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Signs and Symptoms of Alzheimers Disease - Case Study Example

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The paper "Signs and Symptoms of Alzheimer’s Disease" argues in a well-organized manner that Alzheimer’s disease is the most common form of dementia. The disease first described in 1906, worsens with time and eventually leads to death (Molsa, Marttila &, Rinne 1986, p. 105). …
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Extract of sample "Signs and Symptoms of Alzheimers Disease"

ALZHEIMER’S DISEASE Name Course Professor Institution: City and State Date Alzheimer’s disease Introduction Alzheimer’s disease is the most common form of dementia. The disease first described in 1906, worsens with time and eventually leading to death (Molsa, Marttila &, Rinne 1986, p. 105). The disease is named after the German neuropathologist, ALOIS Alzheimer’s. Dementia is a condition where one losses the brain function due to certain diseases. Dementia affects language, behavior, thinking, judgment and memory. The effects of the disease are nonreversible and cannot be turned back. There are several types of dementia. For example, MCI (mild cognitive impairment), DLB, Vascular dementia and Lewy body dementia. The causes of dementia also differ, for example, if an individual suffers many small strokes, this could most likely cause vascular dementia. Some medical conditions are the root causes of dementia (Berchtold & Cotman 1998, p.171 ). These include, picks disease, multiple sclerosis, HIV/AIDS, Lyme disease, Huntington’s disease and progressive supra nuclear palsy. However, some causes of dementia can be reversed if detected at the early stages. These include chronic alcohol abuse, brain injury, brain tumor, level change in blood sugar, sodium and calcium, low vitamin B12 amount and normal pressure hydrocephalus. This essay will focus on Alzheimer’s disease. This type of dementia has no cure, and it slowly progresses and eventually the victim dies. AD causes brain cell damage and death (Molsa, Marttila &, Rinne 1986, p. 104), reducing the level of connection among the cells that are yet to be affected. The brain shrinks in the process. This disease mostly affects older people although it might kick in at an earlier age. AD is not really age related, but chances of this disease development are high if an individual has a close blood relative with AD, is older or has the allele EPOE epsilon4 which is linked to AD. This brain disorder hinders an individual from carrying out daily activities. When the brain is not function well especially memory and judgment a lot of errors are likely to happen, and some can be very devastating leaving no one to blame. Alzheimer’s is a disease that is yet to be understood fully. Although, there are several factors that predispose an individual to the development of AD. Age is one of those factors that contribute to the development of AD. Every 5 years after reaching the age of 65, the risk of developing AD doubles. At the age of 85, the risk is ranging around 50%. Although it is rare, individuals in middle ages, which are 30, contribute to 10% of AD cases. The condition in younger patients tends to worsen quicker. Research also shows that women are more prone to AD as compared to men (Dubois 2007, p. 735). Family is also an important factor. The risk of AD development is higher when a family member, maybe father, mother or sibling is suffering from AD. The risk is even higher when the number of relatives with the condition is more. This is influenced by either environmental conditions or hereditary conditions. Hereditary factors that influence the development of AD are categorized into two. These include the risk genes and deterministic genes. Risk of AD development increases with availability of risk genes although it doesn’t guarantee disease development. Three such genes have been identified. These genes are APOE-e4, APOE-e3 and APOE-e2. APOE-e4 has the strongest impact on AD development and was the first among these genes to be identified. This gene may cause symptom development at an early age. Every one inherits a copy of this gene from each of the parents but those who inherit two copies have an increased risk. Any individual who inherits deterministic genes is guaranteed development of AD. Rare genes have been isolated by researches, and it is suggested that they cause less than 5% AD in extended families worldwide (Dubois 2007, p. 745). These genes are considered to cause what researchers call ‘familial Alzheimer’s ’. The discovery of these new genes is providing novel ideas on development of drugs that slow the progress of AD. This is an important advancement since the role of genes in AD has been unclear. Signs and symptoms One of the major symptoms of AD is memory loss. Memory loss in AD is more than that experienced normally by old people. The individual begins to forget more frequently and is unable to recall frequent events. Since there are no clear signs, it is advisable for an individual to be checked out earlier. Planning and performance of daily tasks (Eskelinen et al. 2009, p. 87) becomes difficult to the individual. Tasks that were part of their daily recent lives become hard to perform. These individuals find it hard to communicate and understanding them is difficult thus, care givers are forced to be keen in learning and monitoring their behavior. Their expression by language and writing becomes poor thus, substituting words for others, which are less meaningful. For most of them, time and space disorientation becomes evident. They can ask where they are and yet they are in the same house they have spent the last 25 years or so in. Their judgments deteriorate. They may dress inappropriately and see nothing wrong with it. Some can wear very heavy clothing in a very hot day or inappropriately give out large sums of money. Such individuals tend to misplace things and place them in odd places. For example, an individual may place his wallet in the oven. Problems may also occur in abstract thinking; one may forget what numbers are and wonder or ask what their purposes are. Changes in mood and behavior are more frequent and rapid. An individual may be extremely happy, and then all of a sudden becomes angry and is screaming at somebody else, for no apparent reason. An individual may also have change in personality. Such people may become dependent on somebody else and become suspicious and fearful. They also tend to loss initiative and become very passive, wanting to indulge in unusual activities. They may also sleep more than usual and/or may spend hours in front of the television. The individuals also tend to loss interest in a lot of other things. AD is a disease that progresses through simple signs and symptoms, then worsening of the condition and eventually leading to death (Molsa, Marttila &, Rinne 1986, p. 106). Accordingly, AD is a condition with various stages. The initial stage or the normal stage is where the individual is free of subjective or objective symptoms, and the individual considered mentally healthy. The second stage involves normal aged forgetfulness. In this stage, those of 65 years and above develop cognitive and functioning difficulties. Most of them find hard to recall names, which in the past was not so problematic. This stage includes forgetfulness of where things or items were placed. Some of these cases are just normal aged forgetfulness. The 3rd stage is mostly mild cognitive impairment. Individuals in this stage exhibit deficit subtle which is manifested through several ways. For those who are still working their performances become poor and mastery of new skills become almost impossible. Such individuals cannot be looked up to organize social events. Those who are not working or aren’t involved in organizing events the symptoms may not be evident to family and friends. Individuals who exhibit MCI are advised to seek clinical consultations. Counseling is helpful for such individuals and for those who are working retirement may be a helpful solution in controlling anxiety. The fourth stage is considered as the mild AD stage and patients in this stage are unable to write correct dates and also correct amounts in checks. Mostly this stage may last for 2 years. Patients tend to forget recent happenings and events. For those live alone bill payments become a difficult task and for those who cooked for their families, a notable decrease in these skills can be accounted for. Shopping for groceries also becomes a difficult task to execute for patients in this stage. The patient becomes less responsive emotionally as compared to the past. This may be attributed to the patients’ denial towards the deficit. The patient’s denial does not allow him, or her to reveal their deficit and hence less emotional responsiveness developed. The 5th stage also termed as the moderate AD. They mean duration of this stage is one and half years. Patients in this stage dress inappropriately and may wear the same clothes every day unless they are reminded to change. At this stage, a patient cannot survive alone, and they require a care giver. The magnitudes of deficits (Antoine C et al 2004, p. 571) are higher in this stage and the patient requires being in constant company of another person for reasons of error elimination and guidance. Most patients are very suspicious and may loss their temper especially in the presence of predatory strangers. The patient is forgetful in this stage and recalling of recent events is very rare (Doody 2008, p. 209). On some occasions, individuals may remember information, but on others, they may forget. Independent survival within a community becomes impossible due to the high magnitudes of deficit. Stage 6 is considered as the moderately severe AD. The ability to carry out daily activities becomes more compromised. For example, dressing without supervision becomes very difficult. This is stage 6a. Stage 6b will involve inability to take a bath without supervision and help (Doody 2008, p. 212). The patient may have problems in adjusting the water temperature. This stage evolves and other aspects of hygiene become poor. Other stages are 6c, 6d and 6e. The ability to go to the toilet by them becomes compromised. Urinary incontinence is first experienced, and then fecal incontinence follows. Absorbent undergarments become imperative to implement at this stage. In Stage 6e, patients have difficulty in identifying close family members and also frequently confusing them. Patients are unable to recall recent events like the head of states and also they cannot recall any of the schools or institutions they attended. Neurochemical basis and psychological response towards the changes affect the emotional changes of the patients. The mean duration for the sixth stage is 2.3 years. The 7th stage is termed as the severe AD stage. The patients’ power of speech becomes poor. Eventually speech is lost, but proper care for the individual can postpone this. The patient is unable to ambulate and sit upright without