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Y5 Psychiatry > Dementia and Huntington's > Flashcards

Dementia and Huntington's Flashcards

1
Q

Define Dementia.

A

Acquired, chronic, and progressive cognitive impairment, sufficient to impair ADLs.

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2
Q

What are the generalised signs and symptoms of Dementia?

A
  • 1st: Forgetfulness
  • 2nd: Disorientation (time then place then person)
    • Wandering
    • Sleep-disturbance
    • Delusions
    • Hallucinations
    • Calling out
    • Inappropriate behaviour / aggression
  • Behavioural and Psychological Symptoms
    • Mood changes
    • Abnormal behaviour
    • Hallucinations / delusions
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3
Q

What are the appropriate investigations for suspected Dementia?

A
  • Cognitive Assessment:
    • Screening - AMTS, GPCOG
      • AMTS (score <7 suggests cognitive impairment)
      • GPCOG (GP Assessment of Cognition)
    • Detailed - Addenbrooke’s, MMSE, MoCA
      • MMSE = 30 questions (18-23 is mild; <18 severe)
      • ACE-R = 100 questions
  • Dementia/delirium screen:
    • TFTs
    • LFTs (Korsakoff’s)
    • U&Es and dipstick (infection, diabetes)
    • HbA1c
    • Vitamin B12 and folate
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4
Q

What additional tests can be ran for suspected Alzheimer’s?

A
  • FDG-PET
  • CSF
  • MRI
    • Grey matter atrophy
    • Wide ventricles & sulci
    • Temporal lobe atrophy
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5
Q

What additional tests can be ran for suspected Vascular Dementia?

A
  • ECG (AF with emboli)
  • MRI/CT
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6
Q

What additional tests can be ran for suspected Lewy Body?

A
  • 123I-FP-CIP SPECT (DaTScan; a tracer 123I-FP-CIP used in Single Photon Emission CT)
  • I-MIBG
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7
Q

What additional tests can be ran for suspected Frontotemporal?

A
  • FDG-PET
  • Perfusion SPECT
  • MRI - frontal lobe shrinkage
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8
Q

Define Alzheimer’s Disease.

A

Dementia with a steady progression

  • Most common - 70%
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9
Q

What are the 3 theories of Alzheimer’s pathophysiology?

A
  • Amyloid
    1. APP cleaved by b-secretase
    2. sAPPb released and the C99 fragment remains
    3. C99 is digested by g-secretase releasing b-amyloid (Ab) protein
    4. Ab protein forms the toxic aggregates
  • Tau
    1. Hyperphosphorylated tau is insoluble so self-aggregates
    2. The self-aggregates form neurofibrillary tangles (neurotoxic)
    3. The tangles result ultimately in microtubule instability and neurotoxic damage to neurones
  • Inflammation
    1. Increased inflammatory mediators & cytotoxic proteins
    2. Increased phagocytosis
    3. Decreased levels of neuroprotective proteins
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10
Q

What are the risk factors of Alzheimer’s Disease?

A
  • Biological
    • Age – 1% at 60yo, risk doubles every 5 years
    • Sex – 2:1 Female to Male
    • Genetics (8% of risk, 92% sporadic – Presenilin 1 gene (Chr14), Presenilin 2 gene (Chr1), Beta-amyloid precursor protein (APP) gene (Chr21)
      • Co-existent Down’s syndrome increases risk
    • Head Injury
    • Vascular Risk Factors – HTN ect
  • Psychological
    • Low IQ
    • Poor education level
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11
Q

What are the signs and symptoms of Alzheimer’s Dementia?

A
  • Presentation: “The Four A’s”
    • Amnesia - recent memories lost first; disorientation occurs early
    • Aphasia - Broca’s, speech muddled/disjointed
    • Agnosia - typically “visual” (i.e. prosopagnosia – recognising faces)
    • Apraxia - typically “dressing” (skilled tasks, despite normal motor functioning)
  • BPSD = mood change, abnormal behaviour, hallucinations/delusions
    • Psychiatric presentations - delusions (15%), depression (20%), GAD
    • Behavioural disturbances - aggression, wandering, sexual disinhibition, explosive temper
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12
Q

What are the good and bad prognostic factors for Alzheimer’s Dementia?

A
  • Good prognostic indicator = female
  • Bad prognostic indicators = male, depression, behavioural problems, severe focal cognitive deficit
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13
Q

What is the management of Alzheimer’s Dementia?

A
  • Biological
    • 1st line: Anticholinesterases
      • Donepezil
      • Galantamine
      • Rivastigmine
    • 2nd line: NMDA (Glutamate) partial receptor agonist
      • Memantine
  • Psychological
    • Structural group cognitive stimulation sessions
    • Other: group reminiscence therapy, validation/reassure therapy, multisensory therapy (improve other senses)
  • Social
    • Explain diagnosis
    • Optimise health in other areas (i.e. hearing aids, glasses)
    • Identify future wishes (i.e. advanced directives, lasting power of attorney)
  • Follow-Up (every 6 months) - with yourself and a single named care manager
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14
Q

What are the side effects of Anticholinesterases?

A
  • GI - N&V, diarrhoea, anorexia
  • Fatigue
  • Dizziness
  • Headache
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15
Q

What are the absolute and relative contraindications of Anticholinesterases?

