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HCoLL > Psychiatry > Flashcards

Psychiatry Flashcards

1
Q

What is Mild Cognitive Impairment (MCI) defined as?

A

Evidence of early memory decline on formal memory tests (e.g. MMSE) without clinical evidence of other features of dementia

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2
Q

What can MCI be due to (4)

A

Early stages dementia (10-15% → dementia in 1yr)
Depression/anxiety
Stress
Physical problem

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3
Q

What are the functions of the frontal lobe? (3)

How may problems manifest

A
  • Voluntary motor activity (learning/initiating/stopping)
  • Speaking ability
  • Elaboration of thought (behaviour, logic, personality)

Problems: disinhibition, initiating action, reasoning/abstract thought

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4
Q

What are the functions of the parietal lobe? (3)

How may problems manifest

A
  • 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

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5
Q

What are the functions of the temporal lobe? (3)

How may problems manifest

A
  • Attention
  • Recording and storing verbal and visual memory
  • Learning of information

Problems: diminished attention, short term memory probs + producing speech

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6
Q 
What proportion (%) of >65s have dementia?
What % of >80s?
What % of >95s
What % of those in care home?
What M:F ratio?
A

5% >65s
20% >80s
1/3 >95s have dementia (doubles every 5yrs)

  • 64% in care homes have dementia
  • 2/3 with dementia are women
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7
Q

What are the main 8 types of primary dementia? (+ proportions)

A 
Alzheimers (62%)
Vascular (17%)
Mixed dementia (10%) - mixed AD/Vascular
Lewy body (4%)
Parkinsons Disease (2%)
Fronto-temporal (2%)
Huntington's
Progressive supranuclear palsy
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8
Q

What are some different types/causes of vascular dementia (8)

A 
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)
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9
Q

How are secondary causes of dementia classified?

A 
Infections
Trauma
Toxic/Metabolic
Intracranial malignancy (primary/metastatic)
Hydrostatic causes (hydrocephalus)
Endocrine
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10
Q

List some infective causes of dementia (6)

A 
o	Syphillis
o	Cryptococcus
o	Sclerosing panencephalitis (SPE)
o	Progressive multifocal leukoencephalopathy (PML)
o	HIV
o	Creutzfield-Jacobs disease (CJD)
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11
Q

List some Toxic/Metabolic/Endocrine causes of dementia (8)

A 
Alcohol-Korsakoff / Thiamine defc
Drug intoxication / medication SEs
Heavy metals
Paraneoplastic
Hypothyroidism
Inherited metabolic disorders (eg. Wilsons)
VitB12 + Folate defc
Anoxia (post-cardiac arrest)
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12
Q

What are the clinical features of the early phase of dementia (3)
How many years usually in this phase?

A
  • Difficulty embracing change
  • Short term memory loss
  • Repetition of questions

3-4yrs

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13
Q

What are the clinical features of the middle phase of dementia (5)

A
  • Difficulty with daily tasks
  • Failure to recognize people
  • Needs prompting
  • Disorientation in time, place and person
  • Memory for distant past often remains good
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14
Q

What are the clinical features of late stage dementia (5)

How many years usually in this phase?

A
  • Aggression
  • Wt loss, poor appetite, dysphagia
  • Incontinence
  • Decline in speech
  • Increased frailty

1-2yrs (intensive care needs)

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15
Q

List some RFs for dementia (7)

A
  • 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
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16
Q

List the Dx criteria of Alzheimer’s (4)

What is the mean life expectancy after Dx

A 
1. Evidence of memory impairment plus ≥1 of:
Agnosia
Language problems
Coordination problems (apraxia)
Impaired exec func
  1. Present >6m
  2. Impairment of functioning
  3. No other medical/psychiatric explanation
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17
Q

What are the 3 genes involved in early-onset AD

How is it inherited

A
  • Amyloid precursor protein (APP) chromosome 21
  • Presenilin gene 1 (PSEN-1), chromosome 14
  • Presenilin gene 2 (PSEN-2), chromosome 1

Autosomal dominant

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18
Q

What brain changes may be seen in Alzheimers disease (compared to a normal brain) (3)
What chemical structures would be found (under microscopy) (2)

A

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)

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19
Q

How do plaques + tangles affect the brain?

A

Plaques → block signalling/activate inflamm → cell death

Tangles → destroy cell transport system (func)

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20
Q

What are the Dx criteria for vascular dementia (3)

A

Same cognitive impairments as AD

Deficits → limitation with ADLs (+ not due to physical effects of stroke alone)

Evidence of cerebrovascular disease O/E + imaging

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21
Q

What is the risk increase + % incidence (within 1yr) of dementia after a stroke?

A

Increased risk x9

25% stroke pts develop new dementia after 1yr

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22
Q

What is the difference b/wn cortical + subcortical vascular dementia

A

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

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23
Q

List the RFs for vascular dementia (9)

A

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

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24
Q

What are the clinical features of vascular dementia / cerebrovascular disease (10)

A

‘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
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25
Q

What are the genetic contributions to vascular dementia (3)

A

Notch 3 - CADASIL
APP variations - HCHWA (heritable cerebral haemorrhage with amyloidosis)
Hyperchol/HTN/DM all have genetic components

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26
Q

M:F ratio of Lewy Body Dementia

Average life expectancy after Dx

A

Slightly higher in males

Av life expectancy 5-7yrs after Dx

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27
Q

What may cause downwards fluctuations in Lewy Body Dementia (3)
What are the main aims/focus of management

A

Medications
Infections
Natural course of disease

Managing neuropsychiatric disturbances + movement disorders

28
Q

What are lewy bodies?

How do Lewy Bodies cause brain changes?

