Michael Mistric, PhD, RN, FNP, BCNurse PractitionerMichael E. DeBakey VA Medical Center
Describe the demographics associated with Alzheimer’s dementia
Describe the clinical features of Alzheimer’s dementia
Describe the medical management of Alzheimer’s dementia
Describe caregiver support services for individuals with Alzheimer’s dementia
Describe caregiver’s basic social process of formulating expectations of dementia care
A syndrome that has multiple reversible and irreversible causes and requires systematic evaluation of the patient presenting with a cognitive complaint
An acquired, persistent decline (not secondary to delirium) involving at least three of the following five domains: language, memory, visiospatial skills, executive function, and personality and mood
Cummings, Benson, LoVerme (1980) Reversible dementia. JAMA, 243(23)
Approximately 5 million Americans have Alzheimer’s disease (AD). Unless a cure or prevention is found, that number will increase to 14 million by 2050.
An estimated 280,000 Texas have Alzheimer’s disease.
One in eight persons over 65 and nearly half of those over 85 have AD. A small percentage of people as young as their 30s and 40s get the disease.
AD is degenerative disease of the brain from which there is no recovery.
AD is now the seventh leading cause of death in adults.
2010 Alzheimer's Disease Facts and Figures (alz.org)
Direct and indirect costs of AD and other dementia’s amount to more than $148 billion annually.
Almost 10 million Americans are caring for a person with AD or another dementia; approximately one out of three of these caregivers is 60 years or older.
In 2005, it was estimated that unpaid caregivers of people with AD and other dementias provided 8.5 billion hours of care valued at almost $83 billion dollars.
More than half the states in the United States provide more than a billion dollars in unpaid care each year – Texas $5.8 billion.
2010 Alzheimer's Disease Facts and Figures (alz.org)
The primary pathologic features of AD are amyloid deposition, neurofibrillary tangle formation, and neuronal loss
Plaques and Tangles: The Hallmarks of AD
The brains of people with AD have an abundance of two abnormal structures:
An actual AD plaque An actual AD tangle
• beta-amyloid plaques, which are dense deposits of protein and cellular material that accumulate outside and around nerve cells
• neurofibrillary tangles, which are twisted fibers that build up inside the nerve cell
AD and the Brain
Beta-amyloid Plaques
Amyloid 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.
AD and the Brain
In AD, many of these clumps form, disrupting the work of neurons. This affects the hippocampus and other areas of the cerebral cortex.
Neurofibrillary Tangles
Neurons have an internal support structure partly made up of microtubules. A protein called tau helps stabilize microtubules. In AD, tau changes, causing microtubules to collapse, and tau proteins clump together to form neurofibrillary tangles.
AD and the Brain
Memory loss
Difficulty with familiar tasks
Problems with language
Disorientation to time and place
Poor or decreased judgment
Trouble with abstract thinking
Misplacing things
Changes in mood or behavior
Changes in personality
Loss of initiative
Memory impairment and 1 or more: Aphasia (language disturbance) Apraxia (inability to carry out motor activities Agnosia (failure to recognize objects) Disturbed executive function (planning,
organizing) Cognitive deficits Gradual onset, continued decline Deficits not due to another condition Deficits not exclusive to delirium
The Changing Brain in Alzheimer’s Disease
No one knows what causes AD to begin, but we do know a lot about what happens in the brain once AD takes hold.
Pet Scan of Normal Brain
Pet Scan of Alzheimer’s Disease Brain
AD and the Brain
Treat a reversible condition
Treat co-morbid conditions
Avoid exacerbation
Limit complications
Relieve symptoms
AD no longer a diagnosis of exclusion
Drugs & programming depend on staging
Caregivers can be secondary victims: provide for them as well
Providers today use a number of tools to diagnose AD:
• a detailed patient history
• information from family and friends
• physical and neurological exams and lab tests
• neuropsychological tests (MMSE, GDS, Global Deterioration Scale, Affect Balance, BEHAVE-D
• imaging tools such as CT scan, or magnetic resonance imaging (MRI), PET scans
AD Research: Diagnosing AD
Complete PE & History
Mini-Mental State Exam (MMSE) or Physical Self-Maintenance Scale (PSMS) to establish baseline cognition and functional ability
Global Deterioration Scale – useful for
staging Affect Balance or Geriatric Depression Scale Katz ADLs – IADLs BEHAVE-AD
Members of various ethnic groups, cultures, and races manifest and cope differently with the disease, care-giving, and related stresses Some Asian/Pacific Islanders view AD as a
normal part of aging
Some Hispanics view AD as a spiritual test or punishment for a past deed.
Some African Americans rely on their spiritual faith to deal with the illness and care-giving.
