Old age psychiatry (dementia and delirium) Flashcards

1
Q

Definition of delirium?

A

Delirium is an acute, transient, global organic disorder of CNS functioning resulting in impaired
consciousness and attention. There are different types of delirium: hypoactive, hyperactive and
mixed depending on the clinical presentation

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2
Q

Features of ageing

A

Most OA services start at age 65

A normal phase of life
- Cognitive changes
Reduced abilities versus accumulated wisdom
Physical changes
- Reduced function/complex needs versus positive adaptation
Social changes
- Loss and isolation versus freedom from responsibility

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3
Q

What are the cognitive and social changes that come with ageing?

A

Cognitive changes
Reduced cognitive ability, memory impairments, sometimes less agile thought processes. Wiser older adult + respected elder is found throughout various societies.
Physical changes
Complex needs! Multiple physical comorbidities. Sometimes able to adapt positively to this and requirement for adaptation, however. OA running groups/exercise etc
Social changes
- Loneliness big burden on OA populations. Loss of family members, social ties, friendships. No longer have to think about mortgages, looking after children, etc etc

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4
Q

Why do we need Older Adult services?

A

Differences in presentation

Differences in needs

Impact of (often deteriorating) physical health
- Causation/Differential Diagnosis
- Management
Impact of mental health condition
- Physical Health
- Suicide

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5
Q

Impact of physical health on old age psychiatry

A

Bidirectional relationship
- Physical illnesses as aetiological/risk factors
- Consequences of mental illness on physical health

Sensory Impairments are direct risk factors for MH problems

Considerations for treatment
↑body fat; ↓ body muscle; ↓ relative body water
↓ renal blood flow and function

Physical illnesses as risk factors – Diabetes, cardiac risk factors
Mental Health Problems as direct consequences of physical illnesses – stroke, thyroid disease, Parkinson’s Disease
Mental Health causing physical health problems
Through direct problem of MH problem, e.g. self-neglect
Through problems associated with treatment, e.g. lithium causing renal failure

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6
Q

74 year old man
BG: Type 2 Diabetes, Osteoarthritis,
CKD 3, Previous stroke

“I don’t know why I’m here, everything’s fine”

Clerking notes – fall at home

Examination – largely normal
Fall – tripped over his dog at home, pressed citywide alarm as couldn’t get himself up.

History – appropriate answers to all of the questions, but they’re very vague. Doesn’t remember the fall at home yesterday. Spends a lot of the conversation asking where his razor is and recurrently coming back to how he hasn’t been getting on with his son-in-law, as he’s moving things about the house.
Blood tests – normal
CT Head – no acute changes, no intracranial haemorrhage, stroke or space occupying lesion

Ring daughter
Mild confusion started 18m ago
Slowly getting more confused over this time
Remembers his childhood without any problems
Can’t tell her what he does with his day when she rings
Generally still very cheery and enjoys seeing family

What are the DDs?

A

Alzheimer’s Dementia

Lewy Body Dementia

Depression

Hypoactive Delirium

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7
Q

Causes of delirium

A

PINCH ME
Pain
Infection
Nutrition
Constipation
Hydration
Medication/Metabolism
Environment/Electrolytes

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8
Q

Treatment for delirium

A

Recovery can take 3-6 months!

Treatment
Treat the cause
Supportive environment
May need benzodiazepines or antipsychotics

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9
Q

Features of Hypoactive (40%) delirium

A

Lethargy, dec motor activity, apathy and sleepiness
Most common type of delirium but often unrecognised
Can be confused with depression

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10
Q

Features of hyperactive (25%) delirium

A

Agitation, irritability, restlessness and aggression
Hallucinations and delusions prominent
Maybe confused with functional psychoses

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11
Q

Mixed (35%) delirium features

A

Both hypo- and hyperactive subtypes co-exist and therefore there are signs of both

