Alzheimer's disease(redirected from Alzheimers Disease)
Also found in: Dictionary, Thesaurus, Legal, Encyclopedia, Wikipedia.
Causes and symptoms
- memory loss that affects job skills
- difficulty performing familiar tasks
- problems with language
- disorientation of time and place
- poor or decreased judgment
- problems with abstract thinking
- misplacing things
- changes in mood or behavior
- changes in personality
- loss of initiative
Nursing care and safety
Care for the caregiver
Outside help, nursing homes, and governmental assistance
Diagnosis is tentatively made on the basis of the symptoms presented and their progression over a period of time. Confirmation of the diagnosis of Alzheimer's disease can be made only by postmortem examination of brain tissue. The defining characteristics noted on autopsy are neurofibrillary tangles in the cytoplasm of neurons, neuritic plaques or deposits resulting from degeneration in the neural processes, and granulovacuolar degeneration in the neurons.
Perseveration, or continuous repetition of words or gestures, is characteristic of Alzheimer's disease in its later stages. Personality changes, incontinence, voracious appetite, and a compulsion to put everything in the mouth are other manifestations of the disease.
Family members and other caregivers encounter emotional outbursts and progressive intellectual and physical deterioration that make the tasks of care even more challenging. Part-time or full-time help in the home usually is needed to give some respite to caregivers. They will also need guidance in the management of incontinence and help in coping with role reversals and their own feelings about the loss they have suffered and the burden of care that they bear. Eventually, it may be necessary to institutionalize the person with Alzheimer's disease. This can bring on feelings of guilt and a sense of failure on the part of the caregiver.
Educational materials and information on clinical trials are available from the Alzheimer's Disease Education and Referral Center (ADEAR) by writing them at P.O. Box 8250, Silver Spring MD 20807-8250, calling them at 1-800-272-3900, or consulting their web site at http://www.alzheimer.org.
Alzheimer's disease(älts′hī-mərz, ălts′-, ôlts′-, ôlz′-)
Alzheimer's disease (AD)
Alzheimer's diseaseAlzheimer's dementia Neurology A progressive, neurodegenerative disease, which is the most common cause of dementia, and characterized by progressive mental deterioration accompanied by disorientation, memory and language defects, confusion, leading to progressive dementia, which may be accompanied by dysphasia, and apraxia; in the DSM-IV, AD '…is …a diagnosis of exclusion, and all other causes (of) cognitive defects … must first be ruled out.' AD affects 3% in those aged 65–74; 18% aged 75–84; 47% > age 85; AD has been linked to a form of apolipoprotein E, those with 1 defective APOE ε4 gene–located on chromosome 19 are at an ↑ risk of AD, and those with 2 copies have AD of early onset; A68 protein is present in AD brain homogenates, and linked to formation of neuritic plaques and neurofibrillary tangles–68 kD; one Alzheimer's amyloid precursor–APP may inhibit serine proteases, and is generated by alternative enzyme splicing, releasing an intact β fragment, possibly explaining the deposition of these fibrils in AD brains Management Tetrahydroaminoacridine-THA, aka tacrine, an acetylcholinesterase inhibitor, may improve the quality of life in AD Pts. See Tacrine.
Alzheimer's diseaseA brain disorder that is by far the commonest cause of DEMENTIA. A common disorder with important genetic elements featuring severe brain shrinkage from loss of nerve tissue, accumulation of plaques of AMYLOID beta (A-beta) peptide in the brain cells and tangled masses of fibres of tau protein. The A-beta peptide is cleaved from the natural AMYLOID PRECURSOR PROTEIN (APP). A mutation of the gene on chromosome 21 for APP is a cause of Alzheimer's disease. Mutations in the genes for presenilin 1 and 2, which have a role in the cleavage of A-beta peptide from APP can also cause the disease. There is progressively worsening dementia. People with DOWN'S SYNDROME develop this disorder 10 to 30 years earlier than other people. Down's syndrome is caused by an extra chromosome 21 and features slow accumulation of A-beta peptide. Acetylcholinesterase inhibitor drugs can help temporarity as can glutamate inhibitors such as memantine. Research is progressing on ways of inhibiting the production of A-beta. (Alois Alzheimer, German neurologist, 1864–1915).
