Psychiatry- Dementia Flashcards

1
Q

What is Alzheimer’s disease

A

• Cerebral atrophy due to neuronal loss
◦ Extracellular beta-amyloid protein plaques form
‣ Intracellular tau neurofibrillary tangle formation
• Cholinergic loss

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2
Q

What part of brain affected in Alzheimer’s disease

A

• Hippocampi in temporal lobe affected

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3
Q

Onset and progression of Alzheimer’s disease

A

• Insidious onset
• Slow progression of cognitive decline with gradual loss of function

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4
Q

What are 4 A’s of Alzheimer’s disease

A

4 A’s:
◦ Amnesia: Recent memories lost first (immediate recall spared in early disease)
◦ Aphasia: Difficulty finding right words (Broca’s), speech muddled
◦ Agnostic: Typically visual (prosopagnosia- recognising faces)
◦ Apraxia: Typically dressing (skilled tasks, despite initial normal motor functioning)

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5
Q

Investigations for Alzheimer’s disease

A

• MMSE

(ACE-III is the most detailed)
MoCA
AMTS cut off is 8 (max score is 10)

• Dementia/delerium screen: TFTs, FBC, U&Es, LFTs, CRP/ESR, HbA1c, B12, Folate

• MRI: grey matter atrophy, wide ventricles and suicidal, temporal lobe atrophy

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6
Q

MMSE cut offs (no impairment, MCI, SCI)

A

‣ >24= no impairment
‣ 18-23= mild cognitive impairment
‣ <18= severe cognitive impairment

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7
Q

Alzheimer’s referral

A

• Referral to memory clinic

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8
Q

Mild or moderate Alzheimer’s disease management

A

1) Acetylcholinesterase inhibitors:
◦ DONEPEZIL
◦ Galantamine
◦ Rivastigmine
◦ Can cause cholinergic side effects: nausea, vomiting, diarrhoea, urinary incontinence, bradycardia
◦ Contraindicated in prolonged QTc

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9
Q

Moderate to severe Alzheimer’s disease management

A

1) Memantine:
• NMDA antagonist

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10
Q

Psychological support for Alzheimer’s disease

A

• Social support: orientate the patient with clocks, calendars. Help with ADLs. Can refer for structural group cognitive stimulation sessions
• Follow-up every 6 months

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11
Q

What is vascular dementia

A

• Dementia precipitated by a cerebrovascular event (e.g stroke)

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12
Q

Causes of vascular dementia

A

‣ Thromboembolism
‣ Atherosclerotic disease of large arteries
‣ Cerebral small vessel disease

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13
Q

Presentation of vascular dementia

A

• Sudden onset: typically after cerebrovascular event
• Stepwise decline of cognitive function
• Emotional and minor personality changes:
◦ Lability emotion

• Neuro symptoms:
◦ Upgoing plantars

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14
Q

Vascular dementia investigations

A

• CT: can show lacunary infarcts

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15
Q

Vascular dementia management

A

• Daily Aspirin:
• Indicated if cerebrovascular event or AF risk

• Reduce risk factors (exercise, HTN management, diet, smoking cessation etc)

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16
Q

What are Lewy bodies

A

• Eosinophilic intracytoplasmic inclusions (Lewy Bodies) that contain alpha-synuclein

17
Q

Where are Lewy bodies found

A

• Found in the brain stem, cingulate gurus and neocortex
◦ In Parkinson’s, only found in brain stem

18
Q

Lewy body dementia presentation

A

• TRIAD:
‣ Fluctuating cognitive impairment:
◦ Marked variations in alertness levels
◦ Associated with lucid intervals

	‣ Hallucinations:
				‣ Typically visual
				‣ Lilliputian hallucinations (animals or people)

	‣ Parkinsonism:
				‣ Shuffling gait
				‣ Bradykinesia
				‣ Tremor 
				‣ Rigidity 
				‣ Anosmia (early sign of Parkinson’s)

• Worsened by antipsychotics
• Frequent falls
• Rapid Eye Movement (REM) sleep behaviour disorder: can cause sleep walking

19
Q

Management of Lewy body dementia

A

1) Acetylcholinesterase inhibitors:
◦ Donepezil
◦ Rivastigmine

• Melatonin or Clonazepam for sleep disturbances

• DO NOT offer antipsychotics

20
Q

What is frontotemproal dementia

A

• Atrophy of fronto-temporal regions

21
Q

Age of onset of frontotemporal dementia

A

• Occurs in mid-life:
◦ 45-65 years old

22
Q

Two types of frontotemporal dementia

A

2 Pathologies, but no difference in presentation:
◦ Tau Positive: Presence of Pick’s bodies (Pick’s disease)
◦ Tau Negative

23
Q

Presentation of frontotemporal dementia

A

• Personality and Behaviour changes:
• Hallmark feature
• Disinhibition:
◦ Socially inappropriate behaviour
◦ Invade personal space
◦ Make offensive remarks
◦ Lack of social awareness

					• Apathy + Loss of empathy:
						◦ Losing interest and/or motivation for activities and social relationships
						◦ Cold or unfeeling towards others
						◦ Lack of filter
						◦ Aggression

					• Compulsive behaviours:
						◦ Hoarding, checking, cleaning
						◦ Simple repetitive movements

• Altered food preferences and binge eating
• Most lack insight
• Memory affected much later

24
Q

Pharmacological management of frontotemporal dementia

A

• Antidepressants: To treat frontal lobe syndrome

• Short-acting Benzodiazepines: to treat aggression, restlessness or agitation (Lorazepam)

25
Q

Psychological management of frontotemporal dementia

A

• Behavioural interventions + Environmental Modifications

26
Q

What not to give in frontotemporal dementia

A

• Do not offer Acetylcholinesterase inhibitors or memantine

27
Q

What is delirium

A

Disturbance in attention, develops over a quick period. Awareness and attention flactuate during the day (worse at night)
Cognition can be affected

28
Q

Risk factors for delirium

A

RISK FACTORS:
• Elderly (typically >65yo)
• Pre-existing dementia
• Post-op
• Substance dependence
• Serious illness
• Burn victims

29
Q

Subtypes of delirium

A

‣ Hyperactive: agitated, very active
‣ Hypo active: very tired, excess sleeping, quiet
‣ Mixed: Flactuating during the day

30
Q

Causes of delirium

A

‣ Change of location
‣ Analgesia
‣ Pain
‣ Dehydration
‣ Constipation
Infection

31
Q

Management of delirium

A

establish cause and treat
Provide environmental and supportive measures (use same staff member, clocks, hearing aids, glasses, educate those that interact with patient, adequate lighting
Avoid sedation