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Dementia Flashcards

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1
Q

What is dementia?

A

An organic syndrome characterized by the loss of cognitive functioning — thinking, remembering, and reasoning — to such an extent that it interferes with a person’s daily life

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2
Q

What age does dementia occur?

A
  • <65yo = early-onset dementia
  • 5-10% population over 65yo; 20% population over 80yo
  • Alzheimer’s disease (70% dementia) > Vascular Dementia (VD) > Dementia with Lewy Bodies (DLB)
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3
Q

What are the general S/S of dementia?

A

1st: forgetfulness (stepwise or progressive)

2nd: disorientation (time > place > person) > management problems…

  • Wandering
  • Sleep-disturbance
  • Delusions
  • Hallucinations
  • Calling out
  • Inappropriate behaviour / aggression
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4
Q

What is BPSD?

A

Behavioural and Psychological Symptoms of Dementia:
(1) Mood changes
(2) Abnormal behaviour
(3) Hallucinations / delusions

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5
Q

What are the investigations for dementia?

A

Screening tools:

  • Risk assess patient
  • The abbreviated mental test score (AMTS)
    Score <7 suggests cognitive impairment
  • The mini-mental state examination (MMSE)

Bloods:

  • FBC
  • TFTs (hypothyroid > cognitive decline)
  • LFTs (Korsakoff’s)
  • U&Es and dip (infection, diabetes)
  • HbA1c / glucose (diabetes)
  • Vitamin B12 and folate

CT/MRI:

  • AD: Generalised atrophy
  • VD: Multiple luciencies
  • DLB: Mild atrophy
  • FT: Frontal lobe shrinkage

Memory Assessment Clinic referral (after GP):

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6
Q

What is AD?

A

A progressive degenerative disease of the brain accounting for the majority of dementia seen in the UK (70%)

  • Onset usually after 65yrs
  • Relentlessly progressive
  • Early onset > more rapid progression
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7
Q

What are the RFs for AD?

A

Biological:

  • AGE
  • Genetics - APEN, APP, ApoE, etc
  • FHx of AD
  • Caucasian ethnicity
  • Head injury
  • Vascular RFs e.g. HTN
  • Down Syndrome associated with EOS

Psychosocial:

  • Low IQ
  • Poor education level
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8
Q

What are the pathological changes that occur in AD?

A

Macroscopic:

  • Widespread cerebral atrophy, particularly involving the cortex and hippocampus

Microscopic:

  • Cortical plaques due to deposition of type A-Beta-amyloid protein
  • Intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
  • Hyperphosphorylation of the tau protein

Biochemical:

  • There is a deficit of acetylcholine from damage to an ascending forebrain projection
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9
Q

What are the S/S of AD?

A

“The Four A’s”

  • Amnesia - recent memories lost first; disorientation occurs early
  • Aphasia - in finding correct words (Broca’s), speech muddled/disjointed
  • Agnosia - typically “Visual” (i.e. prosopagnosia – cant recognise faces)
  • Apraxia - tpically “Dressing” (skilled tasks, despite normal motor functioning)

BPSD
Psychiatric presentations

  • Delusions (15%)
  • Depression (20%)
  • GAD

Behavioural disturbances

  • Aggression, explosive temper
  • Wandering
  • Sexual disinhibition
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10
Q

What is the management of AD?

A

BIOPSYCHOSOCIAL APPROACH

Pharmacological:

  • 1st line (mild to moderate): Cholinesterase inhibitors
    e.g. Donepezil, Galantamine, Rivastigmine
  • 2nd line (moderate or 1st line in severe): NMDA antagonist
    e.g. Memantine

Psychological:

  • 1st line: Structural group cognitive stimulation sessions (mild to moderate AD)
  • Exclude depression or GAD
  • NICE recommend offering ‘a range of activities to promote wellbeing that are tailored to the person’s preference’
  • Other: group reminiscence therapy, validation (reassure) therapy, multisensory therapy (improve other senses)

Social:

  • Explain diagnosis and signpost support
  • Optimise health in other areas (i.e. hearing aids, glasses)
  • Personal care support, meal support, day centre availability
  • Identify future wishes (i.e. advanced directives, lasting power of attorney)

FOLLOW-UP

  • Every 6 months with yourself and a single named care manager (with a clearly defined care plan)

Also

  • GENERAL: always wear ID, Dossett boxes, change gas to electricity, assistive technology in the house
  • CARERS: identify and support any carers involved (signpost information and support; carer’s assessment)
  • Legally required to inform DVLA and insurers (if diagnosed with any form of dementia; MCI does not need to inform DVLA)
  • Outcome > renew licence each year, revoked licence, maintain licence
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11
Q

What needs to be checked when using cholinesterase inhibitors?

A

(Raise the ACh available)
Check:

  • 1st > ECG
  • Side effects – GI (N&V, diarrhoea, anorexia), other (fatigue, dizziness, headache)
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12
Q

What are contraindications to using AChI’s?

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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13
Q

What is vascular dementia?

