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Psychiatry > Y4 - Dementia > Flashcards

Y4 - Dementia Flashcards

1
Q

What is required for the diagnosis of dementia?

A

Evidence of cognitive decline (e.g. MOCA/MMSE) and functional decline with a clear consciousness and duration > 6months

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2
Q

What are some examples of cognitive dysfunctions common in dementia?

A

Dysmnesia (tends to be short term)
Dysphasia
Dysgnosia
Dyspraxia
Problems with orientation (in time, place, person)
Constructional ability issues
Executive dysfunction (initiation, inhibition, abstraction, problem solving etc.)

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3
Q

What activities of daily living may be affected in dementia?

A 
Finances
Food - eating food that is in date? buying food? cooking? 
Care of children/pets
Health/medication 
Use of telephone/television 
Basic ADL - washing, dressing, eating
Driving
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4
Q

When assessing someone’s functional ability for a diagnosis of dementia what must you do?

A

Consider a change from baseline

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5
Q

What must you do in relation to driving when someone is diagnosed with dementia?

A

Tell them to inform the DVLA

If they do not, you can go above their head if you feel their driving would put them/others at risk

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6
Q

Name some reversible types of dementia

A 
Normal pressure hydrocephalus 
Subdural haematoma (tends to be fluctuating) 
Tumours
Neurosyphillis/HIV
Vitamin deficiencies 
Hypothyroidism
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7
Q

When might you think of a vitamin deficiency causing a reversible dementia?

A

Poor cognition, low mood

This is why GPs must always check haematinics and FBC

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8
Q

What vitamin deficiencies can lead to a reversible dementia?

A

B12

Folate

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9
Q

How are dementias typed?

A

Based on clinical decision

Scans may be used to back it up

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10
Q

What are the types of dementia?

A 
Alzheimer's
Vascular
Mixed AD and VD
Lewy body dementia 
Frontotemporal/Pick's
Alcohol related brain damage - e.g. Korsakoff's
Subcortical, e.g. Parkinson's, Huntington's, HIV
Prion protein, e.g. CJD
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11
Q

What is typical in the presentation of Alzheimer’s?

A

Progressive deterioration over a long period of time
V. little insight
Confabulation
Memory issues

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12
Q

What is typical in the presentation of vascular dementia?

A

Step wise deterioration

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13
Q

What is typical in the presentation of Lewy body dementia?

A

Dementia
Parkinsonism
Hallucinations (visual)
Fluctuation

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14
Q

What is Pick’s disease?

A

Type of frontotemporal dementia
Neurodegeneration of frontal and temporal lobes due to accumulation of proteins in the brain

Tends to affect behaviour and personality a lot (e.g. become hypersexualised, rude)

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15
Q

What causes ARBD?

A

Thiamine deficiency

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16
Q

What is the pathology of Alzheimer’s?

A

Abnormal accumulation of proteins (beta-amyloid plaques, tau tangles)
Atrophy of key brain regions (temporal in Alzheimer’s)
Neurochemical disruption - acetylcholine is reduced

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17
Q

What is the aetiology of Alzheimer’s?

A

Genetic and environmental factors

Early onset more associated with genetic factors, late onset more associated with environmental factors

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18
Q

What are RFs for Alzheimer’s?

A

Age
F>M
Vascular RFs
Head injury

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19
Q

What are risk factors for vascular dementia?

A 
Age
HTN 
Smoking
Hyperlipidaemia
M
IHD
DM
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20
Q

How do you treat vascular dementia?

A

No specific Rx

Modify RFs

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21
Q

What is the difference between LBD and dementia in Parkinson’s?

A

Onset of motor and cognitive decline within 1y = LBD

Onset of cognitive decline 1y after motor symptoms = DPD

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22
Q

What is the pathology of LBD?

A

Lewy body accumulation leads to reduced dopamine due to alpha synucleic protein

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23
Q

Why can people with LBD get differing symptoms?

A

Predominant site in brain confers symptoms

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24
Q

What are classical features of LBD?

A

Visual hallucinations
Fluctuating course
Parkinsonism

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25
Q

What drug should be avoided in those with LBD?

A

Antipsychotics

Makes motor symptoms a lot worse

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26
Q

How do you treat LBD?

A

Cholinesterase inhibitors (e.g. rivastigime)

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27
Q

What are some differentials for dementia?

A

Normal
Delirium
Depression
Mild cognitive impairment

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28
Q

What things may make you lean towards delirium as a diagnosis as opposed to dementia?

