core conditions - 2 Flashcards
Definition of old age psych?
who to always ask about with patients with dementia?
anyone referred to mental health services who is over 65 years
always ask about CARERS and how they’re doing
- for every pt with dementia there is almost always at least one carer
CAUSES OF COGNITIVE IMPAIRMENT? 6
- dementia
- delerium
- organic brain disease (eg CVA, encephalitis)
- psychoactive substance misuse
- psychosis
- depression
Types of dementia:
- common? 5
- rarer? 3
COMMON
- alzheimers
- vascular
- mixed alzheimers + vascular
- lewy-body
- fronto-temporal
RARE
- parkinson’s-disease dementia
- HIV dementia
- huntington’s dementia
ICD-10 definition of dementia? (incl timescale)
Syndrome due to disease of the brain
progressive neurodegenerative condition
Consciousness not clouded
Disturbance of multiple higher cortical functions:
- Memory & learning = Registration, storage and retrieval of new information
- language
- orientation
- abstract thinking
- problem solving
- attention and concentration
- Judgement and thinking,
- Processing of information,
- Emotional control,
- Social behaviour or motivation.
Can affect reason and communication skills - Difficulty attending to more than one stimulus at a time
Diagnosis = must impair ADLs, usually >6 months.
—> Dementia is NEVER part of ‘normal aging’.
What are the 5 ‘A’s of dementia?
ie the 5 main groups of features / symptoms
1) aMNESIA
2) aPHASIA
an impairment of language, affecting the production or comprehension of speech and the ability to read or write
3) aGNOSIA
inability to interpret sensations and hence to recognize things, typically as a result of brain damage. eg “visual agnosia”
4) aPRAXIA
loss of the ability to execute or carry out skilled movements and gestures, despite having the desire and the physical ability to perform them
5) aSSOCIATED behaviours – Behavioural and psychological symptoms of dementia.
THREE types of assessment of cognition?
what are each used for?
what 2 things must you always ensure a patient has before assessing cognition?
INFORMAL ASSESSMENT
Crude description of cognitive function based on your history taking (e.g. “orientated to time, place and person”)
FORMAL SCREENING TEST
Tests with high sensitivity used to screen whether further investigation / referral is warranted (e.g. AMTS)
FORMAL DIAGNOSTIC TEST
Tests with high specificity used as tools for diagnosis (e.g. MoCA / ACE-III)
make sure pt has:
1) glasses
2) hearing aids
ASSESSMENT OF SUSPECTED DEMENTIA:
- where normally referred to?
- two histories to take? 2
- bedside test to do? 1
- bloods to do? 7
- imaging? 1
referred to MEMORY CLINIC
histories:
- from pt
- collateral
cognitive test (eg ACE-3)
BLOODS:
- FBC
- U+E
- LFT
- folate
- ferritin
- B12
- TFTs
(also cholesterol + lipids if suspect vascular?)
Imaging = norm CT (but can use MRI if need more detail or younger person)
Differentials for dementia in older people to rule out? 8
incl acronym
DEMENTIA (=acronym)
D = Drugs / Delirium E = Emotions (ie depression) M = Metabolic disorders E = Eye + Ear impairment N = Nutritional disorders T = Tumours, Toxins, Trauma I = Infection A = Alcohol, Arteriosclerosis
nb around 25% of over 65yo have depression
BEHAVIOURAL + PSYCHOLOGICAL SYMPTOMS of DEMENTIA (BPSD):
- what dementias found in?
BEHAVIOURAL symptoms:
- communication / towards others? 4
- other emotional? 4
- physical? 3
PSYCHOLOGICAL symptoms
- mood? 2
- psychotic symptoms? 2
- other? 2
BPSDs are found in all types of dementia
BEHAVIOURAL
1) COMMUINCATION (/towards others)
- apathy
- repetitive questions / behaviour
- disinhibition / culturally inapprpriate behaviour
- swearing + aggression (incl physical)
2) OTHER EMOTIONAL
- agitation
- restlessness
- crying
- screaming
3) PHYSICAL
- Wandering
- Pacing
- Hoarding
PSYCHOLOGICAL
1) MOOD
- anxiety
- depression
2) PSYCHOTIC SYMPTOMS
- delusions
- hallucinations
3) OTHER
- misidentification
- insomnia
ASSESSMENT OF BPSD:
- what charts to use? how work?