A

Second most common form of dementia after AD.

It is not a single disease but a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease.

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14
Q

What is the aetiology of vascular dementia?

A
  • Infarcts caused by thromboemboli
  • Narrowing of arteries due to HTN
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15
Q

What is the epidemiology of vascular dementia?

A
  • Prevalence of dementia following a first stroke varies depending on location and size of the infarct, interval after stroke, age etc
  • Overall, stroke doubles the risk of developing dementia
  • Incidence increases with age
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16
Q

What are the RFs for vascular dementia?

A

(CVD RFs):

  • Age
  • Male
  • Obesity / lack of exercise
  • Smoking
  • AF
  • DM
  • HTN
  • CVA history (stroke, TIA)
  • Hyperlipidaemia
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17
Q

What are the main subtypes of VD?

A

Stroke-related VD – multi-infarct or single-infarct dementia

Subcortical VD – caused by small vessel disease

Mixed dementia – the presence of both VD and Alzheimer’s disease

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18
Q

What are the S/S of VD?

A

Patients typically present with several months/years hx of sudden or stepwise deterioration of cognitive function (may follow CVA)

  • 1st: emotional and minor personality changes (labile emotion – tearful > elation)
  • 2nd: cognitive deficit

Focal neurological signs

  • Visual / sensory / motor disturbance
  • (S/S reflect site of infarct) – i.e. upgoing plantars, some reserved cognition

Also:

  • Co-morbid depression
  • Difficulty with attention and concentration
  • Seizures
  • Memory disturbance
  • Gait disturbance
  • Speech disturbance
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19
Q

What is the management of VD?

A

Treatment is mainly symptomatic with the aim to address individual problems and provide support to the patient and carers

Biological:

  • Daily aspirin (if indicated due to CVA/AF risk)
  • Reduce risk factors (exercise, less alcohol, treat HTN, stop smoking, treat AF, control DM)
  • Only consider AChE inhibitors or memantine for people with vascular dementia if they have suspected comorbid Alzheimer’s disease, Parkinson’s disease dementia or dementia with Lewy bodies.

Psychosocial:

  • Same as per AD
  • Tailored to the individual
  • Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
  • Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication
20
Q

What is DLB?

A

The characteristic pathological feature is alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.

21
Q

What is the aetiology of DLB?

A
  • Lewy Bodies (LB) = a-synuclein with ubiquitin
  • Spectrum of diseases including Lewy Bodies = DLB …all the way to… Parkinson’s disease (PD)
  • In PD, LB are found in the brainstem;
  • In DLB, LB are found in the brainstem, cingulate gyrus and neocortex
22
Q

What are the S/S of DLB?

A

(≥2 of 3) – general gradual decline:

  • Fluctuating confusion with marked variations in alertness levels - may resemble delirium > I.E. has some lucid intervals (unlike other dementias)
  • Vivid visual hallucinations (Lilliputian hallucinations) – animals or humans
  • Parkinsonism (shuffling gait, bradykinesia, rigidity, amimia – n.b. anosmia is an early sign of PD)
  • Frequent falls
  • (Co-morbid depression)
  • “Hallucinations and slow movements”

PD= parkinsonism > dementia
DLB = dementia > parkinsonism

23
Q

What is the management of DLB?

A

Biological:

  • 1st line: acetylcholinesterase inhibitors (Donepezil or Rivastigmine)
  • Do not offer antipsychotics (increased risk of cerebrovascular disease)

Psychosocial:

  • Same as per AD
24
Q

What is the aetiology of front-temporal dementia?

A

Atrophy of fronto-temporal regions

  • Early onset (20% pre-senile cases) – 40 to 60yo
  • 60% sporadic; 40% autosomal inheritance
  • “Early-onset dementia > child-like behaviour”
25
Q

What are the S/S of front-temporal dementia?

A

3 clinical presentations:

  • (1) Frontotemporal dementia > frontal lobe syndrome (disinhibition, social/personality changes)
  • (2) Semantic dementia > progressive loss of understanding of verbal and visual meaning
  • (3) Progressive non-fluent aphasia > 1st: naming difficulties; 2nd: mutism

Memory tends to be affected much later (unlike in AD where it may be the first thing to be affected)

26
Q

What is the pathology of front-temporal dementia?

A

Two pathologies with no correlation to clinical presentations:

  • (1) Tau positive – “Pick’s” bodies (hyperphosphorylated tau) = Pick’s disease (3R), CBD (4R), PSP (4R)
  • (2) Tau negative – no Tau = FTLD-U (Frontotemporal Lobar Dementia with Ubiquinated inclusions)
27
Q

What is the management of front-temporal dementia?

A

Biological:

  • Antidepressants (treat frontal lobe syndrome)

Psychosocial:

  • Same as per AD
  • OT, SALT, physiotherapy
28
Q

What is the prognosis of front-temporal dementia?

A

Death in 5-10 years

29
Q

What factors favour delirium over dementia?

