzheimer Association, 2017). • Cellular Damage:Damage to cellular structures by toxins or free radicals is also characterized with the pathology of AD. Brain inflammation is typical Alzheimer’s Association, 2017). Pathophysiology of Alzheimer’s Disease • Genetic evidence links Amyloid B-peptide (AB) and Bamyloid precursor protein (APP) on chromosome 21q21.3- 22.05. About 10% of AD cases are familial, with early onset (before age 65) and autosomal dominant inheritance. About 70% of familial cases of AD are also linked to mutations in Presenilin 1 on chromosome 14q24.3. Another 14% have been associated with another gene, Presenilin 2 on chromosome 1q31-42 Huether & McCance, 2017). • Alzheimer's disease (AD) disproportionately affects women in both prevalence and severity. In the United States, 3.4 million women compared to 1.8 million / to 65 years have AD (Carter et. al, 2012). • African Americans are about 2x more likely than Whites to have AD, and Hispanics are about 1.5 x more likely than Whites to have AD (Alzheimer’s Association, 2014) Impact of Genetics, Gender, and Ethnicity Pathological Changes in Respiratory System• Experience changes in physical abilities, including the ability to walk, sit and, eventually, swallow • Have increasing difficulty communicating • Become vulnerable to infections, especially pneumonia(