Transcript Chapter_060_Alzheimers_Disease

(Relates to Chapter 60, “Nursing Management:
Alzheimer’s Disease, Dementia, and Delirium” in the
textbook)
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 Three most common in adults
 Dementia
 Delirium—acute confusion
 Depression
• Often associated with dementia and delirium
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 Syndrome characterized by dysfunction or
loss of






Memory
Orientation
Attention
Language
Judgment
Reasoning
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 Other characteristics that can manifest
 Personality changes
 Behavioral problems such as
• Agitation
• Delusions
• Hallucinations
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 Problems disrupt individual’s
 Work
 Social responsibilities
 Family responsibilities
 Physicians usually diagnose when two
or more brain functions are
significantly impaired.
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 Not a normal part of aging
 Affects 15% of older Americans
 ~100 causes of dementia
 >60% of patients with dementia have
Alzheimer’s disease (AD).
 Half of the patients in most long-term care
facilities have dementia.
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 Due to treatable and nontreatable
conditions
 Two most common causes
 Neurodegenerative conditions
• 60% to 80% of cases
 Vascular disorders
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Etiology and Pathophysiology
 Vascular dementia
 Loss of cognitive function due to brain
lesions caused by cardiovascular disease
• Ischemic lesions
• Ischemic-hypoxic lesions
• Hemorrhagic brain lesions
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Etiology and Pathophysiology
 Vascular dementia (cont’d)
 Result of decreased blood supply from
narrowing and blocking of arteries that
supply brain
 Can be caused by a single stroke or by
multiple strokes
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Etiology and Pathophysiology
 Predisposed risks of dementia
 Smoking
 Cardiac dysrhythmias
 Hypertension
 Hypercholesterolemia
 Diabetes mellitus
 Coronary artery disease
 Metabolic syndrome
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Clinical Manifestations
 Onset of dementia depends on cause.
 Insidious and gradual
 Abrupt
• Vascular dementia tends to be abrupt or
progress in a stepwise pattern.
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Clinical Manifestations
 Cause of dementia difficult to distinguish
on the basis of symptoms alone
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Clinical Manifestations
 Acute or subacute pattern of change
may be more indicative of an infectious
or metabolic change.
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Clinical Manifestations
 Classifications
 Mild
 Moderate
 Severe
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Clinical Manifestations
 Initial symptoms are related to
changes in cognitive function.
 Family members often report to doctor
 Memory loss
 Mild disorientation
 Trouble with words and/or numbers
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Diagnostic Studies
 Focused on cause
 Reversible or nonreversible
 Thoroughly evaluate patient history
 Medical
 Neurologic
 Psychologic
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Diagnostic Studies
 Physical examination to rule out other
medical conditions
 Screen for
 Cobalamin (vitamin B12) deficiencies
 Hypothyroidism
 Possibly neurosyphilis
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Diagnostic Studies
 Mild cognitive impairment
 May be able to compensate, making
diagnoses difficult
 American Academy of Neurology
recommends
• Cognitive evaluation
• Ongoing clinical monitoring due to increased
risk of developing dementia
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Diagnostic Studies
 Mental status testing
 Mini-Mental State Examination
 Commonly used tool
 Assesses cognitive functioning
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Diagnostic Studies
 Depression often mistaken for
dementia and vice versa
 Manifestations of depression,
especially in older adults
 Sadness
 Difficulty thinking and concentrating
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Diagnostic Studies
 Manifestations of depression (cont’d)
 Fatigue
 Apathy
 Feelings of despair
 Inactivity
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Diagnostic Studies
 Computed tomography (CT)
 Magnetic resonance imaging (MRI)
 To characterize central nervous system
(CNS) changes:
 Single-photon emission computed
tomography (SPECT)
 Positron emission tomography (PET)
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 State of cognitive and functional
ability below defined norms that does
not meet criteria for dementia
 Memory impaired but function
normally
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 Characteristics
 Memory complaint
 Abnormal memory for age
 Intact activities of daily living
 Normal general cognitive functioning
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 10% to 20% of individuals >65 years
old have MCI.
 15% of those with MCI will develop
dementia.
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 Presently no widely accepted
guidelines for treatment
 Insufficient evidence
 Research is being conducted.
