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CSI > CSI 4: Mild Cognitive Impairment > Flashcards

CSI 4: Mild Cognitive Impairment Flashcards

1
Q

Describe MCI

A

→ Minor problems with cognition
→ Affects around 5-20% over 65s
→ Puts person at greater risk of developing dementia
→ Not guaranteed though (only 5-15% of those with MCI and gradual memory loss develop dementia)

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2
Q

Similarities between MCI and dementia [3]

A

→ Both impact a person’s cognitive abilities
→ Neither impact a person’s consciousness
→ Both can have a big impact on a person’s daily living

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3
Q

Differences between MCI and dementia [3]

A

MCI - may be a normal part of ageing
Dementia - definitely not a part of normal aging

MCI - describes a set of symptoms not a disease which do not always have and underlying cause
Dementia - Chronic syndrome resulting from a variety of diseases and illness

MCI - No drugs approved for treatment
Dementia - Drugs are available

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4
Q

What do MCI symptoms usually affect?

A

→ Memory
→ Reasoning
→ Planning and problem solving
→ Attention
→ Language
→ Visual depth perception

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5
Q

How can you reduce risk of developing dementia?

A

→ Physical activity
→ Mediterranean diet
→ Not smoking
→ Not drinking to excess
→ Remaining socially active
→ Engaging in cognitive stimulation
→ Prompt treatment of infection or depression

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6
Q

How do we diagnose MCI?

A

Six item cognitive impairment test
→ Responses translate to a score, which determines whether to refer them or not

0-7 Normal → Referral not necessary
8-9 MCI → Probably refer
10-28 Severe Cognitive Impairment → Refer

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7
Q

What are the benefits of the 6-CIT?

A

Quick, easy to implement, doesn’t have any cultural references

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8
Q

What does the 6-CIT test?

A

Orientation, short-term memory, attention and focus

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9
Q

Define a multidisciplinary team

A

Combination of professionals from different clinical disciplines and specific expertise that work together to optimise a patient’s care

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10
Q

What would a MDT for patient with dementia look like?

A
  1. Dementia social worker - make sure patient is well supported and safe at home
  2. Dietician - assess patient’s diet and suggests any necessary modifications
  3. Carers - update staff on how patient is on a day to day basis
  4. Volunteer - company to patients, offered by charities
  5. Specialist nurse - expertise in dementia, administer medications, help suggest ways to prevent forgetting
  6. Occupational therapist - assess safety of a patient’s home environment and suggest modifications e.g. to avoid falls, stair lift
  7. Consultant - make diagnosis and monitor clinical progression
  8. Physiotherapist - help patients with mobility issues and recommend exercises to minimise fall risks
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11
Q

Define capacity

A

The ability to use and understand information to make a decision and communicate any decision made

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12
Q

What is the Mental Capacity Act?

A

Applies to anyone over 16
→ Protects people who may lack capacity to make their own decisions as far as possible

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13
Q

The MCA says a person is unable to make a decision for themselves if they can’t:

A

→ Understand information relevant to decision
→ Retain that information i.e. recall it and communicate it back
→ Use or weigh up the information as part of the decision making process

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14
Q

What does the MCA allow for, if someone lacks capacity?

A

→ People can appoint a trusted person to make decisions on their behalf in the future and provides an independent advocate to support them in situations when serious restrictions are being put on their rights and freedom

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15
Q

How does the MCA assess capacity?

A

Assume everyone has capacity until proven otherwise

  1. Does the person have an impairment of their mind or brain, whether as a result of an illness or external factor e.g. drug use?
  2. Does this impairment mean the person is unable to make a specific decision when they need to?

Time and situation dependent

No to either → patient can make decision
Yes to both → patient’s medical team decided what is in their best interest

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16
Q

Examples of people who may lack capacity

A

→ Dementia

→ Severe learning disability

→ Brain injury

→ Mental health illness

→ Stroke

→ Unconsciousness due to anaesthesia or sudden accident

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17
Q

How is the nature of capacity both time and situation dependent?

