Older Persons Mental Health Flashcards

1
Q

Delirium/acute confusional state: Predisposing factors and precipitating events

A

Predisposing factors include:
age > 65 years
background of dementia
significant injury e.g. hip fracture
frailty or multimorbidity
polypharmacy

The precipitating events are often multifactorial and may include:

infection: particularly urinary tract infections

metabolic: e.g. hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration

change of environment

any significant cardiovascular, respiratory, neurological or endocrine condition

severe pain

alcohol withdrawal

constipation

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2
Q

Presentation of delirium?

A

memory disturbances (loss of short term > long term)
may be very agitated or withdrawn
disorientation
mood change/personality changes
visual hallucinations
disturbed sleep cycle
poor attention

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3
Q

Causes of acute confusional state - DELERIUMS

A

D - Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)
E - Eyes, ears and emotional
L - Low Output state (MI, ARDS, PE, CHF, COPD)
I - Infection
R - Retention (of urine or stool)
I - Ictal
U - Under-hydration/Under-nutrition
M - Metabolic (Electrolyte imbalance, thyroid, wernickes
(S) - Subdural, Sleep deprivation

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4
Q

Delirium management

A

Optimise environment:

Provide a calm, quiet environment.
Keep inside lighting appropriate for the time of day.

Plan for uninterrupted periods of sleep at night.
Help the person keep a regular daytime schedule.
Encourage self-care and activity during the day.

TREATMENT OF UNDERLYING CAUSE

the 2010 NICE delirium guidelines advocate the use of haloperidol or olanzapine

Minimise risk of self harm or harm to others with appropariate supervision (1:1, 2:1)

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5
Q

Delerium management specifically in Parkinsons

A

management can be challenging in patients with Parkinson’s disease, as antipsychotics can often worsen Parkinsonian symptoms
careful reduction of the Parkinson medication may be helpful
use lorazepam rather than haloperidol
if symptoms require urgent treatment then the atypical antipsychotics quetiapine and clozapine are preferred

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6
Q

DSM 5 criteria for delerium

A
  • Due to another medical condition
  • Substance intoxication
  • Substance withdrawal
  • Delirium due to multiple eiteologies
  • Medication related

Further specifiers:
Time: Acute - hours/days Persistent: weeks/months

Level of activity:
Hyperactive (increased psychomotor activity - e.g. myocolonus)
Hypoactive (psychomotor retardation)
Mixed (fluctuations between both

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7
Q

Highest prevelance of delirium

A

In increasing order:
Post repair of fractured hip
Post CABG
Nursing homes
ICU elderly
Terminally ill patients

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8
Q

Clinical course of delerium

A

Abrupt of acute onset - within days
Fluctuation in symptom severity:
Waxinag and waning, worse at night, may result in diagnostic uncertainty

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9
Q

Clinical course of delirium

A

Abrupt of acute onset - within days
Fluctuation in symptom severity:
Waxinag and waning, worse at night, may result in diagnostic uncertainty

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10
Q

Symptoms of hyperactive delrium?

A

Acting disorientated
Anxiety
Hallucinations
Rambling
Rapid changes in emotion
Restlessness
Cognitive defects

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11
Q

Symptoms of hyperactive delirium?

A

Acting disorientated
Anxiety
Hallucinations
Rambling
Rapid changes in emotion
Restlessness
Cognitive defects

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12
Q

Symptoms of hypoactive delirium?

A

Apathy
Decreased responsiveness
Flat affect
Laziness
Withdrawal
Cognitive defects

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13
Q

Delirium vs depression vs dementia

A

Delerium: abrupt, fluctuating, hours to weeks, alertness increased or decreased, activity increased or decreased, attention impaired, orientation impaired

Dementia: slow and incidious, usually stable daily course, lasts years, clear conciousnes, alertness normal, acitivty variable, attention usually normal and orientation is impaired

Depression: Variable onset, stable daily course, variable length, conciousness is clear, alertness normal, acitvity is variable, attention is usually normal, orientation is normal

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14
Q

How might you investigate an acute confusion?

A

Capillary Blood Glucose
CT head
FBC
LFT
TSH, B12, Folate
RPR
ABG
Levels of any drugs if appropriate (e.g. digoxin)
Urine dip +/- culture
MRI brain (focal neyroloigcal signs, head trauma, no clear cause found)
ECG
EEG (usually generalised slowing, low voltage fast activity in alcohol or sedative hypotonic withdrawal)
Cardiac enzymes
HIV
CXR
ANA RF CRP

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15
Q

Donepezil adverse effects?

A

is relatively contraindicated in patients with bradycardia
adverse effects include insomnia

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16
Q

Management of the non-cognitive symptoms of dementia?

A

NICE does not recommend antidepressants for mild to moderate depression in patients with dementia

antipsychotics should only be used for patients at risk of harming themselves or others, or when the agitation, hallucinations or delusions are causing them severe distress

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17
Q

Pharmacological management of Alzheimer’s disease?