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12
Q

Causes of delirium

A

HE IS NOT MAAD
Hypoxia - resp failure, MI, HF, PE
Endocrine - Hyper+Hypo T, hyper + hypoglycaemia, cushings
Infection - UTI, Pneumonia, encephalitis, meningitis
Stroke - Stroke, raised ICP, intercranial haemorrhage, space occupying lesions
Nutritional- Dec thiamine, nicotinic acid, vitamin B12
Others - pain, sensory deprivation, sleep deprivation
Theatre - Anaesthetic, opiate analgesics
Metabolic - Hypoxia, hyponatraemia, hep + renal impairment
Abdominal - faecal impaction, malnutrition, urinary retention
Alcohol
Drugs - benzos, opioids, anti-Parkinsonism, steroids

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13
Q

Most common cause of delirium

A

UTI

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14
Q

Epidemiology of delirium

A

Delirium occurs in about 15–20% of all
general admissions to hospital.
Delirium is the most common complication of hospitalization in the elderly population.
Up to two-thirds of delirium cases occur in inpatients with pre-existing dementia.
15% of >65s are delirious on admission to hospital.

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15
Q

RFs for delirium

A

Older age ≥65
Multiple co-morbidities
Dementia
Physical frailty
Renal impairment
Male sex
Sensory impairment
Previous episodes
Recent surgery
Severe illness (e.g. CCF)

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16
Q

Clinical features of Delirium

A

DELIRIUM
Disordered thinking: Slowed, irrational, incoherent thoughts.
Euphoric, fearful, depressed or angry.
Language impaired: Rambling speech, repetitive and disruptive.
Illusions, delusions (transient persecutory or delusions of misidentification) and
hallucinations (usually tactile or visual).
Reversal of sleep-wake pattern: i.e. may be tired during day and hyper-vigilant at night.
Inattention: Inability to focus, clouding of consciousness.
Unaware/disoriented: Disoriented to time, place or person.
Memory deficits.

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17
Q

ICD-10 criteria for the diagnosis of delirium

A

Impairment of consciousness and attention
Global disturbance in cognition
Psychomotor disturbance
Disturbance of sleep-wake cycle
Emotional disturbances.

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18
Q

Delirium Key facts

A

Sleep-wake cycle Disrupted
Attention Markedly reduced
Arousal Increased/decreased
Autonomic features Abnormal
Duration Hours to weeks
Delusions Fleeting
Course Fluctuating
Consciousness level Impaired
Hallucinations Common (especially visual)
Onset Acute/subacute
Psychomotor activity Usually abnormal

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19
Q

Dementia key facts

A

Sleep-wake cycle Usually normal
AttentionNormal/reduced
Arousal Usually normal
Autonomic featuresl Normal
Duration Months to years
Delusions Complex
Course Stable/slowly progressive
Consciousness level No impairment
Hallucinations Less common
Onset Chronic
Psychomotor activity Usually normal

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20
Q

Historical questions to ask in delirium

A

Much of the history may be collateral as obtaining the history from the patient may
prove very difficult.
Identify rate of onset and course of the confusion.
Any symptoms of underlying cause, e.g. symptoms of infection or of intracranial
pathology?
Having an understanding of their premorbid mental state is important.
Are they hypo-alert or hyper-alert?
Do they have hypersensitivity to sound and light?
Is there any perceptual disturbance (misidentification, illusions and
hallucinations)?
Take a thorough drug history and a full alcohol history

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21
Q

MSE for delirium

A

Appearance &
Behaviour
Hypo- or hyper-alert. Agitated, aggressive, purposeless
behaviour.
Speech Incoherent, rambling.
Mood Low mood, irritable or anxious. Mood is often labile.
Thought Confused, ideas of reference, delusions.
Perception Illusions, hallucinations (mainly visual), misinterpretations.
181
Cognition Disoriented, impaired memory, reduced
concentration/attention.
Insight Poor

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22
Q

Investigations for delirium

A

Routine investigations: Urinalysis (UTI); Bloods: FBC (infection); U&Es
(electrolyte disturbance); LFTs (alcoholism, liver disease); calcium
(hypercalcaemia); glucose (hypo-/hyperglycaemia); CRP (infection/inflammation);
TFTs (hyperthyroidism); B12, folate, ferritin (nutritional deficiencies); ECG
(cardiac abnormalities, acute coronary syndrome); CXR (chest infection);
Infection screen: blood culture (sepsis) and urine culture (UTI).
2. Investigations based on history/examination: ABG (hypoxia), CT head (head
injury, intracranial bleed, CVA), and you may consider lumbar puncture
(meningitis), EEG (epilepsy).
3. Diagnostic questionnaire (helps with diagnosis but also monitoring):
Abbreviated Mental Test (AMT): A quick easy tool (see OSCE tips 3).
Confusion Assessment Method (CAM): Usually performed after AMT (see
OSCE tips 3).
Mini-Mental State Examination (MMSE)

