Old Age Psychiatry Flashcards

1
Q

How common is depression in older adults, what is it associated with

A
  • 15% of older people, and 30% of older hospital inpatients are depressed at any time.
  • Depression in later life may be associated with cerebrovascular disease, vascular RFs and current or future cognitive deficits
  • Depression in older adults is also associated with bereavement, isolation, poverty, chronic pain, physical illness, and polypharmacy
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2
Q

How does a presentation of depression in older adults differ from younger patients

A
  • Older people may present in a similar way to younger people, but may show: physical symptoms (constipation, insomnia, fatigue), psychomotor agitation/ retardation, memory problems, executive dysfunction. Suicidal ideation should be taken very seriously (high completion %)
  • Pseudodementia occurs where depression mimics dementia
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3
Q

What is the prevalence of anxiety disorders and psychosis in old age

A
  • The prevalence and incidence of anxiety disorders fall with age, possibly due to under-reporting. They are more common in women and isolated people.
  • Many people with psychosis first become unwell in their youth, however, functional psychosis can develop for the first time in old age. This is called ‘late onset psychosis’ above the age of 40 and ‘very late onset’ above the age of 60 (paraphrenia.)
  • Positive symptoms are more common than negative symptoms and occur ore commonly in women (lose protective factor of oestrogen.)
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4
Q

Definition of dementia, when can it be diagnosed

A

An acquired progressive degenerative disorder giving global impairment of all mental functions in clear consciousness (must be present in clear consciousness for 6 months.)

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5
Q

Definition of mirror sign and sun downing

A
  • Mirror sign = autoprosopagnosia, inability to recognise own reflection.
  • Sun-downing = confusion worsening as in the evening
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6
Q

What is the prevalence of dementia in over 65 and over 80 year olds

A

5% over 65 and 20% over 80

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7
Q

Describe the geenral presentation of dementia

A

Problems are often attributed to ‘normal ageing’ or absent-mindedness at first

  • Dementia often begins with forgetfulness of recent events (anterograde amnesia.) This may first present with uncharacteristic mistakes (muddling up appointments.) With time, this then progresses to loss of long-term memory (retrograde amnesia.) Disorientated to time then place then person.
  • Problems with speech and language include both receptive and expressive aphasia.
  • May also get subcortical and behavioural symptoms
  • Behavioural and psychological symptoms of dementia: Behavioural= restlessness, disturbed sleep/day-night reversal, shouting, screaming, swearing sexual disinhibition, aggression. Psychological= delusions, hallucinations, depression/ anxiety
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8
Q

Prevalence of Alzheimer’s dementia. What are the RFs for AD

A
  • Most common form of dementia- 50-70% of dementia in older people
  • Risk factors: Down’s syndrome, previous head injury, hypothyroidism, family Hx, female sex, low IQ, vascular risk factors
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9
Q

What predisposes AD genetically? Why are patients with Down’s Syndrome more at risk

A
  • 40% have a positive family history of AD. Heritability (70%) is even greater if there is a history of early onset dementia (<55 y/o).
  • Inheritance is autosomal dominant and involves mutation of chromosome 21 (Gene APP (Amyloid precursor protein) and chromosome 19 (Apolipoprotein E- involved in breaking down β-Amyloid.)
  • People with Down’s syndrome are at greater risk of alzheimer’s due to having three copies of the APP gene on chr21
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10
Q

Describe the common neuropathology of AD

A
  • Amyloid plaques (beta amyloid deposits which can form beta pleated sheets in the hippocampus, amygdala) disrupt signalling between neurones, trigger immune-mediated inflammation and damage blood vessels to cause haemorrhage
  • Neurofibrillary tangles form after plaques trigger abnormal tau phosphorylation.
  • This accompanies atrophy, first in the hippocampus, then in the temporal and parietal lobes. Plaques and tangles lead to a loss of cholinergic neuronal function.
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11
Q

What is the cholinergic hypothesis of AD

A
  • Pathological changes lead to degeneration of cholinergic nuclei in the basal forebrain- nucleus basalis leading to a decrease in Ach.
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12
Q

What is the presentation of AD

A

Slow progressive decline in memory with a late pattern of onset. Poor spatial navigation can be an early sign. Usually get short term memory loss followed by long term memory loss. Causes a decline in judgement, thinking, planning and organising. Are aware of the environment and consciousness is preserved.

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13
Q

What are the FOUR As of AD

A

_A_mnesia, _A_phasia, _A_gnosia, _A_praxia

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14
Q

What can be seen on MRI or CT in AD

A
  • Hippocampal atrophy (medial temporal lobe atrophy). In end-stage there is widespread atrophy, which is no different from other end-stage dementias. Therefore, in imaging we have to identify AD in earlier stages and concentrate on the hippocampus and medial temporal lobe.
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15
Q

Prevalence and causes of vascular dementia

A
  • 2nd most common cause of dementia after AD
  • Results from small strokes, caused by thromboemboli or arteriosclerosis (stroke-related dementia.) On imaging, arteriosclerosis, cortical ischaemia and infarcts predominate (multiple lucenscies)
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16
Q

RFs for vascular dementia

A
  • Risk factor are the same as for strokes, cardiovascular risk factors include (history of TIA/ CVA/ Hypertension/ Diabetes/ Hypercholesterolaemia)
17
Q

Disease progression in VD

A
  • Acute onset/stepwise progression > periods of stability followed by sudden declines in cognitive function (but can be insidious progression due to small vessel disease), therefore sometimes distinguished from AD by progression
  • In some cases a single, importantly located stroke can cause a sudden dementia (strategic infarct stroke)
18
Q

