N512-19A Module Four Discussion: Disorders of the Nervous System Across the Life Span
N512-19A Module Four Discussion: Disorders of the Nervous System Across the Life Span
N512-19A Module Four Discussion: Disorders of the Nervous System Across the Life Span
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Discussion 4
Marisol Arroyo, age 23 y.o., and unmarried, accompanies her mother, Julia, who is a 68 y.o., divorced Latina female, to her appointment with her primary care Nurse Practitioner. N512-19A Module Four Discussion: Disorders of the Nervous System Across the Life Span. Both Marisol and her mother, who live together, have noted that her ever-present forgetfulness seems to be worsening. Just yesterday she walked to the corner store for a few items, which she obtained, but even though she had been to this store many times over the years, she found herself unable to get home without directions. Marisol also notes that her mother’s hygiene is changing, that she is becoming more and more quarrelsome, and that she forgets information she had been told as little as 10 minutes earlier. The Nurse Practitioner is attempting to rule out whether this patient may have some form of dementia or delirium.
In this discussion:
- Describe and discuss the unique pathophysiology of Dementia of the Alzheimer’s Type.
- If this patient is diagnosed with Alzheimer’s dementia, describe and discuss with your colleagues a potential clinical course, and prognosis for her.
- Describe and discuss your plan of care for this patient with both short-term and long-term plans considering current social supports and health-care access.
Include citations from the text or the external literature in your discussion posts.
Remember to respond to at least two of your peers. Please refer to the Course Syllabus for Participation Guidelines & Grading Criteria.
Sample Approach for Discussion 4 (N512-19A Module Four Discussion: Disorders of the Nervous System Across the Life Span)
Dementia of the Alzheimer’s Type
Pathophysiology:
Alzheimer’s disease (AD) is a neurodegenerative disease that progresses slowly and is one of the most common causes of dementia (Hammer & McPhee, 2018, pp. 203-206). Alzheimer’s disease can be familial, occurring via genes/genetic or sporadically when there is no correlation with family genetics, this occurs more commonly and is less predictable (Pathophysiology Made Incredibly Easy!, 2019, pp. 143-148).
The onset of AD beginning in your 30’s to mid 60’s is caused by one of three single-gene mutations increasing abnormal protein production which are: amyloid precursor protein (APP) on chromosome 21, presenilin 1 (PSEN1) on chromosome 14, and presenilin 2 (PSEN2) on chromosome 1 (Alzheimer’s Disease and Related Dementias, 2019). As the disease progresses, the number of APP plaques increases which is known as the “hallmark of AD” (Alzheimer’s Disease and Related Dementias, 2019). Almost all of the individuals with Down’s syndrome (trisomy 21), due to having an extra copy of the chromosome 21, will develop changes seen in AD since there is an increased APP segment of the gene (Hammer & McPhee, 2018, pp. 203-206). Late-onset AD occurs from the mid to late 60’s with the variant genetic risk factor being apolipoprotein (APOE) on chromosome 19 (Alzheimer’s Disease and Related Dementias, 2019). The responsibility of the APOE gene is to make protein to carry fat and cholesterol through the bloodstream (Alzheimer’s Disease and Related Dementias, 2019). There are three different alleles of the APOE protein which you can inherit, potentially one from your each of your parents: APOEe2, relatively rare, APOEe3, more common, and APOEe4 which increases your risk for developing early-onset AD if you are even going to get AD (Alzheimer’s Disease and Related Dementias, 2019).
Diagnosis/Clinical Features of Alzheimer’s Dementia:
As previously stated, AD is a neurodegenerative disease that progresses slowly and may run its course over approximately 5-10 years (Hammer & McPhee, 2018, pp. 203-206). As a caregiver or daughter, as seen by Julia’s daughter Marisol, you begin to notice subtle changes in the person’s character. At first, you question whether these signs are the normal progression everyone goes through at one time or another; forgetting where they placed their keys, going into a room, and coming out without the item you intended to grab as you were distracted by someone. With Julia forgetting how to get home from the corner store, this confirmed Marisol’s thoughts of her mom’s forgetfulness was getting worse.
