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PS2028 - Mental Health & Clinical Psychology > dementias > Flashcards

dementias Flashcards

1
Q

what is the global impact of dementia?

A
  • 1 million people in UK
  • the older we get = the higher the chances
  • 1 in 3 will develop dementia
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2
Q

what is dementia?

A
  • major neurocognitive disorder
  • ‘deprived of mind’ (aka senility)
  • serious loss of cognitive ability in a previously unimpaired person, affects behaviour, mood an personality
  • slow progressive decline in range of cognitive and behavioural aspects
  • generally irreversible and unremitting
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3
Q

dementia vs Alzheimer’s?

A
  • Alzheimer’s is a form of dementia
  • it is the most common form of dementia
  • increases with age
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4
Q

what are some differential diagnoses of dementia?

A
  • vascular dementia
  • parkison’s disease
  • pick’s disease
  • huntington’s disease
  • FTD
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5
Q

what is vascular dementia?

A
  • poor blood flow in brain
  • mixed cognitive effects - dependent on pathology/location
  • 20-25% of dementias are this one
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6
Q

what is Lewy body dementia?

A
  • closely related to Parkinson’s disease
  • appears to be rare (<10% dementias)
  • possibly under-diagnosed
  • improved methods of detection
  • build up of protein: alpha-synuclein
  • neural loss
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7
Q

what are some central and core features of Lewy body dementia?

A
  • central = progressive dementia severe enough to interfere with normal social or occupational function and deficits on tests of attention, EF and visuospatial ability
  • core = fluctuating cognition, recurrent visual hallucinations, spontaneous parkinsonism
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8
Q

what is the pattern of spread of lewy body dementia?

A
  • motor cortex
  • brainstem
  • limbic system
  • neocortex
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9
Q

what is the aetiology of Lewy body dementia?

A
  • sporadic
  • maybe rare family linkage
  • maybe APOE4 risk effect
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10
Q

what changes have been made to ‘dementia’ in the DSM-5 criteria?

A
  • replaced the term ‘dementia’ with ‘major neurocognitive’ disorder and ‘mild neurocognitive’ disorder
  • this aims to help reduce the stigma associated with the term ‘dementia’
  • new terms focus on a decline, rather than deficits in function
  • focus on memory impairment is reduced - more broad diagnosis includes variables commonly associated with conditions that begin with declines in speech or language usage ability
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11
Q

what is mild vs major neurocognitive disorder?

A
  • mild = cognitive deficits are present, but the ability to be independent remains; less severe presentation, but can progress from mild to major
  • major = cognitive deficits are present that interfere with independence
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12
Q

what does the criteria for mild neuro-cognitive disorder intend to promote?

A

early detection and treatment of cognitive decline

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13
Q

what is Alzheimer’s disease?

A
  • progressive, unremitting, irreversible, major deficits in aspects of: memory (episodic, semantic), attention, learning and behavioural control (apathy, disinhibition)
  • basic sensory/motor function relatively intact until end-stages
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14
Q

why can Alzheimer’s disease lead to high co-morbidity of depression?

A

because people understand what is happening to them

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15
Q

what is the mini-mental state exam (MMSE)?

A
  • simple questions and problems: the time and place of the test, repeating lists of words,
    arithmetic tests, language use and comprehension, basic motor skills (copying/tracing pictures)
  • max 30
  • normal results is 27
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16
Q

what are the MMSE scores for mild cognitive impairment, mild AD, moderate AD and severe AD?

A
  • MCI = 25
  • mild AD = 21
  • moderate AD = 15
  • severe AD = 5
17
Q

what is the DSM-5 criteria for AD?

A
  • major or mild neurocognitive disorder due to AD
  • diagnostic criteria for major/mild neurocognitive disorder fulfilled
  • diagnostic criteria for either possible or probable Alzheimer’s Dementia are fulfilled: presence of causal Alzheimer’s Dementia genetic mutation based on family history or genetic testing
  • or the following 3 indicators are present: decline in memory or learning, and one other cognitive area, based on history or trials of neuropsychological testing, steady cognitive decline, without periods of stability, no indicators of other psychological, neurological, or medical problems responsible for cognitive decline
18
Q

what is major probable AD?

A

genetic mutation + memory decline + other cognitive decline

19
Q

what is minor probable AD?

A

genetic mutation

20
Q

what is mild possible AD?

A

progressive memory decline

21
Q

what must someone show for a full accurate AD diagnosis?

A

brain pathology

22
Q

what are the 4 categories to know if someone has AD?

A
  • define AD
  • probable AD
  • possible AD
  • unlikely AD
23
Q

what does AD brain pathology look like?

A
  • expect to see amyloid plaques (made of beta-amyloid) and neurofibrillary tangles post-mortem
  • regional brain shrinkage (near the end stages)
  • increased ventricular size (but this is also seen in other disorders e.g., SZ)
24
Q

how to use blood test to check for AD?

A

check beta-amyloid markers in blood

25
Q

what are some aetiologies of AD?

A
  • genetics (deterministic genes, familial AD, APOE4 mutation)
  • sporadic AD
  • other risk factors
26
Q

what is the most likely reason people get sporadic AD?

A

APOE4 gene mutation

27
Q

is age a risk factor in getting AD?

A
  • population ageing is the main driver of projected increases
  • increases in causes of dementia = increase in AD
28
Q

how does familial AD pose a risk to getting AD?

A
  • common variants conferring small increased risk
  • unless other things happen, we may not get AD
  • low frequency variants with intermediate effects
  • deterministic genes, autosomal dominant - will defo cause AD
29
Q

on what chromosome is APOE found, how many alleles does it have, which are least/most common and is having them good or bad?

A
  • chromosome 19
  • 3 diff alleles (e2, e3, e4)
  • e3 most common = normal
  • e2 least common
  • e4 confers some risk, but having e2 may be protective
  • e4 only = bad
  • no e4 = better
30
Q

what functions does APOE have and what could having more e4 lead to?

A
  • synaptic plasticity
  • synaptic repair
  • cholesterol transport
  • more e4 could lead to = tangle formation, neural toxicity, amyloidogenic processing
31
Q

a dysfunction in the tau protein can lead to?

A

neuronal damage

32
Q

in which 4 brain areas do tau derived tangles occur?

A
  • frontal cortex
  • parietal cortex
  • temporal lobe
  • amygdala
33
Q

what are some other causes/risks of acquiring AD?

A
  • head injury
  • heart problems
  • stress
  • diet
  • cholesterol
  • gender
  • exercise
  • education level
  • environment
  • aluminium (toxins)
34
Q

is living near major roads and the incidence of dementia linked?

A

YES

35
Q

what is Leqembi and how does it work?

A
  • a drug that has been shown to slow the decline in memory and thinking that defines AD by targeting the disease’s underlying biology
  • the FDA have approved is specifically for patients with mild or early cases of dementia
  • binds beta-amyloids in the brain and stops it from forming plaques
36
Q

what are 3 other putative treatments?

A
  • moderating how enzymes work
  • beta-amyloid aggregators
  • moderating pathways and channels
37
Q

what effects does acetylcholine have on AD?

A
  • effects of Ach seem to be important
  • only cortical neurons affected - temporal lobe most severely
  • part of limbic system (hippocampus etc.)
  • affects most probably late on in disorder
  • lead to development of drugs
  • don’t do anything to AD pathology
  • prevent degradation of Ach in the synapses
  • help in early stages of AD, keeps them independent
  • may also help in Lewy body dementia

PS2028 - Mental Health & Clinical Psychology (13 decks)

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