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z. z. PSY3032 Lectures - Abnormal Psychology > Week 4 Lecture 4a - Late Life Disorders (DN) > Flashcards

Week 4 Lecture 4a - Late Life Disorders (DN) Flashcards

1
Q

Delirium

A

A disturbance of consciousness and a change in cognition that develop over a short period of time 3:10

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2
Q

Dementia

A

Multiple cognitive deficits that include impairment in memory

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3
Q

What is the new way of referring to Late-Life Disorders in DSM-5?

A

Mild Cognitive Disorders or Major Cognitive Disorders

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4
Q

How is a cognitive disorder determined to be ‘Mild’?

A

SD’s below cognitively normal range

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5
Q

How is a cognitive disorder determined to be ‘Major’?

A

3 or more SD’s below cognitively ‘normal’ range

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6
Q

Once it is determined whether the cognitive disorder is ‘Mild’ or ‘Major’, what is the next stage of diagnosis?

A

then specify whether associated with Alzheimer’s disease Frontotemporal lobar degeneration Lewy body disease Vascular disease Traumatic brain injury Substance/medication use HIV infection Prion disease Parkinson’s disease Huntington’s disease Another medical condition Multiple etiologies Unspecified

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7
Q

Compare Dementia & Delirium?

A

Dementia gradual deterioration of abilities Delirium rapid onset

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8
Q

What should be considered when looking at disorders of old age?

A

Physical Health Mental Health Social Implications

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9
Q

What is a gerontologists concept of old age?

A

Young old 65-74 Old old 75-84 Oldest old 85+ 6:00

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10
Q

How has the number of people 85+ increased over the last 2 decades?

A
  1. 6% increase
    7: 30
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11
Q

What are some positive & negatives of aging?

A

Negatives

  • lonely
  • death of loved ones
  • declining health
  • cognitive decline
  • social stresses (change in appearance)
  • medication issues (side effects)
  • sleep issues
  • loss of loved ones
  • cumulative stress effects

Positives

  • social selectivity (fewer but closer friends)
  • less reactivity to negative stimuli - protected by some stresses & anxieties
  • many wouldn’t want to be young again
    • financially secure
    • less family pressures
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12
Q

What is MCI?

A
  • Mild Cognitive Impairment
    11: 15
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13
Q

What are the three levels of cognitive functioning that older people tend to experience?

A
  1. 1 in 100 aging people show **no cognitive decline **
    • (referred to as aging successfully)
  2. cognitive decline can be a normal function of aging
  3. more than ‘normal’ decline classified as Mild Cognitive Impairment (MCI)
  • read article by Peterson (summarises what MCI is)
    11: 50
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14
Q

What process would lead to a diagnosis of MCI?

A
  • report of cognitive impairment by patient
  • change in condition
    • not normal
    • not dementia
    • cognitive decline
    • preserved functional abilities
  • memory impairment
    • YES
    • NO

Peterson (2011)

11:50

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15
Q

What are the two sub-types of MCI?

A
  1. Amnestic MCI
    • memory impairment
  2. Nonamnestic MCI
    • no memory impairment
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16
Q

What is the Peterson’s Criteria?

A
  • level of cognition required to meet criteria for MCI (relative to mean)
    • 1.5 standard deviations below the norm
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17
Q

What is Amnestic MCI?

A
  • one of the two subtypes of MCI
  • memory impairment
    • either alone or alongside other cognitive decline

14:00

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18
Q

What is Nonamnestic MCI?

A
  • one or more areas of cognitive decline
  • no memory impairment

14:30

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19
Q

What is a critical distinction between an individual diagnosed with dementia and an individual diagnosed with MCI?

A
  • no functional decline
    • i.e., performing in every day life
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20
Q

What is the Prevalence of MCI?

A
  • 10-20% of individuals over 65yrs
  • Amnestic more common than Nonamnestic MCI
    • 11% to 4%
  • dont need to know percentages for exam - just know that Amnestic is more prevalent*
    15: 40
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21
Q

What are the possible outcomes for an individual diagnosed with MCI?