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23
Q

Presentation of delirium

A

Sudden onset, different to usual self
Fluctuating course
Disorientation
Poor concentration, inattention
Poor STM
Abnormal perception; Hallucinations
Abnormalities of Sleep-wake cycle
Psychotic thoughts
Agitation
Emotionally labile

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24
Q

Delirium vs dementia

A

Look at slide 33 old age psychiatry

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25
Q

DDs of delirium?

A

Dementia.
Mood disorders: depression or mania (bipolar).
Late onset schizophrenia.
Dissociative disorders.
Hypothyroidism and hyperthyroidism (may mimic hypo- and hyperactive delirium
respectively).

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26
Q

Management of delirium

A

Person centred care
Identify and manage the possible underlying cause or combination of causes.
Ensure effective communication and reorientation

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27
Q

Supportive management of delirium

A

Clear communication – explain what you are doing slowly and clearly, remember their STM is impaired so they might not remember. Try to use questions that need a ‘yes or no’ rather than asking them questions that rely on their memory as this can be distressing.
Reminders of the day, time, location and identification of surrounding persons.
Have a clock available.
Have familiar objects from home, especially glasses, walking aids and hearing aids.
Staff consistency - both doctors and nurses. Try not to move beds/wards.
Involve the family and carers.
Remove catheters etc where possible.
Quiet environment with low lighting.
Uninterrupted sleep – do they really need obs overnight?
Mobilise regularly with physio – NICE recommends no cot side, encourage walking/motion exercises 3x daily

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28
Q

Questions for Abbreviated Mental Test

A
  1. Age? (1)
  2. Time to the nearest hour? (1)
  3. Recall address at end: ‘42 West Street’
    (1)
  4. ‘What year is it?’ (1)
  5. ‘Where are you right now?’ (1)
  6. Identify two people. (1)
  7. ‘What is your date of birth?’ (1)
  8. ‘Date of First World War?’ (1)
  9. ‘Who is the current monarch?’ (1)
  10. ‘Count backwards from 20 to 1.’ (1)
    ≥8 → cognitive impairment unlikely
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29
Q

Question for Confusion Assessment Method

A

The Confusion Assessment tool (CAM)
involves assessing a patient for four features.
The diagnosis involves the presence of 1 and
2 + either 3 or 4:
1. Acute onset and fluctuating course.
2. Inattention (e.g. using the serial 7s test
where 7 is subtracted from 100 and then
7 is taken from each remainder, i.e. 100,
93, 86, 79, 72…).
3. Disorganized thinking (e.g. incoherent
speech).
4. Alteration in consciousness.

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30
Q

Management of delirium

A

Treat underlying cause - Treat infections, correct electrolytes, stop potential offending drugs, Laxatives for faecal impaction
Reassurance and re-orientation
Provide appropriate environment - Quiet, well-lit side room, consistency in care and staff, reassuring nursing staff
Managing disturbed, violent or distressed behaviour - encourage oral intake and continence, verbal and non- verbal de-escalation, oral low dose haloperidol (0.5-4mg) or olanzapine (2.5-10mg), avoid benzos

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31
Q

What is not first line for delirium?

A

Antipsychotics and benzodiazepines are never first-line for managing delirium and
unfortunately this is a misconception amongst many clinicians. Treating the underlying cause,
providing reassurance and re-orientation and an appropriate environment are the main means
for treating delirium as recommended by NICE guidelines. Low dose antipsychotics should only be used as a last resort in cases of violent or severely distressed behaviour and when
other ways of calming the patient have failed.

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32
Q

What are the outcomes of delirium

A

Full recovery 18-22%
Functional impairment
Increased costs
Institutionalization
Death 30-40%
Prolonged hospitalisation
Psychological stress
Long term cognitive impairment

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33
Q

What is the definition of dementia?

