Older Persons Mental Health Flashcards

1
Q

When taking a history for a pt with cognitive impairment,. what questions do you need to ask?

A

Presenting compliant

  • Duration
  • Onset/course
  • Example questions: forgetfulness, forget names, getting lost etc…
  • Ensure to ask about behavioural & psychiatric symptoms of dementia & any triggers (includes hallucinations, delusions)
  • Impact on life
  • ADLs
    • Washing, dressing, eating/drinking/cooking, shopping, housework, financial/bills
  • Continence
  • Safety

PMH

  • Risk factors
  • PMH
  • Medications
  • Allergies

FH

  • Dementia (and age)

Social

  • Who live with
  • Where live
  • Socialise much
  • Any support at home

ICE

  • Do they have insight
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2
Q

Notes from memory clinic regarding histories

A
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3
Q

What history should you always take when assessing a pt with cognitive impairment?

A

Collateral history

(ask similar questions as to what you would ask person but in different way. Ask about pre-morbid self, memory, personality changes, behaviour changes, ADLs, concerns, rest of hx you can’t get from pt)

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4
Q

State some tools commonly used to assess cognitive ability

A
  • AMTS (abbreviated mental test score): useful as very quick cognition screen
  • MMSE (mini mental state examination): copyright issues so not used as much now
  • ACE-III (Addenbrooke’s cognitive examination III): more in depth, 100 points, need to see pt face to face as some writing involved/need to identify pictures
  • CAM (confusion assessment method): used to support delirium diagnosis
  • MOCA (Montreal Cognitive Assessment): used more than MMSE now due to copyright issues with MMSE
  • MIS-T CHECK!!!
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5
Q

Remind yourself of AMT-10

A

Questions

  • Age
  • Time to nearest hour
  • Year
  • Either name of where they are or their home address
  • Recognise two people (e.g. chef, post-man, doctor)
  • DOB
  • Date WW1 began (can ask WW2)
  • Name of monarch or prime minister
  • Count backwards from 20 to 1
  • Repeat address (should be given after asking time)

Results

0-3 = severe impairment

4-6= moderate impairment

≥ 7 = normal

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6
Q

Remind yourself briefly of what is involved in MMSE

A
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7
Q

Remind yourself of 4 parts of CAM (Confusion Assessment Method)

A
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8
Q

Remind yourself briefly of what is involved in ACE-III

A

Cognitive test that assesses five cognitive domains: attention, memory, verbal fluency, language and visuospatial abilities. Need to see images & draw hence need to do in person

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9
Q

Remind yourself briefly what is involved in GP-COG

A
  • Designed as dementia screening tool for GPs
  • Two parts: one to be completed by pt and one to be completed by informant if results from pt questionnaire inconnclusive
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10
Q

Remind yourself briefly of what is involved in MOCA (Montreal Cognitive Assessment)

A
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11
Q

Summary from memory clinic:

  • GP-COG and MOCA often used in GP settings as quick tool
  • ACE-III or mini-ACE used in memory clinics
  • FAB (frontal assessment battery) used alongside ACE-III in memory clinic if you suspect FTD
A
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12
Q

What is dementia?

Discuss prevalence/epidemiology

A
  • Dementia is a clinical syndrome of generalised, progressive, irreversible decline of memory, intellect and personality- without impairment of consciousness- leading to functional impairment
  • Prevalence:
    • WHO says 50 million people world wide
    • NICE CKS: 885,000 in UK in 2019
    • GOING TO INCREASE
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13
Q

Dementia is irreversible however you may hear people talk about reversible causes of dementia; state some examples of reversible causes of dementia

*HINT: mnemonic for reversible causes is DEMENTIA

A

MANAGEMENT= treat underlying cause

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14
Q

Dementias can be classified as cortical, subcortical or mixed based on where dysfunction is most predominant. Compare cortical and subcortical dementias based on the following:

  • Memory loss
  • Mood
  • Speech & aphasia
  • Personality
  • Coordination
  • Praxis
  • Motor speed

Sate some examples for each

A
  • Cortical: Alzheimer’s dementia, FTD
  • Subcortical: DLB, Parkinson’s disease with dementia
  • Mixed: vascular
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15
Q