1st degree African American relatives have higher risk than Caucasians.
African Americans are 4 times more likely to develop AD by age 90
African Americans and Hispanics may be at higher genetic risk based on APOE-4 allele aberration
Hypertension and hypercholesterolemia each place African American at a 4 times risk for AD
http://www.ethniceldercare.net
African American family members & caregivers may not consider dementia an illness, but rather an expected consequence of aging
Some believe it is a form of mental illness May be believed to be the result of
“worriation” and behaviors may be interpreted as “spells”
First cue may be in the failure to carry out role and social functions (later than desired recognition per professional assessment)
http://www.ethniceldercare.net
Hispanics may be 2 times more likely than Caucasians to develop AD by age 90
Vascular dementia has higher prevalence than AD
http://www.ethniceldercare.net
Female family members are the designated caregivers
Dementia may be viewed as some form of mental illness
Dementia is a source of shame, embarrassment, stigma; and, therefore may be a barrier to getting help
Problem not typically shared in the cultural network
http://www.ethniceldercare.net
Dementia is a form of normal aging
Dementia is a form of mental illness
Dementia is a source of shame
Dementia is a family secret that should not be shared
Dementia is a result of fate
http://www.ethniceldercare.net
Early Dementia“All dressed up and no where to go”
Middle Dementia“I want to go with you”
Late Dementia“In his own little world”
Physical Appearance May still dress self appropriately
Awareness “Lost in Time”
Behaviors Wandering Anxious Resistance to ADLs Sleep disturbance
Preclinical AD • Signs of AD are first noticed in the entorhinal cortex, then proceed to the hippocampus.
• Affected regions begin to shrink as nerve cells die.
• Changes can begin 10-20 years before symptoms appear.
• Memory loss is the first sign of AD.
AD and the Brain
Slide 20
Eating Eats independently May need cueing Remove stimulants from diet
Toileting Needs supervision locating bathroom and
reminders to go Usually continent
Hydration Needs supervision Provide favorite beverages frequently
Dressing Needs help locating and choosing clothing
Coaxing--resistance
Personal Hygiene Needs supervision-is relatively
independent Bathing
Needs supervision
Awareness of need to bathe is variable
Physical Appearance ▪ Looks unfinished; does not want to change
clothes▪ Change in posture
Awareness ▪ May be awareness of past versus present▪ Unable to think in the abstract
Behaviors▪ Wanders, is suspicious, resistant to
caregivers, social butterfly
Mild to Moderate AD• AD spreads through the brain. The
cerebral cortex begins to shrink as more and more neurons stop working and die.
• Mild AD signs can include memory loss, confusion, trouble handling money, poor judgment, mood changes, and increased anxiety.
• Moderate AD signs can include increased memory loss and confusion, problems recognizing people, difficulty with language and thoughts, restlessness, agitation, wandering, and repetitive statements.
AD and the Brain
Slide 21
Eating Trouble using utensils, positioning, and
swallowing--precut food, use prompting/cueing
Toileting Needs assistance with mechanics--wiping,
flushing, pulling down underwear, reminders
Hydration Hydration is dependent on caregiver
attention
Dressing Assistance in dressing due to agnosia, apraxia
Personal Hygiene Assistance due to agnosia, apraxia,
Parkinsonian symptoms
Needs tasks broken down
Bathing Needs supervision
Awareness of need to bathe is dependent on
caregiver
Physical Appearance ▪ Looks abnormal, undresses, looks lost,
posture/balance deficits, loses weight, loss of 3D vision
Awareness▪ Limited to field of vision, seeks sensory
stimulation
Behaviors▪ Hyper/hypo activity, cannot
communicate needs, does not recognize self or loved ones
Severe AD• In severe AD, extreme shrinkage
occurs in the brain. Patients are completely dependent on others for care.
• Symptoms can include weight loss, seizures, skin infections, groaning, moaning, or grunting, increased sleeping, loss of bladder and bowel control.
• Death usually occurs from aspiration pneumonia or other infections. Caregivers can turn to a hospice for help and palliative care.
AD and the Brain
Slide 22
Eating Total loss in eating skills: using
utensils, position, swallowing difficulty Toileting
Total Care May resist
Hydration Unable to pour water or understand
need or mechanics of drinking water
Dressing Needs total assistance
May disrobe or fiddle with clothes
Personal Hygiene Needs total assistance.