Alzheimer's diseasea form of senile dementia in humans which may be associated with genes on chromosome 21.
|Mean LOS:||4.8 days|
|Description:||MEDICAL: Degenerative Nervous System Disorders without Major CC|
Alzheimer’s disease (AD) is a degenerative disorder of the brain that is manifested by dementia and progressive physiological impairment. It is the most common cause of dementia in the elderly but is not a normal part of aging. More than 4 million Americans suffer from AD. AD causes two-thirds of the dementia cases in the United States, and the prevalence of dementia doubles every 5 years in people older than 65, reaching 30% to 50% at age 85. It involves progressive decline in two or more of the following areas of cognition: memory, language, calculation, visuospatial perception, judgment, abstraction, and behavior. Dementia of the Alzheimer’s type (DAT) accounts for approximately half of all dementias. The average time from onset of symptoms to death is 8 to 10 years. The pathophysiological changes that occur in DAT include the following:
- Presence of neurofibrillary tangles, neuritic plaques, and amyloid angiopathy
- Accumulation of lipofuscin granules and granulovacuolar organelles in the cytoplasm of the neurons
- Structural changes in the dendrites of the neurons and in the cell bodies
- Predominant neuronal degeneration in the cortical association areas of the basal ganglia
- Gross cortical atrophy and widening of the sulci
- Enlargement of the ventricles
- Decrease in neurotransmitters (acetylcholine, dopamine, norepinephrine, serotonin), somatostatin, and neuropeptide substance P
The cause of AD is unknown, but knowledge about the hereditary links is growing (see Genetic Considerations). Patients with Down syndrome eventually develop DAT if they live long enough. There is a higher than normal concentration of aluminum in the brain of a person with DAT, but the effect is unknown. A distinct protein, AZ-50, has been identified at autopsy in the brains of patients with DAT. This protein has been isolated from neurons that were not yet damaged, suggesting that its presence early in the degenerative process might cause the neuronal damage. The life expectancy of a patient with DAT is reduced 30% to 60%.
AD is not caused by a single gene. The genetic contributions to the disease are complex because more than one gene mutation can cause AD, and genes on multiple chromosomes are involved. There are two basic types of AD from a genetic standpoint: familial and sporadic (associated with late-onset disease). Familial AD (FAD) is a rare form of AD that has an early onset before age 65 and affects less than 10% of AD patients. FAD is caused by gene mutations on chromosomes 1, 14, and 21 (definitively, within the PSEN2, PSEN1, and APP genes, respectively) and has an autosomal dominant inheritance pattern. Therefore, if one of these mutated genes is inherited from a parent, the person will almost always develop early-onset AD.
The majority of AD cases are late onset (developing after age 65), have no known cause, and show no clear inheritance pattern. Late-onset AD is linked with the apolipoprotein E (ApoE) gene on chromosome 19. It is involved with making ApoE, a substance that transports cholesterol in the bloodstream. The ApoE gene comes in several different alleles, but the three alleles that occur most frequently are ApoE epsilon 2, 3, and 4 (e2, e3, and e4). The e4 allele of the ApoE gene is considered a risk factor for AD and appears to influence the age of onset of the disease. No one really understands the degree of risk of AD based on ApoE status. Specific polymorphisms in the A2M, LRP1, TF, HFE, NOS3, VEGF, ABCA2, and TNF genes are also associated with AD. Scientists continue to search for genetic risk factors for late-onset AD on regions of chromosomes 1, 3, 7, 8, 9, 10, 12, 19, 20, and X. Recent genome-wide association studies (GWAS) identified three polymorphisms significantly associated with AD at the CR1 (1q32), CLU (8p21), and PICALM (11q14) loci. CLU, which encodes clusterin/apolipoprotein J, was identified independently by two separate groups of researchers and therefore likely represents a true genetic risk factor.