As the Certified Nurse Practitioner (CNP), I would obtain valuable information from Marisol which would include family history, physical and emotional history, surgeries, as well as medications her mom is taking. I would rule out any underlying diseases that would mimic signs and symptoms of Dementia such as hypothyroidism, chronic subdural hematoma, deficiencies in vitamins B12, B6, B1 or niacin, brain tumors, neurosyphilis, normal pressure hydrocephalus (NPH) or even depression “pseudodementia” (Hammer & McPhee, 2018, pp. 203-206). I would assess Julia for any head trauma, insect bites, as well as a history of alcohol and illicit drug use while obtaining her interests, and difficulties she may be having with activities of daily living (ADL’s). I would complete a neurological, cognitive, and physical assessment, on Julia including gait and verbal responses to confirm subjective findings discussed during the appointment. I would order a series of tests potentially including, however not all: Positron-Emission Tomography (PET) measuring cerebral cortex activity and early diagnosis confirmation, Magnetic Resonance Imaging (MRI) show plaque presence ruling out any intracranial lesions or NPH, Electroencephalography (EEG) to differentiate from intracranial lesions, evaluating electrical activity, Cerebral Spinal Fluid (CSF) to rule out infection, cerebral blood flow studies as well as biomarkers that could be present due to the accumulation of APP (Pathophysiology Made Incredibly Easy!, 2019, pp. 143-148)
In Conclusion/Plan of Care for Julia:
There is no cure unfortunately for AD; however, there are medications, cholinesterase inhibitors that can potentially slow the progression, Memantine, which will help enhance memory processing, and vitamin E supplements to support brain health (Pathophysiology Made Incredibly Easy!, 2019, pp. 143-148). Many clinical trials are in place to find a potential vaccine that would help the immune system fight the APP plaques from increasing (Pathophysiology Made Incredibly Easy!, 2019, pp. 143-148).
Educating Marisol about AD and the many difficulties that arise when caring for an individual with AD will help prepare her to take care of her mom. Providing Marisol with adequate caregiver/support information, as well as programs that she and her mom can participate in to lessen the daily burden keeping consistency in mind is important with these patients. Safety is the key as you don’t want Julia leaving the house wondering off, leaving the stove on after cooking, forgetting to turn it off before retiring at night. Maintaining a safe environment is essential. Having a place Marisol can call and ask for assistance in caring for her mother is beneficial to set up as soon as possible so that she has it when needed. N512-19A Module Four Discussion: Disorders of the Nervous System Across the Life Span
References
Alzheimer’s Disease and Related Dementias. (2019, December 24). National Institute on Aging.
Hammer, G. D., & McPhee, S. J. (2018). Pathophysiology of Disease: An Introduction to
Clinical Medicine 8E (8th ed.). McGraw-Hill Education / Medical.
Pathophysiology made incredibly easy! (6th ed.). (2019). Cherie R. Rebar, Nicole M.
Heimgertner,
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In reply to Diane
Re: Discussion #4 Dementia of the Alzheimer’s Type
Hi Diane,
Thanks for your post. As you stated, there is no curative therapy for AD just yet. There is a lot ongoing research though in this field. Recent research includes enhancing pharmacotherapy choices, such as anti-amyloid therapies that modify the amyloid development cascade; development of immunization for AD-related antibodies; the use of monoclonal antibodies to prevent further amyloid accumulation; and tau-targeted medications that prevent hyperphosphorylation (Briggs et al., 2016). The effectiveness of these therapies have varied from being largely disappointing to having some modest effectiveness (Briggs et al., 2016).
-Dr. Reynaldo
Reference:
Briggs, R., Kennelly, S. P., & O’Neill, D. (2016). Drug treatments in Alzheimer’s disease. Clinical medicine, 16(3), 247-253.
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In reply to Diane
Re: Discussion #4 Dementia of the Alzheimer’s Type (N512-19A Module Four Discussion: Disorders of the Nervous System Across the Life Span)
Thanks for the informative post. I really liked reading about the pathophysiology of Alzheimer’s dementia. You made it much easier to understand. I found it interesting that people with Down’s Syndrome can potentially develop similar changes seen in AD due to both affecting chromosome 21. I also found it interesting that genetic testing is often discouraged because even if a person has the apolipoprotein E gene-allele (apoE) 2, 3, or 4, it’s possible that the person won’t ever have Alzheimer’s (McCance & Huether, 2019). You’re so right in obtaining a list of medications that can mimic Alzheimer’s, or since she already has the diagnosis, medications that can exacerbate her dementia. I always try to check out the Beers criteria for my older patients. So many of them are over-medicated or taking anticholinergics (By the 2019 American Geriatrics Society Beers Criteria Update Expert Panel, 2019). Simplifying Julia’s medications might help her with compliance as well.Thanks again,
LorriBy the 2019 American Geriatrics Society Beers Criteria Update Expert Panel (2019). American Geriatrics Society 2019 Updated AGS Beers Criteria for Potentially Inappropriate Medication Use in Older Adults. Journal of the American Geriatrics Society, 67(4), 674-694. https://doi.org/10.1111/jgs.15767McCance, K. L. & Huether, S. E. (2019). Alterations in cognitive systems, cerebral hemodynamics. In V. L. Brashers & N. S. Rote (Eds.), Pathophysiology: The biologic basis for disease in adults and children (pp. 546-549). Elsevier Mosby.
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