OPIC - Older Person's Mental Health Flashcards
Capacity
Who Lacks Capacity?
2-Stage Capacity Test
Making Best Interest Decisions
Assessing Capacity
- ) Who Lacks Capacity? - examples include:
- schizophrenia, bipolar, severe learning disabilities
- delirium, dementia, brain damage/injury, LOC
- drowsiness, intoxication with drugs or alcohol - ) 2-Stage Capacity Test - Mental Capacity Act 2005
- 1: cognitive impairment due to illness or drugs/alcohol
- 2: their capacity is time-specific and decision specific, should try to give them time for their capacity to return - ) Assessing Capacity
- understand information relevant to the decision
- retain that information
- weigh that information into their decision-making
- communicate their decision - ) Making Best Interest Decisions - if lacks capacity
- care of the patient is the first concern
- use advocates the patient may have identified
- what the patient would have wanted if had capacity
- treat patients as individuals and with dignity
Legalities in Decision Making
Advance Statements Advance Decision to Refuse Treatment Lasting Power of Attorney (LPS) Deputies appointed by the Court of Protection Deprivation of Liberty Safeguards (DoLS)
- ) Advance Statements - not legally binding
- written statement that sets down your preferences, wishes, beliefs and values regarding your future care - ) Advance Decision (to Refuse Treatment)
- decision to refuse a specific type of treatment at some time in the future. It is legally binding - ) Lasting Power of Attorney (LPS) - a legal document that lets you appoint one or more people to make decisions on your behalf when you lack capacity
- types: health+welfare, property+financial affairs, only health+welfare allows them to make medical decisions - ) Deputies appointed by the Court of Protection
- court of protection assigns a deputy to essentially act as your lasting power of attorney - ) Deprivation of Liberty Safeguards (DoLS)
- A means to protect the rights of patients who lack capacity who are detained in a hospital or care home
- when it’s necessary to deprive a patient (who lacks capacity) of their liberty to keep them safe from harm
- procedure prescribed in law, can only be used in a care home or hospital and must ask the local authority
- can be used for up to 1 year
Sectioning Under the Mental Health Act
Section 2 Section 3 Section 5 Community Treatment Order (Section 17a) Section 135 Section 136
- ) Section 2 - up to 28 days, not renewable
- requires an approved MH professional (AMHP)
- treatment can be given against a patient’s wishes
- section 4 is a 72hr assessment order which is often changed to a section 2 upon arrival at a hospital - ) Section 3 - up to 6 months, can be renewed
- requires an AMHP along with 2 doctors who must have seen the patient within the past 24 hrs
- treatment can be given against a patient’s wishes - ) Section 5 - for voluntary patients in hospital
- 5(4): doctor can legally detain a patient for 72 hours
- 5(2): nurse can legally detain a patient for 6 hours - ) Community Treatment Order (Section 17a)
- used to recall a patient to the hospital for treatment if they do not comply with conditions of the order in the community, such as complying with medication
5.) Section 135 - allows the police to break into a property to remove a person to a Place of Safety
- ) Section 136 - allows the police to take a person from a public place (w/ suspected mental disorder) to a Place of Safety for up to 24 hours
- a Mental Health Act assessment should be arranged
Delirium
Pathophysiology
Precipitating Factors
Clinical Features
Complications
- ) Pathophysiology - acute onset (1-2 days) of confusional state w/ altered level of consciousness
- can be hyperactive, hypoactive or mixed (fluctuating)
- hyperactive is more common but easier to spot
- hypoactive has a worse prognosis
- risk factors: >65s, dementia, significant injury e.g. hip fracture, frailty, multimorbidities, polypharmacy - ) Precipitating Factors - can be multi-factorial
- infection: particularly a UTI or chest infection
- metabolic: ↑/↓ Na+, ↑Ca2+, ↑/↓ BG, dehydration
- severe pain, alcohol withdrawal, environment change
- significant cardio, resp, neuro or endocrine condition
- medications: opioids, anti-cholinergic, antidepressants, antipsychotics, anticonvulsants,
- others: illicit drugs, hypoxia, ↓sleep, hypothermia, malnutrition, organ dysfunction - ) Clinical Features
- duration: days (hours to weeks), can be longer depending on the previous mental state
- fluctuating sx: worse at night, periods of normality