Gender, ethnic/racial, and life span considerations
The onset of DAT may occur at any age but is rare before age 50; the average onset occurs after age 65. Approximately 3% of men and women ages 65 to 74 have AD. More females than males have the disease. It is difficult to determine if there are racial and ethnic differences in the prevalence of AD. However, a unique issue for older blacks/African Americans is that, in contrast with other ethnic/racial groups, they are disproportionately affected by stroke, high blood pressure, and diabetes. These diseases can increase the risk of developing AD.
Global health considerations
Prevalence rates in Canada and the United States in people older than 65 years is approximately 6% to 7%. Lower rates are reported in China and Nigeria, and higher rates are reported in India. Data are not available for most developing countries.
DAT is a slowly progressing disease, and secondary sources are used for diagnosis because the patient is often unaware of a thought-processing problem. Past medical history should be evaluated for previous head injury, surgery, recent falls, headache, and family history of DAT.
The history will help determine which stage the disease process has reached at the time of patient assessment. The following four-stage scale reflects the progressive symptoms of DAT:
- Stage 1 is characterized by recent memory loss, increased irritability, impaired judgment, loss of interest in life, decline of problem-solving ability, and reduction in abstract thinking. Remote memory and neurological examination remain unchanged from baseline.
- Stage 2 lasts 2 to 4 years and reveals a decline in the patient’s ability to manage personal and business affairs, an inability to remember shapes of objects, continued repetition of a meaningless word or phrase (perseveration), wandering or circular speech patterns (circumlocution dysphasia), wandering at night, restlessness, depression, anxiety, and intensification of the cognitive and emotional changes of stage 1.
- Stage 3 is characterized by impaired ability to speak (aphasia), inability to recognize familiar objects (agnosia), inability to use objects properly (apraxia), inattention, distractibility, involuntary emotional outbursts, urinary or fecal incontinence, lint-picking motion, and chewing movements. Progression through stages 2 and 3 varies from 2 to 12 years.
- Stage 4, which may last approximately 1 year, reveals a patient with a masklike facial expression, no communication, apathy, withdrawal, eventual immobility, assumed fetal position, no appetite, and emaciation.
The neurological examination remains almost normal except for increased deep tendon reflexes and the presence of snout, root, and grasp reflexes that appear in stage 3. In stage 4, there may be generalized seizures and immobility, which precipitate flexion contractures.
Appearance may range from manifesting normal patient hygiene in the early stage to a total lack of interest in hygiene in the later stages. Some patients also demonstrate abusive language, inappropriate sexual behaviors, and paranoia. The Folstein Mini-Mental State examination is a quick evaluation tool that can assist in diagnosis and monitoring of the disease’s progression.
The nurse needs to assess the family for its ability to cope with this progressive disease, to provide physical and emotional care for the patient, and to meet financial responsibilities. A multidisciplinary team assessment approach is recommended for the patient and family.
Diagnostic tests will generally be completed to rule out a treatable condition that could be causing dementia, such as thyroid disease, stroke, vitamin deficiency, brain tumor, drug and medication effects, infection, anemia, and depression. Imaging studies such as computed tomography (CT) and magnetic resonance imaging (MRI) help exclude other possible causes for dementia, but clinical criteria rather than biological testing are used to make the diagnosis of AD.
|Test||Normal Result||Abnormality with Condition||Explanation|
|Brain biopsy upon autopsy||Negative||Positive for cellular changes that are associated with the disease||No diagnostic test is definitive for AD. Clinical criteria for diagnosis of DAT: (1) presence of at least two cognitive deficits, (2) onset occurring between ages 40 and 90, (3) progressive deterioration, (4) all other causes ruled out|
Other Tests: Most patients will receive neuroimaging (CT, MRI) as part of the diagnostic work-up to rule out other conditions such as subdural hematoma, brain tumors, stroke, or other conditions. Supporting tests include CT scan, MRI, and positron emission tomography (PET). During the early stages of dementia, CT and MRI may be normal, but in later stages, an MRI may show a decrease in the size of the cerebral cortex or of the area of the brain responsible for memory, particularly the hippocampus. Genetic testing for the ApoE gene is available, and the presence of the gene is a risk factor for AD. Genetic tests may be helpful in diagnosis, but further studies are needed to confirm their reliability.
Primary nursing diagnosis
DiagnosisSelf-care deficit related to impaired cognitive and motor function
OutcomesSelf-care: Activities of daily living—Bathing, Hygiene, Eating, Toileting; Cognitive ability; Comfort level; Role performance; Social interaction skills; Hope
InterventionsSelf-care assistance: Bathing and hygiene; Oral health management; Behavior management; Body image enhancement; Emotional support; Mutual goal setting; Exercise therapy; Discharge planning
Planning and implementation
The initial management of the patient begins with education of the family and caregivers regarding the disease, the prognosis, and changes in lifestyle that are necessary as the disease progresses. Basic collaborative principles include:
- Keep requests for the patient simple
- Avoid confrontation and requests that might lead to frustration
- Remain calm and supportive if the patient becomes upset
- Maintain a consistent environment
- Provide frequent cues and reminders to reorient the patient
- Adjust expectations for the patient as he or she declines in capacity
Generally, therapy is focused on symptoms with an attempt to maintain cognition.
|Medication or Drug Class||Dosage||Description||Rationale|
|Donepezil||5–10 mg PO qd||Cholinesterase inhibitor; elevates acetylcholine concentration in cerebral cortex by slowing degradation of acetylcholine released by intact neurons; other drugs in this class include galantamine and rivastigmine||Improves cognitive symptoms; improves cognitive function in the early stages of the disease only; drug effects diminish as the disease progresses|
|Antidepressants||Varies with drug||Selective serotonin reuptake inhibitors; increases activity of serotonin in the brain||Treat depression, anxiety, and irritability|
|Atypical antipsychotics||Varies with drug||Risperidone, olanzapine, quetiapine, aripiprazole, clozapine, ziprasidone||Treat psychosis but should be avoided in people with the risk of stroke and weight gain; drugs are expensive and may increase mortality but might be better tolerated; use must be weighed carefully|
Other Therapies: Other drugs and preparations currently being investigated are memantine, ginkgo biloba, vitamin E, estrogen, and NSAIDs. Secondary treatments are aimed at treating depression, psychosis, and agitation. To control night wandering and behavioral outbursts, physicians prescribe mild sedatives such as diphenhydramine. Barbiturates are avoided because they can precipitate confusion. Depression is treated with antidepressants (trazodone), and agitation is controlled by anxiolytics (oxazepam or diazepam). Psychotic behaviors are treated with antipsychotics (chlorpromazine or haloperidol). Consider hospitalization for any unstable medical condition, such as an infectious or metabolic process, that may complicate the patient's treatment. If the patient becomes a danger to himself or herself or a danger to others, a short hospitalization may be indicated to adjust psychotropic medications.
Promote patient activities of daily living to the fullest, considering the patient’s functional ability. Give the patient variable assistance or simple directions to perform those activities. Anticipate and assess the patient’s needs mainly through nonverbal communication because of the patient’s inability to communicate meaningfully through speech. Emotional outbursts or changes in behavior often are a signal of the patient’s toileting needs, discomfort, hunger, or infection.
To maximize orientation and memory, provide a calendar and clock for the patient. Encourage the patient to reminisce, since loss of short-term memory triggers anxiety in the patient. Emotional outbursts usually occur when the patient is fatigued, so it is best to plan for frequent rest periods throughout the day.