A

First line: acetylcholinesterase inhibitors (donepezil, galantamine and rivastigmine) as options for managing mild to moderate Alzheimer’s disease

Second line: memantine (an NMDA receptor antagonist) - reserved for
- Pts with moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors
- as an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s
- monotherapy in severe Alzheimer’s

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18
Q

Non-pharmacological management of Alzheimer’s disease

A

NICE recommend offering ‘a range of activities to promote wellbeing that are tailored to the person’s preference’

NICE recommend offering group cognitive stimulation therapy for patients with mild and moderate dementia
other options to consider include group reminiscence therapy and cognitive rehabilitation

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19
Q

What is Alzehimer’s disease?

A

Alzheimer’s disease is degenerative condition of the brain that leads to memory loss and ultimately global impairment of brain function.

Most common form of dementia

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20
Q

Risk factors for development of Alzheimer’s disease?

A

increasing age

family history of Alzheimer’s disease
(5% of cases are inherited as an autosomal dominant trait)
mutations in the amyloid precursor protein (chromosome 21), presenilin 1 (chromosome 14) and presenilin 2 (chromosome 1) genes are thought to cause the inherited form
apoprotein E allele E4 - encodes a cholesterol transport protein

Caucasian ethnicity

Down’s syndrome

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21
Q

Macroscopic pathological changes in Alzheimer’s?

A

widespread cerebral atrophy, particularly involving the cortex and hippocampus

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22
Q

Microscopic pathological changes in Alzheimer’s?

A

cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein

hyperphosphorylation of the tau protein has been linked to AD

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23
Q

Biochemical pathological changes in Alzheimer’s?

A

there is a deficit of acetylcholine from damage to an ascending forebrain projection

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24
Q

Neurofibrillary tangles in AD

A
  • paired helical filaments are partly made from a protein called tau
  • tau is a protein that interacts with tubulin to stabilize microtubules and promote tubulin assembly into microtubules
  • in AD are tau proteins are excessively phosphorylated, impairing its function
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25
Q

‘4 A’s of Alzheimer’s disease’

A

Amnesia (recent memories lost first)
Aphasia (word-finding problems, speech muddled and disjointed)
Agnosia (recognition problems)
Apraxia (inability to carry out skilled tasks despite normal motor function)

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26
Q

Factors favouring 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

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27
Q

Dementia screening tools?

A

NICE recommend:
10-point cognitive screener (10-CS)
6-Item cognitive impairment test (6CIT)

The following are often used but not recommended by NICE in the non-specialist setting:
the abbreviated mental test score (AMTS), MOCA, ACE3, General practitioner assessment of cognition (GPCOG) and the mini-mental state examination (MMSE)
A MMSE score of 24 or less out of 30 suggests dementia

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28
Q

Investigating ?dementia

A

PRIMARY CARE - a blood screen is usually sent to exclude reversible causes (e.g. Hypothyroidism). NICE recommend the following tests: FBC, U&E, LFTs, calcium, glucose, ESR/CRP, TFTs, vitamin B12 and folate levels.

Patients are now commonly referred on to old-age psychiatrists (sometimes working in ‘memory clinics’).

SECONDARY CARE - neuroimaging is performed* to exclude other reversible conditions (e.g. Subdural haematoma, normal pressure hydrocephalus) and help provide information on aetiology to guide prognosis and management

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29
Q

Most common causes of dementia?

A

Alzheimer’s disease
cerebrovascular disease: multi-infarct dementia (c. 10-20%)
Lewy body dementia (c. 10-20%)

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30
Q

Rare causes of dementia?

A

Huntington’s
CJD
Pick’s disease (atrophy of frontal and temporal lobes)
HIV (50% of AIDS patients)

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31
Q

Important differentials for dementia?

A

hypothyroidism, Addison’s
B12/folate/thiamine deficiency
syphilis
brain tumour
normal pressure hydrocephalus
subdural haematoma
depression
chronic drug use e.g. Alcohol, barbiturates

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32
Q

What is Frontal Lobal degeneration? What are the three recognised types?

A

Frontotemporal lobar degeneration (FTLD) is the third most common type of cortical dementia after Alzheimer’s and Lewy body dementia.

There are three recognised types of FTLD:
Frontotemporal dementia (Pick’s disease)
Progressive non fluent aphasia (chronic progressive aphasia, CPA)
Semantic dementia

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33
Q

Common features of frontal lobal dementia

A

Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems

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34
Q

Pick’s disease clinical features including macroscopic and microscopic changes

A

This is the most common type and is characterised by personality change and impaired social conduct. Other common features include hyperorality, disinhibition, increased appetite, and perseveration behaviours.

Focal gyral atrophy with a knife-blade appearance is characteristic of Pick’s disease.

Macroscopic changes seen in Pick’s disease include:-
Atrophy of the frontal and temporal lobes

Microscopic changes include:-
Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques

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35
Q

What is CPA (chronic progressive aphasia)?

A

A recognized type of Frontotemporal lobar degeneration

Chief factor is non fluent speech.

They make short utterances that are agrammatic.

Comprehension is relatively preserved.

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36
Q

What is Semantic dementia?

A

A recognized type of Frontotemporal lobar degeneration

Here the patient has a fluent progressive aphasia.

The speech is fluent but empty and conveys little meaning.

Unlike in Alzheimer’s memory is better for recent rather than remote events.

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37
Q

NICE recommendations re:pharmacological management of frontal-lobal dementia?

A

NICE do not recommend that AChE inhibitors or memantine are used in people with frontotemporal dementia

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38
Q

What is Lewy-Body Dementia and what is the characteristic pathological feature?

A

Lewy body dementia is an increasingly recognised cause of dementia, accounting for up to 20% of cases.

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

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39
Q

What conditions is Lewy Body dementia associated with?

A

The relationship between Parkinson’s disease and Lewy body dementia is complicated, particularly as dementia is often seen in Parkinson’s disease. Also, up to 40% of patients with Alzheimer’s have Lewy bodies.

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40
Q

Features of Lewy Body dementia?

A
  • progressive cognitive impairment
  • in contrast to Alzheimer’s, early impairments in attention and executive function rather than just memory loss
  • cognition may be fluctuating, in contrast to other forms of dementia
  • usually develops before parkinsonism
  • parkinsonism
  • visual hallucinations (other features such as delusions and non-visual hallucinations may also be seen)
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41
Q

Diagnosis of Lewy Body dementia?

A

usually clinical
single-photon emission computed tomography (SPECT) is increasingly used (dopamine uptake scanning)

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42
Q

What drugs can be used to manage lewy body dementia?

A

both acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine) and memantine can be used as they are in Alzheimer’s.

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43
Q

What drugs should be avoided in patients with Lewy Body dementia and why?

A

neuroleptics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism

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44
Q

Three core features of Lewy Body Dementia?

A

Fluctuating cognition
Parkinsonism
Visual hallucinations

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45
Q

What is vascular dementia?

A

Vascular dementia (VD) is the second most common form of dementia after Alzheimer disease. 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. Vascular dementia has been increasingly recognised as the most severe form of the spectrum of deficits encompassed by the term vascular cognitive impairment (VCI)

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46
Q

What are the main subtypes of vascular dementia?

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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47
Q

Vascular dementia: risk factors

A

History of stroke or transient ischaemic attack (TIA)
Atrial fibrillation
Hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A family history of stroke or cardiovascular

Rarely, VD can be inherited as in the case of CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

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48
Q

How does vascular dementia present?

A

Several months or several years of a history of a sudden or stepwise deterioration of cognitive function.

Symptoms and the speed of progression vary but may include:
Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
The difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance

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49
Q

How is vascular dementia diagnosed?

A

A comprehensive history and physical examination

Formal screen for cognitive impairment

Medical review to exclude medication cause of cognitive decline

MRI scan – may show infarcts and extensive white matter changes, can show evidence of significant small vessel disease

NICE recommends that diagnosis be made using the NINDS-AIREN criteria for probable vascular dementia

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50
Q

NINDS-AIREN criteria for probable vascular dementia

A

Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event
- established using clinical examination and neuropsychological testing

Cerebrovascular disease
- defined by neurological signs and/or brain imaging

A relationship between the above two disorders inferred by:
- the onset of dementia within THREE MONTHS following a recognised stroke
- an abrupt deterioration in cognitive functions
fluctuating, stepwise progression of cognitive deficits

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51
Q

Management of vascular dementia?

A

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

Important to detect and address cardiovascular risk factors – for slowing down the progression

Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy

Managing challenging behaviours e.g. address pain, avoid overcrowding, clear communication

Consider pharmacological management if mixed subtype

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52
Q

Pharmacological management of vascular dementia

A

There is no specific pharmacological treatment approved for cognitive symptoms

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.

There is no evidence that aspirin is effective in treating patients with a diagnosis of vascular dementia.

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53
Q

The Deprivation of Liberty Safeguards is the procedure in law used where it is necessary to deprive a patient or resident of their liberty as they lack capacity to consent to treatment or care to keep them safe from harm.

These procedures must be authorised by a supervisory authority e.g. local authority.

What conditions must be met to allow for a DoLS to be put in place?

A

The following conditions must be met to allow a person to be deprived of their liberty under the safeguards:

The person must be 18 or over.

The person must be suffering from a mental disorder.

The person must be a patient in hospital or a resident in a care home.

The person lacks capacity to decide for themselves about the restrictions which are proposed so they can receive the necessary care and treatment.

The proposed restrictions would deprive the person of their liberty.

The proposed restrictions would be in the person’s best interests.

Whether the person should instead be considered for detention under the Mental Health Act.

