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AIP: Acute confusional state > Acute on chronic dementia > Flashcards

Acute on chronic dementia Flashcards

1
Q

What is the most common cause of dementia in the UK?

A

Alzheimer’s disease (followed by Vascular and Lewy Body dementia)

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2
Q

What are the 2 assessment tools recommended by NICE for the non-specialist assessment for dementia?

A
  1. 10-point cognitive screener (10-CS)
  2. 6-item cognitive impairment test (6CIT)
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3
Q

What are 3 assessment tools not recommended for use by NICE for the non-specialist setting that can be used to assess cognition in a patient?

A
  1. AMTS
  2. General practitioner assessment of cognition (GPCOG)
  3. Mini-mental state examination (MMSE)
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4
Q

What MMSE score (despite not being recommended by NICE to screen for dementia) suggests dementia?

A

24 or less out of 30

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5
Q

What are 8 blood tests recommended by NICE to perform in suspected dementia, to exclude reversible causes?

A
  1. FBC
  2. U+Es
  3. LFTs
  4. Calcium
  5. Glucose
  6. TFTs
  7. Vitmain B12
  8. Folate
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6
Q

To which service are patients with suspected dementia commonly referred on to from primary care?

A

old-age psychiatrists, sometimes working in ‘memory clinics’

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7
Q

What investigation is performed in suspected dementia in secondary care and why?

A

Neuroimaging (structural imaging essential in investigation of dementia)

to exclude reversbile conditions e.g. subdural haematoma, normal pressure hydrocephalus, and help provide information on aetiology to guide prognosis and management

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8
Q

After the 3 commonest causes of dementia, what are 4 rare causes?

A
  1. Huntington’s disease
  2. Creutzfeldt-Jakob disease
  3. Pick’s disease (atrophy of frontal and temporal lobes)
  4. HIV
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9
Q

What is Pick’s disease?

A

atrophy of frontal and temporal lobes

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10
Q

What proportion of AIDS patients suffer from dementia?

A

50%

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11
Q

What are 9 potentially treatable differentials when considering a diagnosis of dementia?

A
  1. Hypothyroidism
  2. Addison’s
  3. B12/folate/thiamine deficiency
  4. Syphilis
  5. Brain tumour
  6. Normal pressure hydrocephalus
  7. Subdural haematoma
  8. Depression
  9. chronic drug use e.g. alcohol, barbiturates
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12
Q

What spectrum is vascular dementia considered part of?

A

vascular cognitive impairment (VCI) - spectrum of deficits

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13
Q

What proportion of dementia is accounted for by vascular dementia?

A

17% in UK

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14
Q

What effect dose stroke have on the risk of developing dementia?

A

doubles risk

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15
Q

What are the 3 main subtypes of vascular dementia?

A
  1. Stroke-related vascular dementia - multi-infarct or single-infarct dementia
  2. Subcortical vascular dementia - caused by small vessel disease
  3. Mixed dementia - presence of both vascular dementia and Alzheimer’s disease
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16
Q

What are 9 risk factors for vascular dementia?

A
  1. History of stroke or transient ischaemic attack (TIA)
  2. Atrial fibrillation
  3. Hypertension
  4. Diabetes mellitus
  5. Hyperlipidaemia
  6. Smoking
  7. Obesity
  8. Coronary heart disease
  9. FH of stroke or cardiovascular disease
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17
Q

What is a rare condition in which vascular dementia can be inherited?

A

CADASIL: cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

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18
Q

What is the typical presentation of vascular dementia?

A

several months or years of a history of sudden or stepwise deterioration of cognitive function

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19
Q

What are 7 features of the presentation of vascular dementia?

A
  1. Focal neurological abnormalities e.g. visual disturbance, motor or sensory symptoms
  2. Difficulty with attention and concentration
  3. Seizures
  4. Memory disturbance
  5. Gait disturbance
  6. Speech disturbance
  7. Emotional disturbance
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20
Q

What are 4 requirements for a diagnosis of vascular dementia?

A
  1. Comprehensive history and physical examination
  2. Formal screen for cognitive impairment
  3. Medical review to exclude medical cause of cognitivee decline
  4. MRI scan - may show infarcts and extensive white matter changes
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21
Q

What does NICE recommend that a diagnosis of vascular dementia is formally made based on?

A

NINDS-AIREN criteria for probably vascular dementia

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22
Q

What are the 3 broad aspects of the NINDS-AIREN criteria for probable vascular dementia?

A
  1. Presence of cognitive decline that interferes with activities of daily living
  2. Cerebrovascular disease - neuro signs and/or brain imaging
  3. Relationship between above two disorders inferred by:
    • onset of dementia within 3 months following recognised stroke
    • abrupt deterioration in cognitive functions
    • fluctuating, stepwise progression of cognitive deficits
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23
Q

How is the presence of cognitive decline that interferes with ADLs establishing, based on the NINDS-AIREN criteria for probable vascular dementia?

A

clinical examination and neuropsychological testing

not secondary to cerebrovascular event

24
Q

What are 3 things that imply a relationship between presence of cognitive decline and cerebrovascular disease?

A
  1. Onset of dementia within three months following a recognised stroke
  2. Abrupt deterioration in cognitive functions
  3. Fluctuating, stepwise progression of cognitive deficits
25
Q

What is the general management of vascular dementia?

A
  • symptomatic treatment, addressing individual problems and providing support to patient and carers
  • detect and address cardiovascular risk factors - for slowing down the progression
26
Q

What are 3 aspects of the non-pharmacological management of vascular dementia?

