Friday, December 6, 2019

Alzheimers Disease and Parkinsonism †Free Samples to Students

Question: Discuss about the Alzheimers Disease and Parkinsonism. Answer: Introduction: According to World Health Organization, the life expectancy has been increased dramatically in the last few decades. As evaluated by Union ministry of health and family welfare in India, the normal average lifespan is evaluated 69.6 years in 2011 to 2015. Whether the problem is to improve the quality of life for older adults not only the physical health but also the mental stability is an important issue (Dementia, Delirium, and Alzheimers Disease, 2017). For this purpose, various geriatric problems should be considered properly. In this report, a geriatric mental illness which is Alzheimers disease has been discussed. A German neurologist, Dr Alois Alzheimer, first discovered this problem in 1906. Alzheimers disease is now becoming a common disease in older adults where they are losing their standard of life (Journal of Alzheimers Disease and Parkinsonism, 2017). In this report, the process to diagnose this disease, the difference from other mental disorders, and pathophysiology of the disease, clinical course and treatments, ways to improve the life of the patient at home and in the hospital has been discussed briefly with relevant points. Alzheimers disease is a progressive disease where brain tissues of the patient degenerate, affects the memory of the patient. The patient becomes disabling to socially interact even loses the ability to think logically Alzheimers disease is common in about 1 out of 10 people over the age 65 years and about 1 out of 4 people among the people above 85 years (Alzheimers disease, 2017). To diagnose the Alzheimer disease in a patient properly, the study of symptoms of the disease and brain imaging should be used together. These are as follows: The change in awareness, perception and thinking in contrast to the previous condition of the patient is studied. This can be done by evaluating the data obtained from that patient or the persons very close to that patient and know the patient very well (Valenti, Pantoni Markus, 2014). Several assessments can be performed to check the functionality of one or more than one cognitive domains about the educational and cultural background and age of the patient. According to Bradshaw et al., (2013), in the case of detection of Alzheimer's disease, the change in several cognitive domains such as memory, ability to execute a function, communication skill, language, attention and ability to learn new things reduced drastically. The patient faces problem to finish the daily normal task and confused with the location or passing of time. Gradually the patient may lead to deprivation of the ability to social engagements or works actively (Pedersen, Larsen, Tysnes Alves, 2017). Brain imaging studies such as Computerized Tomography or CT scan produces images which show the cross-sectional view of the brain, which help to study the condition of the patient. MRI or Magnetic Resonance Imaging is very much preferred brain-imaging study to understand Alzheimers disease. Now the more advanced techniques such as Positron Emission Tomography or PET and functional MRI or fMRI is used to study the if the activity of the neuron cells is proper or not (James, Doraiswamy Borges-Neto, 2015). Though the above mentioned processes and tests to diagnose Alzheimers disease have been discussed, one can confirm that a patient is suffering from this disease is possible after the death of the patient, by examination of brain tissue (Richard, Schmand, Eikelenboom Van Gool, 2013). Differences among dementia, delirium and Alzheimers disease: There is a huge confusion that dementia and Alzheimer's disease are the same, but actually, there are some differences. As opined by Breitve et al., (2014), dementia is the brain disorder that affects the performance of daily routine activities and communication whereas Alzheimers disease is a form of or part of dementia, where the parts of the brain which controls memory, thought and language get affected. Thus it can be said that Dementia is the umbrella term, and Alzheimer's disease comes under it. Another difference between dementia and Alzheimers disease is- some forms of dementia are temporary and curable, such as dementia caused by vitamin deficiency and drug interaction. On the other hand, Alzheimers disease is a degenerative non-reversible disease which cannot be cured, and the condition worsens gradually. Delirium has a pattern of abrupt beginning, and it stays for a short duration. Delirium is a temporary condition and also curable, and the symptoms of it include disturbed sleep, jerky movements, anxiety, hallucination, confusion, change in mood, altered pulse rate and blood pressure. As discussed above, Alzheimers disease is totally different from it (Dementia, Delirium, and Alzheimers Disease, 2017). Pathophysiology of Alzheimers disease: As opined by Chen et al., (2015), Alzheimers disease is specified by the loss of neuron cells. It also includes synapses in cerebral cortex area and some specific subcortical regions. This abnormality results in immense