- what treatable causes to look for? 6 (incl acronym)
- exam to do?
- hx to do?
Behavioural ABC charts
A = Antecedent
- What happened BEFORE the behaviour?
B = Behaviour
What was the BEHAVIOUR?
C = Consequence
What was the CONSEQUENCE?
look for causes = PINCH ME
P – Pain IN – Infection C – Constipation H – Hydration M – Medication E – Environmental
- mental state exam
- collateral hx (and pt hx)
Management of BPSD:
- 1st line?
- 2nd line?
- 3rd line?
1st line = TREAT THE CAUSE
- ‘pinch me’ causes
- refer to medics if necessary
2nd line = ENVIRNOMENTAL MODIFICATION
- and practical management
- eg education for family / staff
3rd line = MEDICATION
- use as last resort
- only RISPERIDONE is licensed for management of agitation
- use lowest possible dose for shortest possible time
- if alzheimers, Acetylcholinesterase inhibitors (e.g. Donepezil) can be useful
avoid A/Ps if possible as increased risk of:
- parkinsonism
- falls
- stroke
- cardiovascular event
- death
ALZHEIMERS:
- epidemiology?
- static risk factors? 3
- modifiable / acquired risk factors? 6 (2 medical, 4 social)
most common cause of dementia in ANY age group (about 50% - vascular is 20%)
STATIC RISKS
- advancing age
- trisomy 21
- mutations of amyloid precursor protein (apoprotein E4)
MODIFIABLE /ACQUIRED
- previous head injury
- hypothyroidism
- smoking
- alcohol
- obesity
- social isolation
ALZHEIMERS:
- describe THREE main pathophysiological features?
1) Widespread CEREBRAL ATROPHY – esp. medial temporal lobe = cortex and hippocampus
2) AMYLOID PLAQUES + NEUROFIBRILLARY TANGLES (caused by aggregation of tau protein)
- Accumulation of these = reduction in transmission of information and eventual brain cell death.
3) DEFICIT of ACETYLCHOLINE -> Loss of neurons and synapses
ALZHEIMERS:
- normal presentation and course of illness?
- –> Usually presents with MEMORY LOSS, with evidence of varying changes in:
- planning
- reasoning
- speech
- orientation
- Steady, gradual decline is common in AD with faster deterioration following delirium or physical illness
- memory impairment is usually the most prominent feature
ALZHEIMERS MANAGEMENT:
- bio? 3 (in which order)
- psych? 3
- social? 3
BIO
1) treat reversible causes (eg thyroid, depression)
2) acetylcholinesterase inhibitors (eg DONEPEZIL)
3) NMDA receptor antagnoist (eg MEMANTINE)
nb Both acetylcholinesterase inhibitors and NMDA receptor antagonists work by increasing levels of acetylcholine
- They don’t reverse the decline but can slow the rate of progression
- also used to help with associated BPSDs
PSYCH
- emotional support
- cognitive stimulation / rehabilitation
- treat co-morbid conditions (eg CBT for anxiety)
SOCIAL
- carer support
- occupational therapy
- social care interventions
nb the psych + social is same for all dementias - is only the bio that changes depending on diagnosis
Factors associated with poorer prognosis in alzheimers? 7
- Greater severity at presentation
- Male
- onset <65
- Parietal lobe damage
- Severe focal deficits
- Prominent behavioural problems
- Depression
VASCULAR DEMENTIA
- cause?
- presentation?
- pattern of progression?
- risk factors? 9
2nd most common cause of dementia over 65 years
Dementia due to infarction of the brain due to vascular disease.
Infarcts are usually small but cumulative in effect.