 Primary treatment consists of ongoing
monitoring.
 Observe for 10 warning signs of AD.
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 Chronic, progressive, degenerative
disease of the brain
 Most common form of dementia
 ~5.3 million Americans suffer from AD.
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 Economic cost of care in the United
States is at least $148 billion annually.
 Burden on patient, family, caregivers,
and society as a whole
 Women more likely to develop AD
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Etiology and Pathophysiology
 Exact cause is unknown.
 Age is most important risk factor.
 Familial Alzheimer’s disease
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Etiology and Pathophysiology
 Changes in brain structure and
function
 Amyloid plaques
 Neurofibrillary tangles
 Loss of connections between cells and
cell death
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Fig. 60-2. Pathologic changes in Alzheimer’s disease. A, Plaque with central amyloid core (white arrow) next to
a neurofibrillary tangle (black arrow) on the histologic specimen from a brain autopsy. B, Schematic
representation of amyloid plaque and neurofibrillary tangle.
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Etiology and Pathophysiology
 People develop some plaques in their
brain tissue.
 In AD plaque is greater in certain parts.
 Clusters of insoluble plaque
• β-amyloid, other proteins, remnants of
neurons, non-nerve cells, and other cells
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Etiology and Pathophysiology
Fig. 60-3. Current etiologic theories for the development of Alzheimer’s disease. A, Abnormal amounts
of β-amyloid are cleaved from the amyloid precursor protein (APP) and released into the circulation. The
β-amyloid fragments come together in clumps to form plaques that attach to the neuron. Microglia react
to the plaque and an inflammatory response results. B, Tau proteins provide structural support for the
neuron microtubules. Chemical changes in the neuron produce structural changes in tau proteins. This
results in twisting and tangling (neurofibrillary tangles).
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Etiology and Pathophysiology
 Where plaques develop in the parts of
the brain used for
 Memory
 Cognitive function
• Hippocampus
 Eventually develops in the cerebral
cortex
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Etiology and Pathophysiology
 Neurofibrillary tangles
 Abnormal collections of twisted protein
threads inside nerve cells
 Main component is a protein called tau.
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Etiology and Pathophysiology
 Gradual loss of connections between
neurons
 Leads to damage and then death of
neurons
 Affected parts of brain shrink.
• Brain atrophy
• Significant in final state of AD
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Fig. 60-4. Effects of Alzheimer’s disease on the brain. This figure shows slices from two brains.
On the left is a normal brain from a 70-year-old; on the right is the same region from a 70-year-old
with Alzheimer’s disease. The diseased brain is atrophic with loss of cortex and white matter,
most marked in the hippocampal region (H).
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Genetic Factors
 May play significant role in how the
brain processes β-amyloid protein
 ↑ β-amyloid protein  ↑ risk
 First gene associated with AD
 Epsilon (E)-4 allele of apolipoprotein E
(ApoE) gene on chromosome 19
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Etiology and Pathophysiology
 Researchers interested in link between
inflammation and AD
 Theory suggests that formation of free
radicals damages neurons  loss of
function
 Oxidative damage leads to inflammation.
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Etiology and Pathophysiology
 Researchers (cont’d)
 Another area is focusing on link between
cardiovascular disease and AD.
 Common risk factors for heart disease are
associated with increased risk of AD.
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Clinical Manifestations
 Pathologic changes precede clinical
manifestations by 5 to 20 years.
 Alzheimer’s Association has developed
a list of 10 warning signs.
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Clinical Manifestations
 Early signs of Alzheimer’s disease
 Memory loss that affects job skills
 Difficulty performing familiar tasks
 Problems with language
 Disorientation to time and place
 Poor or ↓ judgment
 Problems with abstract thinking
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Clinical Manifestations
 Early signs of AD (cont’d)
 Misplacing things
 Changes in mood or behavior
 Changes in personality
 Loss of initiative
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Clinical Manifestations
 Categorized similarly to those for
dementia
 Mild
 Moderate
 Late
 Progression is variable from person to
person and ranges from 3 to 20 years.
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Clinical Manifestations
 Initial sign is subtle deterioration in
memory.
 Inevitably progresses to more
profound memory loss
 Manifestations easier to recognize
when family member or patient seeks
medical help.
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Clinical Manifestations
 Recent events and new information
cannot be recalled.
 Behavioral manifestations are not
intentional or controllable because of
ongoing loss of neurons.
 Some develop psychotic
manifestations.
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Clinical Manifestations
 In AD that has progressed,
 Dysphasia
 Apraxia
 Visual agnosia
 Dysgraphia
 Some long-term memory loss
 Wandering
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Clinical Manifestations
 Late stages
 Long-term memory loss
 Unable to communicate
 Cannot perform activities of daily living
(ADLs)
 Patient may be unresponsive and
incontinent, requiring total care.
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Diagnostic Studies
 Diagnosis of exclusion
 No single clinical test
 Made once all other possible conditions
causing cognitive impairment have been
ruled out
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Diagnostic Studies
 Comprehensive patient evaluation
 Complete health history
 Physical examination
 Neurologic assessment
 Mental status assessment
 Laboratory tests
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Diagnostic Studies
 Brain imaging tests
 CT
 MRI
 SPECT
 PET
 Allow monitoring in early stages and
treatment response
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Fig. 60-5. Positron emission tomography (PET) scan can be used to assist in the diagnosis of Alzheimer’s
disease (AD). Radioactive fluorine is applied to glucose (fluorodeoxyglucose), and the yellow areas indicate
metabolically active cells. A, A normal brain. B, Advanced AD is recognized by hypometabolism in many
areas of the brain.
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Diagnostic Studies
 Neuropsychologic testing can help
document degree of cognitive
impairment.
 Mini-Mental State Examination (MMSE)
 Also used to determine a baseline from
which to evaluate change over time
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Collaborative Care
 No cure
 Collaborative management aimed at
 Improving or controlling decline in
cognition
 Controlling undesirable behavioral
manifestations
 Providing care for the caregiver
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Drug Therapy
 Cholinesterase inhibitors
 Used to treat mild and moderate
dementia
 Block cholinesterase, enzyme responsible
for breaking down acetylcholine
 Improve or stabilize cognitive decline but
do not cure or reverse
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Drug Therapy
Fig. 60-6. Mechanism of action of cholinesterase inhibitors. A, Acetylcholine is released from the nerve
synapses and carries a message across the synapse. B, Cholinesterase breaks down acetylcholine.
C, Cholinesterase inhibitors block cholinesterase, thus giving acetylcholine more time to transmit the
message.
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Drug Therapy
 Memantine (Namenda) protects nerve
cells against excess amounts of
glutamate.
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Drug Therapy
 Depression often treated with
selective serotonin reuptake inhibitors
 May help with sleep problems
 Antiseizure drugs
 Manage behavioral problems
 Stabilize mood
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Nursing Assessment
 Subjective data
 Past health history
 Medications
 Health perception
 Nutritional state
 Eliminating properly—incontinence
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Nursing Assessment
 Subjective data (cont’d)
 Activity-exercise habits and state
 Sleep-rest pattern
 Cognitive-perceptual state
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Nursing Assessment
 Objective data
 Disheveled appearance
 Neurologic
• Early, middle, late
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Nursing Diagnoses
 Impaired memory
 Self-care deficit
 Risk for injury
 Grief
 Wandering
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Planning
 Overall goals for patient
 Maintain functional ability as long as
possible.
 Maintain safe environment.
 Personal care needs met
 Dignity maintained
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Planning
 Overall goals for caregiver of a patient
 Reduce caregiver stress.
 Maintain personal, emotional, and
physical health.
 Cope with long-term effects associated
with caregiving.
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Nursing Implementation
 No known method to reduce risk of AD
 Antioxidants may be of benefit.
 Promote safety in physical activities
and driving.
 Recognize and treat depression.
 Genetic testing not performed on a
regular basis
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Nursing Implementation
 Early recognition and treatment
important
 Nurse should inform patients and
family regarding early warning signs.
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Acute Intervention
 Diagnosis traumatic for patient and
family
 Patient often responds with
 Depression
 Denial
 Anxiety and fear
 Isolation
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Acute Intervention
 Nurse should assess for depression and
suicidal ideation.
 Counseling and antidepressants may
be indicated.
