Psych: Old Age Psychiatry and Dementia Flashcards

1
Q

Which patients see old age psychiatry?

A

any person over 65 with mental health problems referred to secondary care services

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Charles Bonnet syndrome? What are the risk factors?

A

complex visual disturbances/ hallucinations a/w eye disease. Usually hallucinations of faces, children and wild animals.
RF: increasing age, M=F

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the differences with telling whether the diagnosis is delirium or dementia?

A

delirium: rapid onset, fluctuating, days to weeks (can be months), altered consciousness, impaired attention, immediate recall memory impaired, hypo or hyperactive, disturbed sleep wake cycle (sundowners), usually reversible
dementia: insidious onset, progressive, months to years, clear consciousness, normal attention (unless severe), immediate recall memory usually normal, no psychomotor changes, usually normal sleep wake cycle, irreversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Give some examples of organic and functional mental disorders/causes?

A

organic: normal ageing, mild cognitive impairment, Alzheimer’s, uncontrolled diabetes, vascular dementia, reduced B12/folic acid (also macrocytic anaemia sign), reduced thiamine, meds eg benzodiazepines can cause memory loss
functional: depression (pseudo-dementia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the features of the MMSE?

A

maximum score is 30 points. a score of 20-24 suggest mild dementia, 13-20 suggests moderate dementia, and less than 12 indicates severe dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What tests are done in screening confusion (to rule out delirium/reversible causes of confusion)?

A

Blood tests
o FBC (infection, anaemia [confusion], malignancy)
o U&Es (hyponatraemia [confusion], hypernatraemia)
o LFTs (liver failure with secondary encephalopathy)
o Coagulation/INR (intracranial bleeding)
o TFTs (hypothyroidism [depression & similar presentation])
o Calcium (hypercalcaemia)
o B12 + folate/haematinics (B12/folate deficiency [cognition problems])
o Glucose (hypoglycaemia /hyperglycaemia)
o Blood cultures (sepsis)
Urinalysis
o UTI is a very common cause of delirium in the elderly
o Positive urine dipstick without clinical signs is not satisfactory
o Look for other evidence (increase WCC, suprapubic tenderness, dysuria, offensive urine, positive urine culture
Imaging
o CT head – concern about intracranial pathology (bleeding, ischaemic stroke, abscess)
o Chest x-ray – may be performed if there is concern about lung pathology e.g. pneumonia, pulmonary oedema)
ECG required for some dementia meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the definition of delirium?

A

acute, transient and reversible state of confusion, usually the result of other organic processes eg infection, drugs, dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 2 types of delirium?

A

hyperactive - typical: agitation, delusions, hallucinations, wandering, aggression
hypoactive - atypical and often missed or confused with depression; lethargy, slowness, excessive sleeping, inattention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the causes of delirium?

A

CHIMPSPHONED
C - constipation
H – hypoxia/hydration
I – infection
M – metabolic disturbance inc dehydration
P - pain
S - sleeplessness
P – prescriptions/polypharmacy
H – hypothermia/pyrexia
O - organ dysfunction
N - nutrition
E - environmental changes* - inc. emotions/depression/anxiety
D - drugs (over the counter, illicit, alcohol and smoking)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the first line diagnostic tool in delirium?

A

SQID: single question in delirium (SQID)
more confused than normal? yes or no
positive > collateral history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

After history and cognitive assessment of suspected delirium, a thorough clinical exam should be performed including what?

A
  • Vital signs (fever if infection, low SpO2 in pneumonia)
  • Level of consciousness (GCA/AVPU) – clouding of consciousness often present in delirium
  • Evidence of head trauma
  • Sources of infection
  • Asterixis (uraemia/encephalopathy)
  • Confusion screen (bloods, urinalysis, imaging)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the definitive, supportive and medical management of delirium?

A

Definitive: Identify and treat the underlying cause

Supportive
* Consistent care team, ensure access to aids, glasses, hearing and walking sticks, Enable independent activity where possible
* Access to a clock and other orientation reminders, have familiar objects (e.g. photos/clothes), involve friends and family, control surrounding noise, adequate lighting and temperature

Medication
* Avoid unnecessary medications where possible, can worsen delirium
* Wandering is not absolute indication for sedation
* Lorazepam is the first line benzo (0.5mg starting dose – 1mg) due to its rapid onset and short half life
o MAX DOSE is 2mg in 24 hours
* If already on benzos or at risk of respiratory depression then haloperidol is first line option (at a low dose in the elderly – 0.5mg)
o Contraindicated in parkinsons, dementia with LB or prolonged Qtc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the prognosis of delirium and what is the prevention?