atrophy of the transformed affected areas and also leads to degeneration of parietal lobe, temporal lobe, some parts of the cingulate gyrus and frontal cortex. Several studies show the formation of plaques around the neurones and outside of neurones also. Plaques are made up of insoluble beta-amyloid peptide and cellular materials (Jucker Walker, 2015). The presence of neurofibrillary tangles has been clearly observed in the brain tissue of the patient of Alzheimers disease. Aggregation of the microtubule associated Tau protein which gets phosphorylated and form tangles, gets accumulated inside the cells. Oxidative damage of neurones, the presence of Lewy bodies and cascade of inflammation are also associated with Alzheimers disease. Recent studies reveal that though there are presences of plaque and tangles in healthy older adults, the number of plaques and tangles are much greater in the brain of a patient with Alzheimer's disease, especially in the temporal lobe portion. According to Hroudov, Singh Fiar (2014), an increase of synthesis of beta-amyloid peptide is related directly to the occurrence of Alzheimer's disease. The main component of plaque, the beta-amyloid peptide is the fragment of the larger Amyloid Precursor Protein or APP. This APP is a trans-membrane protein which invades the membrane of the neurones. APP plays a crucial role in survival, growth and post-injury restoration (Chen et al., 2015). In the case of Alzheimer's disease, beta secretase and gamma secretase act on APP and fragmented it into smaller parts. Prognosis of Alzheimers disease: Prognosis is the medical term that predicts the chance of a patient to survive. As opined by James et al., (2014), Alzheimers disease is not curable till now. A patient of Alzheimers disease survives about eight years in average after the first onset of the symptoms (Research and Prognosis on Alzheimer's Disease - Alzheimers Disease and other Cognitive Disorders, 2017). Sometimes persons with Alzheimers disease have been found to live between 3 to 20 years after the onset of symptoms, but it mainly depends on the age of the patient, severity and type of the other medical conditions. According to Ginis et al., (2017), a patient of this disease often die due to flu or pneumonia, on the other hand, they may die while all the bodily systems stop their activity. According to Castello, Jeppson Soriano (2014), there are three stages of Alzheimer's disease. The first stage is a mild stage or early stage, the second one is moderate, or middle stage and the last one is a severe or last stage. These stages are difficult to identify separately as most of the time they are overlapped and not very easy to distinguish the symptoms of different stages. The treatment depends on the stage and severity of the disease. Two types of drugs are used to treat Alzheimer's disease, i.e. Memantine and Cholinesterase inhibitor (Treatment - Mayo Clinic, 2017). It helps to treat moderate to severe stages of Alzheimers disease. It improves the brain cell communication network and reduces the progress of symptoms. It often used with a Cholinesterase inhibitor (Treatment - Mayo Clinic, 2017) Cholinesterase inhibitor drugs include donepezil or Aricept, galantamine or Razadyne, rivastigmine or Exelon, whereas; Aricept or donepezil is the only drug which is approved by FDA and used in all stages of Alzheimer's disease (Ginis et al., 2017). These drugs boost up neuron to neuron communication (by providing acetylcholine which is a neuro transmitter) which decreases in the brain-tissues of a patient of Alzheimers disease. These drugs are also helpful to reduce the symptoms of depression or agitation as well (Hroudov, Singh Fiar, 2014). It should be remembered that these medications cannot cure or stop the progress of Alzheimers disease; it can only help to lessen the symptoms. Safety intervention for Alzheimers Patient: According to Heller, Gibbons Fisher (2015), Alzheimer's disease is such type of condition where a patient needs full help at their home, and in the hospital, they need special care also. Some special care which should be followed in the hospital has been discussed below: Establishment of an effective communication system with a patient with great patience and also with the patient's family. Frequently examination of the vital conditions of the patient. Observe the patients food and fluid intake to determine the imbalances. Application of required medicines for this disease and the effect should be noted. If the patient has a problem to swallow the medicine, then the medicine should be crushed and mixed in a semi-soft food and then help the patient to intake it (Castello, Jeppson Soriano, 2014). Help the patient to maintain hygiene. Encourage the Alzheimers patient for some exercise under proper observation. There should be proper rest periods between exercises as the patients get easily tired. Proper emotional support should be given to the patient and the patients family. If the patient wants to live in patient's home, then some safety interventions should be applied there (Treatment - Mayo Clinic, 2017). The valuable and important things such as keys, mobile phones should