Psychiatry Flashcards
What is Mild Cognitive Impairment (MCI) defined as?
Evidence of early memory decline on formal memory tests (e.g. MMSE) without clinical evidence of other features of dementia
What can MCI be due to (4)
Early stages dementia (10-15% → dementia in 1yr)
Depression/anxiety
Stress
Physical problem
What are the functions of the frontal lobe? (3)
How may problems manifest
- Voluntary motor activity (learning/initiating/stopping)
- Speaking ability
- Elaboration of thought (behaviour, logic, personality)
Problems: disinhibition, initiating action, reasoning/abstract thought
What are the functions of the parietal lobe? (3)
How may problems manifest
- Processes sensory info – locating/making sense of objects, sequence of actions
- Proprioception
- Calculation and construction
→ Problems recognising faces/objects
Difficulty carrying out a sequence of actions
What are the functions of the temporal lobe? (3)
How may problems manifest
- Attention
- Recording and storing verbal and visual memory
- Learning of information
Problems: diminished attention, short term memory probs + producing speech
What proportion (%) of >65s have dementia? What % of >80s? What % of >95s What % of those in care home? What M:F ratio?
5% >65s
20% >80s
1/3 >95s have dementia (doubles every 5yrs)
- 64% in care homes have dementia
- 2/3 with dementia are women
What are the main 8 types of primary dementia? (+ proportions)
Alzheimers (62%) Vascular (17%) Mixed dementia (10%) - mixed AD/Vascular Lewy body (4%) Parkinsons Disease (2%) Fronto-temporal (2%) Huntington's Progressive supranuclear palsy
What are some different types/causes of vascular dementia (8)
o Post-stroke o Multi-infarct dementia o Subcortical vascular dementia o Mixed subcortical and cortical o Cerebral infarcts o Binswanger’s disease o Cerebral Autosom Dom Arteriopathy w. Subcortical Infarcts and Leukoencephalopathy (CADASIL) o Vasculitis (eg lupus)
How are secondary causes of dementia classified?
Infections Trauma Toxic/Metabolic Intracranial malignancy (primary/metastatic) Hydrostatic causes (hydrocephalus) Endocrine
List some infective causes of dementia (6)
o Syphillis o Cryptococcus o Sclerosing panencephalitis (SPE) o Progressive multifocal leukoencephalopathy (PML) o HIV o Creutzfield-Jacobs disease (CJD)
List some Toxic/Metabolic/Endocrine causes of dementia (8)
Alcohol-Korsakoff / Thiamine defc Drug intoxication / medication SEs Heavy metals Paraneoplastic Hypothyroidism Inherited metabolic disorders (eg. Wilsons) VitB12 + Folate defc Anoxia (post-cardiac arrest)
What are the clinical features of the early phase of dementia (3)
How many years usually in this phase?
- Difficulty embracing change
- Short term memory loss
- Repetition of questions
3-4yrs
What are the clinical features of the middle phase of dementia (5)
- Difficulty with daily tasks
- Failure to recognize people
- Needs prompting
- Disorientation in time, place and person
- Memory for distant past often remains good
What are the clinical features of late stage dementia (5)
How many years usually in this phase?
- Aggression
- Wt loss, poor appetite, dysphagia
- Incontinence
- Decline in speech
- Increased frailty
1-2yrs (intensive care needs)
List some RFs for dementia (7)
- Smoking (atherosclerosis risk + vasc dementia)
- Alcohol → high quantities, mod quantities protective
- Atherosclerosis → risk vascular/ AD
- Hypercholesterolaemia → vascular/ AD
- Age → esp vascular/ AD
- MCI
- Plasma homocysteine
List the Dx criteria of Alzheimer’s (4)
What is the mean life expectancy after Dx
1. Evidence of memory impairment plus ≥1 of: Agnosia Language problems Coordination problems (apraxia) Impaired exec func
- Present >6m
- Impairment of functioning
- No other medical/psychiatric explanation
What are the 3 genes involved in early-onset AD
How is it inherited
- Amyloid precursor protein (APP) chromosome 21
- Presenilin gene 1 (PSEN-1), chromosome 14
- Presenilin gene 2 (PSEN-2), chromosome 1
Autosomal dominant
What brain changes may be seen in Alzheimers disease (compared to a normal brain) (3)
What chemical structures would be found (under microscopy) (2)
Cortex atrophic; damaged areas involved in thinking, planning and remembering
Hippocampus severely atrophic; this area plays a key role in memories and is affected early
Ventricles of brain enlarged
Plaques + Tangles (Beta-amyloid)
How do plaques + tangles affect the brain?
Plaques → block signalling/activate inflamm → cell death
Tangles → destroy cell transport system (func)
What are the Dx criteria for vascular dementia (3)
Same cognitive impairments as AD
Deficits → limitation with ADLs (+ not due to physical effects of stroke alone)
Evidence of cerebrovascular disease O/E + imaging
What is the risk increase + % incidence (within 1yr) of dementia after a stroke?
Increased risk x9
25% stroke pts develop new dementia after 1yr
What is the difference b/wn cortical + subcortical vascular dementia
Cortical = multi-infarct (step-wise decline after series of small strokes in cortex)
Sub-cortical = ischaemic damage from demyelination of nerve shafts
Affects inner parts of brain
Often in people with H/o HTN
List the RFs for vascular dementia (9)
o FH stroke/ vascular dementia
o HTN
o CV disease
o Hypercholesterolaemia
o Diet high in sat fat
o DM
o Lack of physical activity
o Smoking
o XS alcohol
What are the clinical features of vascular dementia / cerebrovascular disease (10)
‘Step wise’ progression with stable disease and then sudden deteriorations
- Memory problems (less apparent earlier on)
- Difficulty with concentration and communication
- Seizures
- Depression
- S+S of stroke disease
- Incontinence
- Emotional lability
- Changes in behavior
- Visual problems and perceptual difficulties
- Early gait disturbance, unsteadiness and falls
What are the genetic contributions to vascular dementia (3)
Notch 3 - CADASIL
APP variations - HCHWA (heritable cerebral haemorrhage with amyloidosis)
Hyperchol/HTN/DM all have genetic components
M:F ratio of Lewy Body Dementia
Average life expectancy after Dx
Slightly higher in males
Av life expectancy 5-7yrs after Dx
What may cause downwards fluctuations in Lewy Body Dementia (3)
What are the main aims/focus of management
Medications
Infections
Natural course of disease
Managing neuropsychiatric disturbances + movement disorders
What are lewy bodies?
How do Lewy Bodies cause brain changes?
Lewy bodies = abnormal structures responsible for disrupting brain function
- made up of alpha-synuclein protein
- They interrupt action of acetylcholine + dopamine
What areas of the brain affected in Lewy Body Dementia
Substantia nigra (= classical Lewy bodies - seen in PD)
Cortex degeneration (= cortical Lewy bodies)
Parietal / temporal lobes/ cingulate gyrus shrinkage
What are the core features (3) + supporting features (5) to Lewy Body Dementia
Core:
Fluctuating cognition
Parkinsonism features – if sig cognitive decline within 1y of Parkisonism = LBD
Visual hallucinations – complex + detailed, not always distressing, may also have delusions
Supportive:
Syncope
Falls
Autonomic abnormalities eg postural hypotension
Sensitivity to neuroleptics (should be avoided)
REM sleep behav (gesture/speak in sleep - yrs before)
What are the Dx criteria for LBD
Progressive cognitive decline (prominent memory impairment may not occur in early stages)
Deficits on tests of attention and frontal-sub-cortical skills and visuospatial ability may be especially prominent
Reduced ability to perform ADLs
2 of core Sx = probable; 1 core Sx = possible
Define the criteria for Delirium (4)
Acute onset w. fluctuating course Disturbance of attention / consciousness Change in cognition i.e. worsening confusion Evidence from H/Ex/Ix consequence from: - General medical condition - Drug withdrawal - Drug intoxication - Multiple aetiologies
List some other associated features of delirium (not Dx criteria) (4)
Motor changes (slowness, restlessness, agitation) Emotional changes (anxiety, fear, depression)
Delusions (paranoid, fleeting)
Hallucinations (usually visual)
What is the prevalence of delirium in general hospitals?
