Psychiatry- Dementia Flashcards

(31 cards)

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
Psychological management of frontotemporal dementia
• Behavioural interventions + Environmental Modifications
26
What not to give in frontotemporal dementia
• Do not offer Acetylcholinesterase inhibitors or memantine
27
What is delirium
Disturbance in attention, develops over a quick period. Awareness and attention flactuate during the day (worse at night) Cognition can be affected
28
Risk factors for delirium
RISK FACTORS: • Elderly (typically >65yo) • Pre-existing dementia • Post-op • Substance dependence • Serious illness • Burn victims
29
Subtypes of delirium
‣ Hyperactive: agitated, very active ‣ Hypo active: very tired, excess sleeping, quiet ‣ Mixed: Flactuating during the day
30
Causes of delirium
‣ Change of location ‣ Analgesia ‣ Pain ‣ Dehydration ‣ Constipation Infection
31
Management of delirium
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