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NSB > Cognitive Impairment and Confused States > Flashcards

Cognitive Impairment and Confused States Flashcards

1
Q

What is cognition?

A

the mental processes involved in making sense of and learning about the world around us, including:

  • memory
  • attention
  • perception
  • knowledge
  • problem solving
  • judgement
  • language
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2
Q

Does cognition decline with age?

A
  • Crystallised cognitive abilities are well
    preserved hence will not decline (as much):
    - cumulative skills and memories;
    preserved on tests of general knowledge
  • Fluid cognitive abilities:
    - processing new info to quickly solve
    problems
    - linear decline from the age of 20
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3
Q

When might young adults without health problems experience cognitive impairment?

A
  • acute illnesses
  • post-surgery
  • sleep deprivation
  • extreme exercise
  • alcohol
  • drugs
  • depression
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4
Q

Delirium: Key Features (4):

A
  • ***acute onset of confusion
  • impairment of attention and awareness
  • fluctuating
  • often worse in the evening
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5
Q

Delirium: Causes:

A
  • usually caused by systemic illness
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6
Q

Delirium: Clinical Features:

A
  • impaired awareness, attention and
    concentration
  • disorientation (person, time, place)
  • memories may be preserved
  • hallucinations, especially visual
  • delusions (complex and distressing)
  • anxious, low, labile mood
  • Behaviour: hyperactive, hypoactive, mixed
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7
Q

Hyperactive Behaviour:

A
  • agitation
  • pacing
  • aggression
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8
Q

Hypoactive Behaviour:

A
  • reduced movement
  • appetite
  • withdrawn
  • sleepy
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9
Q

Mixed Behaviour:

A
  • fluctuates between hypo- and hyper-active
    behaviours
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10
Q

Delirium affects what % of hospital inpatients?

A

> 20%

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11
Q

High prevalence of delirium in:

A
  • up to half of elderly inpatients
  • high prevalence in ITU patients
  • if hospitalised with delirium, two fold
    increased of mortality after
  • often don’t return to full cognition despite
    being classed as reversible
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11
Q

Which of the following is not a risk factor for delirium?

  • older age
  • younger age
  • multiple morbidities/frailties
  • polypharmacy
  • learning disabilities
  • dementia
  • sensory impairment
A

learning disabilties

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12
Q

How can delirium be prevented (7)?

A
  • early detection and treatment of any
    infection
  • orientation
  • preventing dehydration and constipation
  • maximise healthy sleep patterns
  • encourage mobility where possible
  • manage pain well
  • ensure good nutrition (dentures)
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13
Q

Delirium: Management:

A
  • treat underlying cause
  • calm, quiet environment
  • regular reorientation
  • consistent routine
  • promote healthy sleep pattern
  • appropriate lighting
  • aggression meds if needed
  • MDT follow up
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14
Q

What is dementia?

A
  • group of progressive, neurodegenerative
    brain disorders
  • impairment in memory, thinking and
    behaviour that interferes with a person’s
    daily activities
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15
Q

Dementia Terminology:

A
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16
Q

Prevalence of dementia related with ages:

A
  • 1 in 100 people (65-69yrs)
  • 1 in 25 people (70-79yrs)
  • 1 in 6 people (+80yrs)
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17
Q

What % of people living in care homes have dementia?

A

70%

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18
Q

Delirium is the main cause of disability later in life.

True or False?

A

False

Dementia is the main cause of disability later in life

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19
Q

Difference between delirium and dementia.

A
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20
Q

Main types of dementia:

A
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21
Q

Dementia: Pathology:

A
  • misfolding of proteins: amyloid, tau, synuclein
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22
Q

Which misfolding of proteins occur in Alzheimer’s disease?

A
  • amyloid
  • tau
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23
Q

Which misfolding of proteins occur in Parkinson’s disease?

A
  • synuclein
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24
Q

Which misfolding of proteins occur in Alzheimer’s disease?

