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Year 2 - BRS > 2.12 - Dementia > Flashcards

2.12 - Dementia Flashcards

1
Q

What is the commonest cause of dementia?

A

Alzheimer’s disease

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2
Q

What is Alzheimer’s disease?

A

A fatal neurodegenerative disorder characterised by progressive cognitive, social and functional impairment

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3
Q

Is there a cure for Alzheimer’s?

A

No current cure, with acetylcholinesterase inhibitors having modest symptomatic benefit in early stages

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4
Q

What is the difference in prevalence of causes of dementia in young onset dementia (YOD) sufferers vs late onset dementia (LOD) sufferers?

A
  • Alzheimer’s disease is the most common cause in both, but way bigger proportion in LOD
  • YOD sufferers have slightly more prevalence of familial autosomal dominant Alzheimer’s (fAD)
  • Lewy body dementia, frontotemporal dementia and other causes are more common in YOD
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5
Q

What are the four most common causes of dementia?

A
  • Alzheimer’s disease
  • vascular dementia
  • frontotemporal dementia
  • dementia with Lewy bodies
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6
Q

What are some other potentially reversible causes of dementia? (9)

A
  • depression
  • alcohol related brain damage
  • endocrine e.g. hypothyroidism, Cushing’s, Addison’s
  • B1/B12/B6 deficiency
  • benign tumours
  • normal pressure hydrocephalus
  • limbic encephalitis
  • infections - HIV/syphilis, Whipple’s disease
  • inflammatory
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7
Q

What does the continuum of dementia look like?

A
  • in normal ageing - as years increase, cognitive function gradually decreases
  • in dementia - as years increase, cognitive function decreases more steeply and eventually reaches zero
  • the phases of dementia are preclinical (deterioration in function without clinical features) –> mild cognitive impairment –> dementia
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8
Q

What does the continuum of dementia look like in reality and why?

A

Many ups and downs in cognitive function over time but with a general decreasing trend - small ups and downs can be due to changes in eating and drinking, sleep, infection etc

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9
Q

Why is it difficult to diagnose dementia in clinic?

A
  • the disease follows a heterogenous course
  • in old age the disease presentation is of multiple comorbidities
  • lots of mixed and uncertain pictures
  • younger patients are more typical
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10
Q

What is the most important thing for doctors to do in clinic with dementia patients?

A
  • get a clinical history
  • see how well the patient is functioning
  • how they change
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11
Q

What physiological issues may be present in the brain of those with dementia?

A
  • A-beta
  • TDP-43
  • alpha-synuclein
  • neuronal tau
  • parenchymal ischaemic changes
  • vessel wall pathology e.g. cerebral amyloid angiopathy
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12
Q

What is the path a dementia patient takes through NHS?

A
  1. referral (e.g. by GP/psychiatrist)
  2. history (with clinical interview)
  3. examination
  4. investigations
  5. diagnosis
  6. management
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13
Q

What things do we ask/check during the interview with dementia patients?

A
  • memory
  • language
  • numerical skills
  • executive skills
  • visuospatial skills
  • neglect phenomena
  • visual perception
  • route finding and landmark identification
  • personality and social conduct
  • sexual behaviour
  • eating
  • mood
  • motivation/apathy
  • anxiety/agitation
  • delusions/hallucinations
  • activities of daily living
  • do a collateral with children of sufferer
  • look at chronology of each and how symptoms have changed over time
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14
Q

Define dementia?

A

Severe loss of memory and other cognitive abilities which leads to impaired daily function (regardless of the underlying cause)

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15
Q

What examinations happen after the interview for dementia?

A
  • neurological - cranial nerves, upper and lower limb nerve test
  • mental state e.g. speech, mood, behaviour, perception
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16
Q

What investigations are done after the examination for dementia?

A
  • neuropsychology - MMSE, ACE III, MoCA
  • bloods
  • MRI
  • PET
17
Q

What bloods are taken as part of the investigation for dementia?

A
  • full blood count
  • inflammatory markers
  • thyroid function
  • biochemistry and renal function
  • glucose
  • B12 and folate
  • clotting
  • syphilis serology
  • HIV
  • caeruloplasmin
18
Q

What do you see on a sMRI as Alzheimer’s progresses?