A

Dementia is a syndrome of generalized decline of memory, intellect and personality, without
impairment of consciousness, leading to functional impairment.

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34
Q

What are the irreversible causes of dementia?

A

Neurodegenerative: Alzheimer’s disease, frontotemporal dementia, Pick’s disease, dementia with
Lewy bodies (DLB), Parkinson’s disease with
dementia, Huntington’s disease.
Infections: HIV, encephalitis, syphilis, CJD.
Toxins: Alcohol, barbiturates, benzodiazepines.
Vascular: Vascular dementia, multi-infarct
dementia, CVD.
Traumatic head injury

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35
Q

What are the reversible causes of dementia?

A

Neurological: Normal
pressure hydrocephalus,
intracranial tumours,
chronic subdural
haematoma.
Vitamin deficiencies:
B12, folic acid, thiamine,
nicotinic acid (pellagra).
Endocrine: Cushing’s
syndrome,
hypothyroidism.

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36
Q

How can we diagnose dementia?

A

Clinical Syndrome

Exclude Differential Diagnoses
Bloods (confusion screen)
Imaging
CT/MRI
DaT/SPECT

Formal cognitive testing
- ACE-III

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37
Q

What is ACE-III?

A

Assess 5 cognitive domains
“Normal” score 82/100

Sub-scores just as imporant as total score
Change in score is relevant over time

“Normal” score doesn’t exclude dementia

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38
Q

What are the ACE-III Domains/Sub-scores

A

Attention /18
Memory /26
Fluency /14
Language /26
Visuospatial /16

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39
Q

A useful mnemonic for reversible/ preventable causes of dementia?

A

DEMENTIA
Drugs (e.g. barbiturates), Eyes and Ears (visual/hearing impairment may be confused
with dementia), Metabolic (Cushing’s, hypothyroidism), Emotional (depression can
present as a pseudodementia), Nutritional deficiencies/Normal pressure hydrocephalus,
Tumours/Trauma, Infections (e.g. encephalitis), Alcoholism/Atherosclerosis

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40
Q

Most prevalent dementia’s

A

Alzheimer’s (50%)
Vascular dementia (25%)
Lewy Body dementia (15%)
Fronto-temporal dementia (<5%)
Other causes of dementia (<5%)

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41
Q

What is the pathophysiology of Alzeheimers?

A

In Alzheimer’s disease there is degeneration of cholinergic neurons in the nucleus basalis of
Meynert leading to a deficiency of acetylcholine. Other pathophysiological changes can be
divided into microscopic (Fig. 10.2.3) and macroscopic:
Microscopic → Neurofibrillary tangles (intracellularly) and β-amyloid plaque formation
(extracellularly).
Macroscopic → Cortical atrophy (commonly hippocampal). Widened sulci and enlarged
ventricles.

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42
Q

Pathophysiology of vascular dementia?

A

Vascular dementia (VaD) occurs as a result of cerebrovascular disease, either due to
stroke, multi-infarcts (multiple smaller unrecognized strokes) or chronic changes
(arteriosclerosis) in the small vessels

43
Q

History for vascular dementia

A

Onset: Step-wise
Fluctuations: Sometimes
Hallucinations: Sometimes
Progressive: Yes
Personality changes: Yes
Insight: Varies

44
Q

Pathophysiology of Lewy body dementia?

A

In Lewy body dementia (DLB), there is abnormal deposition of a protein (Lewy body) within
the neurons of the brainstem, substantia nigra and neocortex. Outside the brainstem LBs
are associated with more profound cholinergic loss than in AD. Within the brainstem, they
are associated with dopaminergic loss and parkinsonian-like symptoms

45
Q

Fronto-temporal dementia pathophysiology

A

there is specific degeneration (atrophy) of the frontal and
temporal lobes of the brain. One type of fronto-temporal dementia is Pick’s disease, where
protein tangles (Pick’s bodies) are seen histologically

46
Q

Cortical dementias

A

Alzeheimers
Fronto-temporal

47
Q

Subcortical dementias

A

DLB

48
Q

Mixed dementia

A

Vascular

49
Q

Features of cortical dementia

A

Memory loss Severe
Mood Normal
Speech and language Early aphasia
Personality Indifferent
Coordination Normal
Praxis Apraxia
Motor speed Normal

50
Q

Features of subcortical dementia?

