PowerPoint Presentation

CASE STUDY

Allie, a 72 year old lady was brought to see a neuropsychologist for an evaluation of memory loss of a progressive nature. The symptoms had been present for years and were getting worse. Her memory loss originally took the form of a tendency to repeat questions and ideas. As the symptoms progressed, her son, reported that her mother was having trouble reasoning and was disoriented with regards to time, day, month and year. Frequently, Allie did not understand were she was when outside of home.

CASE STUDYHer son described that his mother is still experiencing anxiety and depression, which was signified a personality change in her mother despite multiple courses of medication for depression. She is now also tended to be overall aggressive towards others, which was not her usual manner. In addition, her son reported that his mother had begun to require supervision in dressing, bathing, and grooming and required reminders to change his clothes. Frequently, Allie would wear the same clothes repeatedly. It was also noted that she had become socially withdrawn.

CASE STUDY

During the doctors evaluation, she was very upset when she was examined, because she did not comprehend why she was there. Throughout the visit, she had difficulty finding words. Even without any other medical or neurological evaluations, all these indications made it obvious to the neuropsychologist that she had classic Alzheimers disease in the moderately severe stages.

ALZHEIMERS DISEASE Severe type of mental deterioration, or dementia, usually affects older people.(2007, Seeley et. Al, Essentials of Anatomy and Physiology) Progressive, degenerative brain disease that impairs memory, thinking, and behaviour. (2007, Lippincot Williams & Wilkins)Prognosis for patient is poor. (2007, Lippincot Williams & Wilkins) Causes gradual memory loss, decline in the ability to perform routine tasks, disorientation, difficulty in learning, loss of language skills, impairment of judgement and personality changes. ( 2008, Sabbagh, The Alzheimers Answer)NO ONE IS IMMUNED

ALZHEIMERS DISEASE 1906: Dr. Alois Alzheimer first described the disease.1974:Founding of National Institute on Aging 1980:Alzheimers Association founded. Jerome H. Stone is the President.

ALZHEIMERS DISEASE 1993:Tacrine (Cognex)- First Alzheimer Drug approved by FDA.2000:Alzheimers Disease Association of the Philippines was founded. 2011:President Obama signs National Alzheimers Project Act (NAPA) into law.

1994:Ronald Reagans Alzheimers Disease diagnosis announced.

STAGES OF AD:1. PRE-CLINICAL ALZHEIMERS DISEASEBegins near the hippocampus (structure essential to formation of both short & longterm memories)Affected region begins to shrink.

STAGES OF AD:2. MILD ALZHEIMERS DISEASECerebral cortex begins to shrink.Memory disturbance usually noticed.Poor judgement and problem-solving skills, careless in work and household.Irritable, suspicious or indifferent.Cognitive impairments: Agitation, apathy, dysphoria and aberrant motor behaviour.

STAGES OF AD:3. MODERATE ALZHEIMERS DISEASEClient demonstrate Language disturbance, characterized by impaired word-finding and circumlocution (talking around subject rather than about it directly)Paraphasias (words used in the wrong context)Apraxia (motor disturbance)Hyperorality (desire to take everything into the mouth to chew, suck or taste)

STAGES OF AD:4. SEVERE ALZHEIMERS DISEASEPlaques and tangles are widespread throughout the brain.Clients cant recognize family and loved ones.Voluntary movement is minimal, limbs are rigid with flexor posturing.Aspiration pneumonia is common.

LOCAL STATISTICS 7,900 patients were hospitalized with initial diagnosis of Alzheimers disease. ( Hospital Episode Statistics, DOH, 2000)

GLOBAL STATISTICS

PATHOPHYSIOLOGY

3 HALLMARKS OF AD:Beta-amyloid plaquesComposed of degenerating axons and dendrites.Dense deposits of protein & cellular material that accumulate outside & around nerve cells.

Beta-amyloid PlaquesAmyloid precursor protein (APP) is the precursor to amyloid plaque. 1. APP sticks through the neuron membrane.2. Enzymes cut the APP into fragments of protein, including beta-amyloid.3. Beta-amyloid fragments come together in clumps to form plaques.1.2.3.In AD, many of these clumps form, disrupting the work of neurons. This affects the hippocampus and other areas of the cerebral cortex.

3 HALLMARKS OF AD:2. Neurofibrillatory TanglesFibrous proteinsTwisted fibers that build up inside the nerve cells.

Neurofibrillatory Tangles

3 HALLMARKS OF AD:3. Neuronal Cell Death Composed of degenerating axons and dendrites.Dense deposits of protein & cellular material that accumulate outside & around nerve cells.

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References:

Black, J. (2008). Medical-Surgical Nursing 8th Edition. Singapore: Elsevier Pte. Ltd

Morrison A., Lykestos C. (2005). The Pathophysiology of Alzheimers Disease and Directions in Treatment. Galen Publishing LLC.

Predisposing factors

- elevated homocysteine levels

- inflammation

- Stroke

- Oxidative damage from free radicals.

Risk Factors

- Increasing Age

- Family History & Genetics Factors - Gender (Female)

Brain

(Neurons)

- CT scan

- MRI

- single positron emission computed tomography (SPECT)

-positron emission tomography (PET)

- other lab studies are performed to rule out metabolic and drug related dementia

- neuropsychological tests (MMSE)

- CSF studies

-thickening of leptomeninges

-shrunken gyri

-widened sulci

-enlarged ventricles

- hippocampal shrinkage

- generalized atrophy of the brain (in late stages)

(+) amyloid plaques: present in outside and around the neuron hampering neuron communication

(+) neurofibrillary tangles: protein tau becomes tangled

microtubules degenerate and the neuron itself

- neuronal cell death

Unknown

Cholinergic hypothesis

- acetylcholine memory, mood

Glutamatergic/excitotoxicity hypothesis

-continuous activation of glutamate receptors leads to chronic calcium influx that leads to neuronal damage

Oxidative stress hypothesis

- amyloid plaques also promotes free radicals

- memory disturbance memory impairment

- cognitive and motor impairment

- poor judgment and problem solving

- confusion regarding whereabouts

- confusion to time, day

- lacking the ability to learn

- irritable, agitated

- anxiety and depression

-personality changes

- repeats the questions asked

- needs help with much of their daily personal care, including eating or using the toilet.

Alzheimers Disease

CLINICAL MANIFESTATIONS

References:

http://www.buzzle.com/articles/lobes-of-the-brain-and-their-function.html

Black, J (2008). Medical-Surgical Nursing 8th Edition. pp. 1746-1747

Presence of -amyloid plaques neurofibrillary tangles in and neuronal cell death in:

;

Frontal Lobe

Occipital Lobe

Temporal Lobe (includes the hippocampus)

Parietal Lobe

- challenges in planning

- impairment in mental flexibility and spontaneity

-socialization is impaired

- low problem solving skills

-agitation

- impaired personal care skills

- Trouble understanding visual images and spatial relationships

-impairment of visual memories

-memory disturbance/ impairment (difficulty in remembering short-term memory)

- reduced inhibition of talking

-difficulty in recognizing words

-difficulty in remembering verbal material

LATEST RESEARCH REGARDING AD:

Medscape Medical Newsreported on the latest published research in Alzheimers disease on November 7, 2012 indicating individuals carrying a mutant gene for Alzheimers disease demonstrate markers 20 years before onset of memory changes. In addition to markers in the cerebral spinal fluid, the individuals show structural changes in the brain other than the amyloid plaques and tangles commonly found in patients with the disease.

Dr. Eric M. Reiman, the first author on this recent study, published his results in Lancet Neurology on November 6, 2012. His research group from theBanner Alzheimers Institutein Phoenix, Arizona studied about 5000 people who carry the gene mutation that produces Alzheimers disease as early as age 45 years in Colombia.

Reiman and colleagues compared carriers of the gene with non-carriers and found structural differences in area of the brain called the hippocampus as well as less grey matter in some parietal lobes in individuals with the Alzheimers gene mutation. The parietal lobe resides at the top of the head after the frontal lobe and before the occipital lobe at the back of the head. The researchers used magnetic resonance imaging to uncover the changes in the parietal lobe. These changes occurred 20 years before the onset of memory loss. By knowing these alterations exist early, researchers can study treatments and measure for differences at these sites.According to theCenter for Disease Control and Prevention, Alzheimers disease causes the most common form of dementia that produces loss of thought control, memory and language. The disease usually affects men and women over the age of 60 years. The cause of Alzheimers disease remains presently unknown. Most scientists think several factors such as genetic, environmental and lifestyle contribute to the development of the disease. The discovery of changes in the parietal lobe and hippocampus add significantly to progress in the research.