A
  • narrowed sulci
  • widened gyri
  • dilated and enlarged ventricles
  • medial temporal volume loss
  • bilateral hippocampal volume loss
  • shrunken structures that are replaced by CSF, therefore appearing black
19
Q

What do PET scans for dementia involve?

A

Cannulating patient, injecting them with contrast, travels to brain and lights up amyloid in brain, amyloid and tau are pathognomic for Alzheimer’s

20
Q

What PET scan signs are pathognomonic of Alzheimer’s disease?

A

Amyloid along with Tau proteins

21
Q

What are the common potential diagnoses that can be made related to dementia? (7)

A
  • Alzheimer’s
  • vascular
  • Lewy body
  • frontotemporal
  • depression
  • delirium
  • none
22
Q

What are the potential management strategies for dementia? (5)

A
  • acetylcholinesterase inhibitors (AD)
  • watch and wait (to see how current condition changes)
  • treat behavioural/psychological symptoms
  • OT/social services
  • specialist therapies
23
Q

What signs could you use to identify Alzheimer’s? (3)

A
  • subtle
  • insidious amnesia
  • insidious non-amnestic presentations
24
Q

What signs could you use to identify vascular dementia?

A
  • related to cerebrovascular diseases with step-wise deterioration
  • multiple infarcts i.e. strokes
25
Q

What signs could you use to identify dementia with Lewy bodies?

A
  • cognitive impairment before/within 1 year of Parkinsonian symptoms
  • visual hallucinations and fluctuating cognition
26
Q

What signs could you use to identify frontotemporal dementia?

A
  • behaviour variant FTD
  • semantic dementia
  • progressive non-fluent aphasia
27
Q

What is episodic memory (AD)?

A
  • memory for particular episodes in life
  • dependent on medial temporal lobes, including the hippocampus
28
Q

When can diagnosis of Alzheimer’s be made certain?

A

Only be made certain at post-mortem - diagnosis in life was only probable until recently

29
Q

What are some biomarker patterns in Alzheimer’s? (4)

A
  • primary event - A-beta amyloid
  • Tau proteins
  • changes to brain structure
  • cognition lag
30
Q

How is a lumbar puncture used in the diagnosis of Alzheimer’s?

A

To obtain CSF and see how much amyloid and tau proteins there are

31
Q

What does Alzheimer’s disease typically involve?

A

Initial episodic memory deficits secondary to dysfunction of medial temporal lobe structures (entorhinal cortex and hippocampus)

32
Q

What happens in dementia with Lewy bodies? (6)

A
  • associated with fluctuating cognition
  • different cognitive profile to AD
  • often visual hallucinations
  • REM sleep disorder
  • development of symptoms associated with Parkinson’s disease
  • high risk of falls
33
Q

What is the pathophysiology of dementia with Lewy bodies?

A

Aggregation of alpha synuclein –> deposition of Lewy bodies –> symptoms (Lewy bodies in glial cells = myelin and glial dysfunction and subsequent neuronal degeneration)

(Cerebral atrophy, particularly of the frontal lobe with relative sparing of the hippocampi)

34
Q

How does the MRI scan in dementia with Lewy bodies compare to that in AD?

A

MRI shows that unlike Alzheimer’s, hippocampal volume and medial temporal lobe volume generally preserved

35
Q

How does the PET scan in dementia with Lewy bodies compare to that in AD?

A
  • AD - caudate and putamen lit up, lots of dopamine transporters available
  • LBD - less lit up due to less available dopamine transporters (less dopamine –> Parkinsonian symptoms) - characteristic of LBD
36
Q

What do patients with frontotemporal dementia present with? (3)

A
  • increasing behavioural disturbance
  • agitation
  • reduced speech output
37
Q

What does an MRI for frontotemporal dementia show?

A
  • extensive volume loss in temporal lobes and frontal opercula, more so on right
  • Perisylvian fissure volume loss
38
Q

What is vascular dementia?

A
  • infarction of small and medium-sized vessels (essentially mini-strokes)
  • neuronal death —> location specific deficits —> step-wise deterioration
  • symptoms reflect area of infarction:
    • frontal - executive dysfunction, judgement, DM
    • temporal - anterograde amnesia
    • parietal - aphasia, agnosia, apraxia, confusion, agitation

Year 2 - BRS (84 decks)

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