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Year 3 Exam 2 > Dementia > Flashcards

Dementia Flashcards

1
Q

Definition of dementia

A

A group of chronic, progressive, degenerative organic brain disorders all with a common characteristic: Continuous deterioration in cognitive function leading to a gradual decrease in intellectual capacity.

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2
Q

Clinical features of dementia

A
  • Impaired memory and poor cognitive function
  • Impaired thinking
  • Disturbed behaviour
  • Lack of insight
  • Lack of spontaneity
  • Poverty of speech
  • Low mood
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3
Q

What are features of impaired memory and poor cognitive function?

A
  • Forgetfulness
  • Poor attention
  • Disorientation in time and place
  • Agnosia (not recognising objects, people or themselves)
  • Dysphasia (not remembering names of things)
  • Dyspraxia (not understanding commands)
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4
Q

What are features of impaired thinking?

A
  • Slow
  • Impoverished
  • Incoherent
  • Rigid
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5
Q

What are features of disturbed behaviour?

A
  • Disorganised
  • Inappropriate
  • Distracted
  • Restless
  • Antisocial
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6
Q

What are the risk factors of someone developing dementia?

A
  • Older age
  • Poor cognitive performance
  • Low BMI or overweight
  • Slow physical performance
  • Not eating vegetables
  • Lack of alcohol consumption
  • Diabetes
  • Depression and bipolar
  • apoE4
  • MRI showing white matter disease
  • Ventricular enlargement
  • Carotid artery thickening
  • History of bypass surgery
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7
Q

What is the survival rate of dementia?

A

5-8 years from diagnosis

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8
Q

What are the 6 types of dementia?

A
  • Alzheimer’s disease
  • Lewy Body dementia
  • Vascular dementia
  • Frontotemporal dementia
  • Mixed
    -Other e.g. Parkinson’s/ Huntington’s related dementia, Brain injury, HIV infection
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9
Q

What is the most common type of dementia?

A

Alzheimer’s disease 50-60% of cases

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10
Q

Symptoms of the early stages of Alzheimer’s disease (1-3 years)

A
  • Language difficulties
  • Depression
  • Losing direction when out and about
  • Recent memory impairment and forgetting names
  • Increased number of accidents whilst driving
  • Impaired activity of daily living
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11
Q

Symptoms of mid stage Alzheimer’s disease (2-7 years)

A
  • Aphasia (not recognising objects, people, themselves)
  • Amnesia
  • Inability to bathe, eat, toilet or dress without assistance
  • Inability to calculate solutions and problem solve
  • Behavioural and psychiatric changes
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12
Q

Symptoms of late stage Alzheimer’s disease (years 7+)

A
  • Seizures
  • Short and long term memory loss
  • Double incontinence
  • Mutism or nonsensical speech
  • Complete dependence on others
  • Rigid posture
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13
Q

Onset and progression of Alzheimer’s disease?

A

Gradual onset and continual decline

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14
Q

Onset and progression of Vascular dementia?

A

Sudden onset followed by a step wise progression
Onset is usually around late 60s-70s

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15
Q

What are the focal neurological signs of vascular dementia? (not present in AD)

A
  • Gait disturbance (Shuffling gait)
  • Weakness of extremities
  • Extensor plantar response
  • Pseudobulbar palsy
  • Exaggeration of deep tension reflexes
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16
Q

Onset and progression in Lewy body dementia?

A

Progressive cognitive decline, especially in attention and visuospatial ability

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17
Q

What are the key features of Vascular dementia?

A
  • Emergence of emotional and personality changes, followed by memory impairment
  • Apraxia
  • Agnosia
  • Dysarthria
  • Dizziness
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18
Q

What is apraxia?

A

The inability to perform voluntary motor tasks or movements even though the person has the physical ability to do so.

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19
Q

What is agnosia?

A

The inability to recognise and identify objects, people or sounds despite their senses being otherwise functional.

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20
Q

What is dysarthria?

A

Difficulty speaking due to weakness in the muscles involved.

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21
Q

What is aphasia?

A

Inability to communicate effectively with others due to damage to the brain.

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22
Q

What are the key features of Lewy body dementia?

A
  • Persistent and well-formed visual hallucinations (sometimes auditory)
  • Early gait disturbances
  • Parkinson’s type features
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23
Q

What is gait disturbance?

A

Disruption to the ability to walk.

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24
Q

Aetiology of Alzheimer’s disease

A
  • Increasing age
  • Family history
  • Down syndrome
  • ApoE4
  • Low IQ
  • Previous head injury
  • Cerebrovascular disease
  • Depression
  • Diabetes Mellitus
  • Obesity
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25
Q

Aetiology of Vascular dementia

A
  • Family history
  • Male
  • Hypertension
  • History of stroke or TIAs
  • Diabetes Mellitus
  • Smoking
  • AF
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26
Q

Aetiology of Lewy body dementia

A
  • Family history
  • No known environmental risk factors
  • Closely related to Parkinson’s disease
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27
Q

Onset and progression of Frontotemporal dementia

A

Insidious onset with slow progression

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28
Q

Aetiology of Frontotemporal dementia

A

PRIMARILY UNKNOWN
- Mutations in progranulin (GRN)
- TAU -linked to chromosome 17
- TDP-43 and C90RF72 genes

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29
Q

Key features of Frontotemporal dementia

A
  • Early loss of insight
  • Early signs of disinhibition
  • Distractibility and impulsivity
  • Progressive decrease in speech output
  • Echolalia
  • Perseveration
  • Depression
  • Apathy
  • Emotional blunting
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30
Q

What is perseveration (in speech)?