A

Someone may lack capacity to make decisions about complex relationships but have capacity to decide what groceries to get

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18
Q

What does deciding to withdraw someone’s capacity involve?

A

Two doctors must independently assess a patient and agree

Emergencies → decisions last for 24h before needing review

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19
Q

Key consideration when deciding treatment and care on a patient’s behalf

A

The least restrictive option i.e. it would interfere the least with their basic rights and freedom

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20
Q

Options before losing capacity

A
  1. Advance statement
  2. Advance decision
  3. Legal power of attorney
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21
Q

Advance statement

A

A written statement that sets down a person’s preferences, wishes, beliefs and values regarding their future care

→ Not legally binding but acts as a guide for anyone who might need to make decisions in their best interest if they lose capacity

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22
Q

Advance decision

A

A legally binding decision that allows someone over 18 to refuse specified medical treatment for a time in the future where they may lack capacity to consent or refuse that treatment.

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23
Q

Legal Power of Attorney

A

Enables another person to make decisions about a patient’s health and welfare or properties and financial affairs on their behalf should they lose capacity

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24
Q

4 main types of dementia

A

→ Alzheimer’s dementia

→ Vascular dementia

→ Lewy body dementia

→ Frontotemporal dementia

25
Q

What is Alzheimer’s?

A

Chronic, neurodegenerative disease with progressive and insidious onset
(Slow cognitive decline)

→ Memory impairment comes first

26
Q

What changes do you see as Alzheimer’s progresses?

A

→ Language deficits

→ Impaired visuopatial skills

→ Loss of judgement

→ Inability to conduct daily activities

27
Q

Symptoms attributed to AD [6]

A

→ Amnesia - loss of short term memory

→ Anomia → inability to name objects

→ Apraxia → loss of dexterity

→ Agnosia → inability to recognise things, unable to understand the function of objects

→ Aphasia → inability to talk

→ Misplacing items, forgetting recent events, names and becoming repetitive, uncertainty about date, increased anxiety, irritability

28
Q

What is vascular dementia?

A

Persistent disruption to blood supply due to diseased vessels and multiple infarcts within minor blood vessels

→ Mini strokes in brain cause a very noticeable region-specific function each time - “Stepwise progression”

→ Focal ‘localised’ neurology

Affects to 5-10% of people with dementia

29
Q

What could be the causes of vascular dementia?

A

Hypertension, atherosclerosis, diabetes

E.g. athlerosclerosis → contributes to vascular occlusion and transient ischaemic attacks TAI stroke

30
Q

Symptoms of vascular dementia

A

similar to alzheimer’s

→ Slower thinking

→ Personality changes

→ Movement problems e.g. gait disturbance

→ Bladder problems

31
Q

What is Lewy Body dementia?

A

→ Aberrant deposits of alpha-synuclein protein within the brain, predominantly the primary motor cortex

→ Progressive and insidious onset

→ Similar to Parkinson’s

32
Q

Symptoms of Lewy-Body Dementia

A

→ Visual halluncinations

→ Sleep problems (esp. REM)

→ Memory

→ Movement impairments (cogwheel link rigidity), tremor (Parkinsonian)

→ Fluctuating awareness, attention, ability to regcognise family members

33
Q

Treatment for Lewy-Body dementia

A

Acetylcholinesterase inhibitors

34
Q

What is fronto-temporal dementia?

A

Neuronal atrophy of frontal and temporal lobes due to presence of abnormal proteins within them

→ Chronic and progressive disease

→ Earlier and more rapid onset

Similar incidence to LBD

35
Q

What abnormal proteins are associated with frontotemporal dementia?

