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Ten Warning Signs of Alzheimer's Disease

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Everything you need to know about Alzheimers Disease as a Nurse (Nursing Care Plans)

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This article discusses the diagnosis and treatment of Alzheimer's Disease.

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Jason Weller, Conceptualization, Data Curation, Formal Analysis, Investigation, Methodology, Project Administration, Resources, Software, Validation, Visualization, Writing - Original Draft Preparation, Writing - Review & Editing a, 1, ² and Andrew Budson, Formal Analysis, Project Administration, Resources, Supervision, Writing - Review & Editing 1, ²

Abstract

Alzheimer's disease is the most common cause of dementia worldwide, with the prevalence continuing to grow in part because of the aging world population. This neurodegenerative disease process is characterized classically by two hallmark pathologies: β-amyloid plaque deposition and neurofibrillary tangles of hyperphosphorylated tau. Diagnosis is based upon clinical presentation fulfilling several criteria as well as fluid and imaging biomarkers. Treatment is currently targeted toward symptomatic therapy, although trials are underway that aim to reduce the production and overall burden of pathology within the brain. Here, we discuss recent advances in our understanding of the clinical evaluation and treatment of Alzheimer's disease, with updates regarding clinical trials still in progress.

Keywords: Alzheimer's disease, dementia, amyloid, tau

Background

Dementia is a clinical syndrome characterized by progressive decline in two or more cognitive domains, including memory, language, executive and visuospatial function, personality, and behavior, which causes loss of abilities to perform instrumental and/or basic activities of daily living. Alzheimer's disease (AD) is by far the most common cause of dementia and accounts for up to 80% of all dementia diagnoses 1. Although the overall death rate in the United States from stroke and cardiovascular disease is decreasing, the proportion of deaths related to AD is going up, increasing by 89% between 2000 and 20142. Direct and indirect costs for healthcare related to AD are estimated at nearly $500 billion annually3. The definitive diagnosis of AD requires post-mortem evaluation of brain tissue, though cerebrospinal fluid (CSF) and positron emission tomography (PET) biomarkers combined with several relatively new clinical criteria can aid diagnosis in living patients4. Current treatments available include cholinesterase inhibitors for patients with any stage of AD dementia and memantine for people with moderate-to-severe AD dementia. These medications have been shown to enhance the quality of life for both patient and caregiver when prescribed at the appropriate time during the course of illness; however, they do not change the course of illness or the rate of decline5.

Clinical research is advancing toward more definitive treatment of the hallmark pathology in AD with the expectation that these therapies will attenuate the progressive cognitive decline associated with this illness ( Figure 1 ). This review will attempt to summarize the accepted evaluation methods and describe current and future therapies for patients with suspected AD.

Figure 1.

Evaluation

Building upon the original 1984 diagnostic criteria, the National Institute on Aging-Alzheimer's Association (NIA-AA) revised the clinical criteria for the diagnosis of mild cognitive impairment (MCI) and the different stages of dementia due to AD in 2011 6-8. The use of supportive biomarker evidence (imaging, serum, and CSF) of AD pathology were included to aid in the delineation of AD from other forms of dementia as well as in the diagnosis of MCI due to AD. The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) re-classified delirium, dementia, amnestic and other geriatric cognitive disorders into the more encompassing neurocognitive disorders9. This change was made to better discriminate between different neurodegenerative diseases, such as AD, dementia with Lewy bodies, and frontotemporal dementia, as well as to include both major neurocognitive disorder (equivalent to dementia) and mild neurocognitive disorder (equivalent to MCI)4. Finally, the newer criteria allow for the use of current and future biomarkers in the diagnosis of degenerative brain disease.

The development of non-invasive diagnostic imaging recently resulted in a test which increases the diagnostic accuracy in AD 10. After injection of a radiolabeled tracer agent, patients undergo a specialized PET scan that detects the deposition of amyloid-β (Aβ) peptides into plaques in the living brain. In 2012, clinicians were able to accurately diagnose the disease (later autopsy proven) using this method with up to 96% sensitivity and 100% specificity. Over the next year, this same test demonstrated similar results in patients with milder disease11. Nearly a decade after researchers at the University of Pittsburgh created the first tracer, the US Food and Drug Administration approved the use of florbetapir for the detection of AD pathology. Now, the list of amyloid-specific PET ligands includes florbetaben and flutemetamol in addition to florbetapir, all of which have a similar profile12,13. However, the use of amyloid PET imaging in practice is still limited owing to its cost for most patients, as it is not covered by most insurance carriers. Currently, the majority of patients who undergo amyloid PET imaging do so as part of participation in clinical trials.