A

Memory loss Moderate
Mood Low
Speech and language Can be dysarthria
Personality Apathetic
Coordination Impaired
Praxis Normal
Motor speed Slow

51
Q

Epidemiology of dementia

A

There are currently 800 000 people with dementia in the UK and it is estimated that there
will be over one million by 2021.
Dementia increases with age (rare if <55 years; 5–10% if >65 years; and 20% if >80 years).
Overall prevalence is similar in ♂ and ♀, but AD is more common in ♀, whereas vascular
and mixed dementias are more common in ♂.
See Table 10.2.3 and Key facts 1 for risk factors and genes associated with AD.

52
Q

RFs for Alzeheimers

A

Advancing age The incidence of AD increases with advancing age.
Family history The lifetime risk of AD in first degree relatives of those affected is 25–
50%.
Genetics See Key facts 1.
Down’s
syndrome
The mutations in trisomy 21 are associated with the development of
pre-senile AD.
Low IQ Lower educational attainment and lower IQ scores are associated
with higher risks of developing dementia.
Cerebrovascular
disease
Strong risk factor for vascular dementia which can co-exist with AD.
Vascular risk
factors
E.g. Past stroke/MI, smoking, hypertension, diabetes and high
cholesterol are risk factors for both AD and vascular dementia.

53
Q

Link between genetics and Alzeheimer’s disease?

A

Presenilin 1 (chromosome 14), Presenilin 2 (chromosome 2) and amyloid precursor
protein (chromosome 21) are genes associated with early onset AD.
ApoE-4 (chromosome 19) is a susceptibility gene that contributes to late onset AD. The
ApoE-2 variant is thought to be protective.

54
Q

ICD-10 classification of dementia

A

A. Evidence of the following:
1. A decline in memory, which is most evident in the learning of new information,
although in more severe cases, the recall of previously learned information may
also be affected.
2. A decline in other cognitive abilities, characterized by deterioration in judgement
and thinking, such as planning and organizing, and in the general processing of
information.
B. Preserved awareness of the environment for a period of time long enough to demonstrate
(A).
C. A decline in emotional control or motivation, or a change in social behaviour, manifested
by one of the following:
(1) Emotional lability; (2) Irritability; (3) Apathy; (4) Coarsening of social behaviour.
D. For a confident diagnosis (A) must have been present for at least 6 months.

55
Q

What is the symptomatic progression of AD?

A

Early stages - memory lapses, difficulty finding words, forgetting names of people/ places
Disease progression - Apraxia, confusion, language problems, difficulty with executive thinking,
Later stages - Disorientation to time and place, wandering, apathy, incontinence, eating problems, depression, agitation

56
Q

Dementia history: Alzeheimers

A

Onset: Gradual
Fluctuations: No
Hallucinations: Sometimes
Progressive: Yes
Personality changes: Yes
Insight: Varies

57
Q

What does an MRI show for AD?

A

MRI scan showing clear evidence of hippocampal atrophy and enlarged ventricles in
Alzheimer’s disease (right side) compared to control subject (left side).

58
Q

What can AD be classified into

A

AD can be classified into early onset or pre-senile (<65 yrs, familial) and late onset or senile
(>65 yrs, sporadic), but it usually occurs after the age of 65. It has an insidious onset over
years.

59
Q

What are the examples of impairment of cognitive and executive functions?

A

Executive functions: Problem solving, abstract thinking, reasoning, decision making,
judgement, planning, organization and processing.
Visuospatial abilities: Getting lost, impaired driving, copying figures.
Language disturbances (dysphasia): Word finding difficulties, decreased vocabulary,
perseveration (uncontrollable repetition of a particular response, such as a word,
phrase, or gesture), global aphasia (impairment of language, affecting the production or
comprehension of speech and the ability to read or write).
Apraxia: Inability to carry out previously learned purposeful movements despite normal
coordination and strength, e.g. dressing, unbuttoning shirt.
Agnosia: Impaired recognition of sensory stimuli not attributed to sensory loss or
language disturbance, e.g. object agnosia, auditory agnosia.

