W2 Flashcards
1
Q
what is the purpose of ASC?
A
Alz Society Canada
- AD research and training
- New Canadian Charter of Rights for Dementia Patients
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
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
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
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
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
7
Q
what was the purpose of Canadian Dementia Strategy?
A
emphasized need for strategy - growing no of canadians 65+ living with dementia
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
9
Q
what are the 3 National objectives?
A
prevention
advance therapeutics
improve QOL
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
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
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
13
Q
what are the pillars?
A
collab
research/innovation
surveillance and data
info resources
skilled workforce
14
Q
what are the 4 sources of care providers?
A
- health prof
- first responders
- family/friends
- personal care workers
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
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)
17
Q
is age as a RF modifiable?
A
no it is not
- you can modify health but cant stop agining
18
Q
is sex as a RF modfiable?
A
no it is not
you are born with it - biological sex is given to you
19
Q
what are the 3 RF that cannot be changed?
A
age
sex
genetics
20
Q
what is the RF that can be changed or modified early life?
A
less education
21
Q
what are the RF that can be changed in midlife?
A
hypertension
high alc intake
obesity
hearing loss
tbi
22
Q
what are the RF that can be changed later in life?
A
smoking
depression
social isolation
physical inactivity
air pollution
diabetes
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
24
Q
what will be the total increase in D cases and care partners for them?
A
72-290%
25
which care partners are the most?
family members 58%
26
what is the sandwich generation?
middle-aged adults caring for both parent and own children
27
what are the types of support provided by care partners?
- assistance with daily core activities
- assistance with self care activities
- managing support and home care services
- supporting changes in mood, personality and behavior
- other
28
what are the downsides of informal partner support?
- care partner stress
- partner's own health and impairments
impacts relationships
- costly cycle
29
what is the transitional process to AD?
NA - MCI - AD
30
what is AD?
NDD - neurodegenerative disease with overlap among ADRD
31
how to treat AD?
no known cure
- it is irreversible, progressive and neurobiologically degenerative
32
how was AD discovered?
by a single case done by Alois Alzheimer
- patient had confusing symptoms
- had cog deficits
- progressed to be worse
33
what was the prominent neuropathological signs?
plaques and tangles in brain
34
what is the most common form of dementia?
AD
35
what is dementia?
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
36
what are the 2 neurobiological hallmarks of AD?
- amyloid plaques
- neurofibrillary tangles
37
what causes amyloid plaques?
beta-amyloid fragments clump together in toxic plaques in the hippocampus (memory)
38
where does beta-amyloid stem from?
fragment snipped from larger protein (APP)
39
what type of protein supports microtubules?
tau protein used to guide nutrients and molecules along healthy neurons
40
how are tangles formed?
ad-related chemical changes in tau cause tangles and collapse microtubules and neuron's transport sys
41
what is fAD or EOAD?
familial or early-onset AD
- rare
42
what causes fAD?
mutation of specific genes of specific chromosomes
- PSEN1
- PSEN2
- APP
43
what is the process of fAD?
mutation causes abnormal APP to be produced leading to accelerated beta-amyloid deposition in brain
44
how does genetics relate to fAD?
genetic inheritance - if you inherit one copy of mutation from one parent then affect M and F offspring
-> autosomal dominant
45
what kind of AD is the most common for?
sporadic AD or late-onset
sAD or LOAD
46
what causes sAD?
variety of RF
47
what does the Genome Wide Association Studies state?
numerous genes associated with cog aging decline, MCI, sporadic AD
48
what is the most prominent genetic RF for sAD?
Apolipoprotein (APOE e4)
40% of AD
49
what is the common prognosis for contemporary AD?
3-10 yrs
- inevitable and progressive decline
50
what are the characteristics of AD?
- 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
what are the 2 phases of AD emergence?
cognitively unimpaired/cognitively normal
subjective cognitive/memory decline
52
what is asymptomatic aging?
- also known as cognitively unimpaired or cognitively normal
53
what is the focus of asymptomatic aging?
absence of detected early cog symptoms
54
does aging decline occur in CU?
yes - relatively normal with broad ranges of level and slope
55
when do signals start for CU?
midlife
56
what is the next phase after CU?
subjective cognitive/memory decline
57
how is SC initially diagnosed?
early self-report experiences of memory failures - not clinically significant
58
what are the concerns and research stating?
worries about failures and accumulated losses - can be clinically significant
- subjective concerns/worries associated with later impairment and eventual dementia
59
is it possible to reverse SC?
yes either unaided or with intervention
60
what are the 2 steps of progression?
MCI
clinically diagnosed ad
61
can you diagnose MCI?
no - you can detect and it is well-characterized phase of elevated AD risk
62
what is MCI NOT?
not a disease nor dementia
- elevated risk factor or phase
- select and impactful cog deficits
63
can MCI be revised?
YES
64
how is the progression of AD diff?
difference in rate but not direction or sequence
65
what are the 3 stages of AD?
mild
moderate
severe
66
how is preclinical AD detected?
- 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
what are the concurrent differences b/w preclinical AD and NA?
no striking differences in any differences in any easily detectable or replicable respects
68
what are the retrospective differences b/w preclinical and NA?
detected but not consolidated in systematic neurobiological or cognitive domains
69
what are the prospective longitudinal trajectories for preclinical AD and NA?
gradual decline fxn but PreAD might be detectable
70
what is the detectable precursor developmental phase between NA and AD?
MCI
71
what differentiates normal decline from NDD?
MCO
72
what type of AD is retrospectively detected?
PreAD
73
what type of AD is prospectively classified?
MCI
74
what is an important public health and clinical goal?
to detect AD risk as early and accurately as possible
75
what did Dr. Fratiglioni contribute?
delaying dementia onset by 5 years could reduce prevalence by 50%
- decrease in cases substantially
76
what are the steps to diagnose AD by exclusion?
- 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
what is the first diagnosis for AD?
probable AD or probable mild AD
78
how is health affected by mild AD?
- 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
mild AD cog characteristics
- 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
what is the brain health like during moderate AD?
AD damage spreads through cortex
-> plaques and tangles expand
-> cortex shrinks
-> ventricles enlarge
81
how is cognition during moderate AD?
symptoms impossible to ignore or overlook
- dementia evident and chronic
- awareness slips away
- compensation diminishes
82
how is socialization impacted by moderate AD?
- chronic behavioral problems
- intense supervision required
- family difficulties and challenges
- difficult familial decisions
83
how are the formidable changes described as in moderate AD?
accelerating
spreading
interacting decline
84
what are the cognitive characteristics of moderate AD?
- 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
how does the brain look in severe AD?
- engulfed with damage
- plaques and tangles widespread
- shrinkage of cortex
- ventricles enlarged
86
how is overall health impaired by severe AD?
- weight loss
- difficulty with everyday processes
- groaning, moaning, grunting
- increased sleeping
- cause of death- aspiration or pneumonia
87
what is cognition like in severe AD?
baseline
88
what does a AD diagnosis convo look like?
- 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
