Dementia Flashcards

(46 cards)

1
Q

What is dementia?

A

a progressive irreversible decline in cognitive function over several months

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2
Q

Types of dementia

A
  • Alzheimer disease
  • Vascular dementia
  • Lewy body dementia
  • Frontotemproal
  • Parkinson’s disease with dementia
  • Aids related
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3
Q

Cognitive symptoms of dementia
What lobe is involved?

A
  • impaired memory - temporal
  • impaired orientation - temporal
  • impaired learning capacity - temporal
  • impaired judgement - frontal
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4
Q

Non cognitive symptoms of dementia

A
  • behavioural symptoms - agitation, aggression, sexual disinhibition
  • depression + anxiety
  • insomnia
  • daytime drowsiness
  • visual + auditory hallucinations
  • persecutor delusions
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5
Q

How is dementia diagnosed?

A

By exclusion:
- exclude delirium
- exclude organic causes of cognitive decline:
- hypothyroidism
- hypercalcaemia
- B12 deficiency
.
Look for features of progressive cognitive decline, impairment of daily living in patients with a normal conscious level

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6
Q

What must be excluded when making a diagnosis of dementia?

A
  • exclude delirium
  • exclude organic causes of cognitive decline:
  • hypothyroidism
  • hypercalcaemia
  • B12 deficiency
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7
Q

Diagnosis of Alzheimer’s dementia

A

Clinically but hippocampal atrophy on imaging is supportive

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8
Q

Macroscopic pathological features of Alzheimer disease

A
  • widespread cerebral atrophy esp. cortex + hippocampus
  • Global cortical atrophy
  • Sulcal widening
  • Gyri narrowing
  • Enlarged ventricles (primarily lateral + 3rd)
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9
Q

Microscopic pathological features of Alzheimer disease

A

Plaques
Tangles

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10
Q

What are Alzheimer plaques composed of?

A

Amyloid beta

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11
Q

What is amyloid precursor protein?
How is it normally broken down?
What pathology can occur?

A
  • A protein involved in repairing neurones after damage
  • Normally it is replaced + chopped up into soluble parts by a + gamma secretases
  • In Alzheimer disease, B secretase causes insoluble breakdown > formation of B amyloid plaques
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12
Q

How are plaques formed in Alzheimer disease?

A

Amyloid precursor protein is broken down by B secretase into insoluble parts > forming B amyloid plaques

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13
Q

Outline Alzheimer disease in relation to Tau tangle formation

A
  • B amyloid plaque induce pathological response in neuron > hyperphosphrylation of Tau proteins
  • change in shape of Tau proteins
  • reduced support of cytoskeleton
  • neuron death
  • aggregate into tangles
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14
Q

Function ofTau proteins

A

Play a role in stabilising microtubules within neuronal cytoskeleton

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15
Q

Types of Alzheimer disease

A

Sporadic (most common)
Familial

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16
Q

Outline sporadic Alzheimer disease

A
  • 90-95%
  • causes are poorly understood
  • increasing prevalence with age
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17
Q

Outline familial Alzheimer disease

A
  • 5-10%
  • early onset dementia
  • PSEN1/2 genes implicated > mutation of gamma secretase
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18
Q

Relationship between Down syndrome and Alzheimer disease

A

Disease can present as early as 40 years old

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19
Q

Symptoms of Alzheimer disease

A
  • initially symptoms hard to detect
  • short term memory loss initially
  • motor and language skills affected
  • long term memory loss
  • disorientation
20
Q

What is used to assess severity of dementia?