- hyperactive: sleep-wake disturbance, agitation, wandering, aggression, hallucinations,
- hypoactive: inattention, ↓arousal, lethargy, withdrawal
- others: short-term memory disturbance - ) Complications
- delirium can continue for a period of time after the cause has been treated
- increased mortality, prolonged admission, increased risk of developing dementia
- can take up to 3 months to return to baseline whilst some never get back to their baseline
Delirium vs Dementia
Onset and Progression
Hallucinations
Speech
Consciousness and GCS
- ) Onset and Progression
- delirium: rapid onset with a fluctuating course
- dementia: slow onset and steady decline - ) Abnormal Perceptions - delusions, hallucinations
- can be present in delirium, whilst rare in dementia - ) Speech - can both be slow but delirium can be fast
- ) Consciousness and GCS - reduced in delirium
Management of Delirium
Investigations
Cognitive Assessments
Environmental Management
Pharmacological Management
- ) Investigations
- basic obs/EWS, GCS/AVPU,
- confusion screen: FBC, CRP, blood cultures, U+Es, LFTs, TFTs, clotting, bone profile, haematinics, glucose
- urine dip: must also have clinical sx to diagnose UTI
- imaging: CXR, CT Head - ) Cognitive Assessments
- Abbreviated Mental Test (AMT-10): score of <8 is suggestive of possible confusion, do another test:
- 4AT: a specific delirium assessment tool
- Confusion Assessment Method (CAM) is much longer and more specific
- MMSE can also be used to exclude delirium - ) Environmental Management - first-line
- move into a separate room, clocks to orientate them
- familiar objects and familiar people around them
- ↓noise, adequate lighting, ambient temperature
4.) Pharmacological Management - last-line, persistent wandering and delirium aren’t indications for sedation
- sedatives can actually worsen delirium
- (PO/IM/IV) haloperidol (0.5mg) or olanzapine first-line
- anti-psychotics are contraindicated in Parkinson’s as they worsen sx so haloperidol shouldn’t be used
- lorazepam or atypical antipsychotics (e.g. olanzapine)
are used instead
Dementia
General Information Risk Factors Cognitive Features BPSD - Behavioural and Psychological Sx of Dementia Differential Diagnosis
- ) General Information - progressive, irreversible syndrome with a range of cognitive and behavioural sx
- 850,000 in the UK, 1/14 of over 65s with dementia
- 50-75% Alzheimer’s, up to 20% vascular
- 10-15% Lewy-body, 2% frontotemporal - ) Risk Factors
- ↑age, mild cognitive impairment, LD (e.g. Down’s)
- genetic, cardio/cerebrovascular disease, Parkinson’s
- smoking, alcohol, HTN, diabetes, obesity, depression - ) Cognitive Features
- memory loss: learning new info, recent events, people’s names, vague w/ dates, miss appointments
- dysphasia and dyspraxia, disorientation (time, place)
- ↓executive function: planning, problem-solving - ) BPSD - can fluctuate, can last > 6 months
- difficulties w/ ADLs: eating, hygiene, dressing etc.
- motor disturbance: wandering, restlessness, pacing
- agitation and emotional lability: easily upset, mood swings, argumentative, challenging behaviour
- sleep cycle disturbance, social or sexual disinhibition
- depression and anxiety, withdrawal or apathy
- psychosis: delusion and/or hallucinations
- risks: driving, wandering, leaving stove on etc…
- ) Differential Diagnosis - ‘reversible dementia’
- mild cognitive impairment (MCI): not severe enough to diagnose dementia, ↓impact on ADLs, ↓progression
- depression, delirium, vision and hearing deficits
- thiamine/B12/folate deficiency, hypothyroidism
- medication: polypharmacy, sedatives, anticholinergic adverse effects, antiepileptics, corticosteroids, NSAIDs
- normal pressure hydrocephalus (dementia + urinary incontinence + gait abnormality)
- brain tumour, subdural, HIV
Assessment and Management of Dementia
Examinations
Cognitive Assessment Tools
Investigations
Non-Pharmacological Management
- ) Examinations
- neurological: sensory, motor, visual, auditory sx, coordination and gait abnormalities
- cardiovascular: HTN, arrhythmias, PVD - ) Cognitive Assessment Tools - all only suggestive
- GPCOG: patient score out of 9, 8+ = normal, 0-4 = cognitive impairment, 5-8 = inconclusive
- MMSE: better to exclude dementia, out of 30, 24+ is normal, 19-23 = mild, 10-18 moderate, 0-8 = severe
- others: 10 point cognitive screener (10-CS), test your memory (TYM) - ) Investigations - to exclude reversible causes
- bloods (to exclude reversible causes): FBC, CRP, U+Es, LFTs, TFTs, HbA1c, Calcium, B12/folate