A

post discharge: behaviours can continue for up to 6 months after the cause has been treated - make family and carers aware
prevention: avoid drugs known to preciptate delirium (opiates and benzos), identify patients at high risk and observe for early signs, assess pain control and drugs, employ supportive and environmental management approaches for all patients, regardless of delirium risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Is dementia a normal part of ageing? What is the criteria to be classed as dementia? What is dementia associated with (biologically)?

A

it is NOT a normal part of ageing
must be of at least 6 months duration and affect activities of daily living
associated with decreased amount of acetlycholine in the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the rule of 1/3 of cognitive impairment with dementia patients?

A

1/3 get better
1/3 stay the same
1/3 develop dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 5 A’s of dementia?

A

amnesia - memory impairment
agnosia - recognition
apraxia - motor skills eg dressing
aphasia / agnosia - speech and language
associated behaviours - BPSDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What s the role of the temporal lobe?

A

hearing
language comprehension (wernicke’s area)
memory / information retrieval
facial recognition
feelings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the role of the frontal lobe?

A

motor control (premotor cortex)
problem solving (prefrontal area)
speech production (broccas area)
thinking, planning, emotions, behavioural control, decision making

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the role of the parietal lobe?

A

body orientation / sensory discrimination / visuospacial
touch perception (somatosensory cortex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In which dementia are BPSDs most common?

A

fronto-temporal dementia
can occur in all dementia subtypes but don’t occur in everyone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do you tell the difference between delirium and BPSDs?

A

differentiate with timeline (acute vs progressive) and baseline level with a collateral history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the behavioural and psychological symptoms of BPSDs?

A

behavioural:
Wandering
Restlessness
Pacing
Agitation
Disinhibition
Screaming
Physical aggression
Swearing
Apathy
Repetitive

psychological:
Anxiety
Misidentification
Depressed
Insomnia
Delusions (depth perception issues, forget where they place things and think people are “stealing” from them)
Hallucinations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the causes of BPSDs?

A

PINCH ME
Pain

INfection

Constipation

Hydration

Medication

Environmental

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do you assess BPSDs?

A

Behavioural assessment –ABC
o Antecedents – what happened before?
o Behaviour – what was the behaviour?
o Consequences – what was the consequence?
Physical assessment - e.g. are they in pain?
Mental state assessment to consider alternative causes and treatments – e.g. depression or sleep disturbance
Collateral history
Look at the mnemonic PHONED as a guide for assessing causes of symptoms in people with dementia
Refer if necessary to Medicine for the Elderly or Old Age Psychiatry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the differentials of BPSDs?

A

BIO: pain, delirium, constipation, dehydration, stroke etc.
PSYCHO: depression, anxiety, deterioration of dementia
SOCIAL: links to environmental changes, approach of staff

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the management of BPSDs?

A

Treat the cause
If necessary refer to medics
Environmental modification and practical management (e.g. education for family / staff)
Medication as a last resort
Memantine
o Antipsychotics
 Only Risperidone is licensed for management of agitation
 Side effects are greater in older people
 Avoid using it if possible due to the associated risks:
 Parkinsonism
 Falls
 Stroke risk (2-3 times baseline risk)
 Cardiovascular risks
 Death
 If it is used then the lowest possible dose should be prescribed for a time limited period
 Often inappropriately prescribed to ‘control’ BPSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the differentials of dementia?

A

D – drugs, delirium – drugs causing confusion e.g. opitates/steroids
E – emotions/depression – mood causing them to be slow/deteriorate
M - metabolic disorders - U&E, infections etc
E - eye and ear imparitment – affect concentration and ability to retain information
N - nutritional disorders - underweight
T - tumours, toxins, trauma – brain tumors or anything poisoning them
I - infections - delirium (can be superimposed on dementia so treat delirium and see if dementia persists)
A - alcohol, arteriosclerosis

28
Q

In what circumstance can you not diagnose dementia?