A
  • increased risk of developing Dementia (i.e., MCI is a warning sign)
    • 10% compared to 1% of normal go on to develop Dementia
  • some revert back to ‘normal’ at 6mnth follow up
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22
Q

Risk Factors

A

Genetic - plaques & tangles

Lifestyle

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23
Q

What is the current treatment/management for a person with MCI?

A
  • observation
    • at 6mnth point
  • it is a separate ‘transitory’ phase - not fitting into other treatment

17:40

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24
Q

What is Dementia?

A
  • A deterioration of cognitive abilities such that social and/or cognitive functions are impaired.
    • Mild cognitive impairment – risk factor for dementia
  • third leading cause of death in

18:40

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25
Q

What are the social implications of dementia?

A
  • huge burden not only personally but socially
  • over 300,000 living with dementia in Australia
  • with no current cure, 1 million projected by 2050
  • 3rd leading cause of death in Australia
  • single greatest cause of disability
  • no need to memorise these figures just understand the weight of the burden*
    19: 00
26
Q

What is the prevalence & prognosis of dementia?

A
  • Prevalence
    • Worldwide: 25 million (0.4% population)
    • Australia: 245,000 (quadruple by 2050)
    • Increases with age
  • Prognosis
    • Highly individual
27
Q

What are the stages of progression in Dementia?

A
  • Stage 1 (MILD)
    • Difficulty remembering things; forget simple things; forget words for items;
    • awareness of memory lapses;
    • mood swings
  • Stage 2 (MODERATE)
    • More severe memory impairment; asking repetitive questions;
    • Difficulty in every day life; become messy; social withdrawal;
    • recite the past often;
    • personality changes;
    • inability to recognize familiar people;
    • socially withdrawn;
    • sleep disturbances;
    • loss of inhibition
  • Stage 3 (SEVERE)
    • Oblivious to surrounding environment;
    • Unable to care for self;
    • may lose ability to communicate;
    • Sleep often;
    • Often vulnerable to other illnesses.

20:00

28
Q

What are the three main types of dementia?

A
  • Alzheimers
  • Frontotemporal
  • Vascular
29
Q

When & how was Alzheimer’s Disease first observed?

A
  • Observed by Alzheimer in 1906
    • Brain tissue irreversibly dies
    • marked deterioration on memory & cognition

22:30

30
Q

What are some characteristics of alzheimer’s Disease

A
  • Absentmindedness,
  • irritability
  • attention
  • short-term/working memory

As progresses

  • Language problems, word finding, disorientated
  • socially withdrawn
  • Depression
  • changes in sleep & appetite
  • not recognising others
31
Q

What can be observed in an Alzheimer’s brain on autopsy?

A

Plaques & Tangles

32
Q

What accumulates in an Alzheimer’s brain?

A
  • beta-amyloid accumulates
    • forming abnormal amyloid protein plaques
    • kills the cell (neuron)

25:00

33
Q

Why does beta-amyloid accumulate in an Alzheimer’s brain?

A
  • either too much is produced or
  • not enough broken down
34
Q

What are Tangles

A

from protein Tau

35
Q

What is the difference between a healthy brain & an Alzheimer’s brain?

A
  • Healthy brain
    • produces beta-amyloid (normal cell function)
    • excess is then broken down
  • Alzheimer’s brain
    • accumulation of beta-amyloid
36
Q

How do we test for plauqes & tangles?

What is the current issue with these measures?

A
  • PET Scan
  • Cerebrospins Fluid (CSF)
  • Normally too late by this stage
    • by this stage the disease has normally progressed
  • Need to locate early biomarkers
37
Q

What happens to the brain in Alzheimer’s disease?

A
  1. Accumulation of beta-amyloid plaques (start in PFC)
  2. Tangles (start in Hippocampus)
    • from protein Tau which stabilises axon
    • axons strangle themselves & crumble
  3. Synaptic deficits
  4. Loss of Neurons
  5. Cognitive decline

Physical Appearance of Brain

  • Brain shrinkage
  • Increased Ventrical Size

24:50

38
Q

What area shows great promise in the search for predictive risk factors in Alzheimer’s disease?

