Paper Example on Alzheimer in the Form of Its Pathophysiology

Introduction

Many diseases affect the neurons in the body. These are the communication paths that transmit signals from one area to the other and back. Through such processes, they facilitate the working together of the various parts of the body with one of them being at the center of issuing commands. These neurons may be damaged by physical injury or malfunction when there are problems in other areas, or they may get diseased. This paper will look at one such condition referred to as Alzheimer in the form of its pathophysiology, manifestations, differential diagnosis and test and treatment.

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Alzheimer is a chronic disease that affects neurons and manifests in their malfunction and their deaths, and it does gets worse with time. Over time the person concerned will start exhibiting the inability to remember or think which is referred to as dementia. The individual will tend to forget things that are associated with the short-term memory or those which happened recently (Turkington & Mitchell, 2010). The disease is manifested by the loss of neurons and synapses located in the cerebral cortex and some of the subcortical regions. As a result, there will be reduced functioning of the temporal and parietal lobe and the frontal cortex. McCance and Huether (2010) agree that studies have indicated that the mentioned brain regions start reducing in size. The disease is associated with the protein misfolding disease which comes about as a result of the excess accumulation of plaque and tau protein within the brain. The plaque and tau begin pairing with other thread that then ends up disintegrating the neuron transport system.

Several clinical molestations are exibited in the individuals who are suffering from Alzheimer. The patient will appear to age rapidly with the onset of the disease and is likely to exhibit some cardinal symptoms as well. He will suffer from memory impairment and forget most of the things associated with recent events. He will have reduced ability in solving simple problems and judging scenarios presented with the facts surrounding a given case (Miklossy, 2017). There will be some behavioral changes and some psychologic symptoms indicating things not working well. Some additional signs could be apraxia and olfactory dysfunction. During the night the individual is likely to have sleep disturbances, seizures that will increase in frequency with time and motor signs with impairment.

Several other diseases have similar symptoms implying a need for a differential diagnosis to separate Alzheimer from them. These diseases include CBD cortical basal degeneration, CJD Creutzfeldt-Jacob disease and DLB dementia with Lewly bodies among others (Morimoto & Christen, 2013). Some of the aspects that will be used to differential it with the others are the first symptoms, mental status, and the neuropsy-chiatry. Besides, there is neurology and the imaging. It is the only one whose early symptoms will be associated with memory loss when the others may have apathy, hallucinations, mood swings, and focal weaknesses. According to Verkhratskii and Butt (2013), its mental status will be episodic memory loss as opposed to language, delirium prone, variable memory and cognitive slowing for some of the others. The neuropsy-chiatry and the neurology will be initial normal, and its imaging will be entorhinal cortex and hippocampal atrophy.

The ones suffering from the disease have an accumulation of paired helical filaments within the brain which may not be seen using any lab tests, but this will require a biopsy of the brain after the patient had died or the brain autopsied. The PHF is ways higher in patients who are suffering from Alzheimer than it is with other ailments which imply that in future laboratory tests focusing on the presence of this substance will be possible for the test. A series of blood test to test for the presence of Alzheimer is not in the offing for now but will be available soon. Genetic tests can only tell whether one has the gene that is likely to cause the disease. The genetic analysis can be done at home by the use of a saliva swab without the need or any prescription.

Once one exhibits the symptoms of Alzheimer's disease, there is no form of treatment that can stop or reverse these symptoms. Most of the medicines available are meant to ease the symptoms developed. They are supposed to slow down the onset of the disease and how quickly it spreads and assist the brain in staying in a better state by not forgetting. Therefore the person will end generating at a slower rate than one who is not using any medications at all. One's physician will assist in the section on the best medicine to use based on some factors which include one's age, overall health and disease history. He will also have to take into account the severity of the disease and the response to medicine and the preference of the patient or his caregivers. Aricept is some oral medication that is suitable for all forms and stages of the disease and approved by FDA. Razadyne is for mild and Exelon for mild to moderate cases while Memantine and Namzaric work with all cases of moderate to severe. Some of these medicines will work by altering the composition of the chemicals that favor learning and improved memory like glutamate. Doctors can also prescribe medication to alleviate other associated symptoms.

Conclusion

There has been a discussion on Alzheimer's disease and its pathophysiological perspective. Some clinical manifestations of the disease have mostly had the prevalence of memory loss in the initial stages and differential diagnosis to set it apart from other neurological disorders. There were no specific lab tests for the disease other than a genetic one that could indicate the possibility of getting the disease. Lastly, it was noted that there was no medicine to treat it but the ones that could slow down the symptoms and keep ones brain better for longer.

References

McCance, K. A. & Huether, S.E. (2010). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis: Mosby.

Miklossy, J. (2017). Handbook of infection and Alzheimer's disease. Amsterdam: IOS Press.

Morimoto, R. I., & Christen, Y. (2013). Protein Quality Control in Neurodegenerative Diseases. Berlin, Heidelberg: Springer Berlin Heidelberg : Imprint: Springer.

Turkington, C., & Mitchell, D. R. (2010). The Encyclopedia of Alzheimer's disease. New York: Facts On File.

Verkhratskii, A. N., & Butt, A. (2013). Glial physiology and pathophysiology. Chichester, West Sussex: John Wiley & Sons.