Alzheimer Disease in a 57-Years-Old Patient

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Alzheimer Disease in a 57-Years-Old Patient

Words: 908

Subject: Nursing

Introduction We worked with the 57 years old man who presented with six months history of severe memory and function loss. His chief complaint was forgetfulness about objects’ placement, inability to cook essential dishes, and difficulties in picking up the right words. Magnetic resonance imaging, biomarkers’ assessment, family history, and the physical exam revealed a substantial risk of Alzheimer’s disease (AD) or dementia. Despite the youthful age, the patient’s confirmed diagnosis was early-onset AD caused by mild cognitive impairment.

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Alzheimer Disease Etiology The leading cause of AD is brain cells based on neurotransmitters’ death. Hettiarachchi and Leblanc (2020) state that “the major pathological hallmark of the AD is the extracellular amyloid-beta (Aβ) plaques deposition and the intracellular neurofibrillary tangle-aggregation of hyperphosphorylated tau-proteins” (p. 119). The process of plaques and tangles development in the patient’s brain was abnormally rapid for their age. Alzheimer Disease Epidemiology AD is a severe condition that affects 35% of the world population from age 65 and affects all racial and ethnic groups (Haines, 2018). AD genetic epidemiological factor is mutations in PSEN1, PSEN2, and APP genes that are more common for white non-Hispanic individuals (Haines, 2018). The disease can be developed due to obesity, high blood pressure, and cholesterol levels. More than 50% of the United States’ adult population experiences at least one of the conditions listed above (Haines, 2018). Pathophysiology of Alzheimer Disease: Main Factors The pathophysiology factor of AD is extracellular beta-amyloid deposits that trigger neurodegeneration leading to memory loss. Another pathophysiological cause is intracellular neurofibrillary tangles – severe upbuilding of tau protein in neurons. Neurofibrillary tangles appear due to cytoskeletal microtubules and tubulin-associated proteins loss and are crucial in AD diagnosis (dos Santos et al., 2018). Pathophysiology of Alzheimer Disease: Genetics Although AD has no dominant genetic cause, mutations in the APP gene and allele ε4 of apolipoprotein E (ApoE) are strong disease development factors (dos Santos et al., 2018). One in five humans carries the mutation of the ApoE allele, and 65% of that people will probably have AD (dos Santos et al., 2018). Mutations in the PSEN 1 gene that appeared in relationship with ApoE are identified in 18% to 50% of early-onset AD cases (dos Santos et al., 2018). Clinical Manifestations: Pertinent History Findings The patient retired from work at a media company at age 50 to support his family, not due to any cognitive challenges. There is no history of head traumas, no surgeries, other medical interventions, or car accidents. The patient had long-lasting depression in their late 30s and still experiences mood switches and episodes of anxiety. The patient is a non-smoker, drinks 3-4 glasses of wine every weekend for the last five years and is obese. Family history includes 2 cases of dementia on the maternal side (aunt and grandmother), and the patient’s father died from complications of AD 7 years ago. The patient presented with a son who states that he first noticed his father’s memory loss symptoms and abnormal behavior 16 months ago, but the client denies it. Clinical Manifestations: Pertinent Physical Exam Findings Tests scores: mental state examination 18/30, functional activities questionnaire 16/30, and Patient Health Questionnaire 13/27 – the results support Alzheimer as a prior diagnosis. Neurological examination: muscle tone and power are normal, mild ideomotor apraxia on performing commands – no cerebellar dysfunction, no frontal release symptoms. BP=140/90, HR=80, BMI is 29,3. Overall assessment: the patient is alert, experiences difficulties in formulating sentences, and speaks slowly. Clinical Manifestations: Red Flag History and Physical Exam Findings for Alzheimer Disease Memory loss is detected from the forgetfulness of information gathered from conversations, reading, academic knowledge. Family history of AD and forms of dementia on paternal and maternal sides, the patient’s died from AD. The patient had depression and experienced mood switches, physical exam tests submit the mental abnormalities. Diagnosing Screenings Positron Emission tomography (PET) was chosen as a diagnostic test to clarify the patient’s conditions based on evaluating the patient’s neuronal function. PET is more sensitive to AD’s main biomarkers than magnetic resonance imaging or computer tomography, thus its predictive value is higher. Gobbi et al. (2017) state that “PET is a unique tool to support the development of any novel therapeutic agent targeting pathological forms of tau” (p. 7350). Diagnosing Blood Testing The patient’s history includes a family history of AD, therefore blood tests were taken to reveal any gene mutations. Complete blood count (CBC) and thyroid function were tested and revealed the genetic cause of the patient’s condition. Thyroid dysfunction detected in high-normal level in patient’s blood that is related to the AD’s development (Choi et al., 2020). Patient Education Implement a daily routine of basic activities to perform: brushing teeth, having breakfast, walking, do some garden work. Take medication strictly by prescription, set alarms to take pills. Maintain a schedule for sleeping and eating to stay on track with time and notice abnormalities if they occur. Keep being in contact with family and friends, attend social gatherings. Patient Education: Caregiving Provide the patient with support and the ability to call for help at any time. Watch the eating patterns changes, and help a patient maintain a good appetite by offering various dishes and providing optimal nutrition. The patient might develop the habit of repetitiveness, and his intonations might reveal mood swings. Respond calmly and ask different questions to support conversations. Reach out for medical re-examination and support if the patient experiences severe language difficulties or behaves inappropriately in public. References Choi, B. W., Kim, S., Kang, S., Wong, K. S., Yi, H. A., & Kim, H. W. (2020). Relationship between thyroid hormone levels and the pathology of Alzheimer’s disease in euthyroid subjects. Thyroid, 30(11), 1547-1555. Web.

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dos Santos, P., Lee, C., Ozela, P. F., de Fatima de Brito Brito, M., Pinheiro, A. A., Padilha, E. C., & Rosa, J. (2018). Alzheimer’s disease: a review from the pathophysiology to diagnosis, new perspectives for pharmacological treatment. Current Medicinal Chemistry, 25(26), 3141-3159. Web. Gobbi, L. C., Knust, H., Körner, M., Honer, M., Czech, C., Belli, S., & Grall-Ulsemer, S. (2017). Identification of three novel radiotracers for imaging aggregated tau in Alzheimer’s disease with positron emission tomography. Journal of Medicinal Chemistry, 60(17), 7350-7370. Web. Haines, J. L. (2018). Alzheimer disease: perspectives from epidemiology and genetics. The Journal of Law, Medicine & Ethics, 46(3), 694-698. Web. Hettiarachchi, S. D., & Leblanc, R. M. (2020). Dual targeting nano-approaches for Alzheimer’s disease etiology. Neural Regeneration Research, 16(1), 119. Web.

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