A

Phosphorylated tau
Transactive response DNA-binding protein 43 → TDP-43

36
Q

Inheritance pattern of frontotemporal dementia

A

→ Autosomal dominant

→ Identifiable disease-causing mutations in a third of those affected
→ Mutations associated with microtubule associated tau or progranulin genes

37
Q

Symptoms of frontotemporal dementia

A

→ Frontal lobe - speech problems, behavioural changes, emotional problems, disinhibition

→ Temporal lobe → language affected, semantic dementia → progressive non-fluent aphasia

→ Obsessions

→ Diet → changes in food preferences

→ Lack of interest - lack of taking care of themselves

38
Q

What does the limbic system consist of?

A

Cingulate gyrus (connected to the temporal lobe by cingulum - bundle of neurones-), amygdala, hippocampus, mammillary body

39
Q

What is the posterior cingulate cortex associated with?

A

Orientation (time, place, identity)
(What year, month, time is it?)

40
Q

What is the hippocampus associated with?

A

Short term memory
(Repeat the address)

41
Q

What is the anterior thalamus associated with?

A

Attention
(counting backwards)

42
Q

2 proteins central to dementia’s pathophysiology

A

→ Amyloid precursor protein → extracellular amyloid plaques

→ Tau proteins → intracellular neurofibrillary tangles

43
Q

What is APP?

A

Transmembrane protein assisting in neuronal repair and growth

44
Q

What is APP typically cleaved by?

A

Alpha secretase

45
Q

In AD, what happens differently to APP?

A

→ Aberrant cleavage of APP by beta and gamma secretases

→ Results in surplus of amyloid beta

46
Q

What do amyloid-beta peptides do?

A

They aggregate into oligomers and then fibrils with beta-sheet pairing

→ These diffuse out of cell and deposit as insoluble senile plaques

47
Q

Genetic predisposition for extracellular amyloid plaques

A

Mutations in genes encoding for amyloid precursor protein (Presenilin 1 and 2, ApoE) → increased risk of AD

48
Q

What do amyloid plaques cause?

A

Interference with neuronal communication, inflammation

49
Q

What is the role of Tau protein?

A

Involved in assembly of microtubules, essential for neuronal growth and development

50
Q

How are Tau proteins involved in the pathophysiology of dementia?

A

Hyperphosphorylation causes the protein to oligomerise and aggregates into filamentous neuro-fibrillary tangles NFTs

51
Q

What effects do NFTs have?

A

NFTs disrupt the microtubular systems → impaired neuronal growth, transport and communication

52
Q

Where do NFTs tend to deposit?

A

Hippocampus, medial temporal lobe, frontal cortices and lateral parietotemporal regions
Distinct pathogenesis of Alzheimer’s

53
Q

What do Tau gene mutations cause?

A

Familial frontotemporal dementia

54
Q

Is there a correlation between disease severity and location/density of abnormal protein deposit?

A

NFT - yes both density and location of NFTs correlates to diseases severity
Extracellular amyloid plaques - found in people without dementia too, so not so much

55
Q

How are amyloid-beta plaques related to tau proteins?

A

Amyloid-beta plaques triggers tau phosphorylation, dissociating from the microtubules, accumulating into NFTS.

→ Reduction in neuronal function and apoptosis (atrophy)

*Also amyloid-beta peptides might only be toxic in the presence of NFTs

56
Q

Impacts of NFTs and EAPs on brain

A

→ Loss of synapses and neurones (esp. in nucleus basalis of Meynert)

→ Cerebro-cortical atrophy

→ Deficiency of ACh due to death of neurones which supply hippocampus, neocortex, amygdala (rich in ACh) → loss of memory function

→ Reduction in serotonin and NA levels due to loss of neurones in brainstem’s median raphe and locus ceruleus neurones → effects on mood and sleep

57
Q

What is indicative of Alzheimer’s on MRI scans?

A

Dark circles → cholinergic neuronal atrophy

58
Q

Treatment for Alzheimer’s

A

Acetylcholinesterase inhibitors e.g. Donepezil

CSI (4 decks)

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