Brainscape's Knowledge GenomeTM

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


See full index

Z Year3 Neuro Conditions > Dementia > Flashcards

Dementia Flashcards

1
Q

What are 4 types of dementia and how common are they?

A
  1. Alzheimer’s – most common
  2. Frontotemporal
  3. Vascular (25%)
  4. Lew body (15-25%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are RF for AD?

A
  1. Advanced age
  2. FHx
  3. Genetics
  4. Down’s syndrome
  5. Cerebrovascular disease
  6. Lifestyle factors and medications
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What genes are related to AD?

A

ApoE E4 allele

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

What is the time course of AD?

A

deteriorating course 8-10years

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

What is the patho of AD?

A
  1. Excess of interneural amyloid peptide’s due to overproduction or diminished clearance of beta amyloids
  2. Loss of acetylcholine neurotransmitter
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Where is the neuronal loss in AD?

A

hippocampus, amygdala, temporal neocrortex and subcortical nuceli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does AD overlap with?

A

95% of AD show vascular dementia

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

What are RF for fontrotemporal lobe dementia?

A
  1. FHx
  2. 45-65 usually
  3. Mutations in MAPT gene, GRN gene and C9orf72 gene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What gene mutations are in FTD?

A
  1. MAPT gene
  2. GRN gene
  3. C9orf72 gene
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the patho of FTD?

A

neuronal loss, gliosis and microvascular changes of frontal lobes, anterior cingulate cortex and insular cortex

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

How common is vascular dementia?

A

second most common dementia in old ppl

with large overlap with Alzheimer’s ad people can have mixed

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

What is patho of vascular dementia?

A

loss of brain parenchyma from cerebrovascular causes from infarction and small vessel changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the causes of VD?

A
  1. Infarction
  2. Leukoaraiosis
  3. Haemorrhage
  4. F>M
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are RF for VD?

A
  1. Hx of stroke
  2. Age >60
  3. Obesity
  4. Hypertension
  5. Cig smoking
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are RF for lewy body dementia?

A

older age: 60-95

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

What are the symptoms and signs of AD?

A
  1. Memory loss
  2. Disorientation
  3. Nominal dysphasia
  4. Misplacing items/getting lost
  5. Apathy
  6. Decline in IADLs
  7. Personality change
  8. Unremarkable intial physical examination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the symptoms and signs of FTD?

A
  1. Coarsening of personality, social behaviour and habits
  2. Progressive loss of language fluency or comprehension
  3. Development of memeory impairment, disorientation or apraxias
  4. Progressive self-neglect and abandonment of work, activities and social contacts
  5. Overeating
  6. Emotional blunting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are other symtoms with FTD?

A

50% have parkinsonism and some MND

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

What are symptoms and signs of VD?

A
  1. Difficulty solving problems
  2. Apathy
  3. Disinhibition
  4. Slowed processing of info
  5. Poor attention
  6. Retrieval memory deficit
  7. Frontal release reflexes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the symptoms and signs of LBD?

A
  1. Cognitive fluctuations
  2. Visual hallucination
  3. Motor symptoms
  4. REM sleep behavioural disturbance
  5. Depression
  6. Autonomic dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are some DDx for AD?

A
  1. Mild cognitive impairment (MCI)
  2. Delirium
  3. Depression
  4. Vascular depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are some DDx for FTD?

A
  1. Alzheimer’s
  2. Dementia with Lewy bodies
  3. Vascular dementia
  4. Bipolar
  5. Major depression
  6. OCD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some DDx for VD?

A
  1. Depression
  2. AD
  3. Mild cognitive impairment
  4. Lewy body dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are DDx for LBD?

A
  1. Alzheimer’s disease
  2. Parkinson’s disease
  3. Frontotemporal dementia
  4. Vascular dementia
  5. Prion disorders
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What investigations do you do for AD?

A
  1. Bedside cognitive testing
  2. CT
  3. MRI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What would bedside cognitive testing e.g. MMSE show in AD?

A
  1. impaired recall
  2. nominal dysphasia
  3. disorientation
  4. constructional dyspraxia and impaired executive functioning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What would CT show in AD?

A

exclude SOL and other path

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What would MRI show in AD?

A

generalised atrophy with medial, temporal lobe and lateral parietal predominance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Why do you do bloods in AD?

A

rule out a metabolic induced dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What bloods are done for AD?

A
  1. FBC
  2. Metabolic panel
  3. TSH
  4. Vit B12
  5. Urine drug screen: rule out recreational use
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How do you have diagnostic confirmation FTD?

A

on pathological examination or identification of gene mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What tests are done for FTD?

A
  1. Formal cognitive testing
  2. Brain MRI
  3. Brain CT
33
Q

What would formal cognitive testing show for FTD?

A
  1. poor emotional processing

2. MMSE score normal and MOCA frontal subsets may show abnormality

34
Q

What would imaging show in FTD?

A

oth imaging show focal atrophy in frontal and/or anterior temporal lobes + the atrophy characterised by left-right asymmetry with loss of >70% of spindle neurons

35
Q

Why do you do bloods in FTD?

A

check cognitive decline not due to renal failure etc

36
Q

What bloods do you do in FTD?

A
  1. FBC
  2. Serum CRP: rule out inflammatory conditions
  3. TSH
  4. T4
  5. Metabolic panel
  6. Urea
  7. Creatinine
  8. LFTs
  9. B12
  10. HIV, syphilis, serum enzyme-linked immunosorbent assay (for Lyme)
37
Q

What imaging do you do for VD?

A
  1. CT or MRI brain

2. ECG

38
Q

What would CT or MRI brain show in VD?

