Alzheimer\'s Disease - none PDF

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Objectives Definitions Pathophysiology Etiology Diagnosis Clinical manifestations Goals of care Interventions Summary References

• Understand the definitions of Alzheimer’s disease, dementia and delirium • Explain the pathophysiology and etiology of Alzheimer’s disease • Describe the diagnosis and clinical manifestations of Alzheimer’s disease • Enumerate the interventions for Alzheimer’s disease

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DEMENTIA

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DELIRIUM

Onset

Insidious

Rapid

Progression

Slow

Abrupt

Duration

Years (~8-20)

Days/hour/weeks

Thinking/ Perception

Memory loss, disorientation, impaired word-finding, delusions/hallucinations

Incoherent speech, delusions/hallucinations

Psychomotor

Pacing, hyperactive

Sleep-Wake

Sleeping during the day

Hyperactive, hypoactive or mixed Reversed sleep-wake

Dysphasia: difficulty comprehending language and generating speech Dysphagia: difficulty swallowing Visual agnosia: difficulty interpreting visual information, despite intact vision Apraxia: difficulty executing purposeful activities, despite intact motor function Dysgraphia: difficulty writing coherently Dementia: decline in cognitive function interfering with daily activities 5

Alzheimer’s Disease (AD) • AD is a progressive degenerative disease of the brain • Represents the most common form of dementia • Characterized by memory loss, disorientation, behavioral changes, problems with judgement, language and attention • Pathological changes lead to brain atrophy 6

1 Amyloid plaques • β-amyloid proteins are cleaved in excess from their precursors, APP • β-amyloid form insoluble plaques starting in the brain areas of memory and cognitive function, eventually attacking the cerebral cortex and impacting language and reasoning

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2 Neurofibrillary tangles

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• Tau proteins support neuronal structure by binding microtubules • In AD, chemical changes cause the tau protein to become misshapen • This causes twisting and disintegration of the microtubules, resulting in neurofibrillary tangles Amyloid plaques and neurofibrillary tangles may be present in persons without cognitive impairment but are more abundant in individuals with AD

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3 Structural damage • Loss of connections between neurons and neuronal death cause structural changes that lead to atrophy of the hippocampus and cerebral cortex, and enlargement of the ventricles Cerebral Cortex

Hippocampus

Severely Enlarged Ventricles

Entorhinal Cortex

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• Age: most important risk factor for development of AD (> 60 years old) • Gender: Women are affected more often than men, likely because they live longer • Ethnicity: AD is more prevalent in persons of African or Hispanic descent • Socioeconomic status (SES): AD has been associated with lower SES and education • Genetics: mutations in specific genes are associated with the development of AD • Prognosis: fatal, usually 4-8 years after diagnosis 10

Extreme Shrinkage of Hippocampus

Early

Late

STAGE

DESCRIPTION

Pre-clinical

• Amyloid plaques and neurofibrillary tangles may be present and detectable with PET scans or CSF analysis • No clinical symptoms

Mild Cognitive Impairment

• Noticeable memory problems • Does not interfere with ADLs • May or may not progress to Alzheimer’s disease

Dementia due to AD

• Problems with memory, thinking, behavior, performing ADLs • Terminal stage of dementia

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Montreal Cognitive Assessment (MoCA) • Tests executive functions, such as memory recall, visual-spatial abilities and orientation

Image courtesy of: Mattson M (License)

Mini Mental State Exam (MMSE) • Tests cognitive functions such as orientation, registration, recall, attention, calculation and complex commands 12

MILD • Forgetfulness

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• Anhedonia • Small personality changes

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• Difficulty solving simple math problems • Decreased planning and organizational skills

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MODERATE Obvious memory loss and confusion Difficulty recognizing family members and friends Agitation, aggression, wandering May have trouble with ADLs Delusions, hallucinations, paranoia

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SEVERE Severe cognitive dysfunction Unable to perform ADLs May be unable to walk Incontinence Dysphagia, dysarthria Unresponsiveness

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Function at the highest cognitive ability

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Perform ADLs independently or with assistance

Maintain safety

Minimize caregiver burden and anxiety

Some medications may lead to modest temporary improvements in cognitive function, but do not cure or impact overall disease progression

MEDICATIONS

DESCRIPTION

Cholinesterase inhibitors (ChEIs)

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NMDA receptor Antagonist Selective Serotonin Reuptake Inhibitors Antipsychotics Benzodiazepines

Increases the availability of acetylcholine at the synapse Used for treating cognitive and memory problems Protects the cells from glutamate released from damaged cells May be used in combination with ChEIs for a greater effect • Treating depression associated with AD may improve cognitive function • May be used to manage aggression and agitation (chemical restraints) • Increased risk of death in older dementia patients

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Health promotion • Alzheimer’s disease may not be preventable, but brain health can be promoted by: • Avoiding excessive drinking and drug abuse • Performing mental activities like reading, puzzles, etc. • Getting daily physical activity • Socializing with friends, family, community members • Recognizing and treating depression early 16

Behavioral problems • May include repetitiveness, agitation, aggression, hallucinations, delusions, wandering and resisting care • May be a response to a precipitating factor, e.g. pain, frustration, anxiety • Assess vitals signs, pain, elimination patterns, remove noxious stimuli • Frequent re-orientation and reassurance, redirection and/or distraction • Chemical restraints should not be used unless all other strategies have been exhausted • Sun-Downing: Increased agitation, aggression and confusion in the evening 17

Safety • Monitor closely as the patient with AD may not be able to communicate symptoms • Cover tubes and dressings with stretch gauze and/or remove from the patient’s field of view • Address home hazards to reduce the risk of falls • Install door locks to prevent the wandering patient from getting lost Infection prevention • Urinary tract infection and pneumonia are common causes of death in AD • Monitor for changes in behavior, fever, cough, dysuria 18

Difficulty eating/swallowing • Pureed foods and thickened liquids are used for patients with dysphagia • A quiet environment with low stimulation should be provided during mealtimes • NG or PEG feeding may be explored if the patient cannot tolerate the oral route Elimination problems • Urinary and fecal incontinence occur in moderate/severe AD • Encourage scheduled toileting when possible • Keep skin dry and clean to prevent breakdown 19

Caregiver burden • Caring for a person with AD can cause adverse emotional and physical effects • Work with the caregiver to identify stressors and coping strategies • Discuss advance directives and power of attorney while the patient is still capable • Suggest community resources such as respite care and support groups 20

• Alzheimer’s disease is a progressive, degenerative disease of the brain • Amyloid plaques, neurofibrillary tangles and brain atrophy occur in AD • Age is the most important risk factor for AD • Pharmacological interventions cannot slow disease progression • Interventions are aimed at maintaining comfort and safety, and supporting the caregiver

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1. Ignatavicius DD, Workman ML. Medical-Surgical Nursing: Patient-Centered Collaborative Care, Single Volume. 8 edition. St. Louis: Saunders; 2015. 2. Lewis SL, Bucher L, Heitkemper MM, Dirksen SR. Medical-Surgical Nursing: Assessment and Management of Clinical Problems, Single Volume. 10 edition. Mosby; 2016. 3. LeMone PT, Burke KM, Gubrud P. Medical-Surgical Nursing: Clinical Reasoning in Patient Care. 7th edition. Boston: Pearson; 2019.

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