Describe the epidemiology of delirium in dementia pts
20% prevalence in general hosps (varied in pt grps)
2/3rd dementia pts in hosp have delirium
50% delirium is dementia pts
Dementia pts 5-10x more likely to develop delirium
(+ 3x risk developing dementia with delirium)
List things to be included O/E in delirium (7)
Conscious level: GCS/AVPU
Cognition: AMT (<8) / MMSE
MSE
Infection: any obvious source e.g. cellulitis
Nutrition/Hydration
Retention/Constipation: Abdo Ex/DRE/bladder scan
Neuro Exam inc. speech
List some 1st line (9) + 2nd line (6) investigations into delirium
1st line: CRP* U+Es inc. Ca LFTs / TFTs / FBC / Glucose Urinalysis CXR ECG
2nd line: CT head / MRI head EEG Specific cultures e.g. blood, sputum LP ABG
List some predisposing RFs for delirium (5)
Over 65 Physical frailty Dementia Multiple co-morbidities Sensory impairment
List some management approaches used to prevent delirium (8)
Identify high-risk pts Orientation + familiarity Hydration/nutrition Minimise provocation (tubes, noise) Promote night time sleep Reduce medication (avoid anticholinergics + opiates) Facilitate vision/hearing (glasses/hearing aids) Keep mobile
List some complications of delirium (9)
Medication SEs Incontinence Pressure ulcers Falls Malnutrition Hosp-acquired (nosocomial) infections PTSD Functional decline Death
What advice should be given to family regarding management of delirium
Emphathise with distressing for them (may not recog)
Stress importance of their input in the management
Open visiting hours - encourage to come sit
Orientation tactics e.g. bring objects from home
Help at meal times
In what instances (2) in delirium are sedative drugs used
What are the guidelines of sedative use in frail delirium pts (3)
Haloperidol + lorazepam used
Rapid tranquilisation of agitated pt where immediate risk of harm/danger
Short term control of distress
Only use 1 drug
Start at lowest poss dose
Consider increasing after 2hrs
What info regarding recovery from delirium should be discussed with family
If simple cause, can recover in couple of weeks
More co-morbidities complicates/delays this
1/3rd complete recovery + to baseline
1/3rd recover slower + don’t restore full functioning
1/3rd never really properly recover
What is the prevalence of paranoid disorder in >65s
1% of >65s
List the common features of delusional disorder in the elderly (6)
Persecutory/reference delusions
Ideas of theft / ill-treatment / poisoning
Normal speech
No FH
No Dementia
No prior illness
List some RFs for paranoid disorder in the elderly (7)
Female
Never married
Living alone
Social isolation
Sensory impairment
Paranoid personality
Schizoid personality
List the DDx of elderly paranoid disorder (8)
Delirium (do MMSE to exclude) Dementia (do bloods/Ex to exclude) Delusional disorder (late scz / paraphrenia / psychotic depression / mania)
Organic cause: Post CVA Subdural haematoma Epilepsy Uraemia Hepatic encephalopathy
Age of onset of frontotemporal dementia / Pick’s
+ Normal duration of illness
Usually <65 (rarely 20-30)
Normal duration = 10-15yrs
In frontotemporal dementia, what drugs are used / not used?
Use antidepressants / atypicals
NOT
ACh inhibitors used in Alzheimer’s e.g. donepezil (may worsen)
What is the main chemical involved in FTD (frontotemporal dementia)
Abnormal Tau protein aggregates
How may FTD initially present?
What are some later stage features
Initially present as:
Personality changes e.g. extrovert / disinhibited
Change in eating habits e.g. overindulging→ hyperphagia
Word finding difficulties → Economy of speech, echolalia, mutism
List the Dx criteria of FTD (5)
Insidious onset/progression Early decline in social interpersonal conduct Early decline in personal conduct Early emotional blunting Early loss of insight
How would FTD show O/E + Ix?
Impaired frontal lobe tests
No perceptual deficits
No amnesia
Normal EEG
What is the prevalence of dementia in PD?
How does PD presentation differ to LBD?
30% PD → dementia (often mixed aetiologies - AD/vasc)
PD: unilateral Sx for few years then cognitive decline
LBD: bilateral Sx + cognitive decline within 1yr
What is the prevalence of dementia in Down’s syndrome?
50% Down’s syndrome get Alzheimers in their 50s
What are the 3 characteristic features of normal pressure hydrocephalus?
Worsening confusion
Abnormal gait
Urinary incontinence
CT head would clearly show
What domains does the MMSE examine? (6)
Orientation Registration Attention Calculation Recall Language
What Ix may be done in Dementia?
Bloods - confusion screen:
CRP-ESR (ESR may indicate autoimmune e.g. SLE (ANA)
FBC / U+Es inc. Ca / LFT / TFT / B12-Folate
ECG (indicate CV conditions + needed prior to cholinesterase inhibitors)
EEG
Cultures: blood/urine/CSF
CT head (1st line) / poss MRI
What drugs are available for Alzheimers? (4)
Anticholinesterase inhibitors (AChEIs):
Rivastigmine
Donepezil
Galantamine
NMDA-R antagonists:
Memantine
How is severity of Alzheimer’s classed?
Which drugs are recommended for the diff severities
Mild = MMSE 21-26; Mod = 10-20; Mod-Severe = 10-15; Severe = <10
Mild-Moderate → AChEIs
Moderate + unable to take AChEIs → NMDA-R untags
Severe → NMDA-R antags
What are some of the Behavioural + Psychological Sx of Dementia (BPSD)
What % dementia pts get these Sx
Psychological:
Anxiety / Depression
Hallucinations / Delusions
Behav: Cursing / Screaming Aggression / Agitation Wandering Sexual disinhibition
BPSDs in 2/3rd dementia (80% pts in care homes)
What info must be gathered when looking to manage BPSDs
Identification (what Sx) - from Hx/collateral
Perception - underlying agenda/misperception causing behav?
Psych Hx + premorbid personality
Life events
MSE
Dx - consider alternative e.g. delirium/meds SEs
What are the non-pharm management strategies for BPSDs (8)
Family involvement
Orientation
Familiarity
Communication (use clearer)
Conversation (encourage)
Mobility (encourage)
Senses (ensure no barriers)
Hallucinations (do not rebuke)
What drugs may be used for BPSDs? (5)
Depression → citalopram Agression from psychosis → risperidone (3x risk stroke) Sleep disturbance → zopiclone Agitation from constipation → senna Shouting from pain → paracetamol
What sorts of services can be provided in a care plan (social services) (6)
Home help to assist with ADLs Specific equipment/adaptation Meals on wheels Respite care Day care facilities Care home placement
What types of Dementia are Cortical? (2)
+ Subcortical (8)
+ Mixed (2)
Cortical:
AD + Pick’s (FTD)
Subcortical:
PD, LBD, Huntington’s, progressive supranuclear palsy
HIV-related, Normal pressure hydrocephalus, Wilsons, MS
Mixed:
Vascular
Infective causes (neurosyphillis, CJD, chronic meningitis)
How are Cortical + Subcortical dementias different in terms of: Language Speech Praxia (co-ord) Agnosia Calculation Motor system Extra movements
Cortical // Subcortical
Lang: early aphasia // normal
Speech: normal until late // dysarthritic
Co-ord: apraxia // normal
Agnosia: present // usually absent
Calculation: early impairment // normal until late
Motor system:
normal posture+tone // increased tone + abnorm posture
Extra movements:
none (poss myoclonus in AD) // tremor, tics, chorea
List the psych/behav signs/deficits of FTD/Picks (3)
List the physical signs in FTD/Picks (5)
List the speech/lang signs/defcitis (3)
Personal conduct e.g. hygiene
Social conduct - disinhibited /extrovert/ lack insight
Emotional blunting + distractibility
Akinesia
Primitive reflexes / Incontinence
Low BP / Tremor
Reduced spontaneity / echolalia / economy of speech