- urine dip +/- MC+S, CXR, ECG, HIV/syphilis testing
- CT/MRI: first-line, used to clarify the subtype apart from frontotemporal which can be a clinical diagnosis - ) Non-Pharmacological Management
- risk assessment: driving (patient/doctor must inform DVLA), cooking, neglect, wandering, alcohol, smoking
- MDT approach: GP, psychiatrist, occupational therapist, support worker, carer, Age UK
- tailored activities to the patient to promote wellbeing
- group cognitive stimulation therapy for mild-mod
- group reminiscence and cognitive rehabilitation
- must inform DVLA: either the patient or doctor
Alzheimer’s Dementia
Pathophysiology
Genetics
Clinical Features
Pharmacological Management
- ) Pathophysiology - abnormal proteins kill neurones
- ß-amyloid plaques: accumulate and clump together between neurones due to abnormal breakdown
- neurofibrillary tau tangles: tau protein is abnormal and microtubule structures collapse inside the neurone
- macroscopic changes (CT/MRI): global atrophy, sulcus widening, enlarged 3rd/4th interventricular spaces - ) Genetics - defects in these proteins:
- early onset: ß-amyloid precursor, presenilin 1/2
- late-onset: apolipoprotein E gene
- most cases are sporadic, linked to Down syndrome - ) Clinical Features
- progression: insidious onset with slow progression
- usually presents with cognitive decline: memory loss, difficulty w/ executive function or nominal dysphasia
- 4As: amnesia, aphasia, apraxia, and agnosia - ) Pharmacological Management - AChE inhibitors (donepezil, rivastigmine, galantamine) or memantine
- monotherapy: AChEi or memantine (if severe)
- memantine if AChEi are contraindicated/intolerant or are already on an AChEi for other reasons
- avoid antidepressants, antipsychotics only used if psychosis is causing them severe distress
Vascular Dementia
Pathophysiology
Diagnostic Features
Pharmacological Management
- ) Pathophysiology - cerebrovascular disease causing ischaemia or haemorrhage
- sub-types: stroke-related VD (infarct), subcortical VD (small vessel disease), mixed VD (VD+Alzheimer’s)
- risk factors: h/o of stroke/TIA, AF, HTN, DM, obesity, hyperlipidemia, smoking, coronary heart disease
- initial management involves ↓ these risk factors
2.) Diagnostic Features - step-wise deterioration of cognitive function with focal neurological symptoms
- cognitive decline interfering w/ ADLs
- abrupt deterioration in cognitive functions or
fluctuating, stepwise progression of cognitive deficits
- cerebrovascular disease: on MRI or focal neuro sx: seizures, problems w/ vision, speech, weakness, gait
- onset of dementia w/in 3 months of a stroke
3.) Pharmacological Management - only if they have VD along with Alzheimer’s, Parkinson’s or Lewy-body
Lewy Body Dementia
Pathophysiology (+4 locations)
Clinical Features
Investigations
Pharmacological Management
- ) Pathophysiology - aggregation of alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the brain:
- substantia nigra, paralimbic and neocortical areas - ) Clinical Features
- gradually progressive cognitive impairment
- fluctuating cognition, attention and alertness
- often presents w/ early impairment in cognitive function, memory loss not as apparent in early stages
- parkinsonian features (e.g. bradykinesia, rest tremor, or rigidity) usually develops after cognitive impairment
- recurrent visual hallucinations as well as delusions
- REM sleep behaviour disorder - ) Investigations - clinical diagnosis but can also use:
- SPECT (single-photon emission CT)/DaTscan: scans uptake of dopamine, (90% sensitivity, 100% specificity) - ) Pharmacological Management
- donepezil and/or rivastigmine (both if severe)
- galantamine if others not tolerated
- memantine if AChE inhibitors contraindicated
- avoid anti-psychotics as they can cause irreversible parkinsonism
Frontotemporal Dementia (Pick’s Disease)
Pathophysiology
Clinical Features
Pharmacological Management
- ) Pathophysiology - atrophy of frontal/temporal lobe
- focal gyral atrophy with a knife-blade appearance
- microscopic changes: pick bodies (accumulations of TAU protein that stain with silver), gliosis, neurofibrillary tangles, senile plaques
- insidious and early onset (<65) - ) Clinical Features
- personality change and impaired social conduct
- disinhibition, dysphasia (expressive or receptive)
- ↑appetite, hyperorality (examine objects by mouth)
- perseveration behaviours: get ‘stuck’ on a topic/idea
- relatively preserved memory and visuospatial skills
- primitive reflexes - ) Pharmacological Management
- AChEi and memantine are not recommended for use