Maintain physical safety of the patient by securing loose rugs, supervising electrical devices, and locking doors and windows. Lock up toxic substances and medications. Supervise cooking, bathing, and outdoor recreation. Be sure that the patient wears appropriate identification in case he or she gets lost. Terminate driving by removing the car keys or the car. Provide a safe area for wandering. Encourage and anticipate toileting at 2- to 3-hour intervals. Change incontinence pads as needed, but use them only as a last resort. Bowel and bladder programs can be beneficial in the early stage of the disease.
Provide structured activity during the day to prevent night wandering. If confusion and agitated wandering occur at night, provide toileting, fluids, orientation, night lights, and familiar objects within a patient’s view. Some patients respond calmly when given the security of a stuffed animal or a familiar blanket.
Families should be referred to the Alzheimer’s Association Web site (http://www.alz.org/index.asp) and the many pamphlets and books available to provide information on this disease. Encourage family members to verbalize their emotional concerns, coping strategies, and other aspects of caregiver role strain. Discuss appropriate referrals to local support groups, clergy, social workers, respite care, day care, and attorneys. Provide information about advanced directives (living wills and durable power of attorney for health care).
Evidence-Based Practice and Health Policy
Wilson, R., Rochon, E., Mihailidis, A., & Leonard, C. (2012). Examining success of communication strategies used by formal caregivers assisting individuals with Alzheimer’s disease during an activity of daily living. Journal of Speech, Language and Hearing Research, 55, 328–341.
- There is minimal evidence to support effectiveness of various verbal and nonverbal communication strategies, such as slowed speech rate, verbatim repetition, use of gestures, and guided touch, to improve completion of tasks associated with activities of daily living among patients with AD.
- Findings from one study among 12 AD caregiver dyads revealed that saying encouraging comments was associated with decreased duration of the task (hand washing) (r = 0.56, p = 0.056) and pointing to an object was associated with task success rate (r = 0.57, p = 0.056).
- Asking open-ended questions and verifying questions were associated with an increased average time to complete the task (r = 0.81, p = 0.002 and r = 0.63, p = 0.028).
- Any changes in cognitive function: Confused orientation (time, place, person), emotional outbursts, forgetfulness, paranoia, decreased short-term memory, impaired judgment, loss of speech, disturbed affect, decline of problem-solving ability, and reduction in abstract thinking
- Response to medications (anxiolytics, antipsychotics, cholinesterase inhibitors, antidepressants, sedatives)
- Verbal and nonverbal methods that effectively meet or communicate the patient’s needs
- Caregiver response to patient behaviors and information about DAT
- Ability to perform the activities of daily living
Discharge and home healthcare guidelines
medications.Be sure the caregiver understands all medications, including the dosage, route, action, and adverse effects.
safety.Explain the need to supervise outdoor activity, cooking, and bathing. Lock doors and windows, and lock up medications and toxic chemicals. Make sure the patient wears identification to provide a safe return if she or he becomes lost. Commercially made products are available that trigger an alarm if the patient wanders out of safe territory.
Patient discussion about Alzheimer's disease
Q. My father is 84 and he was diagnosed with Alzheimer’s disease. I would like to share with all of you a common question that I hear a lot regarding Alzheimer. My father is 84 and he was diagnosed with Alzheimer’s disease. Is there anything I can do to affect how long I stay mentally sharp or is it solely determined by my genes?
Q. How can alzheimer's disease be slowed down? My father has alzheimer's disease, but only not for a long time. Is it still possible to stop it from progressing? how to do it? He is still ok, recognizing everybody just not remember many things.
You may read more here:
Q. how do you know if you have early onset of alzheimers? i'm 47. i do have extreme tremors at times and memory l i was told this could be what i have by a psychiatrist. What else can cause me to have these symptoms at my age and how do i know?