A

Mental state examination

21
Q

Treatment of Alzheimer disease

A
  • offer range of tailored activities to promote wellbeing
  • offer group cognitive stimulation therapy
  • Acetyl cholinesterase inhibitors donepezil, galatamine, rivastigmine
  • Memantine (NMDA glutamate receptor antagonist) for advanced cases
22
Q

Early symptoms of Lewy body dementia

A

Progressive cognitive symptoms:
- visual hallucination
- depression
- REM sleep disorders - sleep walking/talking
- symptoms can fluctuate

23
Q

Outline Lewy body dementia

A
  • dementia features early then Parkinsonian features - within 1 year of each other
  • caused by misfolding of alpha synuclein
  • misfolded aggregate into Lewy bodies
  • deposition into cortex (dementia type symptoms) + substantia nigra (Parkinsonian features)
24
Q

Late symptoms of Lewy body dementia

A

Parkinsonian symptoms:
- bradykinesia
- resting tremor
- stiffness

25
Treatment of Lewy body dementia
- Symptom based - Levodopa - acetylcholinesterase inhibitors *e.g. rivastigmine* - *memantine*
26
What is frontotemporal lobe dementia?
Frontal + temporal lobe atrophy Umbrella term for heterogeneous group of disease that can be characterised on the type of glial + neuronal proteinaceous inclusions or underlying genetic mutation
27
How does frontotemporal lobe dementia occur?
- aggregate proteins - Tau protein hyperphosphorylation (Pick’s disease) - frontal + temporal lobe atrophy
28
Features of frontotemporal lobe dementia
- onset before 65 - family history - insidious onset - behavioural + emotional changes - inappropriate social behaviour - loss of motivation without depression - broca type aphasia - relatively preserved memory
29
How does AIDs dementia occur?
- occurs when CD4+ count falls below threshold - entry of HIV infected macrophages into brain > inflammation + neuron damage
30
Clinical features of AIDs dementia
- congitive impairment - psychomotor retardation - tremor - ataxia - dysarthria - Incontience
31
Outline vascular dementia
Cognitive impairment caused by cerebrovascular disease (multiple small strokes)
32
Risk factors for vascular dementia
- previous stroke or MI - hypertension - hypercholesteroaemia - diabetes - smoking - AF - obesity - family history of stroke of CV disease
33
Types of vascular dementia
- **stroke related VD** - multi or single infarct - **subcortical VD** - caused by small vessel disease - **mixed dementia**: presence of VD + alzheimers disease
34
Presentation of vascular dementia
- focal neurological abnormalities *e.g. visual disturbances, sensory or motor symptoms* - difficulty with concentration or attention - seizures - memory disturbances - gait problems
35
Management of vascular dementia
- mainly symptomatic - detect + address CV risk factors to slow progression - cognitive stimulation programmes - clear communication - no pharmacological treatment unless signs of combined VS + alzheimers > AChE inhibitors
36
Difference between Parkinson’s disease + Lewy body dementia
- **Parkinson’s disease**: movement disorder followed by dementia - **Lewy body dementia**: dementia followed by movement disorder (Parkinsonism)
37
Why should you not give anti-psychotics *e.g. haloperidol* in Lewy body dementia?
It can cause neuroleptic malignant syndrome
38
Features of neuroleptic malignant syndrome
Fever Confusion Tachycardia Tachypnoea Fluctuating BP Elevated creatine phosphokinase Rigidity
39
What can be done to reduce the risk of developing dementia?
- exercise - mental stimulation *e..g more mentally challenging jobs* - maintain healthy weight - blood pressure control - blood glucose control
40
Memory screening tools recommended in non-specialist setting
**6CIT** - 6 item cognitive impairment test **10CS** - 10 point cognitive screener
41
Memory tests NOT recommended for non-specialist settings
**AMTs** **GPCOG** - GP assessment of cognition - **MMSE**: mini mental state exam
42
What type of dementia matches this presentation? Middle aged adults with insidious onset of dementia + personality changes/social disinhibition
Frontotemporal dementia
43
Macroscopic features of frontotemproal dementiaa
Atrophy of frontal and temporal lobes
44
What are the three acetlycholinesterase inhibitors for Alzheimer’s management?
- donepezil - galantamine - rivastigmine
45
What type of dementia is most likely to have fluctuating symptoms?
Lewy body dementia
46
What type of dementia is most likely to have visual distubrances?
Lewy body dementia