60
Q

What are the non-cognitive symptoms of AD?

A

Perception (hallucinations), thought content (delusions), emotion
(depression, apathy), behaviour (wandering, aggression, restlessness).

61
Q

ICD-10 Criteria for AD

A

A. The general criteria for dementia A–D must be met.
B. No evidence for any other possible cause of dementia or systemic disorder.
Early onset Alzheimer’s disease
A. General criteria for Alzheimer’s met and age of onset is <65.
B. At least one of the following must be met:
(1) relatively rapid onset and progression;
(2) in addition to memory impairment there is aphasia, agraphia (↓ ability to communicate through writing), alexia (↓ ability to read), acalculia (↓ ability to perform mathematical
tasks) or apraxia.
Late onset Alzheimer’s disease
A. General criteria for Alzheimer’s met and age of onset is >65.
B. At least one of the following must be met:
(1) slow, gradual onset and progression;
(2) predominance of memory impairment over intellectual impairment.

62
Q

Clinical features of vascular dementia

A

Usually presents in the late sixties or early seventies.
Stepwise rather than continuous deterioration, i.e. stepwise increases
in severity of symptoms.
Memory loss.
Emotional (depression, apathy) and personality changes (earlier than
memory loss).
Confusion is common.
Neurological symptoms or signs (e.g. unilateral spastic weakness of
the limbs or increased tendon reflexes, an extensor plantar response
or pseudobulbar palsy).
On examination there may be focal neurology (often upper motor
neurone signs) and signs of cardiovascular disease elsewhere

63
Q

Features of Mixed dementia

A

Features of both Alzheimer’s disease and vascular dementia.

64
Q

Features of Lewy Body dementia

A

Day to day fluctuations in cognitive performance.
Recurrent visual hallucinations.
Motor signs of parkinsonism (tremor, rigidity, bradykinesia).
Recurrent falls, syncope, depression.
Severe sensitivity to neuroleptic drugs.
People with Parkinson’s disease who develop dementia after 12
months are diagnosed as having Parkinson’s disease with dementia
as opposed to DLB where dementia and parkinsonian features within
12 months of one another.

65
Q

Fronto-temporal dementia features (including Pick’s disease)

A

Usually occurs between the ages of 50 and 60 and develops
insidiously.
Family history is positive in 50% of cases.
Early personality changes: e.g. disinhibition (reduced control over
one’s behaviour), apathy/restlessness (see Key facts 4 for frontal lobe tests).
Worsening of social behaviour.
Repetitive behaviour.
Language problems: e.g. difficult to find word, problems
naming/understanding words.
Memory is preserved in early stages whereas insight is lost early.

66
Q

Features of Huntington’s disease

A

Autosomal dominant, therefore strong family history.
Abnormal choreiform movements of face, hands and shoulders and
gait abnormalities.
Dementia presents later.

67
Q

Features of Normal pressure hydrocephalus

A

Average age of onset after 70.
Triad of dementia with prominent frontal lobe dysfunction, urinary
incontinence and gait disturbance (wide gait).

68
Q

Features of Creutzfeldt–
Jakob disease
(CJD)

A

Onset usually before 65.
Rapid progression with death within 2 years.
Disintegration of virtually all higher cerebral functions.
Dementia associated with neurological signs (pyramidal,
extrapyramidal, cerebellar).

69
Q

Historical questions to ask suspected dementia patient

A

Questions to ask the patient
‘Do you find yourself forgetting things? Can you give some examples? When did it
begin?’
‘Do you find yourself forgetting familiar people’s names?’
‘Do you get lost more easily than you used to?’, ‘Are you able to handle money
confidently?’
‘Do you think being forgetful is stopping you from doing anything?’

Collateral history from informant (Also ask about functional status. See Key facts 2)
‘Are they repetitive in conversation?’
‘Has their personality changed, for example, are they more irritable or anxious?’
‘Have you noticed any change in their behaviour, for instance being more
isolated?’
‘Are their memory problems getting in the way of their daily life?’
‘Do you have any concerns about their safety?