A
  • impairment of consciousness
  • fluctuation of symptoms: worse at night, periods of normality
  • abnormal perception (e.g. illusions and hallucinations)
  • agitation, fear
  • Delusions
30
Q

What is the DSM-V definition of delirium?

A
  • A. disturbance in attention and awareness
  • B. disturbance develops over a short period of time (hours to days), represents a change from baseline attention and awareness and tends to fluctuate in severity during the course of the day
  • C. an additional disturbance in cognition
  • D. disturbances in Criteria A and C are not better explained by another condition
  • E. evidence from the history, physical examination or laboratory findings that the disturbance is a direct physiological consequence of another medical condition, substance intoxication or withdrawal

I.E. quick onset, fluctuant, disorientated

31
Q

What is the epidemiology of delirium?

A
  • On admission - 10-30% of acute adult inpatients aged 65+
  • After admission - up to 30% new onset on acute wards, 80% ICU
  • Care homes - 20%
  • 50% never recognised
32
Q

What is the aetiology of delirium?

A
  • Infection (UTI, RTI)
  • Change in environment
  • Medication (anti-ACh, steroids, opiates) memantine (think in AD), steroids
  • Alcohol withdrawal
  • Surgery
  • Pain
  • Liver/renal impairment
  • Hypoxia
  • Hyponatraemia
  • Stroke
  • Encephalitis
  • Constipation
  • Urine retention
  • Dehydration
33
Q

What are 2 assessment tools for delirium?

A

Confusion Assessment Method (CAM):
Delirium requires…

  • Feature 1 PLUS feature 2 PLUS feature 3 OR 4

4AT

  • Rapid clinical test for delirium
  • > 4 suggests delirium
34
Q

What is the management of delirium?

A

General

  • ADMIT (fluctuating)
  • Treat the cause
  • Manage aggravating factors (e.g. pain, dehydration, constipation)
  • Stop unnecessary medications

Behavioural Management

  • Frequent reorientation (e.g. clocks, calendars, verbal reminders)
  • Good lighting (gloomy conditions increase risk of hallucinations/illusions)
  • Address sensory problems (e.g. hearing aids, glasses)
  • Avoid over- or under-stimulation (side room if the main ward is disruptive)
  • Minimise change (don’t keep moving the patient, one staff member to engage with the patient each shift)
  • Establish a routine (regular toileting and sleep hygiene)
  • Remove things that can be thrown or tripped over
  • Silence unnecessary noises (e.g. bleeping alarms)
  • Allow safe or supervised wandering

Medication

  • Small night-time dose of BZN could promote sleep
  • If short-term sedation is needed, low-dose typical antipsychotics (e.g. haloperidol) or benzodiazepines can be used
35
Q

What is delirium associated with causing?

A
  • Increased mortality
  • Longer admissions
  • Higher readmissions rates
  • Subsequent nursing home placement

May take days to weeks to resolve
Some patients do not return to pre-morbid levels

36
Q

How is delirium prevented?

A
  • Good sleep hygiene without medication
  • Minimal moves around hospital
  • Encouraging mobility
  • Proactive management (minimise dehydration, pain, constipation, urinary retention and sensory problems)
37
Q

What is the management of normal pressure hydrocephalus?

A

A ventriculo-peritoneal shunt is first line, to allow CSF drainage into the peritoneal

38
Q

What is the management of psychosis in the elderly?

A
  • Reduction of sensory impairment
  • Exclusion of organic cause or LBD
  • Low-dose antipsychotics
39
Q

How is the MMSE interpreted?

A

> Any score > 24/30 is considered normal

Cognitive Impairment

  • Mild: 18-23 - May require some supervision, support or assistance
  • Moderate: 10-17 - Clear impairment, may require 24-hour supervision
  • Severe: 0-9 - Marked impairment, likely to require 24-hour supervision and assistance with ADLs

> The raw score may need to be corrected based on educational attainment and age

> Note: patients with depression may often answer with ‘I don’t know’ whereas patients with dementia will attempt to answer all questions

40
Q

What is Wernicke’s encephalopathy?

A

A neurological condition due to longstanding thiamine (vitamin B1) deficiency, commonly due to chronic alcohol abuse or malnutrition.

41
Q

How does Wernicke’s encephalopathy present?

A

It manifests as the triad of:

  • Confusion
  • Ataxia (e.g. broad-based gait)
  • Oculomotor dysfunction (e.g. CN 6 palsies and nystagmus)
42
Q

What is a complication of Wernicke’s encephalopathy

A

Korsakoff’s syndrome

  • Manifests as anterograde and retrograde amnesia as well as confabulation (patient unconsciously makes up stories to fill a gap in their memory)
43
Q

How is someone with AD described compared to VD?

A
  • In AD … “mum just isn’t herself anymore”
  • In VD … “mum is a little different and is using her left arm much less”
44
Q

What are people with DLB at risk of?

A

High risk of falls due to fluctuating autonomic instability e.g. fluctuating BP

45
Q

Can you give FGAs in DLB?

A

Not advised as can severely worsen symptoms

Psych (18 decks)

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