Ch 14 (lesson 17): Late life and Neurocognitive Disorders Flashcards

1
Q

aging- what is old?

A
  • in US, aging is dreaded
    • elderly not revered as in other cultures
  • 65 + considered “Old”
    • 12.4% (35 mill) 65 +
    • young-old: 65-74, old: 74-84, oldest: 85+
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2
Q

myths about late life

A
  • aging inolves inevitible cognitive decline
    • sever cog probs don’t occur for most
    • mild declines common
  • late life is a sad time/ most elderly depressed
    • older ppl report less neg emotion
    • more brain activation in key areas when viewing pos images
  • late life is lonely
    • some less likely to ddevelop new friendships
    • social selectivity- focus more on relationships that matter most to us
  • older people lose interest in sex
    • sexual activity don’t decrease from mid to late life for most
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3
Q

Late life problems- probs multiply w age

A
  • physical decline and disabilities
  • sensory and neurological deficits
  • loss of loved ones
  • social stresses such as stigmatizing attitudes towards elderly
  • 80% have 1+ major medical condition
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4
Q

late life problems- sleep disturbances increase w age

A

sleep deteriorates w age

  • insomnia
  • sleep apnea
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5
Q

late life problems- medical treatment

A
  • chronic probs instead of curable disorders
  • polypharmacy: practice of prescribing multiple drugs to patients
  • psychoactive drugs usually tested on younger participants
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6
Q

three kinds of effects in research of aging people

A
  • age effects
  • cohort effects
  • time-of-measurement effects
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7
Q

age effects

A

the effects of being a certain age (eg getting social security)

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8
Q

cohort effects

A

effects of having grown up during particular time (eg: frugality increased among those who lived during great depression)

not to be confused w age effects

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9
Q

time-of-measurements effects

A

effects of testing people at particular time in history (eg: in 1990s ppl became more frank about sexuality in surveys as media discussion of sexuality increased)

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10
Q

types of research designs

A
  • Cross-sectional studies
  • Longitudinal studies
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11
Q

Cross-sectional studies

A
  • researcher tests different age groups at one point in time
  • fails to give info about how ppl change over time/ as they age
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12
Q

Longitudinal studies

A
  • researcher retests same group of ppl w same measures at diff points in time
    • may extend over several years or decades
  • attrition is a potential prob-
    • attrition = ppl dropping out
    • selective mortality (attrition due to death) can lead to biased sample– sample left represent healthy people, can’t draw conclusions about unhealthy people
  • time of measurement can also be confused w aging effects
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13
Q

Neurocognitive Disorder in Late Life

A
  • most elderly do not have cog disorders
    • prevalence has decreased over last 15

most common:

  • Dementia
    • deterioration of cog function
  • Delirium
    • state of mental confusion
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14
Q

psychological disorders in older adults

A

every single disorder is less common in elderly people than younger adults

  • most people with disorder later in life are experiencing a continuation of a disorder they’ve previously had
  • older adults may be uncomfortable acknowledging/ disclosing mental health problems
  • people with psych disorders at risk of dying earlier for variety of reasons
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15
Q

treating psych disorders in elderly

A
  • psychotherapy
  • be careful of side effects of meds, but they can be effective
  • caregiver, if cog decline
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16
Q

Dementia

A
  • Deterioration of cog func
    • impairs social/occupational func
    • progresses over time
      • begins w forgetting recent events
  • deficits can be detected before impairment is obvious
  • Mild cog impairment develops slowly, major happens quickly
17
Q

DSM-5 2 categories of Dementia

A

differentiated by ability to live independently:

  • mild neurocognitive disorder (mild cog impairment)
  • Major neurocognitive disorder (dementia)
18
Q

DSM- 5 Neurocognitive disorders

A
  • Delirium
  • Neurocognitive disorder: specify mild or major
    • Neurocog disorder assoc. w Alzheimer’s disease
    • ” “ fronto-temporal lobar degeneration
    • ” “ vascular disease
    • ” “ traumatic brain injury
    • ” “ Lewy body disease
    • ” “ Parkinson’s disease
    • ” “ HIV infection
    • ” “ substance use
    • ” “ Huntington’s diseease
    • ” “ prion disease
    • other specified neurocog disorder
19
Q

DSM-5 Criteria for Mild Neurocog Disorder

A
  • Minor cog decline from previous levels in 1+ domains based on both of the following:
    • concerns of patient, close other, clinician
    • neurocog performance below appropriate norms (btwn 3-16%) on formal testing/clinical eval
  • The cog deficits don’t interfere w independence, even though greater effort, compensatory strategies, or accommodation may be required
  • cog deficits don’t occur exclusively in context of a delirium and not due to another psych disorder
20
Q

DSM-5 criteria for Major Neurocog disorder

A
  • evidence of sig cog decline from prev levels in 1+ domain based on both:
    • concernts of patient/other/clinician
    • neurocog permorance below 3rd percentile on formal testing/ clinical eval
  • Cog deficits interfere w independence
  • cog deficits don’t occur exclusively in context of a delirium and not due to psych disorder
21
Q

Alzheimer’s Disease

A
  • Alois Alzheimer 1906
  • more than half dementia is alzheimers
  • Irreversible brain tissue deterioration
    • death w/in 12 years
  • Usually begins w
    • difficulty remembering recent events
    • learning new material
    • irritability
  • as disease progresses
    • language probs intensify, word-finding
    • disorientation- time, place, identity confusion
    • agitation
    • depression
22
Q

Brain changes in Alzheimers

A
  • plaques
    • beta-amyloid protein deposits outside neurons
    • primarily found in frontal cortex
  • Neurofibrillary tangles
    • protein filaments composed of protein tau in axons of neurons
    • primarily found in hippocampus
  • measured using PET scans
  • Plaques most dense in frontal cortex; tangles most dense in hippocampus
  • loss of synapses for acetylcholinergic (Ach) and glutaminergic neurons
    • as neurons die, atrophy of cerebral and entorhinal cortices and hippocampus
    • enlargement of ventricles
23
Q

Genetic factors- alzheimers

A
  • heritability 79%
  • ApoE4 allele: gene on chromosome 19
    • one E4 increases risk 20%
    • 2 E4 increases risk substantially more
      • related to over-production of beta-amyloid plaques, loss of neurons in hippocampus and low glucose metabolism in cerebral cortex
  • many genes related to alzheimers also related to immune func and cholestoral metabolism
    • conditions that involve immune and inflammatory processes at greater risk for alzheimers
24
Q

Environmental Factors- Alzheimers

A
  • brain traumas from accidents/ injuries can increase risk
  • smoking, being single, low social support, depression related to greater risk
  • mediterranean diet, exercise, education, cog engagement predict lower risk
  • Cognitive reserve
    • using alt brain networks to compensate for disease
25
Q

frontotemporal Dementia

A
  • loss of neurons in frontal and temporal lobes
    • memory not severely disrupted
  • impairment of exec functions
    • planning
    • prob solving
    • goal-directed behavior
  • Difficulty recognizing and regulating emotion
    • much more profound impact than alzheimers
  • caused by multiple genetic pathways
    • pick’s disease
    • high levels of tau proteins
  • rare, less than 1%
  • begins in late 50’s progresses rapidly
    • death occurs w/in 5 yrs
26
Q

Vascular Demetia

A
  • Typically from stroke (cardiovascular)
    • clot forms and impairs circulation
    • cells die
  • risk factors
    • smoking, high LDL cholesterol high BP
  • Symptoms and severity can vaery greatly depending on type and location of stroke
  • 7% develop dementia after first stroke, risk increases w recurrent strokes
27
Q

Dementia w Lewy Bodies (DLB)

A
  • lewy bodies: protein deposits that form in the brain (olfactory bulb and brain stem) and cause cog decline
  • 2 subtypes
    • w parkinsons
    • no parkinsons
  • Symptoms similar to parkinsons and Alzheimers
    • shuffling gait
    • loss of memory
  • Symptoms
    • fluctuating cog symptoms
    • prominent visual hallucination
    • intense dreams involving movement and vocalizing

less than 10% of dementia is DLB

28
Q

Dementias caused by Disease/ injury

A
  • Encephalitis (inflammation of brain tissue by viruses
  • meningitis (inflammation of covering membranes by bacteria)
  • HIV
  • Head traumas
  • Brain tumors
  • Nutritional deficits (B-complex)
29
Q

treatments for dementia- medications

A
  • no drug reverses
  • some drugs produce slightly less decline
    • cholinesterase inhibitors (prevent breakdown of acetylcholine)
    • donepezil (Aricept)
    • Galantamine (Reminyl)
  • Vitamin E, statins, nonsteroidal anti-inflammatory drugs have failed to find support
  • preventive work focuses on processes involved in creation of amyloid from precursor protein
  • antidepressents for depression

-antipsychotic meds for agitation

30
Q

Psych treatments for dementia

A
  • supportive psychotherapy for family and patient
  • education about disease and care
  • cog interventions when disease in early stages
    • labeling drawers, appliances
    • calendars, clocks, strategically placed notes
  • exercise assoc w cog benefits
  • music reduces agitation and disruptive behavior
31
Q

Delirium

A
  • Clouded state of consciousness
    • extreme trouble focusing attention
    • disturbances in sleep/wake cycle
    • fragmented thinking
    • speech rambling, incoherent
    • disorientation
    • perceptual disturbances
    • memory impairments
    • mood swings
  • secondary to underlying medical condition
  • detection of delirium important but often missed
    • untreated, further cog decline and mortality may occur
32
Q

dementia vs delirium

A
  • dementia gradual deterioration — delirium rapid onset
  • dementia decifits in short term memory – delirium trouble concentrating/ staying on train of thought
  • dementia caused by disease processes that directly influence brain, delirium secondary to anther med condition
  • dementia usually progressive and nonreversible– delirium fluctuations over course of day
  • dementia treatment offers min benefit – delirium usually reversible by treating underlying condition, fatal if not treated
  • dementia prevalence increases w age – prevalence highest in young very young and old
33
Q

etiology of delirium

A
  • drug intoxications and withdrawal reactions
  • metabolic and nutritional imbalances (diabetes, thyroid dysfunction, kidney/liver failure, heart failure, malnutrition
  • neurological disorders (dementia, head trauma, seizures
  • stress of major surgery,
  • physical immobility/ restraints are key risk factors
  • usually has more than one cause

older adults vulnerable bc

  • physical decline, susceptibility to chronic disease, medications, sensitivity to drugs
34
Q

treatment of delirium

A
  • beyond treating underlying medical conditions, most common treatment is atypical antipsychotic medication
  • prevention- reduce risk factors in hospital settings such as sleep deprivation, immobility, dehydration, visual/hearing impairment