A more-invasive but less-costly evaluation involves examination of CSF for Aβ42, hyperphosphorylated tau peptide (p-tau), and total tau protein content 14. This method has slightly less diagnostic accuracy (85-90%), carries the risks and inconveniences involved with a lumbar puncture procedure, and often takes weeks to obtain results because of the dearth of laboratory facilities which perform the fluid analysis. However, a head-to-head comparison showed no difference in diagnostic accuracy between CSF Aβ42:p-tau ratio and amyloid PET imaging biomarkers, suggesting that the best test for individual patients depends upon availability, cost, and patient/provider preference15. Less-invasive serum assays designed to detect the quantity of circulating proteins implicated in AD are currently in development and show promise. In 2017, one test discriminated among normal cognition, MCI, and dementia due to AD in a small number of patients with sensitivities and specificities of 84% and 88%, respectively16. Another blood test that shows promise is the serum microRNA profile screen that demonstrated validity and reproducibility in smaller trials17. With validation by future larger-scale studies, the hope is that a simple blood test may aid in the diagnosis of AD18.

Current treatment

At present, only two classes of pharmacologic therapy are available for patients with AD. The cholinesterase inhibitors donepezil, rivastigmine, and galantamine are recommended therapy for patients with mild, moderate, or severe AD dementia as well as Parkinson's disease dementia 19. Memantine, which has activity as both a non-competitive N-methyl-D-aspartate receptor antagonist and a dopamine agonist, is approved for use in patients with moderate-to-severe AD (mini-mental state examination [MMSE] <15) who show difficulty with attention and alertness20. For patients who choose alternative therapy, the nutraceutical huperzine A has shown benefit in both memory function and activities of daily living21. However, while huperzine A is a government-approved medication outside of the US, it is not regulated by the US Food and Drug Administration and may be subject to fluctuations in potency and purity. Vitamin D deficiency was also identified as an independent risk factor for the development of dementia of any cause, and supplementation is recommended for patients in whom deficiency is diagnosed22. Although many retrospective, observational studies alluded to the role of inflammation in the development of AD by showing a reduced risk of AD with the use of non-steroidal anti-inflammatory drugs, a more-thorough investigation failed to note any significant difference in cognitive performance in patients who took these medications23. In the past decade, omega-3 fatty acid supplements including fish oil have received much attention owing to their cardiovascular benefits. Two recent randomized, controlled, double-blinded studies showed improvement in thinking and memory in patients with MCI who took fish oil supplements, though these studies were limited by small sample size24,25.

Finally, the management of cardiovascular risk factors contributes to overall brain health in both cerebrovascular disease and neurodegenerative disease 26. Recent systematic reviews found that people who adhere to the Mediterranean diet (meals consisting of fresh produce, wholegrains, olive oil, legumes, and seafood while limiting dairy and poultry products and avoiding red meat, sweets, and processed foods) have reduced risk of developing cognitive decline and AD27,28. Regular aerobic exercise, long known to prevent metabolic conditions such as diabetes mellitus and coronary artery disease, also shows preservation of function and reduces caregiver burden in patients with AD29. Not only does physical exercise prevent loss of strength and agility as patients age but it also reduces neuropsychiatric symptoms and the increased care requirements associated with these issues. Recreational physical activity increases cognitive function later in life, with benefit noted regardless of age at the initiation of exercise30. Less atrophy was observed in the brains of patients with genetic risk factors for AD who exercised regularly compared with those who did not, suggesting that aerobic activity prevents neurodegeneration31. Although larger controlled studies are still needed to examine the long-term effects of physical activity in patients with biomarker-proven AD pathology, the inherent systemic benefits and lack of health risks should lead all healthcare providers to recommend regular exercise for their patients, regardless of cognitive function.