A

Can be:
the repetition of words, phrases or sounds.
Can also be:
Being stuck on a topic on conversation, inability to change the subject.

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31
Q

What is the importance of early diagnosis of dementia?

A
  • Patient’s personal affairs can be put in order while they still have insight
  • The patient and their family are able to plan for the future
  • Early access to support groups
  • Access to treatment that may slow the progression of the disease.
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32
Q

What are the clinical screening tools used in the diagnosis of dementia? (4)

A
  • Mini mental state examination (MMSE)
  • Abbreviated mental test score (AMTS)
  • Alzheimer’s disease assessment scale- cognitive subscale (ADAS-cog)
  • Addenbrooke’s cognitive examination 3 (ACE3 or mini ACE)
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33
Q

What investigations can be done in primary care to establish the cause of dementia and potential differential diagnosis?

A
  • FBC
  • U and Es
  • LFT’s
    -CRP
  • Calcium and phosphate
  • Thyroid function
  • Vitamin B12 and folate
  • Urine dipstick
  • Blood glucose
  • Temperature
34
Q

What investigations can be done in secondary care to establish the cause of dementia and potential differential diagnosis?

A
  • MRI and CT scan
  • Urinalysis
  • HIV status
  • Neuropsychological assessment
  • EEG
35
Q

What is the Mini-Mental State Examination and what does it involve?

A
  • Used to assess cognitive function and decline
  • It tests memory, attention, calculation, orientation, language, the ability to follow commands
  • Primarily to aid in the diagnosis of dementia

It takes less than 10-15 minutes to perform and involves 8 questions.
Gives a score between 0 and 30 ( the higher the score the better the patients cognitive function)

36
Q

What are the possible agents used to prevent dementia?

A
  • NSAIDs (started early)
  • Antihypertensives
  • Beer
  • Oestrogen
  • Fish
  • Lithium
  • Statins
  • Vitamins B, C, E, folic acid
37
Q

What medications are commonly used at the onset of Alzheimer’s disease? (3)

A

Donepezil, Galantamine, Rivastigmine
(AChEi’s)

38
Q

What is the dosage of Donepezil in Alzheimer’s disease?

A

5-10mg OD ON

39
Q

What is the dosage of Galantamine in Alzheimer’s disease?

A

4-12mg BD

40
Q

What is the dosage of Rivastigmine in Alzheimer’s disease?

A

1.5-6mg BD

41
Q

If AChEI’s are effective in Alzheimer’s disease, what effects can they have?

A
  • The progression of the disease can be delayed for several months or years
    –This reduces carer burden
    –This delays the need for transfer to a dementia-care home or hospital
42
Q

Which AChEi is licenced for both Alzheimer’s disease and Parkinson’s disease?

A

Rivastigmine

43
Q

What are the common side effects of AChEi’s?

A
  • Nausea, vomiting, diarrhoea, sleep disturbance, abnormal dreams, headache, incontinence, fatigue, agitation
    -Bradycardia (dangerous in certain heart diseases or if taking heart-slowing drugs such as beta-blockers, CCB’s ,digoxin)
44
Q

How to minimise nausea when taking AChEi’s?

A

Take doses after food.

45
Q

How to combat rashes caused by rivastigmine patches?

A
  • If the rash is mild, an emollient cream can be used.
  • If severe the prescriber should be informed.
  • Rotation of the application site
46
Q

How to minimise sleep disturbance and nightmares caused by donepezil?

A

Take the dose in the morning.

47
Q

What is Memantine licenced for?

A

Moderate to severe dementia in Alzheimer’s disease.

48
Q

What is the usual dosing of memantine in Alzheimer’s disease?

A

Initially 5mg OD for one week then is increased by 5mg per week until 20mg OD is reached.
Monotherapy is recommended.

49
Q

What are the common side effects of memantine?

A

Headache, constipation, dizziness, hypertension, dyspnoea

50
Q

What medications are offered to patients with Lewy Body dementia? (Unlicenced use)

A

Donepezil or Rivastigmine

51
Q

When is Galantamine considered for a patient with Lewy Body dementia?

A

When donepezil and rivastigmine are not tolerated.

52
Q

What drugs should not be offered in frontotemporal dementia?

A

AChEi’s or Memantine

53
Q

When can AChEi’s or Memantine be considered for patients with Vascular dementia?

A

When they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or Lewy body dementia.

54
Q

What are the NICE guidelines for first line AChEi in Alzheimer’ disease?

