Alzheimer s Disease and Related Dementias-2014

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ALZHEIMER’S DISEASE AND RELATED DEMENTIAS LEHMAN COLLEGE NUR 409

Transcript of Alzheimer s Disease and Related Dementias-2014

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ALZHEIMER’S DISEASE AND RELATED DEMENTIAS

LEHMAN COLLEGE

NUR 409

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Definition of Dementia

Refers to the loss of memory, reasoning, judgment, and language that it interferes with everyday life.

Changes may occur gradually or quickly

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Cognition Cognition is the act or process of thinking,

perceiving, and learning. Cognitive activities that become impaired in

dementia include: Decision-making Judgment Memory Spatial orientation Thinking, Reasoning Verbal communication

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A client with dementia may undergo behavioral and personality changes as well, depending on the area(s) of the brain affected.

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Alzheimer’s Disease (AD) Most common form of dementia among

persons aged 65 and older Intellectual deterioration severe enough to

interfere with occupational or social performance.

Decline in two or more areas of cognition: Memory, language, calculation, visuospatial

perception, judgment, abstraction, or personality AD constitutes about 50% or all dementias

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Multi-infarct disease is the second most common cause of irreversible dementia

Types of infarct disease Blood clots blocking small blood vessles in the

brain and destroy brain tissue Lewy body dementia is similar to Alzheimer’s

disease but may progress more rapidly Lewy bodies are abnormal brain cells Pick’s disease another form of dementia

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Brain is quickly injured from hypoxia, reduced blood flow or drugs: Alzheimer’s disease Multi-infarct dementia Alcoholic dementia Huntington’s chorea AIDs related dementia Toxic or traumatic brain injury Malignant disease

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Alzheimer’s Disease Etiology and risk factors

Cause of Alzheimer’s disease unknown Increasing age is a risk factor Genetic factors involvement of five

chromosomes Clinical situations associated with AD include:

Elevated homocystein Inflammation Stroke Oxidative damage from free radicals

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Pathophysiology Alzheimer’s disease disrupts:

Communication, metabolism, repair of neurons Presence of beta-amyloid plaques, which are

proteins that are dense and insoluble deposits around the brain.

Neurofibrillary tangles which is an irreversible change in the tracts of healthy neurons, which then begin to degenerate leading to memory failure, personality changes, and problems with activities of daily living.

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Acetylcholine is also decreased in clients with AD

Gross changes in the brain of persons with AD include: Enlarged ventricles, hippocampal shrinkage,

generalized atrophy, shrunken gyri A decline in cholinergic neurons in the basal

nucleus leads to loss of choline acetyltransferase in the neocortex and hippocampus

Also involves neurotransmitter changes. The decline in cholinergic neurons in the basal nucleus leads to loss of choline acetyltransferase in the neocortex and hippocampus.

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Clinical Manifestations Impairment of decision-making beginning

insidiously and progressing. Preclinical Alzheimer’s Disease

Hippocampus—responsible for short and long-term memory

Mild Alzheimer’s Disease Memory disturbance Poor judgment and problem-solving skills Careless in work habits and household chores May become confused and get lost May become irritable, suspicious, agitated or

apathetic

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Moderate Alzheimer’s Disease May demonstrate language disturbance,

characterized by impaired word-finding Motor disturbance apraxia—difficulty in using

everyday objects: toothbrush, comb, razor Hyperorality: put things in the mouth Worsening irritability and depression, psychosis,

incontinence may occur Severe Alzheimer’s Disease

Inability to recognize familiar faces Voluntary movement is minimal

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Clinical Manifestations

AD characterized by relentless impairment of decision-making that generally begins insidiously and usually progresses slowly

Onset of AD typically occurs in late middle age, 65 years or older; some familial cases can occur in ages 40’s—50’s

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Classification of Alzheimer’s Disease Preclinical Alzheimer’s Disease

Begins near the Hippocampus Affected regions begin to shrink leading to

memory loss Mild Alzheimer’s Disease

Memory disturbance, confused and disoriented at times. Clients begin to get lost. Routine activities take longer

Person may become irritable, suspicious, indifferent, moody, agitated, apathetic

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Moderate Alzheimer’s Disease Client may demonstrate language disturbance,

impaired word finding Apraxia—difficulty in motor activities—doing

everyday activities. Resulting in safety issues. Hyperorality, depression and irritability may worsen. Wandering at night is common.