Future treatment

Research into future treatments of AD involve targeting of the etiologic pathologies: neurofibrillary tangles (composed of p-tau) and senile plaques (Aβ). However, there remains debate as to which abnormality is the best target to slow or halt neurologic decline as well as how soon treatment should be initiated 32,33. Another approach aims to fortify transcortical networks and enhance inter-neuronal connections in order to enhance cognitive function34. From previous studies, we learned that early identification of an at-risk population and subsequent treatment in the pre-clinical stage is the approach most likely to slow or halt the progression of AD35. Clinical trials are underway that aim to recruit asymptomatic patients with a genetic predisposition or biomarkers suggestive of higher risk of developing Alzheimer's dementia, with results expected early in the next decade. The EU/US/Clinical Trials in AD Task Force in 2016 examined many of these trials in an attempt to identify the most effective measures of patient recruitment and retention, infrastructure development, and patient assessment including biomarkers and objective testing for clinical outcomes35. Some of the persistent challenges identified include the timeline of recruitment and recruitment failures, difficulty in predicting success based upon prior studies for certain drugs, and the overall costs for such large-scale clinical trials. With a more cooperative effort between researchers, private and public funding, and screening of at-risk populations, a better predictor of successful clinical trials can be created.

Anti-amyloid

According to the amyloid cascade hypothesis, toxic plaques are the earliest manifestation of disease, a statement supported by evidence of Aβ up to 20 years prior to the onset of symptoms 36. Researchers found in 2013 that this abnormal amyloid plaque induces the phosphorylation of tau protein, which then spreads almost infectiously via microtubule transport to neighboring neurons, leading to neuronal death37. One class of medications developed using this evidence is the monoclonal antibodies (passive immunotherapy). This type of treatment involves injection of an antibody that targets abnormal Aβ and facilitates its removal from the brain. Two such monoclonal antibodies were initially developed in 2014 to remove these plaques from the brains of people with AD38,39. Neither medication improved cognitive scores in patients with mild-to-moderate disease (MMSE 16-26), leading researchers to conclude that these medications may show benefit only when administered in the early stages of MCI and mild dementia. However, a new study regarding the effect of this class of medication in patients with few to no symptoms (MMSE 20-26) but a positive amyloid PET imaging result also failed to show a significant difference in cognitive outcomes between the study group and asymptomatic controls40. Studies involving similar drugs in this class are ongoing, with the goal of improving or preserving cognition in patients with MCI due to AD.

Another approach to decreasing Aβ plaque burden in the brain is the inhibition of the enzymes that produce the Aβ peptide from its precursor, amyloid precursor protein (APP). Currently, multiple drugs are in development which target β-site APP cleaving enzyme 1 (BACE1), which is thought to be essential for the production of Aβ peptides 41. Though previous studies of BACE1 inhibitors failed to yield meaningful results in human subjects, the novel agent verubecestat recently achieved a more than 40-fold reduction in Aβ levels in the brains of rodents and primates, and it has shown a good safety profile in early human trials42. Currently, another drug is under investigation for its effect on memory and cognitive function in older patients with positive biomarkers or family history of AD, known as the EARLY study.

Researchers showed in 2014 that combination therapy with a monoclonal antibody and a BACE1 inhibitor significantly reduced the amount of Aβ in amyloid-producing mice 43. While there are no current trials underway utilizing this approach in humans, many experts believe that combination therapy employing both approaches to eliminate Aβ will ultimately lead to success in AD treatment44.

Anti-tau

Since p-tau appears to be the downstream pathology and is likely the direct cause of symptoms in AD, drugs to reduce the burden of this protein are also in development 45. Many different tau vaccines have shown both safety and efficacy in animal models46, and, in one recent small study, an anti-tau drug demonstrated a good safety profile and even stimulated a positive immune response in human patients47. Several other early phase trials of drugs which target the tau protein are currently underway, though results are yet to be published48. Table 1 outlines the treatments and targets currently under investigation.

Table 1.