A

cerebrovascular lesion

39
Q

What would ECG show in VD?

40
Q

What bloods are done in VD?

A
  1. ESR
  2. Blood glucose level
  3. Renal and LFTs
  4. Vitamin B12
  5. Folate
  6. Thyroid function
41
Q

What bloods are done for LBD?

A
  1. FBC
  2. Metabolic panel
  3. TSH
  4. Vit B12
  5. Folate
  6. VDRL
  7. Urine drug
  8. Urinalysis
  9. HIV testing
42
Q

What diagnosis of LBD based from?

A

made clinically can only be confirmed pathologically by presence of Lewy bodies – many have AD as well

43
Q

What is the maangement plan for AD?

A

1st line Supportive treatment e.g. career
Plus:
1. Environmental control measures
2. Cholinesterase inhibitors e.g donepezil

44
Q

What medication is used for AD?

A
  1. Cholinesterase inhibitors e.g donepezil

2. Treat associated e.g. depression, psychosis, insomnia (trazodone)

45
Q

What is the 1st line treatment of FTD?

A

supportive cause

46
Q

What medication is use for irritability and agitation FTD?

A

benzodiapseine or antipsychotic

47
Q

What medication is used for compulsion in FTD?

48
Q

What medication is used for ditractability or persevation in FTD?

A

amantadine

49
Q

What medication is used for eating behaviour and euphoria and mania in FTD?

A

valproate semisodium or topiramate (for euphoria, mania) etc) and topiramate for eating behaviour

50
Q

What is the treatment of VD?

A

antiplatelet therapy e.g. aspirin 50-325mg daily

51
Q

What could you add to the general treatment of VD?

A
  1. Lifestyle changes

2. Supportive care

52
Q

What medical treatment could you add to treatment of VD?

A
  1. Carotid enddareterectomy and stenting (with carotid stenosis >70%)
  2. Cholinesterase inhibitor and/or memantine (if AD)
  3. BP control
  4. Statin therapy
  5. Improve glycaemic control
  6. SSRI
  7. Antidepressant
53
Q

How do you treat LBD with acute behavioural disturbances?

A

1st line: short-acting benzodiazepines: lorazepam 0.5mg orally

54
Q

How do you treat LBD without acute behavioural disturbances?

A

1st line: cholinesterase inhibitors e.g. donepezil 5mg

55
Q

What other medication can you add to treatment of LBD?

A
  1. Atypical antipsychotics e.g. risperidone
  2. SSRI
  3. Clonazepam or melatonin (REM sleep behaviour disorder)
  4. Carbidopa/levodopa (motor symptoms)
56
Q

What are possible complications of AD?

A
  1. Pneumonia
  2. Institutionalisation
  3. UTI
  4. Falls
  5. Weight loss
  6. Elder abuse
57
Q

What are possible complications of FTD?

A
  1. Financial crisis
  2. Dangerous driving
  3. Problems with parenting
  4. Falls
  5. Legal crisis
58
Q

What are possible complications of VD?

A
  1. Depression
  2. Agitation/aggression
  3. Wandering
  4. Falls
  5. Aspiration/pneumonia
  6. Decubitus ulceration
59
Q

What are possible complications of LBD?

A
  1. Pneumonia
  2. Institutionalisation
  3. Dysphagia
  4. Antipsychotic sensitivity
  5. Urinary incontinence
  6. Falls
  7. Elder abuse
60
Q

What is the mean survival of AD?

61
Q

What is the patho of dementia?

A

build up of abnormal amyloid precursor protein (APP)

62
Q

How is APP normally formed?

A

alpha and gamma secretase

63
Q

How can APP be formed abnormally?

A

beta and gamma secretase (makes abnormal breakdown product Abeta)

64
Q

What does the Abeta lead to?

A
  1. Extracellular myloid plaques
    -which is abnormal is resistant to degradation
    so leads to build up of abnormal APP
  2. Abeta accumulate outside of cell to form amyloid plaques and lead to phosphorylation of tau
    -so Intracellular neurofibrillary tangles
    -degeneration of Ach neurones
65
Q

Why does this patho lead to dementia?

A

inteferes with neuronal communication (+inflammation)

66
Q

What is tau?

A

protein that supports microfilaments within neurone

67
Q

Where are tau tangles?

A

inside neuron

68
Q

How do tau tangles form?

A

AlphaBeta triggers phosphorylation of tau, causing it to disassociate from the MF and accumulate into neurofibrillary tangles

69
Q

What do the tau tangles lead to?

A

Tangles + weakened microfilaments → ↓neuronal function and apoptosis → atrophy

70
Q

How is Ach affected in dementia?

A

pathological changes leads to degeneration of cholinergic nuceli which lead to decreased cortical Ach

71
Q

What are beta amyloid?

A

extracellular plauques

72
Q

What does the beta amyloid lead to?

A

hyperphosphorylated tau which lead to neurofibrillary tangles and the result in neuronal and synaptic loss

73
Q

What are the 5A’s of Alzheimer’s?

A 
Amnesia
Anomia
Apraxia 
Agnosia
Aphasia
74
Q

What is the most common type of FTD?

A

Pick’s disease

75
Q

What are pick bodies?

A

hyperphosphorylated tau protein

76
Q

What is patho of FTD?

A

involves tau in frontal and temporal lobes but not amyloid beta

77
Q

What is the progression of VD like?

78
Q

What would CSF for AD show?

A
  • high tau and low beta amyloid

- brain tissue required for definitive diagnosis

79
Q

What cognitive tests are used for AD?

A

MMSE, Addenbrooke’s cognitive assessment and MOCA

Z Year3 Neuro Conditions (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions