Dementia Flashcards
(103 cards)
1
Q
What is the definition of a neurodegenerative disease?
A
Systematic symmetrical neuronal death which follows a specific pattern of neuron loss over time and is often the result if the accumulation of abnormal proteins
2
Q
Give an example of a neurodegenerative disease which is always genetic.
A
Huntington’s disease
3
Q
Give an example of a neurodegenerative disease which is often genetic.
A
Cerebellar ataxia
frontotemporal dementia
4
Q
Give an example of a neurodegenerative disease which is often sporadic.
A
Alzheimer’s disease
Parkinson’s disease
5
Q
What normal changes in cognition can be expected with age?
A
Increase in forgetfulness
slowing of response times
changes in vision, hearing, sensory and motor function
6
Q
Dementia affects consciousness level. T/F?
A
False
7
Q
Dementia only affects memory. T/F?
A
False - it affects other cognitive abilities such as visuospatial function,
8
Q
Give examples of reversible causes of cognitive impairment/dementia.
A
Hypothyroidism normal pressure hydrocephalus drugs - opiates, sedatives anticholinergics tumour neurosyphilis chronic subdural haematoma whipple's disease nutrition -vit B3 deficiency psychiatric disorders
9
Q
What are the four main types of dementia?
A
Alzheimer’s
Lewy-body
vascular
frontotemporal
10
Q
What are the risk factors for dementia?
A
Increasing age head injury female downs syndrome genetics - APP, APOE4, presenilin
11
Q
What is the most common type of dementia?
A
Alzheimer’s
12
Q
What is the survival of Alzheimers patients?
A
6-12 years
13
Q
Formal diagnosis of Alzheimers can only be achieved at autopsy. t/f?
A
true
14
Q
What abnormal proteins characterise Alzheimers?
A
Neurofibrillary tangles (tau protein) Beta amyloid plaques
15
Q
There is cerebral atrophy of Alzheimers disease. T/F?
A
True
16
Q
What are the symptoms of moderate Alzheimer’s disease?
A
Memory loss confusion problems recognising people language dificulties restlessness agitation wandering repeptitive statements
17
Q
What are the symptoms of mild Alzheimer’s disease?
A
memory loss confusion trouble handling money poor judgement mood changes anxiety
18
Q
In addition to cognitive symptoms,What are the symptoms of severe Alzheimer’s disease?
A
Seizures
weight loss
increased sleeping
loss of bladder and bowel control
19
Q
How does death often occur in patients with Alzheimers?
A
Infection such as pneumonia
20
Q
What are the symptoms of Lewy-body dementia?
A
Progressive cognitive decline
fluctuating consciousness
visual hallucinations
Parkinsonism
21
Q
Which type of dementia results from accumulation of the same abnormal protein that is seen in Parkinson’s disease?
A
Lewy body dementia
22
Q
What are the symptoms of Parkinson’s disease with dementia?
A
Bradykinesia rigidity tremor autonomic dysfunction cognitive impairment
23
Q
What abnormal protein makes up Lewy bodies?
A
alpha synuclein
24
Q
How can Lewy body dementia and Parkinson’s disease be differentiated pathologically?
A
by where in the brain the primary pathology exists - mainly cortex for LBD, and mainly substantial migrants for PD
25
What age of patients typically get frontotemporal dementias?
45-65 year olds
26
Define frontotemporal dementias
a heterogeneous group of dementias which can be sporadic or inherited
27
What symptoms are particularly associated with frontal lobe dysfunction in frontotemporal dementia?
Behavioural and personality changes
disinhibition
depression
agitation
28
In what type of frontotemporal dementia is there accumulation of abnormal tau protein?
Pick's disease
29
In what type of dementia is there a characteristic stepwise progression in memory impairment and cognitive symptoms?
Vascular dementia
30
What genes are associated with Alzheimers disease?
APOE4
Presenilin 1 and 2
APP
31
Beta amyloid plaques develop within the neuron. T/F?
False - they develop in the extracellular space
32
Neurofibrillary tangles develop in the cytoplasm. T/F?
True
33
Describe the amyloid hypothesis.
The secondary structure of APP changes from an alpha helix to beta related sheet resulting in the formation of alpha beta peptide monomers and oligomers which cause plaque formation
this induces an inflammatory response which results in aggregation of tau proteins, forming tangles
the tangles and plaques together cause synaptic and neuronal loss
34
Which protein are neurofibrillary tangles composed of?
