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Dementia of the Alzheimers Type: The Disease of the Century - Essay Example

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The paper 'Dementia of the Alzheimer’s Type: The Disease of the Century' states that frequently referred to as the “disease of the century,” Alzheimer’s disease is one of the most common causes of dementia (Edwards, Handy, Lancaster & Turnbull, 1998)…
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Dementia of the Alzheimers Type: The Disease of the Century
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Running Head: Alzheimer's Disease Dementia of the Alzheimer's Type: The Disease of the Century Frequently referred to as the "disease of the century," Alzheimer's disease is one of the most common causes of dementia (Edwards, Handy, Lancaster & Turnbull, 1998). It is a type of dementia syndrome that is described as a regression in memory and thinking that results to a considerable impairment in personal, social, and occupatonal function (Draper, 2004). Memory loss is one of its earliest manifestations; however, other cognitive functions that are affected include orientation, comprehension, and calculating ability, learning capacity, language, judgement, reasoning and information processing (Draper, 2004). Barker (2002) more concisely defined the disease as "a progressive neurodegenerative disorder characterized by chronic personality disintegration and cognitive deficits, including confusion, disorientation, and stupor" (655). Furthermore, it is a global worsening of cognitive function in the existence of consciousness wherein persistent impairment of intellect compromises mental activities. Although the explicit causes of Alzheimer's disease are still unbeknownst to professionals in the medical and scientific field, there are several theories that bring light to the etiology of the disease, which point to cell loss. The abnormal beta-amyloid protein theory suggests that accumulations of amyloid-rich proteins in large concentrations in the brain are a possible cause, and this 42-amino acid piece of the amyloid precursor protein cannot be broken down (Barker, 2002). On the other hand, dementia of the Alzheimer's type especially those whose onset is after the age of 65, may have a genetic component (Videbeck, 2004). This genetic predisposition is perceived to ba an autosomal dominant trait, which implies that first degree relatives of a person with Alzheimer's have four times the chance of developing the disease (Edwards et al., 1998). These genetic abnormalities are further related to the development of amyloid plaques in the brain, while other researches have found linkages in the defect of chromosome 21 (involved in Down Syndrome), 14, and 19 (Barker, 2002; Videbeck, 2004). Another study implicated the e4 gene to be one of the causes of the disease. Although the e4 gene can be found in persons without dementia and not found in all persons with dementia, the presence of one copy of the gene in a person increases the likelihood of developing Alzheimer's three times more than in a person who does not have the gene (Sadock & Sadock, 2003). Respectfully, if a person has two copies of the e4 gene, that person's likelihood of developing the disease is four times as much. Although difficult to prove, the slow-virus theory proposes that certain viruses with incubation periods of up to 30 years, enter through a disturbance in the blood-brain barrier. In addition, another unclear theory suggests that aluminum toxicity is relevant in the causes of Alzheimer's disease, since there were aluminum deposits found in the brains of patients with Alzheimer's disease (Barker, 2002). It has also been argued that inflammatory processes stimulate synthesis of the amyloid precursor protein and therefore contributes to its deposition and accumulation in the brain (Barker, 2002). In addition to the above theories, there are several factors that have been known to influence the development of Alzheimer's, such as the role of estrogen in the brain, neurotransmitter deficiencies and dysfunction in brain cell communication and the effects of oxidative stress on brain cells, and the effects of acethycholine and anticholinergic agents in the learning and memory functions of the brain (Barker, 2002). Signs and Symptoms Alzheimer's disease manifests in the individual through a group of symptoms typical of the dementia syndrome (Greutzner, 2001). Giving a list of common symptoms would be a complex task, since the disease can present differently for every individual. However, Kirby, Hart, Cross, and Mitchell (2004) has comprehensively outlined the different symptoms based on the different mental aspects (213). Under the behavioural aspect, there is tactlessness, social withdrawal, loss of receptive and expressive skills, inability to organize and plan activities, inability to set goals, altered concentration levels, lack of purpose, catastrophic reactions, poor self-care skils and the inability to maintain one's own safety (Kirby et al., 2004). The cognitive skills lost on the other hand would be the individual's time orientation, concentration, the ability to make choices and judgement, communication skills, and the individual would also be pre-occupied with himself or herself (Kirby et al., 2004). The perceptual symptoms that may be presented are delusions, hallucinations, short-term memory loss and later on, long term-memory loss, and difficulty in the identification of visual and auditory sensation (Kirby et al., 2004). In addition, there are also mood alterations in the individual. There is emotional instability, frustration, agitation, and violent outbursts either physical or verbal (Kirby et al., 2004). Lifestyle choices painly and highly influence many disease-development risk factors; thus, it just logical to follow commonsense guidelines for disease prevention-follow a healthy diet and keep physically fit (Cooper & Kokjohn, 2005). Factors that promote artherosclerosis may also be traced to promote dementia. Thus, to prevent this, one can avoid a diet high in saturated fats and cholesterol, a measure that is completely humanly controllable (Cooper & Kokjohn, 2005). In addition, since one of the main causes of Alzheimer's disease is the accumulation of amyloid plaques in the brain which then results to degenerating neurons, it is again most logical to inhibit this. Controlling the production of amyloid is a very good prevention measure (Cooper & Kokjohn, 2005). The World Health Organization recommends that a six-month duration of the manifestation of signs and symptoms be given before making a diagnosis (Draper, 2004). A neuropathological examination of the brain tissue is necessary before the final diagnosis of Alzheimer's; however, the Alzheimer's type of dementia is commonly diagnosed in the clinical setting after other causes of dementia is excluded from the diagnostic considerations (Sadock & Sadock, 2003). This exam may be achieved either through post mortem autposy or a brain biopsy. Instead of the typical shrinking of the neuronal volume that is typical in the aging process, in Alzheimer's, there is actual loss of neurons, which may be evident in the brain biopsy (Sadock & Sadock, 2003). A lumbar puncture may also be performed to detect elevated levels of biochemical markers tau and beta-amyloid (Barker, 2002). On the other hand, the diagnosis is not only based on the brain biopsy. The individual's memory impairment and mental functions may also be clinically examined, while a computerized tomography or CT scan and a single phhoto emission computed tomograhic scan may also be performed in order to detect the neurofibrillary tangles between the remaining functioning brain cells (Edwards et al., 1998). Meanwhile, the electroencephalogram or EEG measures the electrical activity of the brain. Alzheimer's is a progressive disease, which has three stages (Barker, 2002). During the first stage, the duration of the disease is just from one to three years and the manifestations are: poor memory, impaired acquisition of new inforamtion, mild anomia or inability to name objects, slight visouspatial impairment, poor word list generation, apathy, irritability and depression ("Mosby's Pocket Dictionary," 2002; Barker, 2002). During this stage, the EEG and CT present as normal. The second stage or phase II occurs within two to 10 of the onset of the disease. The symptoms are profound memory loss, significant impairment of other cognitive aspects, severe impairment of judgement, and indifference and apathy in personality. The EEG is slowing and the CT shows ventricular dilation and sulcular enlargement, yet otherwise normal (Barker, 2002). The third stage or phase, however is very severe in its symptoms and it occurs between eight to 12 years of the disease. There is severe impairment of all cognitive functions with physical impairment as well wherein the individual has an unsteady gait, rigid limb and flexion posture. There is urinary and fecal incontinence as well. The EEG presents to be very slow while the CT has abnormal ventricular dilation and sulcular enlargement (Barker, 2002). At the moment, there are no clinical methods or pharmacological agents that can cure Alzheimer's disease. However, to temporarily enhance cognitive function, five