 Family members may be in denial,
delaying critical early care.
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Acute Intervention
 Nurse should also assess family
members and their ability to cope and
accept diagnosis.
 Ongoing monitoring important
 Work in collaboration with patient’s
caregiver.
 Teach caregiver how to manage care.
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Acute Intervention
 AD patients subject to other health
care problems
 Inability to communicate symptoms
places responsibility on caregiver and
health care professionals.
 Hospitalization can precipitate a
worsening of disease or delirium.
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Ambulatory and Home Care
 Family members and friends care for
most AD patients in their homes.
 Various facilities should be evaluated.
 Consider stage of AD patient when
choosing.
 Nursing care intensifies over time.
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Ambulatory and Home Care
 In early stages, memory aids may
provide benefit.
 Drugs must be taken regularly.
 Drug compliance can be challenging.
 Adult day care can provide
 Caregiver respite
 Stimulation for AD patient
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Ambulatory and Home Care
 Demands on caregiver can exceed
resources, and total care is needed.
 Person may need to be placed in a
long-term care facility.
 Special units for AD patients are growing
in long-term care facilities.
 Emphasis is on safety.
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Behavioral Problems
 Occur in 90% of AD patients
 These problems include
 Repetitiveness
 Delusions
 Illusions
 Hallucinations
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Behavioral Problems
 Problems (cont’d)
 Agitation
 Aggression
 Altered sleep patterns
 Wandering
 Resisting care
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Behavioral Problems
 Behavior is unpredictable.
 Can be challenging for caregiver
 Behaviors are not intentional and are
difficult to control.
 Often lead to placement in
institutional settings
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Behavioral Problems
 Are a patient’s way of responding to
precipitating factor
 Pain
 Frustration
 Temperature extremes
 Anxiety
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Behavioral Problems
 Assess patient’s
 Physical status
 Environment
 Reassure patient about his or her
safety.
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Behavioral Problems
 Nursing strategies to address difficult
behaviors
 Redirection
 Distraction
 Reassurance
 Do not threaten or restrain patient if
frustrated.
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Behavioral Problems
 AD patients can experience
sundowning.
 Specific type of agitation
 Patient becomes more confused and
agitated in late afternoon or evening.
 Cause is unclear.
 Remain calm and avoid confrontation.
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Behavioral Problems
 Nursing interventions: sundowning
 Create a quiet, calm environment.
 Maximize exposure to daylight.
 Evaluate medications.
 Limit naps and caffeine.
 Consult health care provider on drug
therapy.
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Safety
 Risks
 Injury from falls
 Ingesting dangerous substances
 Wandering
 Injury to others and self
 Fire or burns
 Inability to respond to crisis
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Safety
 Special attention to home
environment to decrease risk
 Supervision is needed.
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Safety
 Nurse can help caregiver in assessing
home environment for safety risks.
 Wandering is major concern.
 AD patient can register with Safe
Return.
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Pain Management
 Pain should be recognized and treated
promptly.
 Monitor patient’s response.
 Patients can have difficulty
communicating complaints.
 May exhibit changes in behavior
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Eating and Swallowing Difficulties
 Undernutrition problem in middle and
late stages
 Loss of interest in food
 Decreased ability to self-feed
 Co-morbid conditions
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Eating and Swallowing Difficulties
 When chewing and swallowing
become difficult, use
 Pureed food
 Thickening liquids
 Nutritional supplements
 Quiet and unhurried environment
 Easy-grip utensils
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Eating and Swallowing Difficulties
 Offer liquids frequently.
 Finger foods may allow self-feeding.
 Short-term possibilities
 Nasogastric (NG) feedings
 Percutaneous endoscopic gastrostomy
(PEG) tube
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Oral Care
 In late stages, patient will be unable to
perform oral self-care.
 Dental problems are likely to occur.
 Patient may pocket food, adding to
potential tooth decay.
 Inspect mouth regularly, and provide
mouth care.
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Infection Prevention
 Common
 Urinary tract infection
 Pneumonia
• Ultimate cause of death in many AD patients
 Manifestations need prompt
evaluation and treatment.
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Skin Care
 In late stages, patient are at risk for
skin breakdown.
 Incontinence, immobility, and
undernutrition
 Tend to rashes, areas of redness.
 Keep skin dry and clean.
 Change patient’s position regularly.
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Elimination Problems
 Urinary and fecal incontinence during
middle to late stages
 Habit or behavioral retraining may
↓ episodes
 Constipation may relate to immobility,
dietary intake, ↓ fluids
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Caregiver Support
 AD disrupts all aspects of personal and
family life.
 Very stressful
 Caregivers also exhibit adverse
consequences.
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Caregiver Support
 Work with caregiver to
 Assess stressors
 Identify coping strategies
 Find a support group
• Local Alzheimer Association chapter
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Evaluation
 Patient goals
 Functions at highest level of cognitive
ability
 Performs self-care, bathing, dressing,
and toileting with assistance as needed
 Experiences no injury
 Uses assistive devices appropriately for
ambulation support
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Evaluation
 Patient goals (cont’d)
 Uses effective coping strategies to
manage grief related to diagnosis of AD
 Verbalizes reality of health situation
 Remains in restricted area during
ambulation and activity
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 Lewy body dementia (LBD)
 Characterized by presence of Lewy
bodies in brainstem and cortex
 Common cause of dementia
 Often unrecognized
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 LBD (cont’d)
 Symptoms of
• Parkinsonism
• Hallucinations
• Short-term memory loss
• Unpredictable cognitive shifts
• Sleep disturbances
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 LBD (cont’d)
 Dementia plus two of the following
indicates a possible diagnosis:
• Extrapyramidal signs such as bradykinesia,
rigidity, and postural instability, but not
always a tremor
• Fluctuating cognitive ability
• Hallucinations
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 LBD (cont’d)
 Medications determined on an individual
basis
 Standard treatment plan has not been
determined.
 Nursing care for LBD patients relates to
management of dementia.
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 Creutzfeldt-Jakob disease (CJD)
 Rare and fatal brain disorder
 Caused by a prion protein
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 CJD (cont’d)
 Earliest symptoms
• Memory impairment
• Behavior changes
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 CJD (cont’d)
 Disease progresses rapidly.
• Mental deterioration
• Involuntary movements
• Weaknesses in limbs
• Blindness
• Eventual coma
 No diagnosis or treatment
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 Pick’s disease
 Type of frontotemporal dementia
 Rare brain disorder
 Characterized by
• Disturbances in behavior
• Sleep
• Personality
• Eventual memory loss
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 Pick’s disease (cont’d)
 Major distinguishing characteristic is
marked symmetric lobar atrophy of
temporal and/or frontal lobes.
 Relentless progression
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 Normal-pressure hydrocephalus
 Uncommon disorder
 Characterized by obstruction in the flow
of CSF, causing a buildup of fluid in brain
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 Normal-pressure hydrocephalus
(cont’d)
 Symptoms
• Dementia
• Urinary incontinence
• Difficulty in walking
 Meningitis, encephalitis, or head injury
may cause condition.
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Audience Response Question
The daughter of a patient with early familial Alzheimer’s
disease (AD) asks how AD can be detected. The nurse
describes early warning signs of AD, including:
1. Forgetting a colleague’s name at a party.
2. Repeatedly misplacing car keys or a wallet.
3. Leaving a pot on the stove that boils dry and burns.
4. Having no memory of preparing a meal and forgetting
to serve or eat it.
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Audience Response Question
A patient with Alzheimer’s disease has a nursing
diagnosis of impaired memory related to effects of
dementia. An appropriate nursing intervention for the
patient is to:
1. Let the patient know what behavior is socially
appropriate.
2. Assist the patient with all self-care to maintain selfesteem.
3. Maintain familiar routines of sleep, meals, drug
administration, and activities.
4. At every encounter with the patient, ask the day, time,
and place to promote orientation.
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 72-year-old man was brought in by his
daughter to see his primary physician.
 He was asked to retire because of
erratic performance at work.
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 He has had no appetite or energy since
wife’s death 6 months ago.
 He recently lost his car downtown and
had to take a cab home.
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 He is unable to recognize
surroundings.
 Today, he is unshaven with oversized
slacks and a worn shirt.
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1. What possible problems do his
symptoms suggest?
2. What important teaching should you
do with him and his daughter?
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