Tau
35
What is the physiological role of tau?
neurite growth
axonal transport
microtubule dynamics
36
What pathophysiological role does tau play when hyperphosphorylated in a proteinopathy?
causes formation of tangles
microtubule dysfunction
cell death
37
Other than Alzheimer's give examples of tauopathies
pick disease
frontotemporal dementia
corticobasal degeneration
progressive supranuclear palsy
38
There is a switch from beta pleated sheets to alpha helixes in the misfoldign of alpha synuclein which causes formation of Lewy bodies. T/F?
False - the opposite is true, alpha helixes to beta pleated sheets
39
Give examples of neurodegenerative disease characterised by the accumulation of abnormal alpha-synuclein.
parkinson's
Lewy body dementia
multiple system atrophy
neuroaxonal dystrophies
40
What are the two classes of cognitive enhances used in. the treatment of dementia?
Cholinesterase inhibitors
| Partial glutamate antagonists
41
What severity of Alzheimer's is memantine used to treat?
moderate to severe
42
Give examples of cholinesterase inhibitors used to treat dementia?
Donepezil
galantamine
rivastigmine
43
What severity of Alzheimer's are cholinesterase. inhibitors used to treat?
mild to moderate
44
What is the normal action of cholinesterase?
Breakdown of ACh at the post-synaptic terminal
45
Cholinesterase inhibitors have a high efficacy against dementia. T/F?
False
46
What are the adverse effects of cholinesterase inhibitors?
Nausea, vomiting, diarrhoea, muscle cramps, dizziness, fatigue, anorexia, GI bleeding, cardiac events
47
Cholinesterase inhibitors are used in the treatment of frontotemporal and vascular dementia. T/F?
False
48
Cholinesterase inhibitors are used in the treatment of Lewy body dementia and Parkinson's with dementia. T/F?
True
49
Antipsychotics can be prescribed in dementia with Lewy bodies. T/F?
False
50
Describe the normal functioning of glutamate and AMDA and NMDA receptors.
Glutamate acts on both NMDA and AMPA but initially NMDA channels are blocked by magnesium. During a weak electrical stimulation, EPSP is entirely mediated by AMPA receptors. If there is a stronger presynaptic action potential, AMPA receptors depolarise the membrane, expel the magnesium from the NMDA channel and allow NMDA to also respond to glutamate. this leads to insertion of more AMPA receptors
51
How does the action fo glutamate and AMPA/NMDA result in learning?
Long term potentiation
| calcium activated kinases increase effectiveness of existing receptors and increase number of receptors
52
In Alzheimer's there is glutamate loss in which areas of the brain?
Entorhinal cortex and hippocampus
53
What is the mechanism of action of memantine?
Blocks NMDA receptors to stop overactivity of the glutamatergic system
54
In what types of dementia does memantine have no significant effect?
mild dementia
vascular dementia
frontotemporal dementia
55
What are the side effects of memantine?
```
Dizziness
Headache
constipation
somnolence
hypertension
```
56
How can depression be managed in dementia?
SSRIs such as sertraline and citalopram
57
Describe the use of antipsychotics in dementia
atypical antipsychotics (risperidone, aripiprazole) can be used in severe agitation or aggression
these increase mortality and increase risk of cerebrovascular accident so should be used sparingly
not used to treat insomnia, wandering or abnormal vocalisation
if patient stable for three months on antipsychotics then cautiously withdraw
58
How can dementia be distinguished from learning disability?
In dementia there is a decline from a previously higher cognitive function
59
For a diagnosis, dementia must be impacting on day to day function otherwise it is classified as...?
Mild cognitive impairment
60
In what type of dementia are changes in personality most commonly present in early disease?
Frontotemporal dementias
61
What are the main psychiatric differentials for dementia?
```
delirium
mild cognitive impairment
amnesic syndrome
chronic brain damage
depression
late onset schizophrenia
learning disability
malingering presentations
dissociation
```
62
What are the possible intracranial causes of dementia?
Tumour
| head injury
63
What are the possible infectious causes of dementia?
prion disease
neurosyphilis
His associated dementia
TB
64
What are the possible endocrine causes of dementia?
hypothyroidism
hyperparathyroidism
cushing's
Addison's
65
What are the possible metabolic causes of dementia?