There is no valid advance decision to refuse treatment or support that would be overridden by any DoLS process.

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54
Q

Capacity

A

All patients are initially assumed to have capacity
Capacity is decision-specific e.g. a patient may be able to decide which clothes to wear, but not where is safest to live
Capacity can be impaired permanently, temporarily, or can fluctuate
Patients deemed to have capacity are freely able to make decisions that the healthcare provider thinks unwise or dangerous

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55
Q

What are the 5 principles of the mental capacity act?

A
  1. Every adult is assumed to have capacity unless proved otherwise
  2. A person must be given all practicable help to make their own decisions before they are deemed to lack capacity
  3. Unwise, unsafe or dangerous decisions does not mean that person does not have capacity.
  4. All treatment given to a person who lacks capacity must be in the patients best interests
  5. Anything done for a person who lacks capacity must be done in the least restrictive way possible
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56
Q

An important differential of dementia is pseudodementia, which is primarily associated with cognitive deficits in older patients with depression.
What are the suggestive features?

A

Short duration of dementia
Equal effect on long and short term memory
Amnesia concerning specific events (often events are emotionally charged)
Often patient will very detailed complaint about memory disturbance
Patient may highlight failures in answers to questions relating to memory
Loss of social skills early in the illness
Patient will often answer “don’t know” to questions, as opposed to guessing close answers
Patient may make little effort in performing tasks

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57
Q

How can capacity be maximised?

A

Discuss the options in a time and place that helps them to understand and remember what you say.
Ask whether having a friend or relative with them might help them to remember information, or otherwise help them make the decision.

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58
Q

What is delerium?

A

Acute confusional state, with a sudden onset and fluctuating course.
May be hypoactive or hyperactive - recognised change in conciousness
Onset of 1-2 days.
CHANGE FROM BASELINE

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59
Q

What is Dementia?

A

Progressive decline in cognitive function usually occuring over several months. It affects many different areas of function, including:
Retention of new information, managing complex tasks, language and word finding difficulty, behaviour, orientation, recognitiion, ability to self care, and reasoning

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60
Q

Parkinson’s disease vs Lewy Body Dementis

A

In Parkinson’s disease typical features of Parkinson’s will present and precede confusion by over a year
Lewy Body dementia Parkinsonism tends to be less severe
Both are progressive with prominent auditory or visual hallucinations, delusions are well formed and persistent

61
Q

Which type of dementia presents with fluctuating cognition in comparison to other types?

A

Lewy Body

62
Q

How does frontolobal dementia usually present?

A

Social dishinibition
Family history

63
Q

What bloods are part of the ‘confusion screen/

A

TSH
B12
Folate
Glucose

64
Q

In which patients should haloperidol be avoided and lorezapam instead be considered

A

Patients with Parkinsons disease (promotes dopamine blockade so can result in psychosis and a deterioration in motor function)

65
Q

Lewy body dementia is the presence of dementia alongside two of the three of which core features?

A

Fluctuating attention and concentration
Recurrent well-formed visual hallucination
Spontaneous Parkinsonism

66
Q

What is pseudo-dementia?

A

Depressive dementia
Severe depression leading to psychomotor slowing, memory impairment and difficulties in concentration
Often presents with significant self neglect and weight loss as a result

67
Q

What is cognitive impairment?

A

Disturbance of higher cortical functions (memory, thinking, judgement, language, perception, awareness)
May be single or multiple, and may be static or progressive

68
Q

WHO/CD10 definition - dementia

A

Cognitive impairment: decline in both memory and thinking sufficient to impair ADLs

Problems with processing of incoming information - problems with maintain and directing attention

Clear consciousness

Symptoms present for at least 6 months

69
Q

WHO/CD10 definition - delirium

A

Impairment of cognition, disturbances of attention and consciousness level, abnormal psychomotor behavior, disturbed sleep-wake cycles
Onset is acute (hours/days)
Symptoms fluctuate and are typically worse at night

70
Q

Mental capacity is time specific and decision specific - what is meant by this?

A

Always assess a patient’s capacity to make a particular decision at the time it needs to be made. Don’t assume that because a patient lacks capacity to make a decision on a particular occasion, they lack capacity to make any decisions at all now or in the future.

71
Q

How does the inverse care law apply to dementia?

A

Those who are most dependent and vulnerable often have the least awareness of this disabilities

72
Q

Under what age is dementia considered early onset?

A

65 years

73
Q

What causes of early onset dementia are more common than in dementia affecting elderly patients?

A

FTD
Alcoholic
Huntings Disease

74
Q

What is BPSD?

A

Behavioral and psychological symptoms of dementia (non cognitive)
Including:
Depression
Hallucinations (more common in Lewy Body - NOT CHARLES BONNET - this is related to macular degeneration - these pt have insight)
Adigtation
Delusions
Apathy
Sleep problems

75
Q

BPSD clusters

A

Affective: agitation, screaming/crying, depression or dysphoria, anxiety, hoarding

Apathetic: indifference, lack of emotion, decreased motivation

Psychotic: delusions and hallucinations

Hyperactive: aggression, irritability, lability, resisting care, night time disturbance, pacing/wandering, disinhibiton

76
Q

What is an ABC chart?

