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Dementia Flashcards

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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

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2
Q

Give an example of a neurodegenerative disease which is always genetic.

A

Huntington’s disease

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3
Q

Give an example of a neurodegenerative disease which is often genetic.

A

Cerebellar ataxia

frontotemporal dementia

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4
Q

Give an example of a neurodegenerative disease which is often sporadic.

A

Alzheimer’s disease

Parkinson’s disease

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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

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6
Q

Dementia affects consciousness level. T/F?

A

False

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7
Q

Dementia only affects memory. T/F?

A

False - it affects other cognitive abilities such as visuospatial function,

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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
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9
Q

What are the four main types of dementia?

A

Alzheimer’s
Lewy-body
vascular
frontotemporal

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10
Q

What are the risk factors for dementia?

A 
Increasing age
head injury
female
downs syndrome
genetics - APP, APOE4, presenilin
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11
Q

What is the most common type of dementia?

A

Alzheimer’s

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12
Q

What is the survival of Alzheimers patients?

A

6-12 years

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13
Q

Formal diagnosis of Alzheimers can only be achieved at autopsy. t/f?

A

true

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14
Q

What abnormal proteins characterise Alzheimers?

A 
Neurofibrillary tangles (tau protein)
Beta amyloid plaques
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15
Q

There is cerebral atrophy of Alzheimers disease. T/F?

A

True

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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
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17
Q

What are the symptoms of mild Alzheimer’s disease?

A 
memory loss
confusion
trouble handling money
poor judgement
mood changes
anxiety
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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

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19
Q

How does death often occur in patients with Alzheimers?

A

Infection such as pneumonia

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20
Q

What are the symptoms of Lewy-body dementia?

A

Progressive cognitive decline
fluctuating consciousness
visual hallucinations
Parkinsonism

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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

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22
Q

What are the symptoms of Parkinson’s disease with dementia?

A 
Bradykinesia
rigidity
tremor
autonomic dysfunction
cognitive impairment
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23
Q

What abnormal protein makes up Lewy bodies?

A

alpha synuclein

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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

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25
Q

What age of patients typically get frontotemporal dementias?

A

45-65 year olds

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26
Q

Define frontotemporal dementias

A

a heterogeneous group of dementias which can be sporadic or inherited

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27
Q

What symptoms are particularly associated with frontal lobe dysfunction in frontotemporal dementia?

A

Behavioural and personality changes
disinhibition
depression
agitation

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28
Q

In what type of frontotemporal dementia is there accumulation of abnormal tau protein?

A

Pick’s disease

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29
Q

In what type of dementia is there a characteristic stepwise progression in memory impairment and cognitive symptoms?

A

Vascular dementia

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30
Q

What genes are associated with Alzheimers disease?

A

APOE4
Presenilin 1 and 2
APP

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31
Q

Beta amyloid plaques develop within the neuron. T/F?

A

False - they develop in the extracellular space

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32
Q

Neurofibrillary tangles develop in the cytoplasm. T/F?

A

True

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33
Q

Describe the amyloid hypothesis.

A

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

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34
Q

Which protein are neurofibrillary tangles composed of?

A

Tau

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35
Q

What is the physiological role of tau?

A

neurite growth
axonal transport
microtubule dynamics

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36
Q

What pathophysiological role does tau play when hyperphosphorylated in a proteinopathy?

A

causes formation of tangles
microtubule dysfunction
cell death

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37
Q

Other than Alzheimer’s give examples of tauopathies

A

pick disease
frontotemporal dementia
corticobasal degeneration
progressive supranuclear palsy

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38
Q

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?

A

False - the opposite is true, alpha helixes to beta pleated sheets

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39
Q

Give examples of neurodegenerative disease characterised by the accumulation of abnormal alpha-synuclein.

A

parkinson’s
Lewy body dementia
multiple system atrophy
neuroaxonal dystrophies

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40
Q

What are the two classes of cognitive enhances used in. the treatment of dementia?

A

Cholinesterase inhibitors

Partial glutamate antagonists

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41
Q

What severity of Alzheimer’s is memantine used to treat?

A

moderate to severe

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42
Q

Give examples of cholinesterase inhibitors used to treat dementia?

A

Donepezil
galantamine
rivastigmine

43
Q

What severity of Alzheimer’s are cholinesterase. inhibitors used to treat?

A

mild to moderate

44
Q

What is the normal action of cholinesterase?

A

Breakdown of ACh at the post-synaptic terminal

45
Q

Cholinesterase inhibitors have a high efficacy against dementia. T/F?

A

False

46
Q

What are the adverse effects of cholinesterase inhibitors?

A

Nausea, vomiting, diarrhoea, muscle cramps, dizziness, fatigue, anorexia, GI bleeding, cardiac events

47
Q

Cholinesterase inhibitors are used in the treatment of frontotemporal and vascular dementia. T/F?

A

False

48
Q

Cholinesterase inhibitors are used in the treatment of Lewy body dementia and Parkinson’s with dementia. T/F?

A

True

49
Q

Antipsychotics can be prescribed in dementia with Lewy bodies. T/F?

A

False

50
Q

Describe the normal functioning of glutamate and AMDA and NMDA receptors.

A

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
Q

How does the action fo glutamate and AMPA/NMDA result in learning?

A

Long term potentiation

calcium activated kinases increase effectiveness of existing receptors and increase number of receptors

52
Q

In Alzheimer’s there is glutamate loss in which areas of the brain?

A

Entorhinal cortex and hippocampus

53
Q

What is the mechanism of action of memantine?

A

Blocks NMDA receptors to stop overactivity of the glutamatergic system

54
Q

In what types of dementia does memantine have no significant effect?

