Old Age Psychiatry Flashcards

1
Q

What are MHOA Teams?

A
  • MHOA = Mental health of older adults
  • Serve people aged 65 and over
  • Experts in dementia care
  • Team consists of social workers, nurses, psychologists, occupational therapists, and psychiatrists
  • focus less on symptoms themselves and more on how these symptoms affect everyday life and functioning;
    • they often assess people at home, to under-stand how they’re coping in a familiar environment.
  • Working closely with carers, teams enhance quality of life and support people to stay in their own homes as long as possible
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2
Q

How common is depression in the elderly?

A

About 15% of older people, and 30% of older hospital inpatients, are depressed at any time

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3
Q

What is depression in later life associated with? What are the risk factors?

A
  • Depression inlater life (particularly a first episode) may be associated with cerebrovascular disease, vascular risk factors, and current or future cognitive deficits.
  • Other risk factors more commonly affecting older people include:
  • bereavement
  • isolation
  • poverty
  • chronic pain
  • physical illness
  • polypharmacy (multiple medications, making drug side effects and interactions more likely).
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4
Q

How does depression present in older people?

A

Presents similarly but may show more:

  • Physical symptoms, e.g. constipation, insomnia,fatigue.
  • Psychomotor agitation/ retardation.
  • Memory problems.
  • Executive dysfunction.

Pseudodementia is when memory problems are so bad that depression resembles dementia.

Self- neglect and poor oral intake are important risks in older people and may be the first signs of depression.

Suicide rates are higher (especially in men), so suicidal thoughts should be taken very seriously.

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5
Q

How should we manage depression in the elderly?

A

Similar to that of younger people:

  • Problem-solving, increasing socialisation and day-time activities
  • Psychological therapies (e.g. CBT, psychodynamic therapy, group therapy, family therapy, couple therapy)
  • Antidepressants: SSRIs are first line (e.g. citalopram) though they may cause hyponatraemia → monitor sodium levels
    • Mirtazapine can improve sleep and appetite, so may be preferred in frail, older people with insomnia
  • ECT is sometimes used in psychotic or life-threatening depression
  • Consider social workers, community nurses and carers
  • Recommend Age UK
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6
Q

How common are anxiety disorders in the elderly? Who is it more common in?

A

The prevalence and incidence of anxiety disorders fall with age, possibly because of under-reporting.

They’re more common in women and in isolated people or those who’ve had adverse experiences.

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7
Q

What is the management of anxiety disorders in the elderly?

A

Management is usually through CBT, although SSRIs can help

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8
Q

What is late onset and very late onset psychosis?

A

Functional psychosis can develop for the first time in older people: it’s called ‘late- onset psychosis’ after the age of 40, and ‘very late- onset psychosis’ after 60 (also known as paraphrenia/ late- onset schizophrenia)

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9
Q

Who is at risk of getting psychosis?

A
  • Women are more commonly affected, possibly due to loss of the protective effect of oestrogen after menopause.
  • Risk factors include:
    • social isolation
    • sensory impairment
    • cerebrovascular pathology
    • being single/widowed
    • (for women) without children.
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10
Q

What is the presentation of psychosis in the elderly?

A

Positive symptoms (delusions and hallucinations) are often more prominent than negative symptoms

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11
Q

What is the management of psychosis in the elderly?

A

Reduction of sensory impairment (hearing + vision)

  • Exclusion of organic cause or LBD
  • Low-dose antipsychotics
  • CBT
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12
Q

Define dementia.

A

Dementia is NOT a normal part of ageing. It is an acquired, chronic and progressive global cognitive impairment, sufficient to impair ADLs (activities of daily living).

Problems present in clear consciousness for at least 6 months distinguish dementia from delirium.

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13
Q

What are ADLs?

A
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14
Q

What is the epidemiology of dementia?

A

Risk of dementia increases with age and the prevalence is:

  • 5% over 65 years
  • 20% over 80 years
  • Alzheimer’s disease = most common type (60% of cases), followed by vascular dementia and then lewy body
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15
Q

What are the risk factors of Alzheimer’s Disease (AD)?

A
  • Age = major risk factor
  • F > M

Vascular risk factors

  • Low IQ/poor educational level
  • Hx of depression or Head injury
  • Genetics (Heretability is about 70%)
  • Late- onset or sporadic AD (65+ years) makes up 95% of cases.
    • Multiple genes may be involved, but attention has focused on the apolipoprotein E (APOE) ɛ4 allele on chromosome 19.
      • The APOE protein seems to be involved in breaking down β- amyloid; the ɛ4 allele is less effective, so having one or two alleles increases the risk of AD.
  • Familial or early- onset AD (<65 years) is usually due to rare, autosomal dominant mutations affecting presenilin 1 (chromosome 14), presenilin 2 (chromosome 1),or amyloid precursor protein (APP; chromosome 21) genes. These influence the formation or breakdown of APP, predisposing to β- amyloid deposition
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16
Q

What causes Vascular dementia? What are the RFs?