A

Antecedent-Behaviour-Consequence

77
Q

Implied vs expressed consent?

A

Implied: pt dose not explicity state their consent but their actions suggest it
Expressed: explicitly stated in writing or verbally

78
Q

Why might someone lack capacity?

A
  • Dementia
  • Delerium
  • A learning disability
  • A brain injury
  • A mental health
    condition
  • A stroke
  • Unconsciousness due
    to accident / injury
  • Alcohol / drug use
79
Q

Illusion vs hallucination?

A

Illusion - misinterpretation of a stimulus
Hallucinations - an experience of a stimuli that is not real

80
Q

What is the two stage capacity test?

A

In order to assess capacity, the following two-stage test must have been followed:

Is there an impairment of or disturbance in the functioning of the person’s mind or brain?
Is the impairment or disturbance sufficient that the person lacks the capacity to make that particular decision?
The second stage of the test (or functional test) dictates that the person is unable to make a decision if they cannot:

Understand information about the decision to be made
Retain that information in their mind
Use or weigh-up the information as part of the decision process
Communicate their decision
If a person lacks capacity in any of these areas, then this represents a lack of capacity (Mental Capacity Act 2005: Code of Practice).

81
Q

Why is prognosis of acutely ill patients worse in the presence of delerium

A

Increase length of stay in hospital, increased complications (VTE, HAI)
Increased risk of readmission
Increased risk of instutionalisation
Increased one year mortality

82
Q

How long can delirium take to resolve?

A

Up to 3 months

83
Q

What is an IMHA?

A

Access to an IMHA is a statutory right for people detained under most sections of the Mental Health Act, subject to Guardianship or on a community treatment order (CTO).

When someone is detained in hospital or on a CTO it can be a very confusing and distressing experience.

IMHAs are independent of mental health services and can help people get their opinions heard and make sure they know their rights under the law.

84
Q

Section 2 mental health act

A
  • 2 doctors – at least 1 of whom should be Section 12(2) approved
  • 1 AMHP – not just SW now
  • Can take sometime for the 3 people to meet
  • Community or inpatient (anywhere except
    prison)
  • Section for maximum of 28 days for assessment (and treatment) of a mental disorder - then section 3 which can be refreshed or discharge
  • Appeal within first 14 days – heard within 7 days by a mental health tribunal
85
Q

Section 3 mental health act

A

2 doctors – at least 1 of whom should be Section 12(2) approved + 1 AMHP
- Often following a section two, may use a three straight away if pt known to services and their disorder is well understood
- Community or inpatient (anywhere except prison)
- Section for maximum of 6 months for treatment of a mental disorder, can be extended by 6 months and then by 12
- 1 Appeal to both hospital managers panel and tribunal.

86
Q

Section 136 mental health act

A

Police power to remove to a place of
safety from a public place for an
assessment by an AMHP and 1 doctor.
 Held up to 72 hours to allow
assessment
 Police to stay with person
 If needed second doctor attends for a
MHA assessment for Section 2 or

87
Q

Section S117 mental health act

A

Anyone who has been on section 3 is
entitled to S117 aftercare from local
authority

88
Q

Section 5(4) mental health act

A

Power granted to RMNs to detain an
inpatient (so someone already admitted to
hospital) for up to 6 hours for medical
assessment where mental illness is
suspected. Not for treatment
- Cannot be done in the Emergency Department
- Form to be completed
- Forms to be submitted to hospital manager

89
Q

Section 5(2) mental health act

A

Used for pts who have been admitted informally but then need detaining for assesment but NOT treatment

The RMO - consultant and responsible clinician or nominated deputy (nominated by responsible clinician - won’t be an FY1 - most likely registrar) can detain an inpatient for up to 72 hours under the mental health act

Cannot be done in the Emergency Department

No appeal
Legal form for hospital managers
To allow formal mental health act to be completed

90
Q

Community treatment order

A

Patient on S3 can be considered for a CTO
- Patient is well enough to leave hospital but
may default from treatment/follow up
- Treatment is necessary for the patients
health, safety or protection of others
- Patient can be recalled to hospital if they
do not comply with treatment, attend
appointments etc
- Can still appeal to the tribunal
Lasts 6 months

91
Q

Section 135 mental health act

A

Section 135 allows the police to enter your home and take you to (or keep you at) a place of safety so that a mental health assessment can be done. This could involve keeping you at home.

The police must have a warrant from the magistrate’s court allowing them to enter your home. An application for a warrant must be made by an approved mental health professional (AMHP), and can be given where there is reasonable cause to believe that you:

have a mental disorder, and
are being ill-treated or neglected, or
are unable to look after yourself.
The police must be accompanied by an AMHP and a registered medical practitioner.