Target

Drug

Study phase

Expected completion date

Results

LY3002813 *

2

December 2020

LY3202626 *

2

December 2020

LY450139
3

Completed
April 2011

Not effective

Neural circuitry

The failure of some targeted therapies toward Aβ in large-scale clinical trials has led to the hypothesis that, although the abnormal protein is implicated at the onset of AD, the progression of clinical symptoms is due to more global neural network dysfunction 49. Gamma oscillation, a high-frequency brainwave rhythm, is associated with inter-neuronal communication in virtually all brain networks50 and may help to distinguish between true and false memories51. Recently, researchers at the Massachusetts Institute of Technology found that induction of gamma-frequency oscillations led to reduced Aβ deposition and improved cognitive outcomes in an AD mouse model52. This was done by using a non-invasive 40 Hz photic stimulator to entrain the desired frequency in the mouse cortex. This method is also currently in early phase trials in humans, utilizing both visual and auditory stimulation.

Summary

As recently as 2010, the diagnosis and management of AD relied upon clinical symptom reporting that fit the pattern of memory dysfunction and loss of functional independence in multiple cognitive domains. With the reclassification system devised by the NIA-AA and DSM-5, the spectrum of AD has grown to include pre-clinical disease and MCI, helping to lay the foundation for early identification of at-risk patients. There are now a few widely available diagnostic studies that augment the clinical evaluation for a more accurate diagnosis of AD pathology, including bodily fluids and imaging studies, with good specificity.

However, the treatment options for AD remain supportive and symptomatic without attenuation of the ultimate prognosis. Medications such as cholinesterase inhibitors and memantine improve memory and alertness, respectively, without changing the life expectancy or overall progression of AD dementia. Lifestyle modifications including diet and exercise remain the only interventions with evidence showing lower AD risk and possible prevention of overall cognitive decline, and these interventions are first-line recommendations for all patients regardless of cognitive function. The pathological features associated with AD, Aβ and p-tau, are the current targets for potential treatments; however, early success in comparative studies and smaller clinical trials are thus far not reproducible in larger-scale administrations. Although limited evidence suggests that earlier identification of AD pathology will lead to better and more-definitive treatment, the results of larger-scale interventions are not yet available for review. Given the rising prevalence and mortality of AD coupled with the growing total healthcare costs, there continues to be a sense of urgency in the medical community to develop effective means for the early diagnosis and successful treatment of this progressive neurodegenerative disease.

Abbreviations

Aβ, amyloid β; AD, Alzheimer's disease; APP, amyloid precursor protein; BACE1, β-site amyloid precursor protein cleaving enzyme 1; CSF, cerebrospinal fluid; DSM-5, Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition; MCI, mild cognitive impairment; MMSE, mini-mental state examination; NIA-AA, National Institute on Aging-Alzheimer's Association; p-tau, hyperphosphorylated tau peptide; PET, positron emission tomography

Notes

[version 1; referees: 2 approved]

Funding Statement

The author(s) declared that no grants were involved in supporting this work.

Notes

Editorial Note on the Review Process

F1000 Faculty Reviews are commissioned from members of the prestigious F1000 Faculty and are edited as a service to readers. In order to make these reviews as comprehensive and accessible as possible, the referees provide input before publication and only the final, revised version is published. The referees who approved the final version are listed with their names and affiliations but without their reports on earlier versions (any comments will already have been addressed in the published version).

The referees who approved this article are:

Hemachandra Reddy, Garrison Institute on Aging, Texas Tech University Health Sciences Center, Lubbock, TX, USA

No competing interests were disclosed.

Erik Portelius, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden

No competing interests were disclosed.

References

9. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders. American Psychiatric Association, Arlington, Texas.2013. [ Reference Source Google Scholar]

12. Yeo JM, Waddell B, Khan Z, et al.: A systematic review and meta-analysis of [[ ¹⁸F-labeled amyloid imaging in Alzheimer's disease. Alzheimers Dement (Amst). 2015;1(1):5-13. 10.1016/j.dadm.2014.11.004 PubMed] [ PMC free article] [ CrossRef] Google Scholar]

25. Bo Y, Zhang X, Wang Y, et al.: The [[ n-3 Polyunsaturated Fatty Acids Supplementation Improved the Cognitive Function in the Chinese Elderly with Mild Cognitive Impairment: A Double-Blind Randomized Controlled Trial. F1000 Recommendation Nutrients. 2017;9(1): pii: E54. 10.3390/nu9010054 PubMed] [ PMC free article] [ CrossRef] Google Scholar]