A 
Rapid onset & decline 
Very fluctuant 
Worse at night
Psychomotor disturbance
Disrupted sleep wake cycle 
Florid psychotic symptoms 
Clouding of consciousness
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29
Q

What things may make you lean towards depression as a diagnosis as opposed to dementia?

A 
Trigger/life event
Subjective complaints of memory loss
Sleep/appetite disturbance
Worse in morning
Distressed & unhappy
'Don't know answers'
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30
Q

What is involved in the clinical assessment of someone with suspected dementia?

A 
Hx, collateral Hx
Functional ability
Ex - physical, MSE, cognitive Ex
Risks
Bloods - FBC, UE, LFTs, glucose, B12, folate
CT/SPECT
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31
Q

How should you treat Alzheimer’s?

A

Anticholinesterase inhibitors for mild to moderate AD (MMSE 10+)

NMDA antagonist, GABA for moderate to severe AD (14 or less on MMSE) or second line if AChI not tolerated

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32
Q

How do anticholinesterases work?

A

Reduce breakdown of ACh

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33
Q

What are the anticholineasterases?

A

Donepezil
Galantamine
Rivastigime

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34
Q

What is the NMDA antagonist used for moderate-severe Alzheimer’s?

A

Memantime

35
Q

How is the severity of dementia assessed/

A 
Consider functional level 
MMSE:
Mild - 21-30
Moderate - 10-20
Moderately severe - 10-14
Severe <10
36
Q

What are BPSD?

A

Behavioural and psychological symptoms in dementia

Challenging behaviours (unreasonable and challenging the norms and rules of the context in which they occur)

37
Q

What are the kinds of BPSD?

A

Lack of behaviour
Exaggerated normal behaviour
Abnormal/undesirable behaviours

38
Q

What are the five major BPSD symptoms?

A

Agitation (restlessness, wandering)
Psychosis
Affective (depression, lability, anxiety, hypomania, apathy)
Disinhibition (aggression, sexual)
Behaviour (eating, toileting, dressing, sleep wake cycle)

39
Q

What is involved in BPSD management?

A 
Hx, Obs, monitoring 
Environment 
Personal history and personality 
Physical health 
Intervention
40
Q

What is the ABC approach to BPSD management?

A

Antecedent - circumstances & precipitating factors at onset of behaviour

Behaviour - description of behaviour

Consequences - what occurs after behaviour, how everyone responds to behaviour

41
Q

How is BPSD managed pharmacologically?

A

Antipsychotics, e.g. risperidone

42
Q

What are the SEs of using antipsychotics in dementia patients?

A

Sedation, falls, confusion, postural hypotension

Make EPSE worse

43
Q

Which part of the brain does Alzheimer’s largely affect?

A

Temporal lobes

44
Q

What are the two main theories of Alzheimer’s pathology?

A

Beta-amyloid plaques which interfere with neuronal signalling, cause inflammation –> neuron damage, and deposit in BVs weakening their walls and predisposing to haemorrhage

TAU tangles - TAU proteins become misshapen, cannot support the cytoskeleton & clump together to form neurofibrillary tangles
Non-functioning neurons cannot signal and undergo apotosis –> brain atrophy, sulci and ventricles widen, gyri shrink

45
Q

What are the main clinical features of Alzheimer’s?

A 
Loss of short term memory 
Loss of motor skills
Language problems
Long term memory problems
Disorientation 
Bed ridden
46
Q

How is the definitive diagnosis of Alzheimer’s made?

A

Brain biopsy on autopsy

47
Q

What is Parkinson’s?

A

Movement disorder where dopamine producing neurons in the substantia nigra undergo degeneration

48
Q

Give two risk factors for PD

A

Pesticide exposure

DNA variants in genes

49
Q

Where are the SN?

A

One either side of midbrain

They are part of the basal ganglia

50
Q

What is the role of the basal ganglia?

A

Control movement via its connections to the motor cortex

51
Q

What part of the brain tends to disappear in PD?

A

Substantia nigra

52
Q

What is the pathophysiology of PD?

A

Lewy bodies appear in the affected substantia nigra before they die

53
Q

What are Lewy bodies?

A

Eosinophilic, round lesions made of alpha synuclein proteins

54
Q

What other disease are Lewy bodies found in?

A

LBD among others

55
Q

What are the two parts of the SN?