Presentation of VD

A
  • Cognitively – impaired attention and frontal features predominate. Fluctuations in performance and nightime confusion are common
  • Personality and insight relatively preserved
  • May be focal neurological signs
  • Emotional lability, pseudobulbar palsy, gait disturbance, incontinence
19
Q

WHat is a lewy body? What predisposes to development of LBD

A
  • Lewy Bodies are abnormal eosinophilic, intracytoplasmic neuronal structures composed of alpha synuclein with ubiquitin. PD shares a problem in metabolising a-synuclein.
  • Men are more commonly affected, and although it may not be strongly genetic, risk increases in those with the APOE 4 allele.
20
Q

How can LBD be differentiated from Parkinson’s Disease

A
  • In Parkinson’s Lewy Bodies are confined to the substantia nigra, in DLB they are more widespread and involve cortical regions. In LBD, cognitive impairment precedes movement symptoms, or occurs within a year of their onset (contrasting with PD where movement disorder precedes cognitive impairment by at least a year.)
21
Q

How does DLB present

A
  • Often thought of hybrid of PD and AD with visual hallucinations, REM behavioural sleep disorder and autonomic dysfunction (postural hypotension)
  • Memory problems are often less prominent than in AD, at least at first. Two of the following alerts LBD:
    • Fluctuating cognition and alertness
    • Vivid visual hallucinations
    • Parkinsonism
  • Have neuroleptic sensitivity- antipsychotics are not indicated in LBD and may make symptoms worse, similar to PDD
  • SPECT – may show disproportionately severe occipital hypoperfusion
22
Q

What investigation will differentiate between DLB and PD

A

DatSCAN (shows reduction in dopamine transportation in PD)

23
Q

What are some differentials for dementia

A
  • Mild cognitive impairment
  • Delirium (sudden and fluctuating confusion),
  • Pseudodementia (low mood usually precedes cognitive problems- give don’t know answers when questioned),
  • Reversible causes (brain injury, endocrine, vitamin deficiency.)
24
Q

How does mild cognitive impairment present, how does this differ from dementia

A
  • A dementia-like syndrome, but not severe enough to be classified as dementia
  • Still able to function independently so cognitive impairment is not having a significant effect on their daily life
  • About 30% will develop dementia in 3 years
25
Q

What investigations (including cognitive tests) should be used to assess for dementia

A
  • Comprehensive History (including collateral) > PMH (head injury, vascular disease, CVD) and rule out other psychiatric illness (e.g ask about mood, psychotic symptoms)
  • Cognitive tests: AMTS, MMSE, MOCA, Addenbrooke’s Cognitive Assessment
  • Blood screening (Confusion Profile – FBC, U+E, TFT, B12, Folate, Ca, Glucose/HbA1c, Lipids +/- VDRL and HIV) to rule out reversible causes
  • Neuroimaging- CT Brain/MRI usual practice
26
Q

What score indicates AD in an MMSE

A
  • Mild AD: 21-26
  • Moderate AD: 10-20
  • Severe AD: < 10
27
Q

What important factors should be indentified in a dementia history

A
  • Timeline (gradual, progressive vs. stepwise vs. acute)
  • Ability to perform ADLs/attend to finances/manage household- are they able to look after themselves? Driving? Cooking? Leaving the tap on?
  • Language skills (speech, comprehension, revert to mother tongue)
  • Visuospatial (reading, writing, disorientation, getting lost)
  • Insight - Importance of COLLATERAL HISTORY
28
Q

First stage in the management of any dementia patient

A
  • Referral to Memory Clinic for MDT approach (Old Age Psychiatrists, Neurologists or Geriatricians working with Nurses, OT, Psychologists, Social Workers).
    • Assessment and diagnosis of dementia
    • Management of anti-dementia medication and BPSD
    • Post diagnostic support
29
Q

What biological interventions can be offered in each type of dementia

A
  • 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- Rivastigmine
  • Vascular- none; AChEI only if co-morbid Alzheimer’s or DLB
30
Q

What are some examples of reversible anticholinesterases, what are some side effects of their use

A
  • Reversible inhibitors of acetylcholinesterase- Denepezil, Rivastigmine and Galantamine- slow rate of cognitive decline and possible BPSD. ‘start low, go slow’
  • 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
31
Q

What is memantine

A

Non-competitive Glutamate receptor antagonist. Recommended for moderate Alzheimer’s disease intolerant to or with contraindication to AChE inhibitors or severe Alzheimer’s. Can also add to a Cholinesterase inhibitor if they have moderate disease

32
Q

How can you manage the behavioural and psychological symptoms of dementia

A
  • BPSDs are managed with behavioural and environmental strategies- medication is reserved for BPSD causing severe or immediate risk to person or others (antipsychotics/ benzos.)
33
Q

What psychological therapies exist for dementia

A

Includes Reminiscence therapy (encouraging someone to talk about their life, often using prompts from the past), cognitive stimulation therapy (activities that stimulate thinking concentration, memory), validation therapy (validates emotions behind behaviour) multisensory therapy (as speech is lost, non-verbal stimuli can soothe.)

34
Q

What social interventions exist for dementia

A
  • Age UK- befrienders society and Alzheimer’s society are useful organisations/ resources.
  • If not coping with ADLS, may need social services to complete a needs assessment including OT and PT.
  • May need a package of care at home.
  • If increased needs, may need alternative accommodation (sheltered, residential).
  • Need to support carers (again Alzheimer’s society is a good resource.)
  • Dossett boxes, assistive technology and reality orientation are all useful interventions
35
Q

What are the rules for driving with dementia

A
  • Do not automatically have to stop driving
  • 1/3 people with dementia still drive
  • If diagnosed, a driver must inform DVLA and insurers
  • Outcome- license renewed annually, license revoked or driving assessment