A
  • Genetics
  • Heritability estimates – 79%
    • meaning 79% variance in Alzheimer’s is attributable to genetics
    • 21% to other factors (e.g., environmental)

Early-onset (risk sits on different gene to late-life onset)

  • Single gene identified for early-onset Alzheimer’s – chromosome 21.
    • same as Down Syndrome (3rd pair) - more likely to develop early onset Alz
    • extra risk on that chromosome

Risk Factor in Later Life

  • Chromosome 19 – APOE-4. (alipo protein gene)
    • APOE is polymorphic (APOE 2, 3) but the inc risk is on 4
    • Increased risk from one E 4 allele = ~30%
    • Increased risk from two E 4 allele = ~90%
    • ~50% of Alzheimer’s patients have one E 4 allele,
    • ~30% are APOE- 4 negative.
    • so clearly it is not causal, but contributory

28:25

39
Q

What is a possible early bio-marker for Alzheimer’s disease?

A
  • beta-amyloid
    32: 30
40
Q

WHat is the large study investigating bio-markers for disease of ageing?

A

Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing (AIBL)

41
Q

What are some contributory & protective factors for Alzheimer’s disease?

A

Risk Factors

  • Environment
    • smoking, being single, depression, low social support

Protective Factors

  • Use it or lose it
  • Cognitive enhancement
    • people engaged cognitively have fewer deposits of bet-amyloid plaques
  • Nun study - kept diaries
    • coded diaries for linguistic ability
    • 90% of those with low linguistic ability - developed Alz
    • 10% of those with high linguistic ability - developed Alz
  • Protection of Puzzles
  • Mediterranan diet, exercise, education
42
Q

Some facts about Fronto-temporal Dementia?

A
  • Progressive neurodegenerative disorder
    • loss of neurons in frontal and temporal regions
  • Typical onset – mid-late 50s
    • Mean age 52.8y
    • M:F ratio – 14:3
  • Prevalence
    • 4-20% of Dementia’s
  • Characteristics:
    • Executive Dysfunction
      • due to changes in PFC
    • Emotional regulation
      • massive personality & mood changes
      • difficult to care for a person with this
  • Prognosis
    • Poor (death within 5yrs)
  • Strong genetic component

38:25

43
Q

What is a difference in the prevalence of Alzheimer’s disease compared to Fronto-temporal Dementia?

A

Fronto-temporal Dementia

  • earlier onset mid-late 50’s
  • more male

**Alzheimers **

  • later onset
  • more female
44
Q

What are the two main treatments for Dementia?

A
  • Pharmacological
    • TREAT: Drugs that increase levels of acetycholine (Alzheimers)
      • as Alzheimer’s destoys cells in cholinergic system
    • PREVENT: Production of an antibody which binds to APP – prevents beta amyloid.
    • Antipsychotics/Antidepressants/Benzodiazepines/Sedatives
  • Psychological
    • Psychotherapy (especially for family members)
    • Exercise
    • Behavioural intervention to reduce agitation & anxiety
    • Cognitive enhancement

40:30

45
Q

Vascular Dementia

A
  • Clare referred us to text
  • said if its in the text, yes its examinable
  • didn’t spend any time on this in lecture
46
Q

What did Clare suggest could be a possible cure for Dementia?

A
  • an antibody which binds to the amyloid precursor protein
    • which is the precursor to beta-amyloid
  • if can stop that process, may be able to stop the disorder

41:25

47
Q

Is sleep impacted in people with Alzheimer’s dsease?

What is the most notable change?

A
  • Changes in sleep due to natural ageing
  • Prevalence*
  • 25% of mild-moderate AD and
  • 50% moderate-severe = sleep disturbance
  • What problems do they experience?*
  • Sundowning - wander around, almost like a delirium
  • Does this provide insight into cognitive functioning?*
  • sleep impacts cognitive function of healthy adults
  • sleep takes a hit in normal ageing
  • AD sufferers are ageing & have already got cognitive dysfunction
  • add poor sleep to the mix!!!
48
Q

What is the most notable sleep related problem experiencing Dementia?