State some different types of dementia

**These are ones you need to know more about

A
  • Alzheimer’s dementia
  • Vascular dementia
  • Dementia with lewy body
  • Frontotemporal dementia
  • Parkinson’s disease with dementia
  • Mixed dementia
  • Reversible dementia
  • AIDs-dementia complex
  • Huntington
  • Other neurodegenerative dementias
    • CJD,
    • Syphilis)
    • AIDs dementia complex
    • Huntington’s
    • Wernicke-Korsakoff syndrome
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16
Q

State the 4 most common types of dementia

A
  1. Alzheimer’s disease (50–75%), more common in women, often co-exists with other forms of dementia such as vascular dementia.
  2. Vascular dementia (up to 20%), more common in men
  3. Dementia with Lewy bodies (10–15%).
  4. Frontotemporal dementia (2%).
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17
Q

Discuss the ICD-10 criteria for diagnosing dementia

A
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18
Q

What is early onset dementia?

A

Dementia before 65yrs

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19
Q

What investigations would you request for someone with suspected dementia and why?

(Not including cognitive assessment tools)

A
  • Investigations to exclude potential reversible causes (may often be done in primary care):
    • Urine dipstick
    • FBC: ?infection or anaemia
    • U&E: ?impaired renal func
    • Calcium: if not on U&Es
    • LFTs: ?impaired liver function
    • Coagulation/INR: ?bleeding risk
    • Glucose: ?hypoglycaemia or hyperglycaemia
    • Calcium: ?abnormalities
    • ESR/CRP:?infection
    • TFTs: ?hypothyroidism
    • Vit B12: ?deficiency
    • Folate: ?deficiency
    • May also consider others such as urinalysis, blood cultures, CXR, thiamine, drug levels (it pt on digoxin, lithium, quinidine), thiamine
  • Referral to old age psychiatrist (often refer to memory clinics)
  • In secondary care, neuroimaging (e.g. CT head)
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20
Q

Discuss whether dipsticks are reliable for diagnosing UTIs in the elderly

A
  • Urine dipstick not reliable for pts >65yrs or those with catheter
  • A positive urine dipstick without clinical signs is NOT satisfactory to diagnose urinary tract infection as a cause of delirium
  • Look for other evidence supporting the diagnosis (WCC↑/supra-pubic tenderness/dysuria/offensive urine/positive urine culture).
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21
Q

What do we mean by BPSD?

A

Behavioural and psychiatric symptoms of dementia, including:

  • Agitation
  • Restlessness, pacing and wandering
  • Anxiety
  • Elation
  • Irritability
  • Depression
  • Apathy
  • Disinhibition
  • Delusions
  • Hallucinations
  • Sleep or appetite change
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22
Q

For Alzheimer’s dementia, discuss:

  • Pathogenesis
  • Risk factors
  • *
A

Pathophysiology:

  • Macroscopic: widespread cerebral atrophy
  • Microscopic:
    • Type A-beta amyloid plaques due to wrong enzymes degrading amyloid protein forming insoluble beta amyloid which aggregates outside neurones to form plaques
    • Intraneuronal neurofibrillary tangles due to abnormal aggregation of TAU protein
  • Biochemical: deficiency of acetylcholine

Risk factors:

  • Advancing age
  • FH
  • Genetics (see separate FC)
  • Down’s syndrome (associated early onset)
  • Low IQ/learning disability
  • Cerebrovascular disease (strong risk factor for vascular dementia which can co-exist with AD)
  • Vascular risk factors (see above)
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23
Q

What genes are associated with Alzheimer’s disease; be specific about which genes are associated with early onset and late onset

A

Early onset

  • Presenilin 1
  • Presenilin 2
  • Amyloid precursor protein

Late onset

  • ApoE-4
24
Q

Discuss presentation of Alzheimer’s disease (focusing on late onset)

A

Gradual onset of:

  • Memory loss
    • Initially inability to recall new info
    • Long term memory declines as disease progresses
  • Disorientation to time and place
  • Impairment of executive functions
  • Visuospatial impairment (i.e. get lost)
  • Language disturbances/dysphasia (i.e. can’t find words, decreased vocabulary, repeating same word or gesture, global aphasia)
  • Apraxia (inability to carry out previously learned movements e.g. buttoning a shirt)
  • Agnosia (impaired recognition of sensory stimuli not attributed to sensory loss e.g. can’t recognise familiar faces, can’t recognise sound)
  • Non-cognitive/behavioural:
    • Abnormal perceptions (e.g. hallucinations, delusions)
    • Emotion (e.g. depression, apathy)
    • Behaviour (e.g. wandering, aggression, restlessness)

