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Psych year one > dementia > Flashcards

dementia Flashcards

1
Q

on aevrage how long does Alzheimers last

A

7-8 years

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1
Q

what percentage of dementia cases are Alzheimers

A

60%

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2
Q

what sex is most likeley to get dementia?

A

females

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3
Q

general symptoms of AD

A
  • Forgetful. Problems with episodic memory (events)
  • semantic memory (names of words, places, familiar faces, how objects should be used)
  • Basic thinking skills, maths etc due to deterioration of working memory
  • Can live indecently with support
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4
Q

symptoms of moderate AD

A
  • Confusion, time of day?
  • Poor judgement
  • Disturbed sleep, sundowning
  • Personality changes
  • Hallucinations
  • Paranoia, threatened because they don’t remember who people are
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5
Q

symptoms of severe AD

A
  • Lose mobility
  • Forget themselves
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5
Q

clinical assemement for AD

A

Questions, simple tasks, memory games, write sentences, count back from 100 in 7s,

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6
Q

mini mental state examination (MMSE)

A

intersecting pentagons, they can’t do it since they can’t compute complex visual-motor mappings.

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6
Q

what is happening to the brain in people with AD?

A
  • atrophy of the brain, cells die
  • less glucose and energy
  • reduced use of NT
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6
Q

what are the two key changes in the brain of people with AD

A

beta amyloid plaques
Neurofibrillary tangles

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7
Q

what are beta amyloid plaques?

A

beta amyloid is released and forms big molecules. Do they disable the function of other neurons? Both symptom and cause.

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8
Q

what are Neurofibrillary tangles?

A

protein, tau abnormal tangle

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9
Q

how do sulci between gyris change in AD brain

A

in an unaffected brain the gaps is small but in the brains of people with AD theres a great loss of tissue and ventricles get bigger. this can observed using an MRI/

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10
Q

first case of AD

A

Alois Alzheimer’s. Auguste d first patient. First symptom , rapid loss of memory, paranoia

Did scans and found tangles

neural networks are important

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11
Q

how many people have familial AD?

A

less than 1% of people with AD

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12
Q

Familial alzheimers is aasociated with mutations of how many genes?

A

3

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13
Q

what are the 3 diffferent gene mutations associtaed with familial AD?

A

presenilin 1 (PS1) on chromosome 14

presenilin 2 (PS2) on chromosome 1

amyloid beta A4 precursor protein (APP) on chromosome 21

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14
Q

what do the gene mutations cause?

A

amyloid plaques in the brains of affected individuals.

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15
Q

what can genetic testing tell us about people liklihood of developing AD?

A

Genetic testing can tell you if you are carrying a mutant form of one of the genes. If you know you have the gene then you know you will go on to develop AD AND YOU WILL KNOW THAT YOUR CHILD HAS A 50% CHANCE OF DEVELOPING IT AS WELL.

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16
Q

what gene is associated with late-onset AD?

A

APOE on chromosome 19 and comes in 3 forms
APOE2/3/4

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17
Q

which of the three forms of APOE incareses the risk of AD by 4x

A

APOE4

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18
Q

is APOE defo the cause of AD

A

no because there are people with even two copies of APOE4 and do not go on to develop AD

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19
Q

how many people with AD have the APOE4 allele

A

35%

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20
Q

how does diet influence development of AD

A

Environment also lead to AD. Diet. Mediterranean diet reduces the risk of AD. Gu et al found that diet correlates to the development of AD. Saturated fats etc had an increased risk. Smoking may increase the risk of APOE4 carriers.