70
Q

MSE for dementia

A

Appearance
&
Behaviour
May appear unkempt with poor self-care. Behaviour may be
inappropriate, e.g. in fronto-temporal dementia due to disinhibition.
Uncoordinated or restless.
Speech Slow, confused. Difficulty finding right word. Repetitive.
Mood Low or normal. Disturbance of affect more common in VaD.
Thought May have delusions.
Perception Hallucinations are a core feature in DLB. May have illusions.
Cognition Affected in all dementias but to varying degrees depending on the type
and severity of dementia. Memory impairment is most severe in
cortical dementias. There is usually impaired attention and
disorientation.
Insight May be preserved initially but is invariably lost in the latter stages of
the disease.

71
Q

Routine investigations for dementia

A

Blood tests: FBC (infection, anaemia); CRP (infection, inflammation); U&Es
(renal disease); calcium (hypercalcaemia); LFTs (alcoholic liver disease); glucose
(hypoglycaemia); vitamin B12 and folate (nutritional deficiencies); TFTs
(hypothyroidism).

72
Q

Non-routine investigation for dementia

A
  1. Urine dipstick: Rule out UTI.
  2. Chest X-ray: Pneumonia, lung tumour.
  3. Syphilis serology and HIV testing: Only if there are atypical features or special
    risks.
  4. Brain imaging: Imaging is only indicated for dementia if there is early onset (<60
    years), sudden decline, high risk of structural pathology, focal CNS signs or symptoms (to rule out space-occupying lesions, e.g. subdural haematoma,
    abscess and tumour), or to monitor disease progression.
    CT scan: usual imaging modality. Can identify hippocampal atrophy.
    MRI: identifies posterior circulation vascular pathology with much greater
    sensitivity.
    SPECT: rarely used in specialist centres to reliably differentiate between
    Alzheimer’s disease, vascular dementia and fronto-temporal dementia.
  5. ECG: If cardiovascular disease suspected.
  6. EEG: If fronto-temporal lobe dementia or CJD is suspected, or where seizure
    activity is a possibility.
  7. Lumbar puncture: If meningitis or CJD is suspected.
  8. Genetic tests: For Huntington’s disease and familial dementia.
  9. Cognitive assessment: Folstein Mini-Mental State Examination (MMSE, see Key
    facts 3), the Abbreviated Mental Test (AMT), the Addenbrooke’s Cognitive
    Examination (ACE), General Practitioner Assessment of Cognition (GPCOG) or
    the Montreal Cognitive Assessment (MOCA).
73
Q

DDs for dementia

A

Normal ageing and mild cognitive impairment.
Delirium.
Trauma: Stroke, hypoxic or traumatic brain injury.
Depression (‘pseudodementia’): Poor concentration and impaired memory are
common in depression in the elderly. Identify whether the low mood or poor
memory came first.
Late onset schizophrenia.
Amnesic syndrome: Severe disruption in memory with minimal deterioration in
cognitive functioning.
Learning disability.
Substance misuse.
Drug side effects: Opiate, benzodiazepine

74
Q

MMSE and AD

A

Normal: MMSE 25–30
Mild: MMSE 21–24
Moderate: MMSE 10–20
Moderate–severe: MMSE 10–14
Severe: MMSE <10

75
Q

The Folstein Mini-Mental State examination (MMSE)

A

Generally speaking, a quick and informal cognitive assessment can be carried out by
recording the following:
Orientation in time, place, and person
Attention and concentration, e.g. serial sevens test. Record the time taken and the
number of errors
Memory:
short-term memory
recent memory
remote memory
Grasp, e.g. name the prime minister and reigning monarch
If cognitive impairment is suspected, you can carry out the Folstein Mini-Mental State
Examination (MMSE). The MMSE is scored out of 30. Scores of less than 22 are indicative of
significant cognitive impairment, while scores of 22 to 25 are indicative of moderate cognitive
impairment. The result is invalid if the patient is delirious or has an affective disorder. Due to
recent copyright restrictions only some of the items on the MMSE can be reproduced here.
Sample items from the Folstein Mini-Mental State Examination
Orientation to time
“What is the date?”
Registration
“Listen carefully. I am going to say three words. You say them back after I stop. Ready? Here
they are …
APPLE (pause), PENNY (pause), TABLE (pause). Now repeat those words back to me.”
[Repeat up to five times, but score only the first trial.]
Naming
“What is this?” [Point to a pencil or pen.]
Reading
“Please read this and d