Severe Alzheimer’s Disease Plaques and tangles are widespread. Patients do

not recognize family or friends. Do not communicate in any way. Voluntary movement is minimal; limbs become rigid with flexor posturing. Urinary and fecal incontinence is frequent. Aspiration and aspiration pneumonia are frequent

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Diagnostic Findings Diagnosis made by exclusion (although there

are many types of tests under study) r/o known causes: toxic or metabolic

abnormalities, drug side effects, cerebrovascular disease, neoplasm, infection.

CT scan useful to identify ventricular dilation and sulcal enlargement and cerebral atrophy

MRI, PET scans also helpful Laboratory data to support or dispute other

treatable causes: CBC, ESR, BUN, Creatinine, thyroid and liver function studies, calcium, B12, syphillis, HIV

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Other Dementias

Multi-infarct dementia (MID) Blockage of small cerebral vessles (lacunar) Confusion, memory loss, emotional lability. Occurs more commonly in men than women Onset ages 60--75

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Lewy body dementia Clinical manifestations range from traditional

parkinsonianism effects to loss of spontaneous movement (bradykinesia), rigidity, confusion or fluctuating cognition.

Visual hallucinations may be one of the first manifestations noted.

Other psychiatric symptoms may occur: delusions and depression

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Outcome Management

Diagnosis best made by a multidisciplinary group that can assist the client and family

Goals: Helping maintain mental function Slow the process of deterioration

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Outcome Management:

Multidisciplinary team to assist client and family

No cure Helping to maintain function and slowing the

process of deterioration

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Medical Management Pharmacotherapy

Medications that retain acetylcholine in the neurojunctions such as Tacrine (Cognex), Donepezil (Aricept), Galathamine (Reminyl)

Drugs can have small but noticeable effects, depending on the stage of the disease, differences in the way the drugs act in different clients

None of the medications prevent the progression of the disease

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Exelon Patch

Start with 4.6 mg for four weeks, then increase to 9.5 mg/24 hours. For moderate to severe Alzheimers may increase to 13.3 mg.

May need to lower dosage for patient’s with Hepatic disease, or for clients with weight less than 100 pounds.

Change site of patch daily

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Side Effects

Gastrointestinal—Nausea, vomiting, diarrhea, anorexia, weight loss Skin Reactions—may cause mild irritation to dermatitis. Change patch site daily, clean

with cool water Neurological—May cause tremor or worsen tremor in Parkinson’s clients

.

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Combat oxygen-free radicals Use of vitamin E and selegiline have been

studied. Do support in assisting to delay the later stages of Alzheimer’s and show some improvements in levels of independence

Ginko biloba May improve cognitive function fro 6—12

months; some research does not support this claim

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Other medications Anti-anxiety, antipsychotics, antidepressants Should minimize use of these medications

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Nursing Management

Complete history including use of secondary resources

Mini Mental State Examination Usual behaviors Impact on family

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Nursing Diagnosis: Impaired Verbal Communication Outcome

Client’s needs will be communicated (early stages); later stages focus on interpretation of client’s expressions

Interventions Early: speak slowly and simply. Use the patient’s

language. Use calming tone of voice. As disease progresses use of other techniques

Nonverbal behavior also important—frustration, anger, hostility

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Decrease environmental stimuli Approach the patient calmly Limit demands on patinet Use distraction Elicit listening behavior—hold hand, maintain

physical contact Pain assessment and management

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Disturbed Thought Process

Outcome Client will have appropriate thought processing

Retention of information Interventions

Reorient client Allow client’s to reminisce Use of repetition

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Risk for Injury

Outcome Client’s physical and environmental safety will be

maintained as evidenced by the absence of physical injury and the existence of a safe living environment

Interventions Safety in the home: electrical wiring, toxic

substances, loose rugs, hot tap water, inadequate lighting, dangerous objects

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Self-Care Deficit

Outcomes Client will maintain self-care ability as evidenced

by completing the tasks they are capable of performing and receiving assistive with ADL they are incapable of performing

Interventions Encourage the client with AD to do as much as

possible, as long as it is safe and appropriate Give client plenty of time to complete tasks Remind client that step-by-step process is

required

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Urge Urinary Incontinence

Outcomes Client will have optimal continence bladder and

bowel as evidenced by the client having clean clothing and bedding as much as possible having intact

Interventions Toileting schedule Bright signage for the bathroom Limit fluid intake after dinner

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Caregiver Role Strain Outcomes

Family will demonstrate decreased role strain as evidenced by voicing their emotional concerns, seeking appropriate assistance, and providing adequate care for the client.

Interventions Allow family members to grieve the loss of the

person that they knew Provide formal supports as indicated Refer to support groups Respite care, Adult day care Nursing home care

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Advanced Directives

Living wills Advanced directives Durable power of attorney