A

CANNOT diagnose dementia on top of depression > treat the depression first

29
Q

What is the ICD-10 definition of dementia?

A

It is a syndrome due to disease of the brain, usually of a chronic or progressive nature. There is a disturbance of multiple higher cortical functions, including a decline in memory and learning new information. No clouding of consciousness.
It is also accompanied by deterioration in judgment and thinking, processing of new information, emotional control, social behaviour or motivation. For more than 6 months

30
Q

What does ICD-10 class as mild, moderate and severe dementia?

A

mild: memory loss is sufficient to interfere with everyday activities but they are able to live independently
moderate: memory loss is a seriosu handicap to independent living and only highly learned or very familiar material is retained. They are unable to function without the assistance of another in daily living.
severe: there is a complete inability to retain new information. There is a virtual absence of intelligible ideation. The mind can no longer tell the body what to do.

31
Q

What is the most common type of dementia?

A

Alzheimer’s

32
Q

What is the pathophysiology of Alzheimer’s? What are the 4 pathologies?

A

Progressive degeneration of the cerebral cortex (widespread cortical atrophy)
Affected neurons contain amyloid plaques, neurofibrillary tangles (tau) & produce less acetylcholine
1. amyloid plaques
2. cerebral atrophy - most pronounced in the medial temporal lobes (hippocampus is here which is responsible for memory)
3. neurofibrillary tangles
4. reduced levels of acetylcholine

33
Q

What are the RFs of Alzheimer’s?

A

Age! W>M
Genetics:
ApoE is a gene related to late-onset Alzheimer’s
APP (amyloid precursor protein): found on chromosome 21 (3 of them in Downs Syndrome) – APP produces amyloid plaques which is a feature of AD. Increased plaques = increased risk of AD

Modifiable: social isolation, risk-factors associated with vascular disease (smoking/alcohol, hypercholesterolaemia, HTN, obesity & diabetes), head injury

34
Q

What is the overall feature of Alzheimer’s?

A

insidious and gradual onset with progressive cognitive decline

35
Q

what are the early features of Alzheimer’s?

A

memory loss, leading to confusion
e.g. forgetting names of people & places, difficulty finding the words for things, getting lost mid-sentence, inability to remember recent events, getting lost, misplacing things, forgetting appointments

36
Q

what are the intermediate features of Alzheimer’s?

A

Difficulties with language (struggling to follow a conversation or repeating themselves)
Visuospacial skills – problems judging distance, stairs, parking, 3D
Apraxia (the inability to perform learned movements) – need to be given step by step instructions
Problems with planning & decision making
Orientation – confused or losing track of the day or date

37
Q

What are the features of Alzheimer’s in the later stages?

A

Psychiatric: depression, hallucinations, delusions, insomnia
Behavioural: disinhibition, aggression, agitation, irritable
Wandering & disorientation
Less aware of what is happening around them
Apathy
Altered eating habits, difficulty with walking, increasing frailty
Urinary incontinence
Expressive dysphasia

38
Q

What are the pathological findings of Alzheimer’s?

A
  • Cerebral atrophy on MRI – most pronounced in the medial parietal temporal lobe (predominantly involves in memory)
  • Vascular ischaemic changes
  • Widened sulci and dilated ventricles on CT/MRI
  • Senile/amyloid plaques deposition. Extraneuronal deposits of amyloid beta protein. Plaques cause inflammation  cell death
  • Neuro-fibrillay tangles. Intraneuronal hyperphosphorylated tau protein, disrupts cell functions
  • Acetylcholine levels reduced (loss of cholinergic neurons
39
Q

What are the investigations of Alzheimer’s?

A
  1. Comprehensive history & physical exam:
  2. Medication review: are there any contributing factors?
  3. Formal screen for cognitive impairment: e.g. MMSE/ GPCOG – neuropsychodynamic test can be done by psychologist if borderline score on the ACE
  4. Exclude reversible organic causes: rule out infection (urine dip, inflammatory markers, FBC), metabolic (TFT, U+Es, calcium)
  5. Consider MRI, cultures, CXR
  6. Very important to identify depression!!
40
Q

What are the NICE general managements?