A
  • Absolute contraindications
    • Anticholinergics (block ACh from binding)
    • Beta-blockers
    • NSAIDs
    • Muscle relaxants
  • Relative contraindications
    • Asthma
    • COPD
    • GI disease
    • Bradycardia
    • Sick sinus syndrome
    • AV block
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16
Q

Define Vascular Dementia.

A

Infarcts caused by thromboemboli or narrowing of arteries due to HTN leading to step-wise deterioration in cognitive function

17
Q

What are the risk factors for Vascular Dementia?

A
  • Age
  • Male
  • Obesity
  • Lack of exercise
  • Smoking
  • AF
  • DM
  • HTN
  • CVA history - stroke, TIA
18
Q

What are the signs and symptoms of Vascular Dementia?

A
  • Sudden onset (may follow CVA) with stepwise deterioration
    • 1st: emotional and minor personality changes (labile emotion)
    • 2nd: cognitive deficit
  • Focal neurological signs (S/S reflect site of infarct) –
  • Co-morbid depression
  • Relatively preserved personality
19
Q

What is the management of Vascular Dementia?

A
  • Biological:
    • Daily Aspirin (if indicated due to CVA/AF risk)
    • Reduce risk factors (exercise, less alcohol, treat HTN, stop smoking, treat AF, control DM)
  • Psychological
    • Structural group cognitive stimulation sessions
    • Other: group reminiscence therapy, validation/reassure therapy, multisensory therapy (improve other senses)
  • Social
    • Explain diagnosis
    • Optimise health in other areas (i.e. hearing aids, glasses)
    • Identify future wishes (i.e. advanced directives, lasting power of attorney)
  • Follow-Up (every 6 months) - with yourself and a single named care manager
20
Q

Define Dementia with Lewy Bodies.

A

Dementia with the presence of Lewy Bodies - a-synuclein with ubiquitin

21
Q

What is the distribution of Lewy Bodies in DLB and Parkinson’s?

A
  • DLB - LB are found in the brainstem, cingulate gyrus and neocortex
  • Parkinson’s - LB are found in the brainstem
22
Q

What are the signs and symptoms of Dementia with Lewy Bodies?

A
  • ≥2 of 3 – general gradual decline:
    • Fluctuating confusion with marked variations in alertness levels - may resemble delirium
    • Vivid visual hallucinations (Lilliputian hallucinations) – animals or humans
    • Parkinsonism - shuffling gait, bradykinesia, rigidity, amimia
    • Frequent falls
    • Co-morbid depression
23
Q

What is the management of Dementia with Lewy Bodies?

A
  • Biological:
    • 1st line: Acetylcholinesterase inhibitors - Donepezil or Rivastigmine
    • Do not offer antipsychotics (increased risk of cerebrovascular disease)
  • Psychological
    • Structural group cognitive stimulation sessions
    • Other: group reminiscence therapy, validation/reassure therapy, multisensory therapy (improve other senses)
  • Social
    • Explain diagnosis
    • Optimise health in other areas (i.e. hearing aids, glasses)
    • Identify future wishes (i.e. advanced directives, lasting power of attorney)
  • Follow-Up (every 6 months) - with yourself and a single named care manager
24
Q

Define Frontotemporal Dementia.

A

Atrophy of fronto-temporal regions

25
Q

What are the signs and symptoms of Frontotemporal Dementia?

A
  • Frontotemporal dementia - frontal lobe syndrome (disinhibition, social/personality changes)
  • Semantic dementia - progressive loss of understanding of verbal and visual meaning
  • Progressive non-fluent aphasia - 1st: naming difficulties; 2nd: mutism
  • Memory tends to be affected much later
26
Q

What is the management of Frontotemporal Dementia?

A
  • Biological:
    • Antidepressants (treat frontal lobe syndrome)
  • Psychological
    • Structural group cognitive stimulation sessions
    • Other: group reminiscence therapy, validation/reassure therapy, multisensory therapy (improve other senses)
  • Social
    • Explain diagnosis
    • Optimise health in other areas (i.e. hearing aids, glasses)
    • Identify future wishes (i.e. advanced directives, lasting power of attorney)
  • Follow-Up (every 6 months) - with yourself and a single named care manager
27
Q

What is the prognosis of Frontotemporal Dementia?

A
  • Death in 5-10 years
28
Q

What is Huntington’s Disease?

A

Autosomal dominant trinucleotide expansion disorder resulting in abnormal Huntington protein and the triad of movement, cognitive and psychiatric disease

29
Q

What is the typical age of onset of Huntington’s Disease?

A
  • Onset 30-50yo
    • Onset and severity may be younger and greater in successive generations
      • A feature of all trinucleotide expansion disorders
30
Q

Name 2 trinucleotide expansion disorders.

A

Huntington’s

Fragile X syndrome

31
Q

What are the signs and symptoms of Huntington’s Disease?

A
  • Movement – chorea, speech/swallowing, stumbling/clumsiness
  • Cognitive – organising tasks, flexibility, impulse control, learning new information, difficulty concentrating
  • Psychiatric – depression, irritability/mood swings, suicide in 9% of cases, personality change
  • Lack of insight
32
Q

What investigations should you do for suspected Huntington’s?

A
  • Genetic analysis (HTT gene)

Y5 Psychiatry (11 decks)

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