A
  • amyloid
  • tau
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25
Q

Dementia: Assessment:

A
  • no single diagnostic test
  • clinical history
  • physical examination (neuro)
  • basic blood tests: FBC, U&E, LFTs, Thyroid, Ca2+,
    Glucose, B12, folate, ESR
  • neuroimaging: CT, MRI, advanced imaging
  • cognitive testing
  • lumbar puncture sometimes (young onsert)
26
Q

Alzheimer’s Disease:
- incidence
- survival from diagnosis

A
  • most common form of dementia (62%)
  • 4-20 years
27
Q

Alzheimer’s: Pathophysiology:

A
  • amyloid cascade hypothesis
  • amyloid plaques are an insoluble protein that is
    extracellulary deposits
  • Neurofibrillary Tangles (intracellular)
    - Tau = normal intracellular proteins, binds to
    microtubules, supports axonal transport,
    maintenance of cytoskeleton
    - abnormal phosphorylation: paired helixes,
    neurofibrillary tangles
  • reduced cholinergic activity in cortex
28
Q

Amyloid Cascade Hypothesis:

A

Beta-Amyloid is cleaved from a transmembrane protein called amyloid precursor protein (APP).

APP is usually broken down into non--amyloid peptides by what has been called the -secretase pathway.

The amyloid cascade hypothesis suggests that there is more breakdown of APP by other pathways (called - and -secretase pathways), leading to overproduction of -amyloid.

-Amyloid is insoluble and is normally cleared from the brain via several different mechanisms. Overproduction results in aggregation and plaque formation.

29
Q

Alzheimer’s: Clinical Features:

A
  • amnesia: short-term impairment, later affects
    long-term memory
  • disorientation
  • apraxia (loss of motor skills)
  • agnosia (disturbances in recognition of objects
    and faces)
  • difficulty in performing complex tasks: planning,
    organisation, sequencing, abstraction
  • behavioural and psychological disturbances
30
Q

Genetic Causes of Alzheimer’s Disease:

A
  • complicated, generally different for young and
    late onset
  • young onset clusters withing families are rare
  • mutations in the amyloid precursor protein
    (APP) genes and two presenillin genes (PSEN-1
    and PSEN-2), autosomal dominant
  • late onset = more complex
  • small but growing number of risk genes but are
    NOT mutations
31
Q

What is the largest known risk factor (genetic) of late onset alzheimer’s?

A
  • apolipoprotein epsilon4
32
Q

Alzheimer’s disease: Investigation:

A
  • most important factor = history
  • cognitive testing is helpful
  • CT/MRI: global cortical atrophy, hippocampal
    atrophy
  • lumbar puncture@ beta-amyloid ratios in csf,
    other measures
  • amyloid PET
33
Q

Vascular Dementia is caused by

A

cerebrovascular disease

34
Q

Vascular Dementia: Clinical Features:

A
  • diverse presentation
  • classically stepwise progression: rarely seen,
    gradual decline also possible, abrupt onset can
    occur
  • focal neurology may be present
  • patchy cognitive impairment
  • slowing of gait and falls
35
Q

Dementia with Lewy bodies & Parkinson’s Dementia:

A
  • both conditions are cause by Lewy bodies:
    • intracellular inclusions
    • alpha-synuclein
    • subcortical lewy bodies in parkinson’s
    • cortical lewy bodies in dementia with lewy
      bodies
  • DLB diagnosed if congitive symptoms onset
    before or about same time as movement
    symptoms; not everyone develops movement
    symptoms
36
Q

Dementia with Lewy Bodies: Core Features:

A
  • one or more of cardinal motor features of
    Parkinson’s Disease
  • visual hallucinations
  • marked fluctuations in cognition and alertness
  • REM sleep behaviour disorder
37
Q

Note for patients of dementia with Lewy Bodies:

A
  • high sensitivity to antipsychotic medication
  • risk of falls
38
Q

Dementia with Lewy Bodies: Investigations:

A
  • MRI/CT often normal, may atrophy
  • SPECT imaging using a ligand for the dopamine
    transported protein has high sensitivity and
    specificity
39
Q

What is Frontotemporal Dementia (FTD)?

A
  • diverse group of conditions that are collectively
    a common cause of young onset dementia
  • selective progressive atrophy involving the
    frontal or temporal lobes or both
  • aka frontotemporal lobar degeneration
40
Q

Frontotemporal Dementia (FTD): Pathology:

A
  • three major pathogenic proteins:
    • phosphorylated Tau
    • Transactive response DNA-binding protein 43
      (TDP-43)
    • Fused in sarcoma protein (FUS)

not needed knowledge

41
Q

What is Pick’s disease?