*SEE image for early onset. Idea that early onset is more rapid onset and intellectual impairment predominates

25
Q

Discuss disease progression of Alzheimer’s disease

A
26
Q

Discuss the management of Alzheimer’s dementia

A

MDT management involving old age psychiatrist, specialist nurses, occupational therapists, physiotherapists, social workers, pharmacists etc…

Non-pharmacological

  • Education & support (charities include age UK, Alzheimer’s UK etc..)
  • Ensuring inform DVLA
  • Advancing care planning
  • Occupational therapy input to help with ADLs and safety (e.g. labels on cupboards & doors, motion sensors)
  • Support from carers/care workers
  • Activities
    • Promote wellbeing tailored to person’s preferences
    • Cognitive stimulation therapy
  • Mental capacity act

Pharmacological

  • First line= acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine)
  • Second line= NMDA receptor antagonist (memantine)
  • Adjuncts:
    • Antipsychotics (e.g. risperidone, & haloperidol. Only to pts at risk of harming themselves or experiencing distress due to hallucinations or delusions)
    • Antidepressants (don’t routinely offer if mild-mod depression)
27
Q

For vascular dementia, discuss:

  • Pathogenesis
  • Risk factors
  • *
A

Several subtypes based on pathogenesis:

  • Stroke related VD”- Multiple (often small) cerebrovascular infarcts
  • Subcortical VD”- Small vessel disease
  • Mixed”- VD and Alzheimer’s

Risk factors:

  • Hx stroke or TIA
  • AF
  • Hypertension
  • Diabetes
  • Hyperlipidaemia
  • Smoking
  • Obesity
  • Coronary heart disease
  • FH of stroke or cardiovascular disease
28
Q

Describe typical presentation of vascular dementia

A

Usually presents in older men (late 60’s/early 70’s) with stepwise deterioration in symptoms such as:

  • Difficulty with attention & concentration often predominates
  • Emotional disturbance (depression, apathy) often earlier than memory loss
  • Personality changes often early than memory loss
  • Memory loss
  • Gait disturbance
  • Speech disturbances
  • Seizures
  • Focal neurological abnormalities
  • Signs of CVD
29
Q

Discuss the management of vascular dementia

A

Management via MDT focusing on treating symptoms and risk factors to slow disease progression:

Symptomatic/supportive management

  • Education & support (charities include age UK)
  • Ensuring inform DVLA
  • Advancing care planning
  • Occupational therapy input to help with ADLs and safety (e.g. labels on cupboards & doors, motion sensors)
  • Support from carers/care workers
  • Activities
    • Promote wellbeing tailored to person’s preferences
    • Cognitive stimulation therapy
  • ONLY consider AChE inhibitors or memantine in pts with vascular dementia AND comorbid Alzheimer’s
  • Mental capacity act

Reducing risk factors

  • Lifestyle:
    • Weight loss
    • Stop smoking
    • Reduce alcohol
    • Healthy diet
  • Antihypertensive
  • Lipid modification e.g. statins
  • Diabetic medication
30
Q

What imaging is preferred for vascular dementia?

A

MRI head

31
Q

Discuss the pathogenesis of Lewy body dementia

State some risk factors

*

A
  • Pathogenesis: abnormal deposition of a alpha-synuclein protein (Lewy Body) in neurones of brainstem, substantia nigra and neocortex (outside brainstem associated cholinergic loss, within brainstem dopaminergic loss)
  • Risk factors:
    • Advancing age
    • FH of LBD or Parkinson’s disease

***NOTE: Lewy bodies also present in 40% Parkinson’s pts- mainly in substantia nigra whereas they are more widespread in LBD

32
Q

Describe typical presentation of Dementia with Lewy Body

A
  • In early stages, impairments in attention & executive function predominate over memory loss
  • Fluctuating cognition
  • Visual hallucinations
  • Parkinsonism
  • Sleep disorders common

NOTE: If physical symptoms precede cognitive decline by more than a year, the diagnosis is often Parkinson’s, with superimposed cognitive decline.