The police can keep you at the place of safety for up to 24 hours, which can be extended for another 12 hours if it was not possible to assess you in that time. The time starts when you arrive at the place of safety, or whenever the police arrived if you are not taken somewhere else.

92
Q

What is the confusion assement method?

A

CAM diagnostic algoerithm

Feature 1 - acute onset fluctuating course
Feature 2- Inattention
Feature 3 - Disorganized thinking
Feature 4 - altered level of conciousness

Validated told for diagnosing delirium

93
Q

Normal aging vs cognitive impairment vs dementia

A

Normal aging

Not being able to remember of details of a conversation that took place a year ago, forgetting the name of an acquaintance, forgetting things and events occasionally, occasionally having difficulty finding words, family members generally not concerned

MCI

May affect memory, problem-solving, planning, visuospatial awearenes and language but DOES NOT interfere with daily life

Dementia

Progressive decline in cognitive function usually occuring over several months. It affects many different areas of function, including:
Retention of new information, managing complex tasks, language and word finding difficulty, behaviour, orientation, recognitiion, ability to self care, and reasoning

94
Q

What happens in memory clinic?

A

Dementia and sub-type diagnosis
Review after diagnosis
Care co-ordination
Interventions to promote cognition, independence and wellbeing
Pharmacological interventions

95
Q

Hx and collateral history in ?dementia

A

Course of cognitive impairment over time
Enquiry into specific cognitive domains
Functional disability - explore both basic and instrumental ALDs
Why now? Precipitant/life evnt/physical health change
Timeline - what changed first
Symptoms and impact (memory anterograde/retrograde, knowledge of current events, continence, falls, hallucinations, personality changes, sleep, appetite)
Another culprit? PMHx medication substance abuse, depression PTSD< menopause, vitamin def, polypharmacy, pain

96
Q

Key cognitive domains?

A

Concentration/attention
Patient/collateral rating of memory loss out of ten
Episodic memory impairment - new information (anterograde) and past events (retrograde)
Semantic memory
Language
Executive ability
Personality change
Use of memory aids

97
Q

Aspects of mini mental state examination (MMSE)

A

Appearance and behaviour
Speech
Mood (subjective/objectives)
Thought (form/content)
Perception
Cognition
Insight

98
Q

Rapid onset of dementia ‘symtpoms’ might be what?

A

Normal pressure hydrocephelus

99
Q

Managing driving and dementia dgx?

A

Fear of loss of infependence can be a barrier to early diagnosis
Well learned activity
Risk to pt and general public - must inform DVLA
Annual review
Pt and collateral may be complicit to conceal issues
Restrict driving repitore - e.g. no night driving, no long distance driving

100
Q

How to ensure a diagnosis of dementia is broken well?

A

Preperation
involvement of family
Explore pt perspective
Discolsure of dgx - not always appropriate but ideal
Response to pt reactions
Focus on QoL
Future planning
Effective communication

101
Q

Questions to ask in ?early onset dementia?

A

MEMORY LOSS

Memory - recent/remote
Employement - affect
Motor symptoms
Over eating
Risk (driving, wandering, cooking, impusivity, disinhibition, neglect, carer strain, being left alone, self harm, sucide, agression to others)
Y (U) Usual self - changes, over what time

Language (comprehension, expression, modality)
Accidents (continence)
Night (sleep disturbance)
Exclude other illness (mental/physical)
Sight (cortico-visual distrubance)

102
Q

What type of physical examination is important in ?dementia?

A

Neurological

103
Q

General management of dementia?

A

Explain diagnosis/prognosis

MDT referals - CMHT for aftercare, SALT psychologist,
Refferal to social services,
Refferal to age UK
Drivability assessment
UCL young dementias group (young onset)

Psychopharmacology: cholinesterase inhibitors +/- memantine depending on type, antispychotics/antidepressants for BPSD

104
Q

How might a patient with ?dementia be assesed?

A

Baseline blood tests (for Rx and to exclude ddx)
Neuroradiology - structural and function - MRI
Neuropsychology
OT functional assesment
SALT
+/- CSF genetic councilling and testing (early onset)

105
Q

Types of dementia classified by aetiology?