34. Kosik KS: Diseases: Study neuron networks to tackle Alzheimer's. [ Nature. 2013;503(7474):31-2. [ PubMed] Google Scholar]

43. Jacobsen H, Ozmen L, Caruso A, et al.: Combined treatment with a BACE inhibitor and anti-Aβ antibody gantenerumab enhances amyloid reduction in APP [[ London mice. J Neurosci. 2014;34(35):11621-30. 10.1523/JNEUROSCI.1405-14.2014 PubMed] [ PMC free article] [ CrossRef] Google Scholar]

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Current understanding of Alzheimer's disease diagnosis and treatment

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Alzheimer's disease is the most common cause of dementia worldwide, with the prevalence continuing to grow in part because of the aging world population. This neurodegenerative disease process is characterized classically by two hallmark pathologies: ...

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This graph includes the correlation between memory and Alzheimer's disease.

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Stages of Dementia in Alzheimer's and More

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Stages of Dementia in Alzheimer's and More

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Understand Alzheimer's Disease in 3 Minutes

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Theofanidis, D., Fountouki, A., & Kotrotsiou, S. (2021). Nursing Interventions in Alzheimer’s Disease: A Concise Practical Guide for Everyday Use. International Journal of Caring Sciences, 14(1), 106–114.

Weller, J., & Budson, A. (2018). Current understanding of Alzheimer's disease diagnosis and treatment. F1000Research, 7, F1000 Faculty Rev-1161. https://doi.org/10.12688/f1000research.14506.1

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I found this to be a very informative slide show which discusses many ways in which we can manage patient's with Alzheimer's.

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Alzheimer's disease: Management

1. 1. Alzheimer's Disease<br />

2. 3. Alzheimer's disease<br />A progressive degenerative disorder of the cerebral cortex (especially the frontal lobe)<br /> Most common form of dementia<br />5% of people older than age 65 have a severe form of this disease<br />12% suffer from mild to moderate dementia<br />

3. 5. Alzheimer's disease<br />Characterized by:<br />Progressive impairment in memory, cognitive function, language, judgment, and ADL<br />Ultimately, patients cannot perform self-care activities and become dependent on caregivers<br />Prognosis: poor<br />

4. 6. Pathophysiology and Etiology<br />

5. 7. Gross pathophysiologic changes:<br />cortical atrophy<br />enlarged ventricles<br />basal ganglia wasting<br />Microscopically:<br />Changes in the proteins of the nerve cells of the cerebral cortex<br />accumulation of neurofibrillary tangles and neuritic plaques (deposits of protein and altered cell structures on the interneuronal junctions) <br />granulovascular degeneration<br />loss of cholinergic nerve cells (important in memory, function, cognition)<br />

6. 11. Biochemically:<br />neurotransmitter systems are impaired<br />Cause: unknown<br />Risk factors:<br />genetics and female gender<br />Viruses, environmental toxins, silent brain infarcts, and previous head injury may also play a role<br />

7. 12. Clinical manifestations<br />

8. 13. Disease onset: subtle and insidious<br />Initially, a gradual decline of cognitive function from a previously higher level<br />Short-term memory impairment is commonly the first characteristic in earliest stages of the disease<br />Forgetful and difficulty learning and retaining new information<br />Difficulty planning meals, managing finances, using a telephone, or driving without getting lost<br />

9. 15. Functional deficits:<br />Language disturbance (word-finding difficulty)<br />Visual-processing difficulty<br />Inability to perform skilled motor activities<br />Poor abstract reasoning and concentration<br />Personality changes:<br />Irritability<br />Suspiciousness<br />Personal neglect of appearance<br />Disorientation to time and space<br />

10. 16. Middle stage:<br />Repetitive actions (perseveration)<br />Nocturnal restlessness<br />Apraxia (impaired ability to perform purposeful activity)<br />Aphasia (inability to speak)<br />Agraphia (inability to write)<br />Signs of frontal lobe dysfunction:<br />Loss of social inhibitions<br />Loss of spontaneity<br />