33
Q

What additional investigations may be used to diagnose Lewy body dementia

A

Diagnosis usually clinical but may do SPECT/DaTscan (radioisotope that attaches itself to dopamine receptor; decreased signal in PD & LBD)

34
Q

Discuss the management of Lewy body dementia

A

MDT management involving old age psychiatrist, specialist nurses, occupational therapists, physiotherapists, social workers, pharmacists etc…

Non-pharmacological

  • Education & support (charities include age UK, Alzheimer’s UK etc..)
  • Ensuring inform DVLA
  • Advancing care planning
  • Occupational therapy input to help with ADLs and safety (e.g. labels on cupboards & doors, motion sensors)
  • Support from carers/care workers (with ADLs or may be in form of community services such as day centres, meals-on-wheels etc..)
  • Activities
    • Promote wellbeing tailored to person’s preferences
    • Cognitive stimulation therapy
  • Mental capacity act

Pharmacological

  • Acetylcholinesterase inhibitors (donepezil, rivastigmine, galantamine)
  • NMDA antagonist (memantine)
35
Q

What medications should NOT be used in Lewy body dementia?

A

Neuroleptics (antipsychotics) as LBD pts are extremely sensitive and hence may have severe adverse effects including sensitivity reactions or worsening of pyramidal features (Passmed says irreversible parkinsonism)

36
Q

Discuss the prognosis of Lewy body dementia

A
  • Rapidly progressive
  • Most pts die within 7yrs of diagnosis
37
Q

For frontotemporal dementia, discuss:

  • Pathogenesis
  • Risk factors
  • Presentation
    *
A
  • Deposition of abnormal proteins (usually TAU proteins) in neurones of frontal & temporal lobe causing atrophy of frontal & temporal lobes
  • Main risk factor= FH
  • Presentation:
    • Onset before 65yrs
    • Insidious onset
    • Early personality changes (e.g. disinhibition, apathy, restlessness, worsening social behaviour)
    • Language problems (difficulty finding words, poor articulation)
    • Memory is preserved in early stages
38
Q

Discuss the management of FTD

A

Non-pharmacological

  • Education & support (charities include age UK, Alzheimer’s UK etc..)
  • Ensuring inform DVLA
  • Advancing care planning
  • Occupational therapy input to help with ADLs and safety (e.g. labels on cupboards & doors, motion sensors)
  • Support from carers/care workers (with ADLs or may be in form of community services such as day centres, meals-on-wheels etc..)
  • Activities
    • Promote wellbeing tailored to person’s preferences
    • Cognitive stimulation therapy
  • Mental capacity act

Pharmacological

  • Antidepressants e.g. SSRIs may help control the loss of inhibitions, overeating and compulsive behaviours
39
Q

Discuss the prognosis of FTD

A

Great variation in progression, but average life expectancy is 8 years post-diagnosis.

40
Q

What is Pick’s disease?

A

Pick’s disease is a type of fronto-temporal dementia where protein tangles (Pick’s bodies) are seen histologically

Characterised by personality change & social misconduct (other features= hyperorality, disinhibition, increased appetite

41
Q

Discuss the management of challenging behaviour in dementia

A
  • Identifying and avoiding triggers
  • Distraction
  • Fun activities that person enjoys e.g. socialisation
  • Therapies e.g. life-story work, animal therapy, music therapy etc…
  • Pharmacological if above doesn’t work e.g. haloperidol, risperidone
42
Q

What is the triad seen in normal pressure hydrocephalus?

A
  • Dementia with prominent frontal lobe dysfunction
  • Urinary incontinence
  • Gait disturbance (wide gait)
43
Q

REMEMBER dementia is a psychiatric condition and buzz word in those answers is BIOPSYCHOSOCIAL

A
44
Q

Describe the mechanism of action of Acetylcholinesterase inhibitors

State some common side effects

A
  • Inhibit Acetylcholinesterase enzyme which breaks down Acetylcholine to increase Acetylcholine concentration at neuromuscular junction
  • ADRS:
    • GI upset (nausea, vomiting, diarrhoea)
    • Muscle spasm
    • Bradycardia
    • Drowsiness/fatigue
    • Insomnia
    • Urinary incontinence
45
Q

Describe the mechanism of action of NDMA antagonists e.g. memantine

State some common side effects

A
  • Antagonists of NMDA receptors (main excitatory receptors in CNS)
  • ADRS:
    • Constipation
    • Drowsiness
    • Dizziness
    • Balance impaired
    • Headache
    • Dyspnoea
    • Hypertension
46
Q

What is delirium?

