Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Psych year one > dementia > Flashcards

dementia Flashcards

You may prefer our related Brainscape-certified flashcards:
Psychology 101 flashcards GRE® Psychology flashcards
1
Q

on aevrage how long does Alzheimers last

A

7-8 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

what percentage of dementia cases are Alzheimers

A

60%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what sex is most likeley to get dementia?

A

females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

symptoms of severe AD

A
  • Lose mobility
  • Forget themselves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

clinical assemement for AD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

mini mental state examination (MMSE)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

beta amyloid plaques
Neurofibrillary tangles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are Neurofibrillary tangles?

A

protein, tau abnormal tangle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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/

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how many people have familial AD?

A

less than 1% of people with AD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Familial alzheimers is aasociated with mutations of how many genes?

A

3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what do the gene mutations cause?

A

amyloid plaques in the brains of affected individuals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what gene is associated with late-onset AD?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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

A

APOE4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how many people with AD have the APOE4 allele

A

35%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

how do we diagnose AD?

A

mild cognitive impairment
deficit in two areas of cognitive thinking
12% with MCI = AD

22
Q

cognitive reserve

A

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
Q

Nun study

A

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
Q

treatments for AD

A

cognitive stimulation
reminiscence therapy
drugs

25
Q

what is cognitive stimulation?

A

exercise and improved nutrition can aid development in the short term, or even boost mood even if their cognition doesn’t change much.

26
Q

what is reminiscence therapy?

A

make most of current memories show photos and music

27
Q

what vitamine is important for people with AD

A

vitamine B

28
Q

results of study with vitamin b vs placebo

A

people who took vitamin b had 30% less atrophy in the brain than placebo

29
Q

what drug for AD

A

cholinesterase inhibitors

30
Q

how do cholinesterase inhibitors work

A

they block glutamate
which is released in high quantities and is thought to become toxic to remaining brain tissue

31
Q

what do AD drugs do?

A

boost acetylcholine (NT associated with memory function)
boost muscle choline

32
Q

who are AD drugs pescribed to

A

people with mild-moderate AD not severe as tehy dont seem to work and theyre expensive

33
Q

describe advances in AD treatment

A

stop it from progressing
drug that stops amyloid plaques

34
Q

amyloid hypothesis

A

is it amyloid itself or is abnormal time causing it but when it is attacked people seem to improve suggesting it is amyloid

35
Q

problems with new drugs for AD

A

Would require frequent checkups on the brain using MRI which would be expensive

36
Q

episodic memory has atrophy in the …

A

Atrophy in medial temporal lobe
early stage of AD

37
Q

Semantic memory and language (understanding and producing words)

A

Atrophy in anterior temporal and inferior frontal cortex

37
Q

Controlling thought and behaviour

A

Atrophy in frontal cortex

38
Q

AD is bilateral meaning …

A

atoprhy effects hemisphers equally

38
Q

what does damage to anterioir temporal lobe and inferiori frontal lobe lead to

A

semantic language defictis

38
Q

TMS study

A

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
Q

what areas of the brain suffer first in AD

A

hippocampus in the temporal lobe bc memory loss

39
Q

frontal lobe

A

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
Q

behavioural symptoms of AD

A

Irritability, agitation, outbursts, shouting, restlessness, pacing, fidgeting, repetitive behaviours

41
Q

other dementias

A
  • Vascular dementia
  • Focal dementias
  • Subcortical dementias
42
Q

what is the second most common dementia

A

vascular dementia

43
Q

most common cause of vascular dementia

A

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
Q

who is more vulnerable to stroke

A

high blood pressure, blood supply from one artery

45
Q

symptoms of vascular dementia

A
  • poor conentraion
    -organisation of thoughts
  • apathy
  • restlessness
  • weakness due to damage of motor cortex
46
Q

what is frontotemporal dementia

A

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
Q

types of frontotemporal dementia

A
  1. Frontal-variant (fvFTD)
  2. Semantic dementia (SD)
  3. posteriori cortical atrophy
48
Q

how is frontotemporal different to AD

A

Different from AD rather than amyloid plaques there are pick bodies insides cells.

49
Q

FTD symptoms

A

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
Q

semantic dementia symptoms

A

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
Q

PCA sypmtoms

A

pathology in posterior paritetal cortex
blured vision
agnosia
impaired reading/writting

52
Q

subcortical dementias

A

Huntington’s disease – excessive movement (inhibitory failure)

Parkinson’s disease – problems initiating movements

53
Q

cause of Parkinsons disease

A

Degeneration in substantia nigra causes deficit in neuromodulator dopamine. defiict make it hard to start movement

54
Q
A

Psych year one (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions