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W2 Flashcards

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1
Q

what is the purpose of ASC?

A

Alz Society Canada
- AD research and training
- New Canadian Charter of Rights for Dementia Patients

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2
Q

what occurred in 2018?

A

New Charter of Rights for Freedom
- right to no discrimination, access legal help, participate in policy development and care decision making, access appeal procedures

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3
Q

what are the 10 dementia research priorities?

A
  • stigma
  • emotional well-being
  • impact of early treatment
  • healthy sys capacity
  • caregiver support
  • access to info and services post-diagnosis
  • care provider education
  • dementia-friendly communities (built)
  • implementation of best practices for care
  • non-drug approaches to managing symptoms
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4
Q

what is EDM HQ used as?

A
  • regional resource
  • mission: heighten awareness about AD and related dementias, provide support services and encourage research
  • support groups, library, volunteers
  • First Link: link b/w individuals and families to support
  • Seeds of Hope: 7-week program for knowledge, skills/coping/support network
  • Help for Dementia: online community
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5
Q

what does ASC website define AD as?

A
  • progressive NDD
  • shrinkage of cerebral cortex and increasing appearance of irregularly shaped plaques and tangles
  • cascading neurodegenerative process -> cascades gradually until greater portions of brain shrink, become riddled with plaques and tangles and compromise memory and other adaptive life functions
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6
Q

what are the 10 warning signs on ASC website?

A
  • memory loss that affects day to day fxn
  • everyday difficulty
  • language problems
  • disorientation of time and place
  • poor or decreased judgement
  • abstract thinking problems
  • misplacing things
  • mood changes
  • personality shifts
  • passivity - loss of initiative
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7
Q

what was the purpose of Canadian Dementia Strategy?

A

emphasized need for strategy - growing no of canadians 65+ living with dementia

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8
Q

what are the stats found in the Strategy?

A
  • 63% of W 65+ live with dementia
  • 26+ hours spent as caregivers
  • 16+ billion by 2030 for costs
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9
Q

what are the 3 National objectives?

A

prevention
advance therapeutics
improve QOL

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10
Q

what are the areas of focus for the Prevention?

A
  • identify and assess RF and PF
  • build evidence base to inform and promote interventions
  • expand awareness of RF and PF and effective interventions
  • support measures that promote healthy living and adoption of healthy living
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11
Q

what are the areas of focus for Therapies and Cure?

A
  • establish and review research priorities
  • increase research
  • develop approaches
  • engage ppl and caregivers in developing therapies
  • increase adoption of research findings that support strategy
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12
Q

what are the areas of focus for improved QOL?

A
  • eliminate stigma and promote measures that create communities
  • promote and enable early diagnosis to support planning and action
  • address importance of access to quality care
  • build capacity of care providers
  • improve support
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13
Q

what are the pillars?

A

collab
research/innovation
surveillance and data
info resources
skilled workforce

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14
Q

what are the 4 sources of care providers?

A
  • health prof
  • first responders
  • family/friends
  • personal care workers
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15
Q

what is the international implication of the national dementia strategy?

A

national dementia objectives and strategies should be integrated with global perspectives and collab opportunities

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16
Q

what are the 2 goals from Landmark that are in regards to dementia risk and risk reduction?

A
  • improve knowledge: D is complex with RF. Report has aim to breakdown complexity and highlight RR
  • create action: inspire various types of ppl to support and work toward programs and policies that promote better brain health (health brain aging)
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17
Q

is age as a RF modifiable?

A

no it is not
- you can modify health but cant stop agining

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18
Q

is sex as a RF modfiable?

A

no it is not
you are born with it - biological sex is given to you

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19
Q

what are the 3 RF that cannot be changed?

A

age
sex
genetics

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20
Q

what is the RF that can be changed or modified early life?

A

less education

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21
Q

what are the RF that can be changed in midlife?

A

hypertension
high alc intake
obesity
hearing loss
tbi

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22
Q

what are the RF that can be changed later in life?

A

smoking
depression
social isolation
physical inactivity
air pollution
diabetes

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23
Q

what are the two goals from Landmark for caregiving and care sys?

A
  • advocation for individuals, families, care partners, service providers. ppl contributing need formal and informal care
  • push for change. need for action. more money, changes, recognition, reducing discrimination, stigma, stereotypes, implement equitable solutions
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24
Q

what will be the total increase in D cases and care partners for them?