A

Delirium (also called acute confusional state) is an acute, fluctuating syndrome of inattention, impaired consciousness and disturbed cognition

47
Q

Delirium can be hypoactive, hyperactive or mixed; explain the difference

A
48
Q

State some risk factors for delirium

A
  • Advancing age (≥65yrs)
  • Dementia
  • Physical frailty
  • Previous episodes
  • Renal impairment
  • Sensory impairment
  • Recent surgery
  • Multiple co-morbidities
  • Drugs (e.g. opiates, benzodiazepines, antipsychotics, antidepressants, antiparkinsonism drugs, anticholinergics, diuretics)
49
Q

State some common causes of delirium- highlighting most common

*HINT: CHIMPS PHONED

A

Most cases of delirium are multifactorial. MOST COMMON CAUSE IS UTI. Common causes include:

  • Constipation
  • Hypoxia
  • Infection
  • Metabolic disturbance
  • Pain
  • Sleeplessness
  • Prescriptions
  • Hypothermia/pyrexia
  • Organ dysfunction (hepatic or renal impairment)
  • Nutrition
  • Environmental changes
  • Drugs (over the counter, illicit, alcohol and smoking)

*NOTE: A change in environment coupled with sensory impairment (common in the elderly) increases the risk of developing delirium.

50
Q

Describe typical presentation of delirium

A

Acute onset of symptoms, fluctuating course often worse at night

Presentation will vary dependent on if hypoactive, hyperactive or mixed delirium

51
Q

What investigations would you do for someone with suspected delirium and why?

(Following hx, collateral hx, cognitive assessment & physical examination)

A
  • FBC (e.g. infection, anaemia, malignancy)
  • U&Es (e.g. hyponatraemia, hypernatraemia)
  • LFTs (e.g. liver failure with secondary encephalopathy)
  • Coagulation/INR (e.g. intracranial bleeding)
  • TFTs (e.g. hypothyroidism)
  • Calcium (e.g. hypercalcaemia)
  • B12 + folate/haematinics (e.g. B12/folate deficiency)
  • Glucose (e.g. hypoglycaemia/hyperglycaemia)
  • Blood cultures (e.g. sepsis)
  • Urine culture: (e.g. UTI)

May consider others such as CXR, head CT

52
Q

Discuss the management of delirium (hint, think about 4 key categories of management)

A
  • *Also having photos/other familiar objects around bedside*
  • *Other sources say low dose lorazepam not olanzapine*

Antipsychotics & benzodiazepines are NOT first line management. Treating underlying cause, reassurance, re-orientation & appropriate environment are main means for treating delirium. Should only use pharmacological agents in last resort in cases of violent or severely distressed behaviour when other management strategies have failed

53
Q

Compare dementia & delirium in terms of:

  • Sleep-wake cycle
  • Attention
  • Arousal
  • Autonomic features
  • Duration
  • Delusions
  • Course
  • Conscious level
  • Hallucinations
  • Onset
  • Psychomotor activity
A
54
Q

Describe mechanism of action of haloperidol

State some ADRs

A
  • 1st generation antipsychotic that blocks dopaminergic receptors in brain
  • ADRs:
    • Extrapyramidal symptoms
    • Drowsiness
    • Constipation
    • Dry mouth
    • Galactorrhoea
    • Gynaecomastia
    • Agitation
    • Insomnia
55
Q

Describe the mechanism of action of benzodiazepines

State some ADRs

A
  • GABA agonists
  • ADRs:
    • Concentration impaired
    • Confusion
    • Drowsiness
    • Vomiting
    • Ataxia
56
Q

How is mild cognitive impairment different to dementia?

A

Term used to describe stage between normal ageing and dementia; does not interfere significantly with daily life

57
Q

Manchester assessment tool/ WHAT IS IT

A