A

type of FTD caused by Tau

42
Q

Frontotemporal Dementia (FTD): Risk groups:

A
  • 4-15 per 100,000 under 65 West
  • onset typically 50s-60s but varies
43
Q

Causes of Frontotemporal Dementia (FTD:)

A
  • often genetic
  • can be sporadic
44
Q

Frontotemporal Dementia (FTD): Two Variants:

A
  • behavioural variant (frontal lobe)
  • language variant (temporal lobe)
45
Q

Behavioural Frontotemporal Dementia: Clinical Features:

A
  • frontal lobe affected
  • affects personality or behaviour
  • relative preservation of memory
  • often misdiagnosed as psychiatric condition or
    personality disorder
46
Q

Language Frontotemporal Dementia (FTD): Clinical Features:

A
  • temporal lobe affected
  • affects language
  • different subtypes affect language differently
47
Q

Frontotemporal Dementia (FTD): Investigations:

A
  • MRI/CT: frontal/temporal lobe atrophy
  • amyloid-PET negative
  • perfusion studies (FDG-PET): reduced perfusion
    in frontal/temporal lobes
  • Lumbar Puncture: normal alzheimer’s
    biomarkers, elevated neurofilament light
  • Genetics Testing: specific mutation identification
48
Q

Dementia: Behavioural and Psychological Symptoms:

A
  • cognitive impairment
  • disturbed perception
  • disturbed thought content
  • disturbed mood
  • disturbed behaviour
49
Q

Dementia: Management:

A
  • psychological and social support (particularly
    isolation)
  • some meds: cholinesterase inhibitors,
    memantine
  • mild-dementia do not need dementia-specific
    services
50
Q

Dementia: Practical and Social Interventions:

A
  • care package
  • OT assessments
  • daycentres and clubs
  • one to one support
  • sitting services
  • carer support
51
Q

Dementia: Psychological Interventions:

A
  • pre and post diagnostic support
  • cognitive stimulation therapy
  • individual and group work
52
Q

Cognitive Stimulation Therapy:

A
  • can improve cognition
  • ## mainly evidenced for mild dementia
53
Q

Dementia: Post-diagnosis support groups: How many sessions?

A

4-6 sessions

54
Q

Medications for cognitive symptoms of dementia:

A
  • symptomatic treatments to reduce rate of
    decline, modest effects
  • Cholinesterase Inhibitors: block breakdown of
    ach, helpful for mild to moderate dementia in
    Alzheimer’s
  • Alzheimer’s leads to loss of cells and nerve
    endings that produce ach, so there is less
    available
  • Memantine: moderate to severe dementia in
    Alzheimer’s disease
    • excess glutamate activates NMDA receptors
      • increases Ca2+ influx
      • leads to cell death
    • memantine blocks receptors to reduce
      glutamate mediated excitotoxicity
55
Q

What medications are licensed for use in dementia?

A
56
Q

There are many medications that are effective in managing behavioural and psychological symptoms of dementia (BPSD).

True or False?

A

False
medications have a very small role to play
often furthers effects of polypharmacy

57
Q

Dementia: Depression:

A
  • antidepressants are not effective for treating
    depression in dementia in most cases
  • may reduce impulsivity in frontotemporal
    dementia
  • sometimes used for the bejvioural symptoms
58
Q

Antipsychotic use in dementia treatment:

A
  • massive initiative to reduce prescribing due to
    risk of stroke and mortality
  • used in very specific situations
59
Q

Sedative medication in dementia treatment:

A
  • benzodiazepines
  • generally avoided due to risk of adverse effects
60
Q

What is shown below?

insert picture

A

Cortical atrophy of the temporal/frontal lobe

FTD

61
Q

Young Onset Dementia:

A
  • <65 year old onset
  • atypical presentatons
  • rare and genetic causes more frequent
  • typically takes 4.4 years from symptom onset to
    diagnosis compared to 2.2 in late onset
    dementia
  • very few specialist service that can be used
62
Q

Can we prevent dementia?

A
  • may risk factors are modifiable:
    - limited education
    - hypertension
    - obesity
    - hearing loss
    - smoking
    - diabetes
    - depression
    • social isolation
63
Q

What is cognitive reserve?

A
  • higher level of cognitive function reduces risk of
    dementia
  • brain more able to compensate for pathological
    changes
  • cognitive reserve linked to number of years of
    education
  • cognitively stimulating activity as adults can
    boost cognitive reserve

NSB (50 decks)

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