A

Neurodegenerative: AD, VD, FTD, PD, Lewy body, Korsakoff, Parkinsons, Mixed
Infective: HIV, HSV, syphillis, toxoplasmosis
Prion: CJD, FI
Inflammatory: vasculopathies, sarcoid, autoimmune
Metabolic: poorly controlled endocrine disease, metal exposure, vitamin deficiencies
Genetic: AD, MND, FTD, HD, Downs Syndrome

106
Q

Dementia in over 65s vs under 65s

A

Aetiology
Under 65s: AZ, VD Lewy Body, FTD, rarer types
Over 65s: AZ, VD Lewy Body

Presentation:
Under 65: more varied, memory less prominent, more likely to present with visual, motor, language or behavioral symptoms
Over 65:Typical memory, orientation and loss of executive skills more prominent

Prognosis/course
Under 65: Weeks- years
Over 65s:Typically year

107
Q

Alzheimer’s disease: course and onset, early presenting symptoms, neurological symptoms, mood and behavioral changes, structural brain imaging

A

Course and onset: Gradual, insidious, slow progression
Early presenting symptoms:
Neurological features:
Mood and behavioral changes:
Structural behavioral imaging:

108
Q

Alzheimer’s dementia: course and onset, early presenting symptoms, neurological symptoms, mood and behavioral changes, structural brain imaging

A

Course and onset: Gradual, insidious, slow progression
Early presenting symptoms: Memory impairment
Neurological features: Absent
Mood and behavioral changes: May be minimal initially but pre-existing anixety etc may worsen
Structural behavioral imaging: Volume loss in MEDIUM TEMPORAL LOBE, POSTERIOR CINGULATE

enlargement of cerebral sulci, loss of gyral volume and mild dilation of the ventricular system

109
Q

Frontal temporal dementia: course and onset, early presenting symptoms, neurological symptoms, mood and behavioral changes, structural brain imaging

A

Course and onset: Gradual with quick progression (particularly in younger patients)
Early presenting symptoms: Loss of executive ability and impaired social behaviours
Neurological features: + frontal release signs
Mood and behavioral changes: Apathy, loss of volition and disinhibition may be early features
Structural behavioral imaging: Frontotemporal atrophy

110
Q

Vascular dementia: course and onset, early presenting symptoms, neurological symptoms, mood and behavioral changes, structural brain imaging

A

Course and onset: Gradual, OR more abrupt onset with erratic course
Early presenting symptoms: Variable, there may be prominent dysexecutive features
Neurological features: +/- highly variably
Mood and behavioral changes: Depression common after stroke, emotional lability
Structural behavioral imaging: Maybe evidence of infarcts, bleeds, white matter ischemia

111
Q

Lewy Body: course and onset, early presenting symptoms, neurological symptoms, mood and behavioral changes, structural brain imaging

A

Course and onset: Fluctuating episodic course (may imitate delerium)
Early presenting symptoms: Perceptual disturbance (hallucinations) and parkinsonism, sleep disturbance
Neurological features: ++ (Parkinsonism)
Mood and behavioral changes: Paranoia and suspicious arising from psychotic symptoms
Structural behavioral imaging: No specific abnormalities

112
Q

Alcoholic dementia: course and onset, early presenting symptoms, neurological symptoms, mood and behavioral changes, structural brain imaging

A

Course and onset: Onset may be gradual but cognitive status fluctuates with drinking and withdrawal episodes
Early presenting symptoms: Memory problems and dysexecutive (frontal) features
Neurological features: -
Mood and behavioral changes: Depression commonly associated with alcohol misuse problems
Structural behavioral imaging: Age disproportionate cortical and white matter atrophy

113
Q

What is Posterior Cortical Atrophy?

A

Varient of AD or LBD
50-65 yrs
Problems with visual recognition, reading difficulties judging distances and managing coordination, sometimes light sensitivity, sometime hallucination.
Often acompanied by anxiety
Visual problems subjective despite normal visual examination

114
Q

Dementia mimics

A

Delirium
Functional - depression, anxiety, catatonia, chronic schizophrenia
Substance misuse
Menopause
Fibromyalgia
Normal pressure hydrocephalus
Sensory deprivation

115
Q

?Dementia - red flags

A

Rapid onset
<50 years
Recent trauma
Associate sx: weight loss, headaches, motor sx, seziures incontinence, raised IPC signs
Positive family history

116
Q

Types of memory?

A

Short term - limited in both capacity and duration
- Sensory memory - retaining impressions of sensory information

Long term- function of brain where something is remember for more than a matter of days:
1. Semantic (facts, not drawn from personal experience)
2. Episodic (memories related to specific events and the information related to that experience)
3. Procedural - how to do something, the specific steps to accomplish a task

117
Q

Dementia vs delirium: sleep-wake cycle

A

Dementia: often normal

Delirium: often reversed

118
Q

Dementia vs delirium: attention

A

Dementia: often normal

Delirium: significant inattention and lack of concentration

119
Q

Dementia vs delirium: duration

A

Dementia: months to years (lifelong)

Delirium: hours to weeks (some cases months)

120
Q

Dementia vs delirium: delusions

A

Dementia: systematised

Delirium: transient, poorly organised

121
Q

Dementia vs delirium: course

A

Dementia: slow decline - progressive

Delirium: fluctuations

122
Q

Dementia vs delirium: consciousness level

A

Dementia: alert/stable until terminal stages (earlier in LBD)

Delirium: fluctuations/impaired

123
Q

Dementia vs delirium: hallucinations

A

Dementia: primarily auditory

Delirium: visual and auditory

124
Q

Dementia vs delirium: rate of onset

A

Dementia: insidious - months to years

Delirium: rapid, hours to days

125
Q

Dementia vs delirium: psychomotor activity

A

Dementia: not usually any changes

Delirium: hyperactive, hypoactive, mixed

126
Q

AMT vs MMSE use in what setting

A

Developed by geriatricians, AMT is probably the best known test in general hospital usage. The Abbreviated Mental Test (AMT) score lacks validation in primary care and screening populations; most validity data refer to correlation to the Mini Mental State Examination (MMSE).