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21
how do we diagnose AD?
mild cognitive impairment deficit in two areas of cognitive thinking 12% with MCI = AD
22
cognitive reserve
some brains even though they look similar to the average brain of someone with AD some brains are more resistant to cogtnive effects. high levels of intelligencefunction normally though early AD neural function declines whilst cognitive doesnr
23
Nun study
studied nuns diaries annually and their brains when they died, found that nuns who had the most graamatic inacrrucies were more likely to develop AD.
24
treatments for AD
cognitive stimulation reminiscence therapy drugs
25
what is cognitive stimulation?
exercise and improved nutrition can aid development in the short term, or even boost mood even if their cognition doesn’t change much.
26
what is reminiscence therapy?
make most of current memories show photos and music
27
what vitamine is important for people with AD
vitamine B
28
results of study with vitamin b vs placebo
people who took vitamin b had 30% less atrophy in the brain than placebo
29
what drug for AD
cholinesterase inhibitors
30
how do cholinesterase inhibitors work
they block glutamate which is released in high quantities and is thought to become toxic to remaining brain tissue
31
what do AD drugs do?
boost acetylcholine (NT associated with memory function) boost muscle choline
32
who are AD drugs pescribed to
people with mild-moderate AD not severe as tehy dont seem to work and theyre expensive
33
describe advances in AD treatment
stop it from progressing drug that stops amyloid plaques
34
amyloid hypothesis
is it amyloid itself or is abnormal time causing it but when it is attacked people seem to improve suggesting it is amyloid
35
problems with new drugs for AD
Would require frequent checkups on the brain using MRI which would be expensive
36
episodic memory has atrophy in the ...
Atrophy in medial temporal lobe early stage of AD
37
Semantic memory and language (understanding and producing words)
Atrophy in anterior temporal and inferior frontal cortex
37
Controlling thought and behaviour
Atrophy in frontal cortex
38
AD is bilateral meaning ...
atoprhy effects hemisphers equally
38
what does damage to anterioir temporal lobe and inferiori frontal lobe lead to
semantic language defictis
38
TMS study
they fired certain regions in the brain repeatedly, which makes use of the area decrease when brain area is impaired matches the effects of AD
38
what areas of the brain suffer first in AD
hippocampus in the temporal lobe bc memory loss
39
frontal lobe
The frontal lobes are especially important for controlling thought and behaviour (“***executive function***”). AD patients have trouble **concentrating**, making **decisions** and **planning** complex actions.
40
behavioural symptoms of AD
Irritability, agitation, outbursts, shouting, restlessness, pacing, fidgeting, repetitive behaviours
41
other dementias
- **Vascular dementia** - **Focal dementias** - **Subcortical dementias**
42
what is the second most common dementia
vascular dementia
43
most common cause of vascular dementia
Blocked arteries are the most common cause of vascular dementia, the blockage can be small and effect a small region of the brain. people who have one stroke are likely to have another and cause a deterioriation which causes dementia over time. Infarct is when an area of the brain has cell loss due to oxygen deprivation.
44
who is more vulnerable to stroke
high blood pressure, blood supply from one artery
45
symptoms of vascular dementia
- poor conentraion -organisation of thoughts - apathy - restlessness - weakness due to damage of motor cortex
46
what is frontotemporal dementia
focal dementias are dementias that have atrophy in specific brain regions unusual dementia, 40-65 years old is its higher diagnosis age In Alzheimer’s, pathology and atrophy is widespread, affecting temporal, parietal and frontal lobes.
47
types of frontotemporal dementia
1. Frontal-variant (fvFTD) 2. Semantic dementia (SD) 3. posteriori cortical atrophy
48
how is frontotemporal different to AD
Different from AD rather than amyloid plaques there are pick bodies insides cells.
49
FTD symptoms
Personality changes: rudeness, apathy, impatience. Lack of inhibition; inappropriate language and behaviour. Loss of empathy. Compulsive/ritualised behaviour – obsessions with time/numbers; hoarding. Overeating; preference for sweet foods.
50
semantic dementia symptoms
Atrophy restricted to anterior temporal lobes bilaterally. Semantic impairment that gets progressivley worse. They wouldnt understand the question ‘tell me about your hobies’. They wouldn’t recognise a watering can or be able to name the capital of France. Yet they maintain language skills and memory of recent events (episodic memory).
51
PCA sypmtoms
pathology in posterior paritetal cortex blured vision agnosia impaired reading/writting
52
subcortical dementias
*Huntington's disease*  – excessive  movement (inhibitory failure) *Parkinson's disease*   – problems  initiating movements
53
cause of Parkinsons disease
Degeneration in substantia nigra causes deficit in neuromodulator dopamine. defiict make it hard to start movement
54

Psych year one (19 decks)

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