- Deterioration is step wise, not continuous
- onset more acute (often following stroke)
- often motor/sensory deficits in VD (depends where the ‘mini-strokes’ are)
- emotional + affective changes common
have vascular risk factors
Risk Factors:
- PMHx of Cardiovascular disease
- Smoking
- Diabetes
- HTN
- Hyperlipidaemia
- Polycythaemia
- Coagulopathies, Sickle cell anaemia
- Valvular disease
- Rare familial onset in 40s.
VASCULAR DEMENTIA
- bio management? 3
- bio option if mixed diagnosis? 1
- psych management? 3
- social management? 3
BIO
- LIFESTYLE changes (smoking cessation, exercise)
- consider daily ASPIRIN / anticoagulants
- consider meds to MODIFY RISK FACTORS (ie manage HTN, ^cholesterol + DM)
- NMDA antagonists (eg memantine) can be used if there’s a mixed diagnosis (nb actyl-cholinesterase inhibitors are not used in VD)
PSYCH
- emotional support
- cognitive stimulation / rehabilitation
- treat co-morbid conditions (eg CBT for anxiety)
SOCIAL
- carer support
- occupational therapy
- social care interventions
nb the psych + social is same for all dementias - is only the bio that changes depending on diagnosis
FRONTOTEMPORAL DEMENTIA
- norm age of onset?
- typical presentation and progression?
- three main features?
—> Uncommon but possibly under diagnosed.
45-64 years at presentation
- higher proportion of those with dementia under 65 have FTD (AD still most common)
- FHx components in 15%
Frontal and Temporal lobes = associated with personality, behaviour and language
Insidious onset and gradual progression
Memory and visuospatial ability spared
Presentation:
1) BEHAVIOUR-VARIANT
- changes in personality, behaviour, interpersonal and executive skills
- Early emotional blunting + apathy
- Early loss of insight
2) PROGRESSIVE NON-FLUENT APHASIA (PNFA)
- loss of language skills (ability to produce or understand language)
3) SEMANTIC DEMENTIA
- loss of semantic memory (knowledge)
FRONTOTEMPORAL DEMENTIA
- investigations used for diagnosis? 2
- bio management options? 1
- what med NOT to use? 1
- psych management? 3
- social management? 3
FRONTAL LOBE TESTS (they do poorly)
MRI
- younger pts so higher level of accuracy
- shows fronto-temporal atrophy
BIO
- some evidence for use of SSRIs in improving disinhibition
DO NOT use acetylcholinesterase inhibitors
emphasis on psychosocial!
PSYCH
- emotional support
- cognitive stimulation / rehabilitation
- treat co-morbid conditions (eg CBT for anxiety)
SOCIAL
- carer support
- occupational therapy
- social care interventions
nb the psych + social is same for all dementias - is only the bio that changes depending on diagnosis
LEWY-BODY DEMENTIA
- three core features?
- additional features? 3
CORE FEATURES
1) FLUCTUATING presentation (cognition, attention + alertness)
2) spontaneous motor features of PARKINSONISM (up to 70%)
3) VISUAL HALLUCINATIONS (about 2/3rds)
OTHER FEATURES
- frequent falls
- nighttime agitation
- depression (50%)
nb also a lot more sensitive to A/Ps (ie neuroleptic sensitivity) and so more likely to have EPSEs and neuroleptic malignant syndrome if given them
Pathophysiology of lewy-body dementia?
- age of onset?
- gender split?
Protein deposits develop in nerve cells (Neocortical Lewy body plaques)
Lewy Bodies are ‘alpha-synuclein cytoplasmic inclusions’ in the substantia Nigra, paralimbic and neocortical areas
onset 50-85 years
- F>M
How to differentiate dementia in Parkinson’s (DPD) vs Lewy Body (LBD)?
For DPD there must have been PD symptoms for at least a year before cognitive symptoms
If cognitive symptoms and Parkinson’s features start within a year of each other (either being present first) then it’s LBD
two types of imaging to do for lewy-body dementia + findings?
CT Head – shows generalised atrophy
SPECT - reduced striatal uptake of ligand for presynaptic dopamine transporter site.