pharmacological agents have been developed for mild to moderate Alzheimer's. tacrine, donepizil, rivastigmine, and galantamine act to increase the amount of acetylcholine neurotransmitter in the central nervous system and inhibits the enzyme cholinesterase. Donepezil is a new drug that has been found to be effective in treating symptoms in memory and cognitive loss, and can give up to two years respite for the patient (Kirby et al., 2004). Through these drugs, there is more effective transmission to the receptors (Melillo & Houde, 2005). However, there are several side effects to these drugs. The common side effects are nausea and vomiting, diarrhea and weight loss, and anorexia. The fifth drug memantine is the first drugs that has presented to be effective in managing moderate to severe cases of Alzheimer's, which blocks the selective receptors that are stimulated by glutamate (Melillo & Houde, 2005). Glutamate is a neurotransmitter that is produced excessively in people with Alzheimer's. Management of Alzheimer's is primarily supportive and symptom focused. It usually includes treatment of the mood disorders, and cares for the individuals as physical and emotional beings, and preserves the individual's dignity not matter the level of their cognition (Barker, 2002). This type of supportive care maintains functional ability instead of producing recovery, which helps to delay the further deterioration of the patient's mental and physical abilities. Since most patients with Alzheimer's are elderly, it is very common for them to acquire disease in the course of their current cognitive state. If not treated promptly, these unrelated diseases may further impair their mental function (Edwards et al., 1998). Thus, prompt and adequate treatment is necessary. Examples of these diseases are heart diseases, pneumonia, obstructive airway diseases and others. It is also important to manage the patient's behavior to control agitation, depression, sleep disturbances, psychotic thiknking, and wandering, and in addition to this, the rate of deterioration must be slowed (Edwards et al., 1998). Alzheimer's is a disease that presents differently in every individual. The exact and direct causes are still unknown, and there is no cure yet. However, the signs and symptoms of Alzheimer's have been enumerated in detail, which are categorized into different phases of the disease in terms of the severity. Several theories have also been presented with regards to the possible causes of the disease. From these theories, prevention methods have been deduced. Various management and treatment measures are also available for patients with the Alzheimer's disease. There are 5 drugs that have been developed to manage cognitive function of the patient. However, proper care and safety measures must always be observed, apart from the medical and nursing interventions. Above everything else, the most important way to manage the disease is the support and affection of the family and friends of the patient, as well as the health care provider. As they say, there is nothing more therapeutic than love. References Allen, M.A. (eds.). (2002). Mosby's Pocket Dictionary of Medicine, Nursing, and Allied Health. (4th ed.). Singapore: Mosby. Barker E. (2002). Neuroscience Nursing: A Spectrum of Care. (2nd ed.). Missouri: Mosby. Cooper K.E. & Kokjohn, T.A. (2005, September-October). The Outlook for Alzheimer's Disease: No Cure Is Yet in Sight, but Preventing Alzheimer's Disease May Be Possible. If the Disease Is Caused by Plaque Buildup, Similar to Cardiovascular Diseases, Then Individuals Might Be Able to Control or Prevent Alzheimer's through Healthier Diet and Lifestyle Choices. The Futurist, 39(5), 34. Draper, B. (2004). Dealing with dementia: A guide to alzheimer's disease and other dementias. Crows Nest, NSW: Allen & Unwin. Edwards, J., Handy, R.C., Lancaster, M.M., & Turnbull, J.M. (1998). Alzheimer's disease: A handbook for caregivers. St. Louis, MO: Mosby. Greutzner, H. (2001). Alzheimer's: A caregiver's guide and sourcebook. New York: Wiley. Kirby, S.O., Hart, D.A., Cross, D., & Mitchell, G. (2004). Mental Health Nursing: Competencies for Practice. New York: Palgrave Macmillan. Melillo K.D. & Houde S.C. (2005). Geropsychiatric and Mental Health Nursing. Massachusetts: Jones and Bartlett. Sadock, B.J. & Sadock V.A. (2003). Kaplan and Sadock's Synopsis of Psychiatry: Behavioral Sciences and Clinical Psychiatry. (9th ed.). Philadelphia: Lippincott Williams & Wilkins Videbeck, S.L. (2004). Psychiatric Mental Health Nursing. (2nd ed.). Philadelphia: Lippincott Williams & Wilkins. Read More
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