A

72-290%

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25
Q

which care partners are the most?

A

family members 58%

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26
Q

what is the sandwich generation?

A

middle-aged adults caring for both parent and own children

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27
Q

what are the types of support provided by care partners?

A
  • assistance with daily core activities
  • assistance with self care activities
  • managing support and home care services
  • supporting changes in mood, personality and behavior
  • other
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28
Q

what are the downsides of informal partner support?

A
  • care partner stress
  • partner’s own health and impairments
    impacts relationships
  • costly cycle
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29
Q

what is the transitional process to AD?

A

NA - MCI - AD

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30
Q

what is AD?

A

NDD - neurodegenerative disease with overlap among ADRD

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31
Q

how to treat AD?

A

no known cure
- it is irreversible, progressive and neurobiologically degenerative

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32
Q

how was AD discovered?

A

by a single case done by Alois Alzheimer
- patient had confusing symptoms
- had cog deficits
- progressed to be worse

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33
Q

what was the prominent neuropathological signs?

A

plaques and tangles in brain

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34
Q

what is the most common form of dementia?

A

AD

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35
Q

what is dementia?

A

abnormal decrements in memory, reason, language, judgements
- cog losses that interfere with everyday life
- IT IS NOT A DISEASE
- group of symptomssssss
- differentiate from normal cog deficits or cog decline in aging

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36
Q

what are the 2 neurobiological hallmarks of AD?

A
  • amyloid plaques
  • neurofibrillary tangles
37
Q

what causes amyloid plaques?

A

beta-amyloid fragments clump together in toxic plaques in the hippocampus (memory)

38
Q

where does beta-amyloid stem from?

A

fragment snipped from larger protein (APP)

39
Q

what type of protein supports microtubules?

A

tau protein used to guide nutrients and molecules along healthy neurons

40
Q

how are tangles formed?

A

ad-related chemical changes in tau cause tangles and collapse microtubules and neuron’s transport sys

41
Q

what is fAD or EOAD?

A

familial or early-onset AD
- rare

42
Q

what causes fAD?

A

mutation of specific genes of specific chromosomes
- PSEN1
- PSEN2
- APP

43
Q

what is the process of fAD?

A

mutation causes abnormal APP to be produced leading to accelerated beta-amyloid deposition in brain

44
Q

how does genetics relate to fAD?

A

genetic inheritance - if you inherit one copy of mutation from one parent then affect M and F offspring
-> autosomal dominant

45
Q

what kind of AD is the most common for?

A

sporadic AD or late-onset
sAD or LOAD

46
Q

what causes sAD?

A

variety of RF

47
Q

what does the Genome Wide Association Studies state?

A

numerous genes associated with cog aging decline, MCI, sporadic AD

48
Q

what is the most prominent genetic RF for sAD?

A

Apolipoprotein (APOE e4)
40% of AD

49
Q

what is the common prognosis for contemporary AD?

A

3-10 yrs
- inevitable and progressive decline

50
Q

what are the characteristics of AD?

A
  • insidious onset - characteristics accumulate over years
  • long-term progressive - gradual shrinkage, accumulate of plaques and tangles
  • degenerative cascade - through brain and compromises fxn
  • histologically fAD and sAD similar - differ in general onset age and genetic role
51
Q

what are the 2 phases of AD emergence?

A

cognitively unimpaired/cognitively normal
subjective cognitive/memory decline

52
Q

what is asymptomatic aging?

A
  • also known as cognitively unimpaired or cognitively normal
53
Q

what is the focus of asymptomatic aging?

A

absence of detected early cog symptoms

54
Q

does aging decline occur in CU?

A

yes - relatively normal with broad ranges of level and slope

55
Q

when do signals start for CU?

A

midlife

56
Q

what is the next phase after CU?

A

subjective cognitive/memory decline

57
Q

how is SC initially diagnosed?

A

early self-report experiences of memory failures - not clinically significant

58
Q

what are the concerns and research stating?

A

worries about failures and accumulated losses - can be clinically significant
- subjective concerns/worries associated with later impairment and eventual dementia

59
Q

is it possible to reverse SC?

A

yes either unaided or with intervention

60
Q

what are the 2 steps of progression?

A

MCI
clinically diagnosed ad

61
Q

can you diagnose MCI?

A

no - you can detect and it is well-characterized phase of elevated AD risk

62
Q

what is MCI NOT?