A

Offer a ‘range of activities to promote wellbeing that are tailored to the person’s preference’ – e.g. group cognitive stimulation therapy for those with mild & moderate dementia. E.g. + Group reminiscence therapy
Emotional and carer support
Familiatiry – photos in room same carers etc
Calm, well lit environment,
Communicate calmly and clearly
DO - talk slowly, ask short questions, stay calm
DO NOT - take offence, blame, argue etc.

41
Q

What is the medical management of Alzheimer’s?

A

mild-moderate: Acetylcholinesterase inh eg donezepil, rivastigmine or galantamine
moderate-severe: memantine (NMDA) > added on top of donezepil when symptoms worsen

42
Q

What are the side effects of acetycholinesterase inhibitors?

A

Decreases anxiety, increases motivation, concentration, ADLs
(Cholinergic side effects) Diarrhoae, incontinence, nausea, vomiting, headache, loss of appetite, dizziness, sleep disorders, GI disturbance = so start at a low dose & titrate up opposite of can’t see, pee, climb a tree
Severe side effects: Slows HR (less so for galantamine), decreases appetite, increased weight loss

43
Q

What are the contraindications of acetylcholinesterase inhibitors?

A

heart block, bradycardia, active asthma/COPD/bronchitis (more frequent use of inhaler/beta blockers contraindicated), active peptic ulcer unless on PPI (as risk of bleeding), epilepsy (lowers seizure threshold)

44
Q

When should acetylcholinesterase inhibitors be given?

A

Taken in the morning – not on an empty stomach (GI disturbance). May make people sleepy, in which case take it at night

45
Q

What are the side effects of memantine?

A

Side effects (less common/severe): Dizziness, constipation, SOB, headache, sedation (taken at bed time), increased BP
Renal function needs monitoring, esp eGFR – must be >49 for more than 10mg
Can affect INR (check if on warfarin)

46
Q

Which meds should be avoided in Alzheimer’s?

A

Avoid anti-cholinergic medications (worsen cognitive impairment) E.g. antihistamines, anti-psychotics & tolterodine

47
Q

What is the second most common type of dementia in over 65s?

A

vascular dementia

48
Q

What is the onset of vascular dementia?

A

sudden onset with stepwise deterioration
fluctuating day to day

49
Q

What makes vascular dementia different to Alzheimer’s with regards to memory?

A

vascular dementia has motor and sensory defects alongside memory decline
AD is memory only

50
Q

What are the RFs for vascular dementia?

A

high BP, smoking, coronary artery disease, hypercholesterolaemia, diabetes, strokes (lots of small events eg lacunar infarcts which accumulate to cause vascular dementia), M>W, age

51
Q

What are the symptoms of vascular dementia?

A

problems with planning, organising, concentrating, memory, language, visuospatial skills; difficulties following steps; slower speed of thought

52
Q

How do you manage the RFs of vascular dementia?

A

statins, antihypertensives, diabetes

53
Q

What are the features of dementia with Lewy bodies?

A

alpha-synuclein forms into clumps inside neurons (aggregation of alpha-synuclein), starting in areas of the brain that control aspects of memory and movement

54
Q

What is the triad of Lewy Body dementia?

A

REM sleep disorder, history of falls (secondary to motor problems) and hallucinations (often of small, non-threatening people/animals [Lilliputian hallucinations])

55
Q

What are the RFs of Lewy body dementia?

A

few RFs other than age - no clear family history

56
Q

What are the clinical features of Lewy Body dementia?

A
  • Progressive ALZ and Parkinsons symptoms
  • Early – attention/alertness issues which fluctuate throughout the day
  • Visual hallucinations (2/3rds) (more than AD/VD) and delusions
  • Parkinsonism (up to 70%) to differentiate between two = what came first the parkinsonism or cognitive decline
    If the memory issues more than 12 months after movement issues - PDD
    If memory issues within 12 months of movement issues (same sort of time) - LBD
    Tactile hallucinations common/”happy” one – animals and babies etc
  • Risk of falls!
  • Fluctuating consciousness
  • REM sleep disorders
  • 70% have systematised delusions, 40-50% have a depressive episode, risk of falls, syncope
  • As it progresses, day-day memory, behaviour challenges and walking gets worse
57
Q

What will the SPECT (DaT)/PET scan show with Lewy Body Dementia?

A

reduced DA (reduced striatal uptae of ligand for presynaptic dopamine transporter site in LBD but not AD)

58
Q

What is the management of Lewy Body dementia?