The National Institute on Aging describes the importance of clinical research for uncovering causes, treatment modalities and disease prevention in Alzheimers disease. Patients or families interested in becoming involved in research trials can go theClinical Trials.govwebsite for more information. The research trial website lists trials available in all 50 states and 181 countries.

Source: http://www.examiner.com/article/remarkable-recent-discoveries-alzheimer-s-disease

PHARMACOLOGY

Research Topic

Alzheimers disease: Abstainers or binge drinkers. Who are the most at risk population?

Treatment1. Patient & Family education regarding memory aids, diet, and safety issues may slow the progression of symptoms.

2. Medications:NamendaRazadyneExelonAricept

Treatment3. Cholinesterase inhibitorsDonezepilRivastigmineGalantamine

4. Vitamin E- may slow progression of death, institutionalization and severe AD

Ethical Considerations

Ethical Issues in the Early Diagnosis of Alzheimer Disease

Matthew E. Growdon

Mattsson N, Brax D, Zetterberg H. To know or not to know: ethical issues related to early diagnosis of Alzheimers disease.Int J Alzheimers Dis. 2010.

While a disease-modifying treatment for Alzheimer disease (AD) remains elusive, recent advances have shed light on its pathophysiology, giving patients and researchers alike hope that a viable treatment will emerge. Research efforts have identified promising drug targets for clinical trials and uncovered cerebrospinal fluid (CSF) biomarkers and imaging studies that allow for preclinical detection of AD pathology. The recognition that the hallmark plaques and tangles of AD are detectable in the brains of individuals more then 10 years before they present with any cognitive changes underscored the need to validate biomarkers that could reliably detect AD and chart its progression.

In April 2011, the Alzheimers Association [1] updated the criteria for the diagnosis of Alzheimers disease dementia for the first time in 27 years. Their report emphasizes biomarker data and lays out research guidelines for the preclinical diagnosis of AD meant to facilitate ongoing clinical research and drug discovery efforts [2].

Implicit in these new guidelines is the hope that effective therapies are around the corner and the belief that interventions should be designed for individuals before their brains are irreversibly damaged. The well-placed optimism of scientific progress can obscure the humanistic dimensions of early diagnosis. In To Know or Not to Know: Ethical Issues Related to Early Diagnosis of Alzheimers Disease, Niklas Mattsson, David Brax, and Henrik Zetterberg examine the ethical issues surrounding the early diagnosis of AD. They emphasize the potentially harmful consequences of early diagnosis to the patient and raise important questions about personal identity and decision-making competence that are central to the diagnosis and management of AD. Their article is a timely reminder about the powerful, life-altering effects of diagnosis and, above all, the enduring need to place the patients desires and preferences at the center of the clinical encounter.

As a point of departure, Mattsson et al. consider the potential for misdiagnosis of AD, even in the era of sophisticated biomarker studies. Several studies underscore the high diagnostic accuracy of cerebrospinal fluid (CSF) biomarkers, with sensitivity and specificity around 85-90 percent in identifying incipient AD in patients diagnosed with mild cognitive impairment, an intermediate stage between the expected cognitive decline of normal aging and the pronounced decline of dementia [3].

However, the authors acknowledge the enduring possibility of misdiagnosis in populations or samples in which there is a low prevalence of disease because of false positive screening results. Furthermore, while severe complications are rare, lumbar punctures to obtain CSF are associated with post-LP headaches in 2-4 percent of patients [4]. Colloquially referred to as spinal taps, lumbar punctures are feared by many patients, to the point that there have been calls within professional circles to rename the procedure and move it into the mainstream of clinical practice in dementia care [5].

The authors offer a balanced analysis of the potential benefits and considerable drawbacks to the early diagnosis of AD. It is difficult to do justice to the intensely personal and wrenching effects for patients and families of a test result that is positive for AD. Mattsson et al. consider many of these effects: extended follow-up for the patient, feelings of hopelessness, agony, and despair, and increased risk of suicide in people with dementia (a subject about which there has been inconclusive research to date).