A

Sundowning

49
Q

What problem normally occurs alongside the cognitive decline in MCI?

A

Sleep disturbance

Dont know which causes which, but we do know the co-occur

45:30

50
Q

What proportion of MCI patients experience poor sleep?

What was poor sleep in MCI patients been associated with in Naismith et al., 2010

A
  • 59% MCI patients have poor sleep
    • consistent across reporting types
  • poor sleep in MCI associated with poorer outcomes on
    • nonverbal learning
    • attention
    • executive function
  • Circadian timing advanced (go to bed earlier & wake earlier)
  • Biological (internal) timing
    • i.e., Melatonin expression shifts forward (associated
    • greater the shift forward, the greater the level of cognitive impairment

45:30

51
Q

What questions are Anna’s study addressing with regard to Melatonin?

A
  • how does delaying biological timing systems
  • preimposed timing systems
  • does this give improved sleep, cognitive outcomes
52
Q

Describe some features of the study by Riemersersma-van der Lek. (2008) in Sweden.

A
  • bright light and melatonin intervention in institutionalised patients with dementia
  • randomised control
  • long term, double-blind, placebo-controlled, 2 x 2
    • Whole day bright light (1000 lux) vs. dim light (300lux)
    • Evening melatonin vs. placebo
  • Assessed at baseline, 6 weeks
  • and every 6mths for 3.5 years

48:10

53
Q

What were the outcomes of the Swedish light & melatonin intervention study?

A

Light

  • Reduction of cognitive deficits by 5%
    • No deceleration of decline
  • Reduced depressive symptomology by 19%
  • Attenuated gradual increase in functional limitations by 53%

Melatonin

  • Reduced mood (ameliorated by the light)
  • Attenuated agitation when combined with light by 9%
  • Reduced sleep onset by 19%
  • Increased total sleep duration by 6%
  • Increased duration of uninterrupted sleep by 25%

50:00

54
Q

The outcomes of the light intervention study were very impressive…..

What other currently used treatment are these results comparable to?

A

comparable to the cholinergic medication currently prescribed to patients with dementia

cost effective, easy to employ, very few side effects with similar outcomes to pharmacological approach

50:20

55
Q

What was the main improvement shown in the melatonin trials

A

aided sleep

56
Q

What are some characteristics of Delirium?

A
  • A clouded state of consciousness
  • Lack of concentration and attention
  • Disturbances in the sleep/wake cycle
  • Perceptual disturbances are frequent
  • Delusions relatively common (~25%)
  • Mood Swings
57
Q

What are some causes of Delirium?

A
  • Drug/Medication Complications
  • Metabolic/Nutritional Imbalances
  • Infections/Fevers
  • Neurological Disorders
  • Extreme Stress

53:00

58
Q

Depression

A
  • Depression in late life
    • can be a myth
    • linked to changing time of life, losses
  • Treatment of Depression in late life
    • Medication versus behavioural intervention
    • 60% successful

56:50

59
Q

How is Anxiety treated in late life?

A
  • similar to younger adults
  • behavioural & pharmacological
  • Implications for medication
    • anxiolitics - short term solution but
    • linked to cognitive decline, morbidity, can be addictive
    • elderly often awake thru night for toilet - drowsy, fall risk
60
Q

What are some issues confronted by researchers of late life disorders?

A
  • Older adults are less likely to have a mental health issue - 10-20% prevalence
    • is this a cohort effect (i.e., stigma - not reporting it having grown up in a different era)
  • If they do have a mental disorder
    • is it a new disorder? - unlikely
    • 97% had experienced GAD & 94% depression before 65yrs old
  • Early mortality for Anxiety & Depressives - so this also impacts elderly population

z. z. PSY3032 Lectures - Abnormal Psychology (20 decks)

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