127
Q

Aspects of AMT

A
128
Q

Detainment and treatment against the patient’s will in a patient lacking capacity is covered by which act?

A

Mental health act (1983, amended 2007)

129
Q

Pathophysiology of vascular dementia

A

Restricted blood flow resulting in damage to the brain

130
Q

What is reversible dementia, and what are some examples of causes?

A

“Reversible dementias” are conditions that may well be associated with cognitive or behavioral symptoms that can be resolved once the primary etiology is treated

Subdural haematoma
Alcoholic
Normal pressure hydrocephalus

131
Q

CJD

A

Creutzfeldt-Jakob disease causes a type of dementia that gets worse unusually fast.

132
Q

LBD diagnostic criteria

A

A diagnosis of Lewy body dementia requires a progressive decline in cognition, as well as at least two of the following:
Fluctuating alertness and cognition
Repeated visual hallucinations
Parkinsonian symptoms

133
Q

Dementia BPSD

A

Usually NEGATIVE delusion - as opposed to manic delusions
Frequently persecutory - someone has stolen something or abandoned you
Misidentification syndromes - misidentifies people, places, objects or events
Related to sensory impairment

134
Q

Apathy vs depression

A

Apathy - sleep ok, appetite ok, etc
Both - chronic loss of motivation, withdrawn, etc

135
Q

Haloperidol vs benzodiazepines in management of delirium/dementia

A

Haloperidol: reduced falls risk, less likely to cause a delirium/worsen delirium - concerns with extrapyramidal symptoms, prolonged QT syndrome

Benzodiazepines: more suitable in Parkinson’s

136
Q

Non pharmacological methods of managing BPSD

A

Psychoeducation (carers/family and potential lot early on)
Specialised nursing care
Psychical activity
Specific therapies - Music therapy (only NICE reccomended therapy), reminiscence therapy, CBT

137
Q

Considerations for BPSD pharmacological intervention

A

Older pts with dementia are particularly vulnerable to side effects
Need to consider polypharmacy
Shorter term for duration of BPSD - lowest effective dose for the shortest time

138
Q

What antipsychotics are licensed to treat BPSD?

A

Risperidone and haloperidol

139
Q
A

Antipsychotics - minimum dose for minimum time - haloperidol or respiridone
Cognitive enhancers - cholinesterase inhibitors and memantine - manage depression and apathy
Benzodiazepines (association with falls, dependency and worsening cognition)
Antidepressants - AVOID TCAs due to side effects , citalopram has the best evidence but sertraline has good cardiac safety

140
Q

How long is a MHA section 2

A

28 days

141
Q

How long is a section 3?

A

Up to 6 months, can be renewed for a further 6 months and then a further 12

142
Q

Five key principals of MCA

A

Presumption of capacity
All practical steps taken to allow autonomy
Best interests
Least restrictive option
Allow unwise decisions

143
Q

Two stage test MCA

A
  1. Impairment of function of mind? (Dementia, delirium, even acute stress)
  2. Are they unable to:
    - Understand the information relevant to the decision
    - Retain the information long enough to make a decision
    - Weigh up the information given in the decision
    - Communicate their decision
144
Q

Safeguards involved with DoLS

A

Legal representation
Access to independent mental capacity advocates
Right of appeal to the Court of Protection

145
Q

Mental state examination components

A

Appearance - appropriate dress, unkempt, signs of self neglect, age, ethnicity

Behaviour - eye contact, appropriateness,

Speech - volume, quantity, tone of voice

Mood - subjective and objective - at present moment in time - are they congruent (euthymic)

Thought - form (delivery) and content (nature) -
Form: flight of ideas - thoughts too fast, pressure of speech - mouth can’t keep up, thought circumstantiallity (taking a long time to express idea), thought tangentiality
Content: delusions

Perception: hallucinations, ALL FIVE SENSES,

Cognition

Insight: lost? Entirely or aspects?

146
Q

Cognitive tests

A

Mini-ACE
MMSE
6CIT
AMT
MOCA
ACE-III

147
Q

What is Paraphrenia

A

Paraphrenia is a type of mental disorder characterized by paranoid delusions

148
Q

What is an encapsulated delusion

A

The definition of encapsulated delusion is “a fixed, circumscribed belief that persists over time and is not altered by evidence of the inaccuracy of the belief.”