A
  • Use the least expensive one first
55
Q

What are the behavioural symptoms of dementia?

A
  • Physical aggression
  • Screaming
  • Wandering
  • Culturally inappropriate behaviour
  • Sexual disinhibition
  • Swearing
56
Q

What are the psychological symptoms of dementia?

A
  • Anxiety
  • Depression
  • Hallucinations
  • Delusions
57
Q

What are the 5 typical delusions patients with dementia can have?

A
  • People are stealing their things
  • Spouse or other care giver is an imposter
  • Abandonment
  • Misidentification
  • Convinced their spouse is unfaithful
58
Q

What are the major adverse outcomes of antipsychotics in dementia?

A
  • They double the risk of death
  • Over-sedation and dehydration
  • Infection risk is tripled
  • Stroke risk is tripled
  • Falls and fractures are doubled
59
Q

What are the adverse effects of antipsychotics?

A
  • Sedation
  • Parkinsonism
  • Gait disturbance
  • Dehydration
  • Falls
  • Chest infections
  • Confusion
  • Movement problems ( tremor, rigidity)
  • Agitation/restlessness
  • Dry mouth
  • Blurred vision
  • Constipation
60
Q

What is Risperidone used for in dementia?

A

To treat/manage the behavioural and psychiatric symptoms of dementia.

61
Q

When is Risperidone appropriate in dementia? (4)

A
  • Persistent aggression
  • Moderate to severe Alzheimer’s dementia.
  • Unresponsive to non-drug approaches
  • There is a risk of harm to themself or others.
62
Q

What is the dosage of Risperidone in Alzheimer’s disease?

A

Initialy 0.25mg BD then can be increased by 0.25 BD every other day.
The optimum dose for most patients is 0.5mg BD but some patients need 1mg BD.
Maximum 6 weeks.

63
Q

Why are benzodiazepines not used for behavioural and psychiatric symptoms of dementia?

A

They increase the patients fall risk 8 fold.

64
Q

What is the first line treatment for the behavioural and psychiatric symptoms of dementia?

A

-Non-drug psychosocial interventions
- Treatment of non-dementia cause e.g. pain, infections, depression

65
Q

What are the pathological findings for Alzheimer’s disease?

A
  • Atrophy in the cerebral cortex and hippocampus
  • Extracellular beta-amyloid plaques
  • Functional losses in cholinergic, GABAergic and monoaminergic transmitter systems
  • Intra-neuronal neurofibrillary tangles made mainly of tau protein
66
Q

APP cleavage pathways:

A

Formed from amyloid precursor protein (APP) and the action of secretases:
—–10% of APP is cleaved by beta-secretase into soluble APP beta (sAPP beta) and C-terminal fragment beta (CTF beta). CTF is then cleaved by gama secretase into A beta 40 (80-90%) and A beta 42 (10-20%).
—–90% of APP is cleaved by alpha secretase into soluble APP alpha and C-terminal fragment alpha (CTF alpha).

67
Q

How is beta amyloid produced?

A

Beta secretase cleavage pathway.
(Cleavage of APP)

68
Q

What are the plaques in Alzheimer’s disease made of?

A

Beta amyloid
(A beta 40, A beta 42)

69
Q

Is A beta 40 or A beta 42 more abundant?

A

A beta 40

70
Q

Is A beta 40 or A beta 42 more insoluble?

A

A beta 42

71
Q

How do beta amyloid plaques cause neuronal cell death? (2)

A
  1. They have direct cytotoxic effects
  2. They cause an inflammatory response (microglial activation + cytokine release)
72
Q

How are neurofibrillary tangles formed?

A

1- Tau becomes hyperphosphorylated
2- This aggregates to form paired helical filaments
3- Microtubules are depolymerised

73
Q

What happens to the amount of ACh in the brain during Alzheimer’s disease?

A

Decreased

74
Q

What causes early onset Alzheimer’s (genetics)?

A
  • Trisomy 21
  • Mutations in APP
  • Mutations in Presenilin 1 and Presenilin 2
  • Mutations in Tau
75
Q

What causes late onset Alzheimer’s (genetics)?

A
  • ApoE4 mutations
76
Q

What are the two classes of drugs used to treat Alzheimer’s disease?

A

Anticholinesterases and NMDA antagonist

77
Q

How do Acetylcholinesterase inhibitors work in Alzheimer’s?

A

They inhibit acetylcholinesterase from breaking down acetylcholine, enhancing the action of acetylcholine.

78
Q

What are the downsides to acetylcholinesterase inhibitors in the treatment of Alzheimer’s?

A
  • They rely on the patient having some in tact cholinergic neurones to synthesise acetylcholine
  • The side effects can be limiting
79
Q

What two enzymes does galantamine inhibit?

A

Acetylcholinesterase and butyrylcholinesterase (BuChE)

80
Q

How does memantine work in Alzheimer’s disease?

A

It is a non-competitive NMDA antagonist.
It reduces neuronal excitation.

81
Q

Do acetylcholinesterase’s need to cross the BBB?

A

Yes

Year 3 Exam 2 (19 decks)

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