be kept in the same place as the patient can find it easily. Encourage the patient to carry a mobile phone with the capability of location. Important phone numbers should be saved so that the patient can call someone in case of emergency. Use calendars and white boards at home which will help the patient to follow the daily schedules and the patient can also check if the daily routine has been performed or not (Jucker Walker, 2015). Sturdy handrails should be installed in bathrooms and on stairways. The patient should be taken to the bathrooms at specific time intervals and should be helped them to locate the bathroom. The number of mirrors should be reduced at home as a patient of Alzheimer's disease may be confused or frightened by the reflection in the mirror. The patient should be given independence as much as possible, but the safety of the patient should be ensured. These safety interventions will help to improve the quality of life of the patient. Conclusion: It is clear from the above discussion that with the increase of average life-span, Alzheimers disease is now an inevitable problem which is drawing the attention of medical professionals. It can be said though it is not curable; many types of research have been going on to find out a proper solution. Now, the main focus is to provide a healthy and standard life and provide the patient with a better way to live. It can be concluded that the best proposal to this disease is awareness, communication, engagement and loving care along with medication. Reference list: Alzheimers disease. (2017).NeuRA. Retrieved 5 May 2017, from https://www.neura.edu.au/health/alzheimers-disease/?gclid=CPHi2MyC1NMCFYMEaAodK9UBFA Breitve, M. H., Chwiszczuk, L. J., Hynninen, M. J., Rongve, A., Brnnick, K., Janvin, C., Aarsland, D. (2014). A systematic review of cognitive decline in dementia with Lewy bodies versus Alzheimers disease. Alzheimer's research therapy, 6(5), 53. Burnham, S. C., Bourgeat, P., Dor, V., Savage, G., Brown, B., Laws, S., ... Masters, C. L. (2016). Clinical and cognitive trajectories in cognitively healthy elderly individuals with suspected non-Alzheimer's disease pathophysiology (SNAP) or Alzheimer's disease pathology: a longitudinal study. The Lancet Neurology, 15(10), 1044-1053. Castello, M. A., Jeppson, J. D., Soriano, S. (2014). Moving beyond anti-amyloid therapy for the prevention and treatment of Alzheimers disease.BMC neurology, 14(1), 169. Chen, X., Kondo, K., Motoki, K., Homma, H., Okazawa, H. (2015). Fasting activates macroautophagy in neurons of Alzheimers disease mouse model but is insufficient to degrade amyloid-beta. Scientific reports, 5, 12115. Dementia, Delirium, and Alzheimers Disease.. (2017).Alzheimer's Dementia Resource Center. Retrieved 5 May 2017, from https://adrccares.org/dementia-delirium-and-alzheimers-disease/ Ginis, K. A. M., Heisz, J., Spence, J. C., Clark, I. B., Antflick, J., Ardern, C. I., ... Middleton, L. (2017). Formulation of evidence-based messages to promote the use of physical activity to prevent and manage Alzheimers disease.BMC Public Health, 17(1), 209. Heller, T., Gibbons, H. M., Fisher, D. (2015). Caregiving and family support interventions: Crossing networks of aging and developmental disabilities. Intellectual and developmental disabilities, 53(5), 329-345. Hroudov, J., Singh, N., Fiar, Z. (2014). Mitochondrial dysfunctions in neurodegenerative diseases: relevance to Alzheimers disease. BioMed research international, 2014. James, B. D., Leurgans, S. E., Hebert, L. E., Scherr, P. A., Yaffe, K., Bennett, D. A. (2014). Contribution of Alzheimer disease to mortality in the United States. Neurology, 82(12), 1045-1050. James, O. G., Doraiswamy, P. M., Borges-Neto, S. (2015). PET imaging of tau pathology in Alzheimers disease and tauopathies.Frontiers in neurology, 6, 38. Journal of Alzheimers Disease and Parkinsonism. (2017).Omicsonline.org. Retrieved 5 May 2017, from https://www.omicsonline.org/alzheimers-disease-parkinsonism.php Jucker, M., Walker, L. C. (2015).Neurodegeneration: Amyloid-[beta] pathology induced in humans. Nature, 525(7568), 193-194. Pedersen, K. F., Larsen, J. P., Tysnes, O. B., Alves, G. (2017). Natural course of mild cognitive impairment in Parkinson disease A 5-year population-based study. Neurology, 88(8), 767-774. Research and Prognosis on Alzheimer's Disease - Alzheimers Disease and other Cognitive Disorders. (2017).Gulfbend.org. Retrieved 6 May 2017, from https://www.gulfbend.org/poc/view_doc.php?type=docid=3249cn=231 Richard, E., Schmand, B. A., Eikelenboom, P., Van Gool, W. A. (2013). MRI and cerebrospinal fluid biomarkers for predicting progression to Alzheimer's disease in patients with mild cognitive impairment: a diagnostic accuracy study. BMJ open, 3(6), e002541. Treatment - Mayo Clinic. (2017).Mayo Clinic. Retrieved 6 May 2017, from https://www.mayoclinic.org/diseases-conditions/alzheimers-disease/diagnosis-treatment/treatment/txc-20167132 Valenti, R., Pantoni, L., Markus, H. S. (2014). Treatment of vascular risk factors in patients with a diagnosis of Alzheimers disease: a systematic review. BMC medicine, 12(1), 160.

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