11. 18. Middle and late stages:<br />Delusions<br />Hallucinations<br />Aggression<br />Wandering behavior<br />Patients in the advanced stage of Alzheimer's disease require total care<br />Urinary and fecal incontinence<br />Emaciation<br />Increased irritability<br />Unresponsiveness or coma<br />

12. 21. complications<br />

13. 22. Increased incidence of functional decline<br />Injury due to lack of insight, hallucinations, confusion, wandering, own violent bahavior<br />Pneumonia and other infections, especially if the patient doesn't get enough exercise<br />Malnutrition and dehydration due to inattention to mealtime and hunger or lack of ability to prepare meals<br />Aspiration<br />

14. 25. Diagnostic evaluation<br />

15. 26. Detailed patient history with corroboration by an informed source<br />to determine cognitive and behavioral changes, their duration, and symptoms that may be indicative of other medical or psychiatric illnesses<br />Noncontrast computed tomography (CT) scan, Magnetic resonance imaging (MRI), single-photon emission computed tomography (SPECT) <br />to rule out other neurologic conditions<br /><ul><li>Neuropsychological evaluation (mental status assessment)</li></ul>to identify specific areas of impaired mental functioning in contrast to areas of intact functioning<br />

16. 29. Laboratory tests:<br />complete blood count, sedimentation rate, chemistry panel, thyroid-stimulating hormone, test for syphilis, urinalysis, serum B12, folate level, and test for HIV<br />to rule out infectious or metabolic disorders<br />Commercial assays for cerebrospinal fluid (CSF) tau protein and beta-amyloid<br />Genetic testing<br />In families with a history of Alzheimer's disease, test to confirm AD or to provide information to at-risk family members regarding their likelihood for development of AD<br />

17. 30. management<br />

18. 31. Primary goals of treatment for Alzheimer's disease:<br />To maximize functional abilities and improve quality of life by enhancing mood, cognition, and behavior<br />No curative treatment exists<br />Cholinesterase inhibitors <br />first treatment for cognitive impairment of AD<br />Improve cholinergic neurotransmission to help delay decline in function over time<br />

19. 32. <ul><li>Donepezil (Aricept)</li></ul>Widely used in mild to moderate cases because it can be given once daily and is well tolerated<br />Starting at 5 mg hs and increased to 10 mg after 4 to 6 weeks<br /><ul><li>Galantamine (Reminyl) </li></ul>Given with food in dosage of 4 to 12 mg bid<br />Should be restarted at 4 mg bid if interrupted for several days<br />Dose should be reduced in cases of renal or hepatic impairment<br />

20. 33. <ul><li>Rivastigmine (Exelon) </li></ul>Given 1.5 mg bid with meals and increased up to 6 to 12 mg per day<br /><ul><li>Memantine (Namenda)</li></ul>NMDA-receptor antagonist<br />The first of a new class approved for moderate to severe Alzheimer's<br />Dosage is 10 mg bid<br />Can be used with a cholinesterase inhibitor<br />

21. 34. Patients with depressive symptoms should be considered for antidepressant therapy<br />Behavioral disturbances may require pharmacologic treatment<br />anxiolytics, antipsychotics, anticonvulsants<br />Nonpharmacologic treatments used to improve cognition:<br />Environmental manipulation that decreases stimulation<br />Pet therapy<br />Aromatherapy<br />Massage<br />Music therapy<br />Exercise<br />

22. 35. Drug Alert<br />Cholinesterase inhibitors <br />initially aimed at improving memory and cognition<br />seem to have an important impact on the behavioral changes that occur in patients with cognitive impairment<br />improves the apathy, disinhibition, pacing, and hallucinations commonly noted in dementia<br />Be alert for drug interactions with NSAIDs, succinylcholine-type muscle relaxants, cholinergic and anticholinergic agents, drugs that slow the heart, and other drugs that are metabolized by the hepatic CYP2D6 or CYP3A4 pathways<br />

23. 36. Nursing assessment<br />

24. 37. Perform cognitive assessment:<br />orientation, insight, abstract thinking, concentration, memory, verbal ability<br />Assess for changes in behavior and ability to perform ADLs<br />Evaluate nutrition and hydration<br />check weight, skin turgor, meal habits<br />Assess motor ability, strength, muscle tone, flexibility<br />