Able to do one step tasks – e.g. washing face
Bathing Unable to comprehend bathing
May resist sponge or bed bath
All are focused on maximizing the potential of the patient and managing symptoms
▪ Support cognitive functioning
▪ Reduce and prevent functional disabilities
▪ Ameliorate and mediate behavioral disturbances
Between 70 to 90% of people with AD eventually develop behavioral symptoms, including sleeplessness, wandering and pacing, aggression, agitation, anger, depression, and hallucinations and delusions. Experts suggest these general coping strategies for managing difficult behaviors:
AD Research: Managing Symptoms
• Stay calm and be understanding.• Be patient and flexible. Don’t argue or try to convince.• Acknowledge requests and respond to them.• Try not to take behaviors personally. Remember: it’s
the disease talking, not your loved one.
Experts encourage caregivers to try non-medical coping strategies first. However, medical treatment is often available if the behavior has become too difficult to handle. Researchers continue to look at both non-medical and medical ways to help caregivers.
Still are people that accept memory loss & confusion as a natural part of aging
Cognitive impairments of any kind are not easy to admit, recognize, or discuss
Patients hide or compensate for early signs
Families deny what is being seen
Requires comparison of cognitive and physical functioning relative to a previous level of performance
Eliminate or reverse any other (vascular, metabolic, etc.) causes
Proceed by clinical criteria and protocols for radiologic & laboratory studies
Refer to neurologist and Alzheimer’s Disease Research Center
What Alzheimer symptoms are most prevalent? What significant changes have you noticed?
Memory Behavior Personality Skills Other
How have you successfully accommodated for these changes?
What caregiving challenges are you facing? What activities does your loved one still enjoy? Describe a special moment you shared with
your loved one recently.
Current treatments for Alzheimer’s are not designed to reverse the disease process totally, yet they can produce some improvements in cognition.
Existing medications can be effective in slowing the progression of the disease and helping patients remain independent for longer periods of time.
Treating symptoms effectively is valuable not only to patients but also to their caregivers and families.
Cholinesterase inhibitorsReceptor agonistsEstrogenAnti-inflammatory drugsAntioxidantsVarious experimental
agentsBehavioral controls
Cholinesterase Inhibitors Donepezil (Aricept): Mild/Moderate Dementia
▪ Start with 5 mg/day; increase to 10 mg/day in 4 weeks▪ Nausea; Diarrhea; Poor Appetite
Rivastigmine (Exelon): Mild/Moderate Dementia▪ Start with 4.6 mg/24 hour patch daily; increase to 9.5
mg/24 hour patch daily in 4 weeks▪ Nausea; Diarrhea; Poor Appetite
Galantamine (Reminyl): Mild/Moderate Dementia▪ Start with 8 mg a day; increase by 8 mg every four
weeks up to 24 mg a day▪ Nausea; Diarrhea; Poor Appetite
N-methyl-D-aspartate (NMDA) Memantine (Namenda):
Moderate/Severe Dementia Start with 5 mg a day; increase by 5 mg a week
up to 10 mg twice a day Headache; Dizziness; Confusion
Tacrine (Cognex): Not used anymore Prototypical cholinesterase inhibitor for the
treatment of Alzheimer's disease
Muscarinic receptor agonists M1-type muscarinic acetylcholine receptors play
a role in cognitive processing. In Alzheimer disease (AD) amyloid formation
may decrease the ability of these receptors to transmit their signals leading to decrease cholinergic activity.
A number of muscarinic agonists have been developed and are under investigation to treat AD.
These agents show promise as they are neurotrophic, decrease amyloid depositions, and improve damage due to oxidative stress.
Nicotinic receptor agonists Nicotine has long been known to improve cognitive
function, but its adverse effects make it problematic as a treatment for diseases of cognitive dysfunction
Recent research has revealed that certain subtypes of nicotinic acetylcholinesterase receptors (nAChRs) in the brain are involved in cognitive function
Agents that target these nAChRs have shown promise in Alzheimer’s disease
Research also suggests that these agents may not only improve cognition but also be neuroprotective
Early studies of estrogen suggested that it might help prevent AD in older women. However, a clinical study of several thousand postmenopausal women aged 65 or older found that combination therapy with estrogen and progestin substantially increased the risk of AD. Estrogen alone also appeared to slightly increase the risk of dementia in this study. Therefore, based on epidemiological correlations, the use of estrogen to prevent or treat dementia has not been supported by follow-up studies and is not recommended.http://www.medicinenet.com
Several studies have found evidence of brain inflammation in AD and researchers have proposed that drugs that control inflammation, such as NSAIDs, might prevent the disease or slow its progression and early studies of these drugs in humans have shown promising results. However, a large NIH-funded clinical trial of two NSAIDS (naproxen and celecoxib) to prevent AD was stopped in late 2004 because of an increase in stroke and heart attack in people taking naproxen, and an unrelated study that linked celecoxib to an increased risk of heart attack. Therefore, based on epidemiological correlations, the use of NSAIDs to prevent or treat dementia has not been supported by follow-up studies and is not recommended.
http://www.medicinenet.com
A recent double-blind, placebo-controlled study of Vitamin E and donepezil for the treatment of mild cognitive impairment was unable to demonstrate benefit form Vitamin E and showed only modest and short-term benefit from donepezil.