A
  1. tailored to individual
  2. includes: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
  3. managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
27
Q

When is the only time pharmacological management should be considered for vascular dementia?

A

only consider AChE inhibitors or memantine for people with vaascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or Lewy body dementia

28
Q

What are 3 types of causes of Alzheimer’s dementia?

A
  1. Most cases are sporadic
  2. mutations in amyloid precursor protein (APP) (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) thought to cause inherited form
  3. Apoprotein E allele E4 - encodes cholesterol transport protein
29
Q

What proportion of cases of Alzheimer’s disease are inherited?

A

5%

30
Q

What is the inheritance pattern of inherited Alzheimer’s disease?

A

Autosomal dominant

31
Q

What is a risk factor for Alzheimer’s dementia?

A

Down syndrome

32
Q

What are the macroscopic pathological changes which occur in Alzheimer’s disease?

A

widespread cerebral atrophy, particularly involving cortex and hippocampus

33
Q

What are the microscopic pathological changes which occur in Alzheimer’s disease? 2 key things

A
  1. cortical plaques due to deposition of type A-beta amyloid protein - amyloid plaques
  2. intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
34
Q

What causes amyloid plaques in Alzheimer’s dementia?

A

deposition of type A-beta-amyloid protein

35
Q

What causes neurofibrillary tangles in Alzheimer’s dementia?

A

intraneuronal tangles caused by abnormal aggregation of tau protein

hyperphosphorylation of tau protein has been linked to AD

36
Q

What biochemical changes occur in Alzheimer’s disease?

A

deficit of acetylcholine from damage to an ascending forebrain projection

37
Q

How do tau proteins form neurofibrillary tangles in AD?

A
  • paired helical filaments are partly made from a protein called tau
  • tau is a protein that interacts with tubulin to stabilise microtubules and promote tubulin assembly into microtubules
  • in AD tau proteins are excessively phosphorylated, impairing the function
38
Q

What are 3 aspects of non-pharmacological management of AD?

A
  1. Offer range of activities to promote wellbeing that are tailored to person’s preference
  2. Offer group cognitive stimulation therapy for patients with mild and moderate dementia
  3. Consider group reminiscence therapy and cognitive rehabilitation
39
Q

What are 4 drugs options for Alzheimer’s disease?

A
  1. Donepezil
  2. Galantamine
  3. Rivastigmine
    • these are the first line options for mild-moderate AD. Acetylcholinesterase inhibitors
  4. Memantine
    • NMDA receptor antagonist - second line for moderate
    • add on or single therapy for severe Azheimer’s
40
Q

What class of drugs do donepezil, galantamine and rivastigmine fall into and when are they used in Alzheimer’s disease?

A
  • Acetylcholinesterase inhibitors
  • for the management of mild to moderate Alzheimer’s disease
41
Q

What class of drug is memantine and when is it used in Alzheimer’s disease?

A
  • NMDA receptor antagonist
  • second-line treatment for Alzheimer’s
    • for moderate AD for patient’s who are intolerance of or have a CI to acetylcholinesterase inhibitors
    • add-on in severe AD
    • monotherapy in severe AD
42
Q

What is the NICE recommendation for managing depression in Alzheimer’s dementia?

A

do not recommend antidepressants for mild to moderate depression

43
Q

What do NICE recommend about the use of antipsychotics in Alzheimer’s dementia?

A

only for patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress

44
Q

When is donepezil contraindicated?

A

relatively contraindicated in patients with bradycardia

45
Q

What is one of the adverse effects of donepezil?

A

insomnia

46
Q

What proportion of cases of dementia is accounted for by Lewy body dementia?

A

20%

47
Q

What is the characteristic pathological feature of Lewy body dementia?

A

alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas

48
Q

Why is the relationsip between Parkinson’s disease and Lewy body dementia complicated?

A

dementia is often seen in Parkinson’s disease, and up to 40% of patients with Alzheimer’s disease have Lewy bodies

49
Q

What are 3 key features of the presentation of Lewy body dementia?

A
  1. Progressive cognitive impairment - early impairment in attention + executive function
  2. Parkinsonism
  3. Visual hallucinations (± delusions and non-visual hallucinations)
50
Q

What are 2 ways that the progressive cognitive impairment of Lewy body dementia differs from Alzheimer’s dementia?

A
  1. Early impairments in attention and executive function rather than just memory loss occur
  2. Cognition may be fluctuating in LBD unlike other forms of dementia
51
Q

When does progressive cognitive impairment occur in LBD in relation to parkinsonism?

A

the cognitive impairment usually develops before parkinsonism

52
Q

What is a diagnosis of Lewy Body dementia typically made based on?

A

clinical diagnosis usually

53
Q

What investigation is increasingly used to aid the diagnosis of Lewy Body dementia?

A

single-photon emission computed tomography (SPECT) increasingly used - commercially konwn as a DaTscan

[Dopaminergic iodine-123-radiolabelled 2-carbomethoxy-3-(4-iodophenyl)-N-(3-fluoropropyl) nortropane (123-I FP-CIT) is used as the radioisotope]

54
Q

What is the sensitivity + specificity of SPECT in diagnosing Lewy body dementia?

A

sensitivity 90%, specificity 100%

55
Q

What is the management of Lewy body dementia?

A

acetylcholinesterase inhibitors and memantine can be used, as in Alzheimer’s

56
Q

Which drugs should be particularly avoided in Lewy body dementia and why?

A

Neuroleptics - patients are extremely sensitive and may develop irreversible parkinsonism

(can deteriorate rapidly following introduction of an antipsychotic agent)

AIP: Acute confusional state (14 decks)

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