A

mild dementia
vascular dementia
frontotemporal dementia

55
Q

What are the side effects of memantine?

A 
Dizziness
Headache
constipation
somnolence
hypertension
56
Q

How can depression be managed in dementia?

A

SSRIs such as sertraline and citalopram

57
Q

Describe the use of antipsychotics in dementia

A

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
Q

How can dementia be distinguished from learning disability?

A

In dementia there is a decline from a previously higher cognitive function

59
Q

For a diagnosis, dementia must be impacting on day to day function otherwise it is classified as…?

A

Mild cognitive impairment

60
Q

In what type of dementia are changes in personality most commonly present in early disease?

A

Frontotemporal dementias

61
Q

What are the main psychiatric differentials for dementia?

A 
delirium
mild cognitive impairment
amnesic syndrome
chronic brain damage
depression
late onset schizophrenia
learning disability
malingering presentations
dissociation
62
Q

What are the possible intracranial causes of dementia?

A

Tumour

head injury

63
Q

What are the possible infectious causes of dementia?

A

prion disease
neurosyphilis
His associated dementia
TB

64
Q

What are the possible endocrine causes of dementia?

A

hypothyroidism
hyperparathyroidism
cushing’s
Addison’s

65
Q

What are the possible metabolic causes of dementia?

A 
uraemia
hepatic encephalopathy
hypoglycaemia
hypo/hyperclacaemia
hyper/hypomagnesiamia
66
Q

What are the possible nutritional causes of dementia?

A

B12, folate, thiamine or niacin deficiency

67
Q

What are the possible toxic causes of dementia?

A

lead

alcohol

68
Q

What is involved in clinical assessment of dementia?

A 
corroborative history
general physical examination
MSE
standard bloods
structured cognitive testing
structural imaging
69
Q

What blood tests are commonly used when investigating possible dementia?

A 
FBC
glucose
U/Es
LFTs
TFTs
bone profile
urinalysis
Vit B12 / folate
erythrocyte sedimentation ate
c reactive protein
70
Q

Other than standard bloods, what further investigations may be used when investigating possible dementia?

A 
HIV and syphillis serology
CXR
lumbar puncture
ECG
EEG
CT/MRI
71
Q

How many points is the mini mental state exam scored out of?

A

30

72
Q

How many points is the addenbrooke’s assessment scored out of?

A

100

73
Q

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?

A

Executive function

74
Q

The mini mental state exam is influenced by age, education and socio-economic status. T/F?

A

True

75
Q

The mini mental state exam is used to diagnose dementia. T/F?

A

False - it is used as a screening tool

76
Q

What factors comprise ‘cognitive function’?

A 
attention
memory
executive function
language
calculation
praxis
visuospatial ability
77
Q

How can attention be tested?

A 
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
Q

What is anterograde amnesia?

A

Loss of recent memories or memories occurring after onset of disease

79
Q

What is retrograde amnesia?

A

Loss of past memories of memories occurring before onset of disease

80
Q

Describe Ribot’s gradient of memory loss?

A

A pattern of memory loss where Patients lose more recent memory first then progressively lose past memories

81
Q

What functions are encompassed by executive function?

A 
goal setting and motivation
judgement
social behaviour
personality
abstract reasoning
planning and organising
problem solving
82
Q

What is Agraphia?

A

inability to write

83
Q

What is Alexia?

A

inability to read

84
Q

Where in the. brain is calculation carried out?

A

Left angular guys of parietal lobe

85
Q

What is acalculia?

A

inability to comprehend or write numbers properly

86
Q

What is anarithmetria?

A

Difficulty with arithmetic

87
Q

What is dyspraxia?

A

Inability to move a body part despite intact motor and sensory functioning

88
Q

Dyspraxia can affect both conception and production of movements. t/f?

A

ture

89
Q

What is meant by visuospatial ability?

A

Ability to process visual information and link this to spatial positioning of objects to their orientation in space

90
Q

Which areas of the brain control visuospatial ability?

A 
Visual cortex
Parietal lobe (tells you where object is)
temporal lobe (tells you what object is)
91
Q

What problems can be caused by visuospatial deficits?

A 
topographical disorientation
difficulties with dressing
misreading for objects
visual neglect
visual object agnosia
prosopagnosia
92
Q

What is prosopagnosia?

A

The inability to recognise familiar faces

93
Q

Give examples of rarer types of dementia.

A 
Corticobasal degeneration
progressive supra nuclear palsy
HIV infection
Niemann Pick disease type C
Cruetfeldt Jakob disease
94
Q

Which enzymes normally break down APP in the brain?

A

alpha and gamma secretase

95
Q

Which enzymes degrade APP in Alzheimer’s disease?

A

beta and gamma secretase

96
Q

What is the term for when plaques build up around the blood vessel walls of the brain?

A

Cerebral amyloid angiopathy

97
Q

Cerebral amyloid angiopathy increases the risk of haemorrhage. T/F?

A

True

98
Q

What gene is associated with late-onset Alzheimers?

A

APOE-E4

99
Q

What genes are associated with early onset Alzheimers?

A

PSEN-1

PSEN-2

100
Q

Other than genetics, what factors can increase the risk fo developing alzheimers?

A

Smoking
midlife obesity
diet high in saturated fats

101
Q

Why does Down syndrome result in an increased likelihood of early onset Alzheimers?

A

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
Q

In vascular dementia, executive functions are typically more prominently affected than memory. T/F?

A

True

103
Q

How is vascular dementia treated?

A

Prevention of further cerebrovascular disease by optimal control of major risk factors - anti platelet therapy, anticoagulation, carotid angioplasty, stenting, risk factor modification

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