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

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Flashcards in Week 4 Lecture 4a - Late Life Disorders (DN) Deck (60):
1

Delirium

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

2

Dementia

Multiple cognitive deficits that include impairment in memory

3

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

Mild Cognitive Disorders or Major Cognitive Disorders

4

How is a cognitive disorder determined to be 'Mild'?

SD's below cognitively normal range

5

How is a cognitive disorder determined to be 'Major'?

3 or more SD's below cognitively 'normal' range

6

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

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

7

Compare Dementia & Delirium?

Dementia gradual deterioration of abilities Delirium rapid onset

8

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

Physical Health Mental Health Social Implications

9

What is a gerontologists concept of old age?

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

10

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

170.6% increase

 

7:30

11

What are some positive & negatives of aging?

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

 

12

What is MCI?

  • Mild Cognitive Impairment

 

11:15

13

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

  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

14

What process would lead to a diagnosis of MCI?

  • 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

15

What are the two sub-types of MCI?

  1. Amnestic MCI
    • memory impairment
  2. Nonamnestic MCI
    • no memory impairment

16

What is the Peterson's Criteria?

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

17

What is Amnestic MCI?

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

14:00

18

What is Nonamnestic MCI?

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

 

14:30

19

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

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

20

What is the Prevalence of MCI?

  • 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

21

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

  • 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

22

Risk Factors

Genetic - plaques & tangles

Lifestyle

23

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

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

 

17:40

24

What is Dementia?

  • 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

25

What are the social implications of dementia?

  • 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

What is the prevalence & prognosis of dementia?

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

27

What are the stages of progression in Dementia?

  • 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

What are the three main types of dementia?

  • Alzheimers
  • Frontotemporal
  • Vascular

29

When & how was Alzheimer's Disease first observed?

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

 

22:30

30

What are some characteristics of alzheimer's Disease

  • 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

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

Plaques & Tangles

32

What accumulates in an Alzheimer's brain?

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

 

25:00

33

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

  • either too much is produced or
  • not enough broken down

34

What are Tangles

from protein Tau

35

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

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

36

How do we test for plauqes & tangles?

What is the current issue with these measures?

  • 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

What happens to the brain in Alzheimer's disease?

  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

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

  • 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

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

  • beta-amyloid

32:30

40

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

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

41

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

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

Some facts about Fronto-temporal Dementia?

 

  • 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

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

Fronto-temporal Dementia

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

Alzheimers 

  • later onset
  • more female

44

What are the two main treatments for Dementia?

  • 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

Vascular Dementia

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

46

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

  • 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

Is sleep impacted in people with Alzheimer's dsease?

What is the most notable change?

  • 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

What is the most notable sleep related problem experiencing Dementia?

Sundowning

49

What problem normally occurs alongside the cognitive decline in MCI?

Sleep disturbance

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

 

45:30

50

What proportion of MCI patients experience poor sleep?

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

  • 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

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

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

52

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

  • 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

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

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

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

What other currently used treatment are these results comparable to?

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

What was the main improvement shown in the melatonin trials

aided sleep

56

What are some characteristics of Delirium?

  • 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

What are some causes of Delirium?

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

 

53:00

58

Depression

  • 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

How is Anxiety treated in late life?

  • 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

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

  • 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

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