From a legal perspective, the diagnosis of dementia can affect rights to hold a drivers license or own a gun; a diagnosis of AD thus represents a stigmatizing label that can severely restrict the autonomy of the patient. Citing an instance in which a participant in a phase 1 clinical trial for an experimental AD preventive vaccine developed meningoencephalitis, the authors invoke the guiding principle of nonmaleficence [6]. As in other areas of medicine where disease-modifying treatments are more readily available, physicians will need to balance the positive effects of future AD treatments against the possible side effects and treatment costs for patients.

In the absence of disease-modifying therapies and in light of the devastating meaning of a diagnosis for patients and families, the benefits of early diagnosis of AD can seem paltry at best. An unambiguous and early diagnosis of dementia can be framed as an opportunity for patients and families to plan for the future in an informed manner. Following this line of reasoning, the knowledge of future cognitive decline enables individuals to set up systems and coping strategies that will support them when they have lost their ability to be competent decision makers. Patients can draw up their wills, arrange for advance directives, and make their wishes known. The authors also argue that investigations aiming at an early diagnosis may lead physicians to uncover other treatable causes of cognitive dysfunction, such as depression and hypothyroidism. Thus, the major benefits of early diagnosis generally fall under the rubric of facilitating advanced planning among patients and families.

In considering the possible benefits of early diagnosis, Mattsson et al. arrive at the most intriguing aspect of their paper: a consideration of decision-making competence and hypothetical consent in the setting of AD. Alzheimer disease strips away an individuals identity, recklessly dissolving memories and fundamentally altering emotional and behavioral traits over its long and insidious course. The ravaging, personality-altering effects of neurodegenerative disease pose a problem for individuals who have been diagnosed at a preclinical stage and who are faced with the challenge of making decisions for their future selves. Given that an accurate, preclinical diagnosis of AD spells a future loss of cognitive function, how can and should these individuals plan for their future well-being?

The authors point out that the notion of psychological continuity has been considered a foundational aspect of personal identity ever since the writings of John Locke. The belief that we will be fundamentally unchanged in the futurethat our present self can reliably predict what will be best for our future selfenables us to plan for the future. An early diagnosis of AD challenges this notion by revealing that our future selves may in fact be quite different from our present selves.

The ethical challenges surrounding decision-making capacity in the context of neurodegenerative disease are far from new, but the authors rightfully argue that these issues are increasingly relevant in light of the current focus on preclinical diagnosis. Since the ability to draw up an advanced treatment directive while still cognitively intact is touted as a potential benefit of the early diagnosis of AD, it is important to examine these tools critically. Advance directives, documents in which patients spell out their future treatment preferences or designate a particular family member or trusted person to act as a future decision maker, rest on the principle of respecting individual patient autonomy (in this case, future-oriented autonomy) [7].

But it is possible to imagine a situation in which individuals specify certain treatment preferences in the present that come into conflict with their welfare in the future. This is particularly possible in the case of the early diagnosis of AD, in which there may be a period of several decades between an individuals diagnosis and the onset of clinical symptoms. How should health care professionals act when an individuals future-oriented autonomy, spelled out in a document that was drawn up at an earlier time, demands administration of a treatment that would be considered inhumane in the present moment? Scholars are split on this question, and Mattsson et al. explicitly state that they offer no solutions to these problems [8].

While the ethical challenges surrounding the early diagnosis of AD are daunting to patients, caregivers, and physicians, the prevailing trend towards early diagnosis suggests that this is not an issue that is likely to go away. Many studies point to the difficulty clinicians face in breaking the news about a diagnosis of dementia, particularly in the pressured environment of many office practices and hospitals [9]. However, as signified by the recent amendments to the Alzheimers Associations diagnostic criteria for AD, it is clear that physicians and professional organizations must devote considerable resources and specific training to ensure that clinicians are confident and compassionate in the diagnosis and management of AD, particularly in the context of early diagnosis.