A

Pars reticulata - receives signals from the striatum, relays messages via GABA neurons to the thalamus

Pars compacta - sends messages to the striatum via dopamingeric neurons (nigrostriatal pathway)

56
Q

What is the nigrostriatal pathway involved in?

A

Stimulating cerebral cortex to initiate movement and calibrating/fine tuning movement

57
Q

What is the striatum?

A

Caudate and putamen

58
Q

What are some clinical features of PD?

A 
Resting, asymmetric, pill rolling tremor
Cogwheel rigidity
Stooped posture
Expressionless face
Bradykinesia, hypokinesia, akinesia
Shuffling gait
Postural instability (can lead to falls)

Depression, dementia, sleep disturbances/difficulties

59
Q

What are some PD treatments?

A 
Levodopa/carbidopa
Amantadine
Dopamine agonists
COMT inhibitors
MAO-B inhibitor
Anticholingerics
Deep brain stimulation
60
Q

Can dopamine cross the BBB?

A

No but levodopa (its precursor can)

61
Q

How is levodopa converted into dopamine?

A

By dopa decarboxylase in the nigrostriatal neurons

NB peripheral dopa decarboxylase is found elsewhere in the body

62
Q

What may lead to some of the unwanted SEs associated with levodopa?

A

May be broken down elsewhere in the body to adrenaline, which can lead to arrhythmias

63
Q

What drug is levodopa always given with and why?

A

Carbidopa (dopa decarboxylase inhibitor that can’t cross the BBB to stop it breaking down before it reaches the brain)

64
Q

How does amatadine work?

A

Increases endogenous dopamine production

65
Q

Give examples of dopamine agonists?

A

Bromocriptine
Pramiprexole
Ropinirole

66
Q

What does the COMT enzyme do?

A

Degrade dopamine and levodopa

67
Q

When are COMT inhibitors given?

A

With levodopa

Used to prevent it being broken down outside the CNS

68
Q

How do MAO-B inhibitors work?

A

MAO-B is an enzyme that metabolises dopamine

69
Q

Why might anticholingeric drugs be given in the treatment of PD?

A

Relative increase in amount of ACh compared to dopamine
This tries to reset the balance
Often helps the tremor

70
Q

What is deep brain stimulation?

A

Implanted device that directly sends electrical signals to the basal ganglia that counteracts the aberrant signalling in PD

71
Q

What is parkinsonism?

A

Symptoms of Parkinson’s, e.g. in other diseases or due to drugs, e.g. antipsychotics or metacloperamide

72
Q

What is vascular dementia?

A

Progressive loss of brain function due to long term poor blood supply (usually a series of strokes)

73
Q

What are the functions of the frontal lobe?

A 
Movement
Personality
Counting
Spelling
Decision making
74
Q

What are the functions of the parietal lobe?

A

Processes sensory information to allow us to know where we are physically
Guides movement in 3D space

75
Q

What are the functions of the temporal lobe?

A

Hearing
Smell
Memory
Recognition of faces

76
Q

What is the main function of the occipital lobe?

A

Visual information processing

77
Q

What is the pathophysiology of vascular dementia?

A

Neurons are aerobic & have no longer term energy supply

Atherosclerosis leads to gradual decrease in BF to the brain –> chronic ischaemia

Small parts of atherosclerosis can break off & occlude small arteries

Once tissue demand > supply ==> ischaemic stroke & tissue damage (which can undergo liquefactive necrosis)

–> loss of mental function

78
Q

What is atherosclerosis?

A

Build up of plaque that thickens the artery wall

79
Q

What are the symptoms of vascular dementia like?

A

Depends on area affected

Symptoms appear suddenly and function decreases with each stroke

80
Q

How do you diagnose vascular dementia?

A

Neuropsychological tests

CT/MRI can show multiple cortical/subcortical infarct & atrophy confirming ischaemia

81
Q

What causes lewy body dementia?

A

Misfolded alpha-synuclein proteins that aggregate to form Lewy bodies that deposit in neurons, especially those in the cortex/SN

82
Q

What are the symptoms of LBD?

A

Early cognitive - difficulty focusing, poor memory, visual hallucinations, disorganised speech, depression

Later motor - resting tremor, stiff movements, reduced facial movements

Sleep disorders

83
Q

How is the definitive diagnosis of LBD made?

A

Brain biopsy

84
Q

How do you manage LBD?

A

Alzheimer’s meds for the cognitive aspects, e.g. donepezil

PD medications for the motor aspects, e.g. levodopa

Psychiatry (26 decks)

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