```
uraemia
hepatic encephalopathy
hypoglycaemia
hypo/hyperclacaemia
hyper/hypomagnesiamia
```
66
What are the possible nutritional causes of dementia?
B12, folate, thiamine or niacin deficiency
67
What are the possible toxic causes of dementia?
lead
| alcohol
68
What is involved in clinical assessment of dementia?
```
corroborative history
general physical examination
MSE
standard bloods
structured cognitive testing
structural imaging
```
69
What blood tests are commonly used when investigating possible dementia?
```
FBC
glucose
U/Es
LFTs
TFTs
bone profile
urinalysis
Vit B12 / folate
erythrocyte sedimentation ate
c reactive protein
```
70
Other than standard bloods, what further investigations may be used when investigating possible dementia?
```
HIV and syphillis serology
CXR
lumbar puncture
ECG
EEG
CT/MRI
```
71
How many points is the mini mental state exam scored out of?
30
72
How many points is the addenbrooke's assessment scored out of?
100
73
The Addenbrroke's assessment is more thorough than the mini mental state exam. In particular, what aspects of cognition does the Addenbrooke's test cover better than the mini mental state exam?
Executive function
74
The mini mental state exam is influenced by age, education and socio-economic status. T/F?
True
75
The mini mental state exam is used to diagnose dementia. T/F?
False - it is used as a screening tool
76
What factors comprise 'cognitive function'?
```
attention
memory
executive function
language
calculation
praxis
visuospatial ability
```
77
How can attention be tested?
```
orientation in time and place
digit span - forwards and backwards
recite months of the year backwards
serial 7s
spell a word backwards
stroop test
```
78
What is anterograde amnesia?
Loss of recent memories or memories occurring after onset of disease
79
What is retrograde amnesia?
Loss of past memories of memories occurring before onset of disease
80
Describe Ribot's gradient of memory loss?
A pattern of memory loss where Patients lose more recent memory first then progressively lose past memories
81
What functions are encompassed by executive function?
```
goal setting and motivation
judgement
social behaviour
personality
abstract reasoning
planning and organising
problem solving
```
82
What is Agraphia?
inability to write
83
What is Alexia?
inability to read
84
Where in the. brain is calculation carried out?
Left angular guys of parietal lobe
85
What is acalculia?
inability to comprehend or write numbers properly
86
What is anarithmetria?
Difficulty with arithmetic
87
What is dyspraxia?
Inability to move a body part despite intact motor and sensory functioning
88
Dyspraxia can affect both conception and production of movements. t/f?
ture
89
What is meant by visuospatial ability?
Ability to process visual information and link this to spatial positioning of objects to their orientation in space
90
Which areas of the brain control visuospatial ability?
```
Visual cortex
Parietal lobe (tells you where object is)
temporal lobe (tells you what object is)
```
91
What problems can be caused by visuospatial deficits?
```
topographical disorientation
difficulties with dressing
misreading for objects
visual neglect
visual object agnosia
prosopagnosia
```
92
What is prosopagnosia?
The inability to recognise familiar faces
93
Give examples of rarer types of dementia.
```
Corticobasal degeneration
progressive supra nuclear palsy
HIV infection
Niemann Pick disease type C
Cruetfeldt Jakob disease
```
94
Which enzymes normally break down APP in the brain?
alpha and gamma secretase
95
Which enzymes degrade APP in Alzheimer's disease?
beta and gamma secretase
96
What is the term for when plaques build up around the blood vessel walls of the brain?
Cerebral amyloid angiopathy
97
Cerebral amyloid angiopathy increases the risk of haemorrhage. T/F?
True
98
What gene is associated with late-onset Alzheimers?
APOE-E4
99
What genes are associated with early onset Alzheimers?
PSEN-1
| PSEN-2
100
Other than genetics, what factors can increase the risk fo developing alzheimers?
Smoking
midlife obesity
diet high in saturated fats
101
Why does Down syndrome result in an increased likelihood of early onset Alzheimers?
In Down syndrome there is an extra copy of chromosome 21. The gene which produces APP is located on this chromosome and so Down syndrome likely causes over expression of APP
102
In vascular dementia, executive functions are typically more prominently affected than memory. T/F?
True
103
How is vascular dementia treated?
Prevention of further cerebrovascular disease by optimal control of major risk factors - anti platelet therapy, anticoagulation, carotid angioplasty, stenting, risk factor modification