A

Lewy bodies = abnormal structures responsible for disrupting brain function
- made up of alpha-synuclein protein

  • They interrupt action of acetylcholine + dopamine
29
Q

What areas of the brain affected in Lewy Body Dementia

A

Substantia nigra (= classical Lewy bodies - seen in PD)

Cortex degeneration (= cortical Lewy bodies)

Parietal / temporal lobes/ cingulate gyrus shrinkage

30
Q

What are the core features (3) + supporting features (5) to Lewy Body Dementia

A

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)

31
Q

What are the Dx criteria for LBD

A

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

32
Q

Define the criteria for Delirium (4)

A 
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
33
Q

List some other associated features of delirium (not Dx criteria) (4)

A 
Motor changes (slowness, restlessness, agitation)
Emotional changes (anxiety, fear, depression)

Delusions (paranoid, fleeting)
Hallucinations (usually visual)

34
Q

What is the prevalence of delirium in general hospitals?

Describe the epidemiology of delirium in dementia pts

A

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)

35
Q

List things to be included O/E in delirium (7)

A

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

36
Q

List some 1st line (9) + 2nd line (6) investigations into delirium

A 
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
37
Q

List some predisposing RFs for delirium (5)

A 
Over 65
Physical frailty
Dementia
Multiple co-morbidities
Sensory impairment
38
Q

List some management approaches used to prevent delirium (8)

A 
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
39
Q

List some complications of delirium (9)

A 
Medication SEs
Incontinence
Pressure ulcers
Falls 
Malnutrition
Hosp-acquired (nosocomial) infections
PTSD
Functional decline
Death
40
Q

What advice should be given to family regarding management of delirium

A

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

41
Q

In what instances (2) in delirium are sedative drugs used

What are the guidelines of sedative use in frail delirium pts (3)

A

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

42
Q

What info regarding recovery from delirium should be discussed with family

A

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

43
Q

What is the prevalence of paranoid disorder in >65s

A

1% of >65s

44
Q

List the common features of delusional disorder in the elderly (6)

A

Persecutory/reference delusions
Ideas of theft / ill-treatment / poisoning
Normal speech

No FH
No Dementia
No prior illness

45
Q

List some RFs for paranoid disorder in the elderly (7)

A

Female
Never married
Living alone
Social isolation

Sensory impairment

Paranoid personality
Schizoid personality

46
Q

List the DDx of elderly paranoid disorder (8)

A 
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
47
Q

Age of onset of frontotemporal dementia / Pick’s

+ Normal duration of illness

A

Usually <65 (rarely 20-30)

Normal duration = 10-15yrs

48
Q

In frontotemporal dementia, what drugs are used / not used?

A

Use antidepressants / atypicals
NOT
ACh inhibitors used in Alzheimer’s e.g. donepezil (may worsen)

49
Q

What is the main chemical involved in FTD (frontotemporal dementia)

A

Abnormal Tau protein aggregates

50
Q

How may FTD initially present?

What are some later stage features

A

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

51
Q

List the Dx criteria of FTD (5)

A 
Insidious onset/progression
Early decline in social interpersonal conduct
Early decline in personal conduct
Early emotional blunting
Early loss of insight
52
Q

How would FTD show O/E + Ix?

A

Impaired frontal lobe tests

No perceptual deficits
No amnesia
Normal EEG

53
Q

What is the prevalence of dementia in PD?

How does PD presentation differ to LBD?

A

30% PD → dementia (often mixed aetiologies - AD/vasc)

PD: unilateral Sx for few years then cognitive decline
LBD: bilateral Sx + cognitive decline within 1yr

54
Q

What is the prevalence of dementia in Down’s syndrome?

A

50% Down’s syndrome get Alzheimers in their 50s

55
Q

What are the 3 characteristic features of normal pressure hydrocephalus?

A

Worsening confusion
Abnormal gait
Urinary incontinence

CT head would clearly show

56
Q

What domains does the MMSE examine? (6)

A 
Orientation
Registration
Attention
Calculation
Recall
Language
57
Q

What Ix may be done in Dementia?

A

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

58
Q

What drugs are available for Alzheimers? (4)

A

Anticholinesterase inhibitors (AChEIs):
Rivastigmine
Donepezil
Galantamine

NMDA-R antagonists:
Memantine

59
Q

How is severity of Alzheimer’s classed?

Which drugs are recommended for the diff severities

A 
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

60
Q

What are some of the Behavioural + Psychological Sx of Dementia (BPSD)
What % dementia pts get these Sx

A

Psychological:
Anxiety / Depression
Hallucinations / Delusions

Behav:
Cursing / Screaming
Aggression / Agitation
Wandering
Sexual disinhibition

BPSDs in 2/3rd dementia (80% pts in care homes)

61
Q

What info must be gathered when looking to manage BPSDs

A

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

62
Q

What are the non-pharm management strategies for BPSDs (8)

A

Family involvement
Orientation
Familiarity

Communication (use clearer)
Conversation (encourage)
Mobility (encourage)

Senses (ensure no barriers)
Hallucinations (do not rebuke)

63
Q

What drugs may be used for BPSDs? (5)

A 
Depression → citalopram
Agression from psychosis → risperidone (3x risk stroke)
Sleep disturbance → zopiclone
Agitation from constipation → senna
Shouting from pain → paracetamol
64
Q

What sorts of services can be provided in a care plan (social services) (6)

A 
Home help to assist with ADLs
Specific equipment/adaptation
Meals on wheels
Respite care
Day care facilities
Care home placement
65
Q

What types of Dementia are Cortical? (2)
+ Subcortical (8)
+ Mixed (2)

A

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)

66
Q 
How are Cortical + Subcortical dementias different in terms of:
Language
Speech
Praxia (co-ord)
Agnosia
Calculation
Motor system
Extra movements
A

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

67
Q

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)

A

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

HCoLL (8 decks)

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