A

not a disease nor dementia
- elevated risk factor or phase
- select and impactful cog deficits

63
Q

can MCI be revised?

A

YES

64
Q

how is the progression of AD diff?

A

difference in rate but not direction or sequence

65
Q

what are the 3 stages of AD?

A

mild
moderate
severe

66
Q

how is preclinical AD detected?

A
  • entorhinal cortex atrophy -> mild declarative memory and spatial disruptions
  • early hippocampus atrophy -> emergence of memory problems, disorientation
  • ventricles gradually enlarge -> begin years before clinically classified MCI or AD, vol a sign
    -> cavities where CSF is produced
67
Q

what are the concurrent differences b/w preclinical AD and NA?

A

no striking differences in any differences in any easily detectable or replicable respects

68
Q

what are the retrospective differences b/w preclinical and NA?

A

detected but not consolidated in systematic neurobiological or cognitive domains

69
Q

what are the prospective longitudinal trajectories for preclinical AD and NA?

A

gradual decline fxn but PreAD might be detectable

70
Q

what is the detectable precursor developmental phase between NA and AD?

A

MCI

71
Q

what differentiates normal decline from NDD?

A

MCO

72
Q

what type of AD is retrospectively detected?

A

PreAD

73
Q

what type of AD is prospectively classified?

A

MCI

74
Q

what is an important public health and clinical goal?

A

to detect AD risk as early and accurately as possible

75
Q

what did Dr. Fratiglioni contribute?

A

delaying dementia onset by 5 years could reduce prevalence by 50%
- decrease in cases substantially

76
Q

what are the steps to diagnose AD by exclusion?

A
  • detailed patient history: symptoms, health, family, milieu
  • informant information:
    -> query: inslights
    -> useful: absence of actual individual’s past change data
  • physical, neurological, neuropsychological tests
    -> minimum: global cognition and memory tests
    -> exclusion: side effects, depression, alc, metabolic imbalances, structural MRI
  • decision
77
Q

what is the first diagnosis for AD?

A

probable AD or probable mild AD

78
Q

how is health affected by mild AD?

A
  • brain shrinkage (hippocampus), plaques and tangles
  • stable or good -> co-morbidities
  • cog health detectably and problematically impaired
    -> awareness and denial of decline
    -> moments of lucidity
    -> initial retention of cog competence
    -> cog compensation
79
Q

mild AD cog characteristics

A
  • typical cog health impairments
  • predictable signs by cognitive domain, but unpredictable (number. sequence, rate, severity)
    -> episodic memory failures
    -> confusion about spatial location
    -> poor judgement
    -> mood swings and personality changes
80
Q

what is the brain health like during moderate AD?

A

AD damage spreads through cortex
-> plaques and tangles expand
-> cortex shrinks
-> ventricles enlarge

81
Q

how is cognition during moderate AD?

A

symptoms impossible to ignore or overlook
- dementia evident and chronic
- awareness slips away
- compensation diminishes

82
Q

how is socialization impacted by moderate AD?

A
  • chronic behavioral problems
  • intense supervision required
  • family difficulties and challenges
  • difficult familial decisions
83
Q

how are the formidable changes described as in moderate AD?

A

accelerating
spreading
interacting decline

84
Q

what are the cognitive characteristics of moderate AD?

A
  • diminishing episodic and semantic memory skills
  • increasing recognition difficulties
  • global cognitive decrements
    -> practical domains
    -> everyday routine impaired
    -> temporal disorientation
  • personal and social difficulties
    -> emotions intensify
    -> confusion
  • interacting processes of decline
    -> interacting and intensifying effects
85
Q

how does the brain look in severe AD?

A
  • engulfed with damage
  • plaques and tangles widespread
  • shrinkage of cortex
  • ventricles enlarged
86
Q

how is overall health impaired by severe AD?

A
  • weight loss
  • difficulty with everyday processes
  • groaning, moaning, grunting
  • increased sleeping
  • cause of death- aspiration or pneumonia
87
Q

what is cognition like in severe AD?

A

baseline

88
Q

what does a AD diagnosis convo look like?

A
  • formal diagnosis: discrete but comprehensive
  • preference: with patient and confidant
  • personal info to share: reason and basis for diagnosis
  • factual info to share: typical disease progression
  • opportunities for conversation: questions

Psych 403 (10 decks)

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