A

Due to small infarcts caused by thromboemboli or arteriosclerosis (stroke-related dementia)

Risk factors = CV risk factors

  • Older age
  • Male sex
  • Smoking
  • HTN
  • DM
  • Hypercholesterolaemia
  • AF
  • Hx of TIA/MI

VD may also be caused by amyloid angiopathy, so can occur with AD.

Multiple genes of small effect probably influence susceptibility to VD.

  • Rare familial forms of VD can occur, e.g. cerebral autosomal dominant arteriopathy with sub-cortical infarcts and leucoencephalopathy (CADASIL)
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17
Q

What are the risk factors of Lewy Body Dementia (DLB)?

A

Men are more commonly affected, and although DLB doesn’t seem strongly genetic, the risk increases in those with the APOE ɛ4 allele

18
Q
A

CT head showing VD: this non- contrasts can shows areas of lower density adjacent to the anterior and posterior horns of the latera ventricles, due to chronic ischaemia.

19
Q

Describe the pathology of AD?

A

Plaque formation

o APP can be abnormally cleaved into beta amyloid → aggregates into insoluble lumps

o Which disrupt signalling between neurons, trigger immune- mediated inflammation, and damage blood vessels increasing the risk of haemorrhage (‘amyloid angiopathy’)

•Intracellular neurofibrillary tangles (NFTs)

o Made of hyperphosphorylated tau

o Tau usually holds microtubules together within a neurone

o When phosphorylated, they accumulate in the cytoplasm into paired helical filaments (plaques tend to abnormally phosphorylate tau)

o Become tangles → fill neuron and kill it (by disrupting cell transport)

o Severity of dementia is closely associated with number of NFTs

Cortical Atrophy due to neuronal loss

o Hippocampus affected early

o Temporal and parietal later

o Sulci and ventricles may appear enlarged on CT

•Cholinergic loss

o Cholinergic pathways are most affected in AD → symptoms such as memory loss

20
Q

Describe the pathology of VD?

A

Arteriosclerosis, cortical ischaemia and infarction

•Latter appear on CT scans as multiple lucencies

21
Q

Describe the pathology of DLB and PD?

A

DLB may be underdiagnosed, as it can only be confirmed postmortem.

PD and DLB - problem in metabolising alpha-synuclein protein → deposition of lewy bodies.

Lewy bodies = eosinophilic intracytoplasmic neuronal structures

  • Composed of alpha-synuclein with ubiquitin
  • In PD the are found in the brainstem - Movement disorder (tremor, rigidity, bradykinesia)predates cognitive symptoms by at least a year
  • In DLB they are seen in cingulate gyrus and neocortex - Cognitive impairment precedes movement symptoms, or occurs within a year of their onset.

It’s been suggested that DLB might be a variant of AD, as they share pathology, e.g. cholinergic loss in DLB, Lewy bodies in AD

22
Q

What is the clinical presentation of dementia?

A

Often begins with forgetfulness for recent events (hard to lay down new memories (anterograde amnesia)

Mistakes in day-to-day activities

With time the long-term memories are lost (retrograde amnesia)

Anxiety/depression often occurs early when insight is intact

Forgetfulness becomes worse and over time new information becomes harder to retain

Disorientation sets in

o First time, then place and finally person

o Difficulty in recognising day or night, easily get lost and fail to recognise family or friends

Language

Thinking and language become impoverished: Receptive and expressive dysphasia

Personality changes

Familiar traits lost or exaggerated and new traits can appear.

Subcortical symptoms

Deep brain structural damage can cause mental slowing (bradyphrenia), movement disorders (e.g. bradykinesia, chorea), depression, and executive dysfunction.

Other functions

Parietal lobe involvement (common in AD) causes various problems, e.g.:

  • Agnosia: difficulties recognizing things, e.g. familiar objects, faces (prosopagnosia).
  • Apraxia: difficulties performing skilled tasks (e.g.drawing, dressing) despite normal sensory and motor function.
  • Dyscalculia: problems using or understanding numbers.

Frontal lobe damage can cause executive dysfunction, socially inappropriate behaviour, and personality change

Behavioural and Psychological Symptoms of Dementia

• Behavioural:

– Restlessness, wandering.

– Disturbed sleep/ day– night reversal.

– Shouting, screaming, swearing.

– Inappropriate/ sexually disinhibited behaviour.

– Aggression.

• Psychological:

– Delusions.

– Hallucinations.

– Depression, anxiety

Risk

To self:

– Suicide/ self- harm (especially early in illness, while aware of prognosis).

– Self- neglect, e.g. poor oral intake/ hygiene, forgetting medications, squalor.

– Getting lost/ wandering.

– Accidents, e.g. leaving gas on (explosion), flooding, fires.

• From others:

– Financial exploitation.

– Neglect/ abuse (emotional, physical, sexual).

• To others:

– Aggression.

– Sexual disinhibition.

– Dangerous driving.

  • Timeline (gradual, progressive vs. stepwise vs. acute)
  • Ability to perform ADLs/attend to finances/manage household
  • Language skills (speech, comprehension, revert to mother tongue) - Visuospatial (reading, writing, disorientation, getting lost)
  • Insight
  • Importance of COLLATERAL HISTORY
23
Q

What is the clinical presentation of AD?

A
  • Gradual decline
  • Spatial navigation problems - people get lost

Presentation = 4 As

• Amnesia

o Recent memories are lost first, disorientation occurs early

• Aphasia

o Word-finding problems occur

o Speech becomes muddled and disjointed

• Agnosia

o Difficulty with recognition of faces = prosopagnosia

• Apraxia

o Inability to carry out skilled tasks despite normal motor function

24
Q

What is the clinical presentation of VD?

A

Stepwise progression – each step represent a sudden deterioration (represent new infarcts)

Many tiny infarcts cause a smoother, more subtle deterioration

Some times, one strategically located stroke → dementia = STRATEGIC INFARCT DEMENTIA

Sx reflect sites of lesions so ppt may be patchy with sparing of certain cognitive abilities.

25
Q

What is the clinical presentation of DLB?

A

• Two of the following three symptoms

o Fluctuating cognition with marked variation in levels of alertness

o Vivid visual hallucinations (often of people or animals)
o Spontaneous (new) parkinsonian signs

Hard to diagnose especially if Parkinsonian signs occur late

Other suggestive features include

o Repeated falls
o Syncope
o Transient losses of consciousness

o Autonomic dysfunction: incontinence, constipation, postural hypotension

o REM sleep disorders (Acting out dreams while asleep)

Short term memory is less affected

Can resemble delirium – do NOT prescribe antipsychotics

Neuroleptic sensitivity → death in DLB

26
Q

What is the differential diagnosis for dementia?

A

• Mild cognitive impairment (MCI) - impairment on cognitive testing which doesn’t cross the threshold for dementia. 10-15% will progress to dementia. Some, never develop dementia and simply need treatment for underlying illness.

• Delirium
o Sudden and fluctuating presentation

• Reversible causes of new cognitive impairment
o Brain: subdural haematoma, SOL, normal pressure hydrocephalus
o Endocrine: hypothyroidism, hyperparathyroidism, Addison’s, Cushing’s

o Vitamin Deficiency: V12, folate, thiamine, niacin

• Pseudodementia
o Memory problems in severe depression

o Low mood precedes dementia sx

27
Q
A
28
Q

What are the investigations for dementia?

A

Basic obs and physical examination

Bloods

o FBC (infection/anaemia)
o U&Es (dehydration, renal failure, hyponatraemia)
o Glucose
o TFTs (hypothyroidism)
o LFTs (alcohol misuse → Korsakoff’s Syndrome or Alcohol-related dementia

o B12 and folate
o Calcium
o VDRL (neurosyphilis → cognitive impairment)

Cogntive testing - M-ACE, MMSE

Collateral hx

Septic screen: MSU, CXR, blood cultures, sputum/stool samples

CT/MRI head if unusual presentation or neuro signs

ECG before starting anti-dementia medication

There are a range of tests that can be done at the bedside:

  • AMTS (Abbreviated Mental Test Score)
  • MMSE (Mini Mental State Exam)
  • MOCA (Montreal Cognitive Assessment)
  • ACE (Addenbrooke’s Cognitive Examination)
  • RUDAS (Rowland Universal Dementia Assessment Scale) - GP-COG
  • 6 CIT
29
Q

What is an AMTS?

A
30
Q

How should we think of managing dementia?

A
  1. Management focuses on quality of life and preservation of independence and dignity
  2. Biological Interventions
    1. Optimise Physical Health
    2. Psychotropic Medications
  3. Psychological Interventions
  4. Social Interventions
    1. Adaptations
    2. Care coordinator
    3. Social support
    4. Support carers
    5. Consider care home
    6. Voluntary sector organisations: Age UK and Alzheimer’s SOCIETY
31
Q

How can we optimise physical health in dementia?

A

o Treat sensory impairment (hearing aids, glasses)

o Exclude superimposed delirium
o Treat underlying risk factors

o Pain management
o Review all medication:

  • Anticholinergics e.g. TCAs, urinary antispasmodics
  • Sedatives e.g. analgesics, antipsychotics
32
Q

What psychotropic medication should we give patients with AD? What should we do before?

