Dementia Flashcards

1
Q

what is dementia

A

severe loss of memory and other cognitive abilities which leads to impaired daily function
chronic neurodegenerative disease with progressive (slow cognitive decline) and an insidious onset
Heterogenous course
Multiple comorbidities in old age
Younger patients more typical
See Causes for detail
No current cure: acetyl cholinesterase inhibitors

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2
Q

what are risk factors for dementia

A
aging 
oral health 
brain trauma 
infections or systemic inflammation 
genetic factors
midlife obesity 
reduced physical activity
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3
Q

what are the most prevalent causes for the 2 types of dementia

A

1) Young onset
2) late
fAD= frontal alzheimer’s disease
AD = Alzhiermer’s disease
VaD= vascular dementia
FtD= frontal lobe dementia
DLD/PD = lewy body dementia

Dementia can be young onset ( <65 yrs) or late onset ( > 65yrs)
Causes of young onset : Familial autosomal dominant alzheimer’s disease caused by AVP and Presnell mutations, More caused by frontal lobe damage
Causes of late onset : Alzheimer’s most prevalent

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4
Q

what are symptoms of dementia

A
Symptoms of dementia 
Head turning sign 
Forgetfulness / episodic memory ( memory for particular periods of their life )  
Get lost easily 
Disinhibition 
Changes in personality 
Poor personal hygiene
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5
Q

what is progression of dementia

A

Cognitive function decreases with age
In dementia you have a preclinical period : deterioration in cellular function w/o clinical manifestation ie forgetfulness
In Preclinical : increases in amyloid, increases in tau protein inflammation → leads to mild cognitive impairment and dementia
Cognitive function fluctuates up and down - it is not a smooth curve and is dependant on sleep, diet, stress etc

Amyloid tau protein may increase if cause in Alzheimer’s

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6
Q

why is dementia hard to diagnose?

A

Generally hard to diagnose as :
Disease follow heterogenous course
Old age means disease presentation is of multiple comorbidities ( ie hypertension , diabetes, CVD)
Can have mixed pathologies ( ie can be a lot of molecules causing dementia
Younger present with more typical symptoms
V important to look at clinical history and how the patient changes over time

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7
Q

what is the clinical diagnosis pathway for dementia

A

1) referral
2) History
3) examination
4) investigation
5) diagnosis
6) management
7 ) repeat

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8
Q

what happens in referal

A

From GP , therapist , geriatrics doctor ect

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9
Q

what must you ask in the history of dementia

A

Interview( ask about) :
Must ask about chronology of each ( aka how it’s changed over time ie improve/ deteriorate)
Large deterioration = usually vascular causes of dementia . Small deterioration = alzheimers
( should ask family members = collateral history )

V important to ask about memory esp short term memories Ie what did you have for breakfast today
Delusion : firmly held fixed ideas that can’t be changed
Hallucinations can be auditory , visual, somatic
Confirm with a relative
Look for “head-turning” sign
Vague about recent news events and sports results
Queen square green book
Luria three stage sequence with alternating hand task

See google docs for more ie 
- memory 
language 
maths skills 
visuospatial skills 
etc
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10
Q

what examinations of dementia should be conducted

A

Neurological - Cranial nerve tests . Lower + upper limb tests. Focus tests ie frontal lobe function tests etc
Mental state → appearance , perception , insight ( all the physciologial stuff etc)

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11
Q

what investigations of dementia should be conducted

A

Neuropsychology : profound impairment of episodic memory esp in relation to recently learned material

MMSE test : +/- ACE III (15 minutes, more memory focussed) 
Can also do the Cambridge cognitive examination which is more memory focused
Or ACE ( addenbrooke's cognitive assessment) 
Bloods 
Full blood count 
Inflammatory markers 
Thyroid function 
Biochemistry and renal function
Glucose 
B12 and folate 
Clotting 
Other causes 
Syphilis serology 
HIV 
Caeruloplasmin: wilson’s disease, copper deficiency (at intervals when monitoring a copper related disease or its treatment)

Basic Imagining ie MRI / PET

CSF ( microbiology)
Taken via lumbar puncture + assess for B amyloid and tau protein