This result suggested there was no role for the use of Vitamin E in the prevention or early treatment of Alzheimer’s Dementia.
Petersen et al. (2005). New England Journal of Medicine (352)
Many researchers believe a vaccine that reduces the number of amyloid plaques in the brain might ultimately prove to be the most effective treatment for AD.
In 2001, researchers began one clinical trial of a vaccine called AN-1792.
The study was halted after a number of people developed inflammation of the brain and spinal cord.
Despite these problems, one patient appeared to have reduced numbers of amyloid plaques in the brain.
Other patients showed little or no cognitive decline during the course of the study, suggesting that the vaccine may slow or halt the disease.
Researchers are now trying to find safer and more effective vaccines for AD.
http://www.medicinenet.com
Look for concurrent illness/problems Look at medications Try non-pharmocologic alternatives Target the dominant symptom Start drugs low and go slow Look at drug with best side effect
profile Review compliance Simplify Give clear and written instructions
Respiridone (Resperdal) 0.5 - 2 mg/day in two divided doses Sedation; Parkinson's Disease symptoms
Haloperidol (Haldol) 0.25 - 2 mg/day. Gradually increase this dose. Use sparingly
only for severe agitation Parkinson's Disease symptoms; Sedation; Falling; Abnormal
Movements Quetiapine (Seroquel)
12.5 - 200 mg/day in two divided doses Sedation; Light headedness
Olanzapine (Zyprexia) 2.5 - 10 mg/day Sedation; Light headedness; Confusion; Dry Mouth;
Constipation
Citalopram (Celexa) 10 - 60 mg/day Nausea; Dry Mouth; Sedation
Mirtazepine (Remeron) 15 - 30 mg at night Sedation; Weight Gain; Dry Mouth
Sertraline (Zoloft) 50 - 200 mg/day Insomnia; Diarrhea; Tremor
People with AD usually die from complications
Without an advance directive executed while the individual was competent, a substitute decision maker makes difficult life and death decisions
End-of-life choices may include the use, limitation, withdrawal or refusal of:
procedures, treatments or technology such as tube feeding
mechanical respirators or ventilators cardiopulmonary resuscitation (CPR) surgery the use of antibioticsA hospice program offers a more humane
and compassionate option than the nursing home or hospital during the final months
Simplify - Simplify - SimplifyMedications: Start SlowLook for concurrent
illness/problemsRemember your goal:
To improve quality of life Do no harm!
Consider the caregiver and family
The specific aims were to: Elicit subjective perspectives of family
members about what constitutes quality LTC for loved-ones with dementia, and
Develop a grounded theory of shared meanings about quality dementia care that reflects the expectations of family members in various stages of giving care and relinquishing care for a loved-one with dementia
Research Question: How do family members describe their
expectations of dementia care in the LTC setting?
Stage 1: Transitions to caregiver role Sees losses
Stage 2: Takes on caregiver role Fills gaps
Stage 3: Relinquishes caregiver role Recognizes limits Acknowledges need for LTC placement Responds to relinquishment of care
Stage 4: Selects and evaluates LTC facility Makes selection Evaluates care
Stage 5: Accepts LTC resident status Accepts LTC status Justifies LTC placement
Patient Care Nutrition, hygiene,
toileting, medications, and activities
Pleasant Surroundings Resident’s room and
facility common areas Competent Staff
Ability to provide dementia care and care of individuals in LTC
Caring Staff Treat with dignity and
respect; free from neglect and abuse
Communication What is communicated
& when communication should occur
Institutional Responsiveness Staff response to
questions and concerns
The Alzheimer’s Association http://www.alz.org
Family Caregiver Alliance http://www.caregiver.org
AgeNet; follow the "Geriatric Health" link http://www.agenet.com/early_alz_guide.html
Mayo Clinic Health Oasis http://www.mayohealth.org/
Alzheimer's Disease Education and Referral Center (ADEAR Center) http://www.alzheimers.org
Alzheimer's Research Forum http://www.alzforum.org
American Academy of Neurology http://www.aan.com
National Institute of Neurological Disorders and Stroke http://www.ninds.nih.gov
Medic Alert http://www.medicalert.org
National Institute on Aging and Eldercare Locator http://www.eldercare.gov
American Health Assistance Foundation (AHAF) http://www.ahaf.org
Ethnicity and Dementia http://www.ethnicelderscare.net
Summary
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