A

Use MMSE in Alzheimer’s Disease

o Mild AD:21-26

o Moderate AD: 10-20

o Severe AD:<10

Psychotropic Medications
o Start doses low and increase slowly with any medication used

o Older people are very sensitive to drug side-effects
o Treat comorbid psychiatric illness(e.g.depression)
o Acetylcholinesterase inhibitors

  • Options: donepezil, rivastigmine, galantamine
  • Used in mild-to-moderate Alzheimer’s disease
  • Can cause symptomatic relief
  • Has no effect on the progression of dementia
  • Side effects
    Common 1 in 10 : GI upset, agitation, fatigue, dizziness, muscle cramps, rash, syncope, headache ▪Uncommon 1 in 100 : Bradycardia, duodenal/ gastric ulcers, G-I haemorrhage, seizures

Rare 1 in 10,000 : AV/sino-atrial block, extrapyramidal symptoms, hepatitis, bladder outflow obstruction

o Memantine (NMDA antagonist) -Used in severe Alzheimer’s disease

  • Or if there is intolerance/contraindication for acetylcholinesterase inhibitors

o Behavioral disturbance may require sedatives as a last resort (e.g. trazodone, sodium valproate, haloperidol)

33
Q

What psychotropic medication should we give patients with DLB?

A

Psychotropic Medications
o Start doses low and increase slowly with any medication used

o Older people are very sensitive to drug side-effects
o Treat comorbid psychiatric illness(e.g.depression)

  • Acetylcholinesterase inhibitors may provide symptomatic relief
    • Consider galantamine if the above are not tolerated
  • Clonazepam used for REM seep disturbance
  • Parkinson’s medications could relieve the tremors, but they could worsen the psychosis
  • Antipsychotics are dangerous and should not be used (they cause severe reactions –confusion, Parkinsonism, death)
34
Q

What psychotropic medication should we give patients with VD?

A

Only consider acetylcholinesterase inhibitors in people with vascular dementia if there is suspected comorbid Alzheimer’s, Parkinson’s dementia or dementia with Lewy bodies

Do not offer to patients with frontotemporal dementia

  • Key is to prevent further cerebrovascular disease by optimal control of major risk factors in people with a history of stroke or TIA
    • Risk Factors: Age, Male, HTN, Hypercholesterolaemia, obesity
35
Q

What are the NICE guidelines on psychotropic medications?

A

NICE GUIDELINES

▪Diagnosis and initiation by clinician with necessary knowledge & skills
Alzheimer’s –AChEI +/- Memantine for mild to moderate, Memantine for moderate

if intolerant to AChEI or 1st line for severe
Dementia with Lewy Bodies- AChEI
Vascular- none; AChEI only if co-morbid Alzheimer’s or DLB▪Do not stop AChE inhibitors because of disease severity alone.

36
Q

What psychological Interventions do we consider in dementia?

A

Psychoeducation and counselling may help people come to terms with a new, early diagnosis of dementia.

o Offer a range of activities

o Offer group cognitive stimulation (memory training and re-learning)

o Consider group reminiscence therapy - encourage someone to talk about their life often using prompt from their past
o Consider cognitive rehabilitation or occupational therapy
o Behavioural approaches - Identify and modify underlying triggers for difficult/risky behaviours (e.g. wandering may be due to disorientation, boredom or anxiety)

o Validation Therapy - Reassure and validate the emotion behind what is said

o Multisensory Therapy - As dementia advances and speech is lost, it may be easier to respond to touch, music etc.

37
Q

What adaptations can be made for patients with dementia?

A

o Always carry ID, address and contact number in case they get lost
o Dossett boxes/blister packs to aid medication compliance
o Reality orientation (visible clocks, calendars)
o Environmental modifications (e.g.patterned carpets can predispose to hallucinations, bad lighting can also increase confusion)
o Assistive technology(e.g.doormat buzzers)
o Do a home safety assessment and ensure that adaptations are made to home (fires, floods, falls)

Explore the person’s wishes for the future, supporting them to formalize these, e.g. writing an advanced decision (‘living will’); appointing a Lasting Power of Attorney (LPA) to manage financial/ health decisions, should they lose capacity to make these.

Driving is discussed early on: independence must be balanced against safety behind the wheel

38
Q

What social support is available for patients with dementia?

A

o Personal care, meal preparation and medication prompting
o Day centres provide enjoyable daytime activities and social contact
o Day hospitals enable daily psychiatric care for more complex patients

39
Q

How can we support carers?

A

o Emotionalsupport

o Offer carer’s assessment
o Educate about dementia
o Train to manage common problems

o Provide respite care

40
Q

What is the prognosis of dementia?

A
  • 2/3 of people with dementia live in their own home or with a carer
  • 5 yr mortality = 65% in men and 59% in women
  • MHOA important to have input
  • Always watch for abuse of the elderly
41
Q

How do we treat BPSD?

A