assistance. The patient experiences neurological changes and develops primitive reflexes. Contractures develop, and this causes permanent damage to the patients’ joints. Rigidity of key joints is also common. Patients can survive for several years while in the 7th stage of AD if provided with life support and proper care. Pneumonia is the most frequent cause of death, and this is mostly caused by aspiration. Alzheimer’s disease has no cure. However, drugs that slow the progression of the disease are available (Klafki 2006, p. 2850). Also, there are drugs that suppress some the symptoms like memory loss. Basically, drugs used in AD are grouped into two. Those that treat cognitive symptoms and those that treats behavioral symptoms. Mental health is improved by treatment of other ailments that accompany AD. For example, administration of antibiotics for urinary tract infection, antidepressants for those who are depressed and anti-inflammatory drugs for those with arthritis. Some of the drugs are Donepezil, Exelon, Reminyl, and Memantine. These drugs improve mental health (Marksteiner, Hinterhuber & Humpel 2007, p. 425). Patients with AD exhibit loss of nerve cells which use the chemical called acetylcholine. Donepezil, Exelon and Reminyl prevent the breakdown of enzymes called acetylcholinesterase. Increased concentration of acetylcholine in the brain significantly improves communication between the surviving nerve cells and that use the chemical acetylcholine as a messenger. The symptoms in this case are either stopped or suppressed for some time and this slows the progress of the disease. Some drugs may have side effects to the patients. The side effects vary in patients and also last for different lengths of time. For example, the most common side effects experienced by taking Donepezil are nausea, loss of appetite, vomiting and diarrhea. Other side effects include insomnia, headache, abdominal cramps and dizziness. The doctor should be consulted on issues regarding drug choice and dosage (Waldemar 1986, p. 104). If the patient stops taking the drugs prescribed by the doctor, the chances of their AD conditioning worsening are increased over several weeks. Patients with this disease require different levels of care depending on the stage they are facing. A patient in the 7th stage requires to be taken care of all time. It may be imperative for a family member to attend to care giving interventions and programs. This enables individuals understand how beat to aid and help a loved one affected by AD (Waldemar 1986, p. 103). The care giver must know how to interact with the sick individual in order for them to help the patient. It is very important to recognize how to manage behavioral problems and aggressions, so as to help the patient. Caregivers should also take care of themselves and circumvent stress, as this has been shown, through research conducted, to reduce immunity and eventually predispose the caregiver to diseases. This slows down the therapeutic process ((Klafki et al 2006, p. 2850) in case of an injury. References Antoine C et al,.2004, ‘Awareness of deficits and anosognosia in Alzheimer's disease’, Encephale, vol. 30, no. 6, pp. 570–7. Berchtold, N, & Cotman, W 1998, ‘Evolution in the conceptualization of dementia and Alzheimer's disease: Greco-Roman period to the 1960s’, Neurobiol Aging, vol. 19, no. 3, pp. 173–89. Dubois, B 2007, ‘Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDS-ADRDA criteria’. Lancet Neurol, vol. 6, no. 8, pp. 734–46. Doody, S, 2008, ‘Effect of dimebon on cognition, activities of daily living, behavior, and global function in patients with mild-to-moderate Alzheimer's disease: a randomised, double- blind, placebo-controlled study’, Lancet, vol. 372, no. 9634, pp. 207–15. Eskelinen M et al. 2009, ‘Midlife coffee and tea drinking and the risk of late-life dementia: a population-based CAIDE study’, J Alzheimers Dis., vol. 16, no. 1, pp. 85–91. Harrington, C 2008, ‘Methylthioninium chloride (MTC) acts as a Tau aggregation inhibitor (TAI) in a cellular model and reverses Tau pathology in transgenic mouse models of Alzheimer's disease’ Alzheimer's & Dementia, vol. 4, no. 4, pp. T120–T121, Klafki, H 2006, ‘Therapeutic approaches to Alzheimer's disease’, Brain, vol. 129, pt. 11, pp. 2840–55. Kukull, A 1995, ‘Solvent exposure as a risk factor for Alzheimer's disease: a case-control study’, Am J Epidemiol, vol. 141, no. 11, pp. 1059–71. Marksteiner, J, Hinterhuber, H & Humpel, C 2007, ‘Cerebrospinal fluid biomarkers for diagnosis of Alzheimer's disease: beta-amyloid(1–42), tau, phospho-tau-181 and total protein’, Drugs Today, vol. 43, no. 6, pp. 423–31. Molsa, P, Marttila, J &, Rinne, U 1986, ‘Survival and cause of death in Alzheimer's disease and multi-infarct dementia’, Acta Neurol Scand, vol. 74, no. 2, pp. 103–7. Shioi, J 2007, ‘FAD mutants unable to increase neurotoxic Aβ 42 suggest that mutation effects on neurodegeneration may be independent of effects on Abeta’, J Neurochem..., vol. 101, no. 3, pp. 674–81. Stahl, S, The new cholinesterase inhibitors for Alzheimer's disease, Part 2: illustrating their mechanisms of action. Waldemar, G 2007, ‘Recommendations for the diagnosis and management of Alzheimer's disease and other disorders associated with dementia: EFNS guideline’ Eur J Neurol, vol. 14, no. 1, pp. 1–26. Wozniak, M, Mee, A & Itzhaki, R 2008, ‘Herpes simplex virus type 1 DNA is located within Alzheimer's disease amyloid plaques’, J Pathol, vol. 217, no. 1, pp. 131–138. Read More
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