The advent of disease-modifying treatments for AD will substantially alter the meaning of a diagnosis of dementia, moving it into the domain of potentially treatable illnesses. In the meantime, clinicians will be well served by paying attention to many of the central considerations raised by Mattsson et al.: a balanced view of the potential benefits and drawbacks to an early diagnosis of AD, an awareness of the conflict between respect for future-oriented autonomy and future welfare in the context of neurodegenerative disease, and, most importantly, an abiding respect for the powerful and life-altering effects of these diagnoses.

References

1. Virtual Mentor, followingThe Chicago Manual of Style, uses the term Alzheimer disease; the Alzheimers Association uses the possessive form.

2. McKhann GM, Knopman DS, Chertkow H, et al. The diagnosis of dementia due to Alzheimers disease: recommendations from the National Institute on Aging-Alzheimers Association workgroups on diagnostic guidelines for Alzheimers disease.Alzheimers Dement. 2011;7(3):263-269.

3. Hansson O, Zetterberg H, Buchhave P, Londos E, Blennow K, Minthon L. Association between CSF biomarkers and incipient Alzheimers disease in patients with mild cognitive impairment: a follow-up study.Lancet Neurol. 2006;5(3):228-234.

4. Andreasen N, Minthon L, Davidsson P, et al. Evaluation of CSF-tau and CSF-Abeta42 as diagnostic markers for Alzheimer disease in clinical practice.Arch Neurol. 2001;58(3):373-379.

5. Herskovits AZ, Growdon JH. Sharpen that needle.Arch Neurol. 2010;67(8):918-920.

6. Bayer AJ, Bullock R, Jones RW, et al. Evaluation of the safety and immunogenicity of synthetic A42 (AN1792) in patients with AD.Neurology. 2005;64(1):94-101.

7. Dresser RS. Treatment decisions for incapacitated patients. In: Ashcroft RE, Dawson A, Draper H, eds.Principles of Healthcare Ethics. 2nd ed. Chichester, England: John Wiley & Sons, Ltd; 2007: 305-310.

8. Mattsson N, Brax D, Zetterberg H. To know or not to know: ethical issues related to early diagnosis of Alzheimers disease.Int J Alzheimers Dis. 2010. http://www.hindawi.com/journals/ijad/2010/841941/. Accessed November 16, 2011.

9. Karnieli-Miller O, Werner P, Aharon-Peretz J, Eidelman S. Dilemmas in the (un)veiling of the diagnosis of Alzheimers disease: walking an ethical and professional tight rope.Patient Educ Couns. 2007;67(3):307-314.

Matthew E.Growdonis a second-year medical student at Harvard Medical School in Boston. Prior to medical school, he was a research coordinator for projects on Alzheimer disease and frontotemporal dementia at the UCSF Memory and Aging Center in San Francisco. His interests include behavioral neurology and the history of medicine. He received a BA in history and literature from Harvard University in 2007.

Reference:

2011 American Medical Association. All Rights Reserved.

http://virtualmentor.ama-assn.org/2011/12/jdsc1-1112.html

Nursing Care PlanNursing diagnosis/problem:

Altered cognitive and perceptual abilities related to loss of nerve cells

Goal: Provide safe, structured environment

Nursing Interventions

Rationale

Outcome Criteria

1. Place patient in location where observation is easy (near nurses station, with reliable roommate, or where family can stay)

2. Establish and maintain consistent environment, including staff personnel.

3. Remove all potentially dangerous objects (e.g., razor, scissors, matches

4. Approach patient in calm, unhurried, firm but tolerant manner.

1. The patient with AD is easily confused by new surroundings.

2. The ability to adjust to a new environment and learn new material is severely limited.

3. .

4. The behavior of others is mirrored in the patients behavior.

1. Patient will remain safe and relatively stable.

References:Black, J. (2008). Medical-Surgical Nursing 8th Edition. Singapore: Elsevier Pte. LtdMorrison A., Lykestos C. (2005). The Pathophysiology of Alzheimers Disease and Directions in Treatment. Galen Publishing LLC. http://www.buzzle.com/articles/lobes-of-the-brain-and-their-function.htmlBlack, J (2008). Medical-Surgical Nursing 8th Edition. pp. 1746-1747Sabbagh, M.D., M (2008). The Alzheimers Answerhttp://www.examiner.com/article/remarkable-recent-discoveries-alzheimer-s-disease