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12
Q

what types of MRT/PET should be done for dementia

A
MRI scan/ structural imaging
Left = cognitive normal 
Middle = mild cognitive impairment 
Right = alzheimer's disease 
In AD :  Ventricles are dilated and enlarged, hippocampal volume loss - replaced with CSF ( appears black on MRI)

Amyloid PET scans
Cannulate patient
Inject patient with contrast ( ATF) which travels to the brain
Contrast lights up amyloid in the brain

Negative: low likelihood of alzheimer’s (low amyloid, low tau)

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13
Q

what can be possible diagnosis of dementia

A
See types + causes below 
Differential list ie : 
Alxheimers 
Vascular 
Lewy body 
FTD 
Depression 
Delirium 
None ?
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14
Q

what are the management strategies of dementia

A

See below !
ACHase inhibitors
Watch and wat ( should see deterioration of patient > 6 months)
Treat behaviour and physiological symptoms
OT / social services
Specialist therapy

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15
Q

what are the different types of dementia

A

In order to diagnose dementia must rule out other conditions

First rule out other conditions: delirium vs dementia vs depression

1) Alzheimer’s
2) vascular dementia
3) dementia with Lewy bodies
4) frontal temporal dementia
5) rapidly progressing dementias

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16
Q

how is delirium different to dementia and depression

A

see google docs

17
Q

what is Alzheimer’s and how does it present on an MRI

A

Subtle, insidious amnestic/non amnestic presentations
(most prevalent)
dysfunction of medial temporal lobe structures (entorhinal cortex and hippocampus)

hippocampal atrophy (replaced by CSF)
→ dilated lateral ventricles
→ widened

18
Q

symptoms of Alzheimer’s

A

gradual onset
Often patients lack insight of their problems
memory loss (names, recent events)
E.g. can still drive but can’t remember the way , forget to take medications/ takes too much
Episodic memory impaired
language deficits
rapid forgetting
impaired visuospatial skills
normal gait and neuro exam early
later affective disturbances; behavioural symptoms such as aggression - increasingly irritable

19
Q

what causes Alzheimer’s

A

(medial temporal atrophy esp in entorhinal cortex + hippocampus)
This causes memory loss

beta amyloid plaques
→ aberrant cleavage of amyloid precursor protein by beta and gamma secretase instead of alpha resulting in surplus of amyloid beta which aggregates and accumulates in amygdala, hippocampus and cerebral cortex as amyloid plaques (interferes with neuron communication and contributes to inflammation)

neurofibrillary tangles
→ plaques trigger tau hyperphosphorylation which aggregates into NFTs in cortex, hippocampus and substantia nigra - leads to reduced neuronal function and atrophy (degeneration of cholinergic nuclei, reduced acetylcholine)

20
Q

what is vascular dementia ? symptoms ? causes?

A

Vascular dementia
→ Related to cerebrovascular diseases with a classical stepwise deterioration +- multiple infarcts

symptoms: abrupt or gradual onset
focal neurological signs
signs of vascular disease

causes: strokes, lacunar infarcts, white matter lesions, vulnerable to cerebrovascular events

21
Q

what is dementia with lewy bodies ? symptoms ? causes

A

→ Cognitive impairment before/within 1 year of parkinsonian symptoms, visual hallucinations and fluctuating cognition

Preserved hippocampal and medial temporal volume, DAT scan: fewer dopamine transporters

symptoms: 
insidious onset, progressive with fluctuations 
fluctuating cognition 
visual hallucinations
REM sleep disorder 
neuroleptic sensitivity 
shuffling gait 
increased tone 
tremors 
falls 

causes
generalised atrophy
lewy bodies in cortex and midbrain
(LB= deposits of alpha-synuclein protein)

22
Q

what is frontotemporal dementia ? symptoms? causes ?

A

Frontotemporal dementia
→ Behavioural variant FTD, semantic dementia, progressive non-fluent aphasia

symptoms: 
insidious onset (50s, 60s), rapid progression
disinhibition 
socially inappropraite 
poor judgemnt 
apathy decreased motivation 
poor executive function 
Limited spontaneous communication
Can’t find the right words

causes:
frontal and temporal atrophy due to hyperphosphorylated tau
pick cells and pick bodies in cortex

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