A

Acetylcholinesterase & memantine are licenced (Rivastigimine) for challenging behaviours (for LBD and Parkinson’s!)
Non-drug management should be tried first – S&L therapy
Avoid antipsychotics!!! > can make parkinsonism much worse. Quetiapine sometimes used with great caution
Treatment is notoriously difficult and is a fine balance between PD and psychotic symptoms
PD and LBD are caused by low levels of DA and are treated by boosting DA - psychosis is caused by high levels of DA and is treated by reducing it
Neurological symptoms may worsen with neuroleptics
psychological interventions are vital in helping manage the condition

59
Q

What is the second most common cause of dementia in those UNDER 65s (AD is first)?

A

frontotemporal dementia (Pick’s disease)

60
Q

What are the key features of frontotemporal dementia?

A

Usually onset <65 years
Insidious onset
Relatively preserved memory
Personality change & social conduct issues
2-10 years prognosis
Later stages similar to later stages of Alzheimer’s dementia

61
Q

what are the 3 subtypes of frontotemporal dementia?

A
  1. behavioural variant FTD (PICKS, 2/3rds) - frontal lobe involvement prominent
  2. progressive non-fluent aphasia (CPA) - slow and progressive (2-3 years); memory etc preserved in early stages
  3. semantic dementia - slow and progressive (2-3 years); memory etc preserved in early stages. peak age of onset = 55-56 years
62
Q

what are the symptoms of the 3 types of frontotemporal dementia?

A
  1. behavioural:
    lose their inhibitions – act in socially inappropriate ways
    lose interest in people and things – lose motivation but are not sad unlike in depression
    lose sympathy or empathy
    show competitive, compulsive or ritualised behaviours
    crave sweet or fatty foods, increased appetite, lose table etiquette – puts random objects into mouth
    perseveration behaviours
  2. progressive non-fluent aphasia (CPA)
    Slow, hesitant speech
    Errors in grammer
    Impaired understanding of complex sentences, but not single word
  3. semantic dementia
    Asking the meaning of familiar words (e.g. what is knife?)
    Trouble finding the right word
    Difficulty recognising familiar people or common objects
63
Q

What is the histology of frontotemporal dementia?

A
  • Picks (20-30%) – marked transcorticol ASTROGLIOSIS, Pick cells (characteristic ballooned neurons) and Pick bodies (tau positive neuronal inclusions)
  • Also atrophy of frontal and temporal lobes and neurofibrillary tangles
  • Non-Picks – spongiform microvacuolation, only mild gliosis
  • ‘Knife-blade atrophy’, gliosis & neuronal loss of the frontal & temporal lobes (younger indivisual so generally more accurately seen
64
Q

What is the management of frontotemporal dementia?

A

Avoid AChE inhibitors & memantine!!
Treat the presenting symptoms, psychosocial interventions
Speech and language therapy
Some evidence in using SSRI to improve disinhibition
Risperidone is the only antipsychotic licensed for persistent aggression/distress. Use at lowest dose for shortest time (up to 6 weeks)
Supportive care + benzos + SSRIS = for agitation

65
Q

What are the differences between depression and dementia?

A

Shorter history, rapid onset
Biologcal symptoms e.g. weight loss, sleep disturbance
Patient worried about poor memory (insight)
Mini-mental test score is variable
Global memory loss (dementia characteristically causes recent memory loss)

66
Q

What is normal pressure hydrocephalus? and what is the treatment?

A

IE wet, wobbly and weird
A reversible cause of dementia that can be seen in predominantly elderly patients.
Due to impaired absorption of CSF at the arachnoid villi  increased ICP  ventriculomegaly. This can be triggered by an insult such as a bleed or head injury.
* Triad of: urinary incontinence, dementia and gait abnormality which develops over several months.
* Neuro-imaging can appear similar to Parkinson’s disease, but being unresponsive to L-DOPA can be used as a sign of normal pressure hydrocephalus.
o Enlarged ventricles with absent sulci [as they are compressed by the sulci] (PD = enlarged ventrciels and prominent sulci)
* Treatment in patients fit for surgery is ventriculo-peritoneal shunting, otherwise they may be managed with conservative treatment and repeated CSF taps.