25. 38. Nursing diagnoses<br />

26. 39. Bathing or hygiene self-care deficit<br />Constipation<br />Disabled family coping<br />Disturbed thought processes<br />Dressing or grooming self-care deficit<br />Feeding self-care deficit<br />Imbalanced nutrition: Less than body requirements<br />Impaired verbal communication<br />Ineffective coping<br />Interrupted family processes<br />Risk for infection<br />Risk for injury<br />Toileting self-care deficit<br />

27. 40. Key outcomes<br />

28. 41. The patient will<br />perform bathing and hygiene needs<br />maintain a regular bowel elimination pattern<br />(Family members will) use support systems and develop adequate coping behaviors<br />remain oriented to time, person, place, and situation to the fullest extent possible<br />perform dressing and grooming needs within the confines of the disease process<br />consume daily calorie requirements<br />

29. 42. The patient will<br />show no signs of malnutrition<br />effectively communicate needs verbally or through the use of alternative means of communication<br />use support systems and develop adequate coping behaviors<br />(Family members will) discuss the impact of the patient's condition on the family unit<br />remain free from signs and symptoms of infection<br />(Family members will) identify strategies to make the patient's environment as safe as possible<br />perform toileting needs within the confines of the disease process<br />

30. 43. Nursing interventions<br />

31. 45. Establish an effective communication system with the patient and his family<br />to help them adjust to the patient's altered cognitive abilities<br />Provide emotional support to the patient and his family<br />Encourage them to talk about their concerns<br />Listen carefully to them<br />Answer their questions honestly and completely<br />Use a soft tone and a slow, calm manner when speaking to him<br />Because the patient may misperceive his environment, <br />

32. 46. Allow the patient sufficient time to answer your questions <br />his thought processes are slow, impairing his ability to communicate verbally<br />Administer ordered medications to the patient and note their effects<br />If the patient has trouble swallowing, check with a pharmacist to see if tablets can be crushed or capsules can be opened and mixed with a semi-soft food<br />Protect the patient from injury <br />Provide a safe, structured environment<br />Provide rest periods between activities because these patients tire easily<br />

33. 47. Encourage the patient to exercise<br />to help maintain mobility<br />Encourage patient independence<br />allow ample time for the patient to perform tasks<br />Encourage sufficient fluid intake and adequate nutrition<br />Provide assistance with menu selection<br />allow the patient to feed himself as much as he can<br />Provide a well-balanced diet with adequate fiber<br />Avoid stimulants, such as coffee, tea, cola, and chocolate<br />

34. 48. Give the patient semisolid foods if he has dysphagia<br />Insert and care for a nasogastric tube or a gastrostomy tube for feeding as ordered<br />Because the patient may be disoriented or neuromuscular functioning may be impaired, take the patient to the bathroom at least every 2 hours<br />Make sure he knows the location of the bathroom<br />Assist the patient with hygiene and dressing as necessary<br />Many patients with Alzheimer's disease are incapable of performing these tasks<br />

35. 49. Patient teaching<br />

36. 50. Teach the patient's family about the disease<br />Explain that the cause of the disease is unknown<br />Review the signs and symptoms of the disease<br />Be sure to explain that the disease progresses but at an unpredictable rate and that patients eventually suffer complete memory loss and total physical deterioration<br />Review the diagnostic tests that are to be performed and treatment the patient requires<br />Advise family members to provide the patient with exercise<br />Suggest physical activities, such as walking or light housework, that occupy and satisfy the patient<br />

37. 51. Stress the importance of diet<br />Limit the number of foods on the patient's plate so he doesn't have to make decisions<br />If the patient has coordination problems, cut his food and to provide finger foods, such as fruit and sandwiches<br />Suggest using plates with rim guards, easy-grip utensils, and cups with lids and spouts<br />Allow the patient as much independence as possible while ensuring his and others' safety<br />Create a routine for all the patient's activities, which helps them avoid confusion<br />If the patient becomes belligerent, advise family members to remain calm and try to distract him<br />Refer family members to support groups<br />

38. 52. Teaching patient about alzheimer's disease<br />

39. 53. Counsel family members to expect progressive deterioration in the patient with Alzheimer's disease<br />To help them plan future patient care, discuss the stages of this relentless neurodegenerative disease<br />Bear in mind that family members may refuse to believe that the disease is advancing<br />Be sensitive to their concerns and, if necessary, review the information again when they're more receptive<br />

40. 54. Forgetfulness<br />The patient becomes forgetful, especially of recent events<br />He frequently loses everyday objects such as keys<br />Aware of his loss of function, he may compensate by relinquishing tasks that might reveal his forgetfulness<br />Because his behavior isn't disruptive and may be attributed to stress, fatigue, or normal aging, he usually doesn't consult a physician at this stage<br />

41. 55. Confusion<br />The patient has increasing difficulty at activities that require planning, decision making, and judgment, such as managing personal finances, driving a car, and performing his job<br />He does retain skills such as personal grooming<br />Social withdrawal occurs when the patient feels overwhelmed by a changing environment and his inability to cope with multiple stimuli<br />Travel is difficult and tiring<br />As he becomes aware of his progressive loss of function, he may become severely depressed<br />Safety becomes a concern when the patient forgets to turn off appliances or recognize unsafe situations such as boiling water<br />At this point, the family may need to consider day care or a supervised residential facility<br />

42. 56. Decline in activities of daily living<br />The patient at this stage loses his ability to perform such daily activities as eating or washing without direct supervision<br />Weight loss may occur<br />He withdraws from the family and increasingly depends on the primary caregiver<br />Communication becomes difficult as his understanding of written and spoken language declines<br />Agitation, wandering, pacing, and nighttime awakening are linked to his inability to cope with a multisensory environment<br />He may mistake his mirror image for a real person (pseudohallucination)<br />Caregivers must be constantly vigilant, which may lead to physical and emotional exhaustion<br />They may also be angry and feel a sense of loss.<br />

43. 57. Total deterioration<br />In the final stage of Alzheimer's disease, the patient no longer recognizes himself, his body parts, or other family members<br />He becomes bedridden, and his activity consists of small, purposeless movements<br />Verbal communication stops, although he may scream spontaneously<br />Complications of immobility may include pressure ulcers, urinary tract infections, pneumonia, and contractures<br />

44. 58. Learning activity<br />

45. 59. True or False: Alzheimer's disease is a memory-related disease that is reversible with medications.<br />

46. 60. FALSE<br />Alzheimer's disease is a progressive degenerative disorder of the brain that is irreversible<br />The exact cause is unknown; initial stages include recent memory loss and impaired judgment, inability to learn and retain new information, and difficulty finding words; later stages include decreased abilility to care for self, wandering, agitation and hostility, and possibly eventually inability to walk, incontinence, and no intelligible speech<br />Medications may help improve memory in early stages, but there is no cure<br />It is typically diagnosed when other dementia-producing conditions have been ruled out<br />

47. 61. http://nurseRD.blogspot.com<br />www.authorstream.com/reynel89/Nursing<br />www.slideshare.net/reynel89/slideshows<br />THANK YOU!Have a nice day : )<br />- RDG<br />

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Alzheimer's disease: Management 1. Alzheimer's Disease 3. Alzheimer's disease A progressive degenerative disorder of the cerebral cortex (especially the frontal lobe) Most common form of dementia 5% of people older than age 65 have a severe form of this disease 12% suffer from mild to moderate dementia 5.

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Nursing Mnemonic for Alzheimer's Disease

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Nursing Mnemonic for Alzheimer's Disease

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This article can be viewed once you log into your Lincoln account. It goes into detail on nursing interventions for patients with Alzheimer's Disease.

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Need Help Logging In to your Account?
You can reach the Information Desk : by calling 573-681-5888, by emailing helpdesk@lincolnu.edu or by Online Form .

Support hours:
Regular Hours: Monday-Friday 8:00 am - 5:00 pm
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Need Help Logging In to your Account? You can reach the Information Desk : by calling 573-681-5888, by emailing helpdesk@lincolnu.edu or by Online Form . Support hours: Regular Hours: Monday-Friday 8:00 am - 5:00 pm Summer Hours: Monday-Thursday 7:30 am - 6:00 pm

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Healthy brain vs. a brain with severe Alzheimer's

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Healthy brain vs. a brain with severe Alzheimer's