76
Q

Frontal Lobe tests

A

There are a number of frontal lobe tests that are useful adjuncts when considering a
diagnosis of fronto-temporal dementia.
Verbal fluency and initiation: Ask the patient to recall as many words as possible in one
minute starting with the letter ‘S’. Fewer than 10 words is abnormal. Should aim for >15.
Cognitive estimates: Ask the patient to make educated guesses to questions which they
are unlikely to know the specific answer to e.g. ‘what is the age of the oldest person in the
country?’
Clock drawing test: Tests executive function. Ask the patient to draw a large clock face,
put the numbers in and then make the clock show ten past five.
Similarities (conceptualization): Ask in what way two objects are alike e.g. banana and
orange (both fruits), table and chair (both items of furniture), tulip and rose (both types of
flower).
Motor sequencing (Luria’s 3 step test): Tell the patient you are going to show them a
series of hand movements. Demonstrate fist, edge, palm 5 times without verbal prompts
and ask them to repeat.

77
Q

General points of the management for AD

A

After a diagnosis of dementia is made, patients are legally obliged to contact the Driver and
Vehicle Licensing Agency (DVLA). They may be able to continue driving subject to medical
reports and annual review.
Early discussions should take place to allow advance planning prior to cognition
deteriorating. Topics include advance statements or decisions, lasting power of attorney and
preferred place of care plans.
In the later stages of the disease, if patients are not competent to make a decision, the
requirements of the Mental Capacity Act 2005 should be adhered to.
Vascular dementia is modifiable and preventable by targeting cardiovascular risk factors

78
Q

What are the management strategies of dementia

A

1st line - Supportive treatment, environmental control measures, Acetylcholinesterase inhibitors
Adjuncts - Antidepress, antipsychotics, insomnia mgmt, mgmt of behavioural and psychological symptoms, adding in or switching to memantine

79
Q

Key drugs that help with treating dementia (AD/LBD)

A

Acetylcholinesterase inhibitors
Donepezil, Galantamine, Rivastigmine
Best for cognitive problems
Side-effects include bradycardia, diarrhoea, headache
NMDA Receptor Antagonists
Memantine
Severe impairment or unable to tolerate AChEI
Better for neuropsychiatric impairment
Can be added to AChEI
Side-effects include confusion and dizziness

80
Q

How do NMDA receptor antagonists work?

A

NMDA receptor antagonists (work on glutamate neurotransmitter) and affect glutamate-mediated toxicity of neurons
- Excessive activation of iGluR (ionotropic glutamate receptors) which leads to loss of post-synaptic dendrites and cell bodies
NMDA receptor antagonist (ketamine)

81
Q

Treating other forms of dementia

A

Vascular
Prevent further damage
Treat vascular risk factors

Alcohol-related
Prevent further damage
Stop drinking alcohol

Fronto-temporal Dementia
No specific treatment

Vascular risk factors, e.g. smoking, weight, hypertension, obesity, Diabetes etc

Stopping drinking alcohol in Alcohol-related dementia can lead to improvement in symptoms

82
Q

Principles of dementia management

A

AChE inhibitors
Treat agitation
Treat low mood and insomnia
Functional support
Social support
Support for carers

83
Q

Community help for dementia

A

Social support including support groups such
as Alzheimer’s Society.
Increasing assistance with day-to-day activities
Information and education
Community dementia teams
Home nursing and personal care
Community services such as meals-on-wheels, befriending services, day centres,
respite care and care homes.
For non-cognitive symptoms or behaviour that challenges, aromatherapy, massage,
therapeutic use of music or animal-assisted therapy may be considered.

84
Q

What is the pharmacological management for dementia

A

The three acetylcholinesterase (AChE) inhibitors (donepezil, galantamine and rivastigmine)
are recommended as options for managing mild to moderate Alzheimer’s disease. They can also be used in dementia with Lewy bodies, in cases where non-cognitive
symptoms cause significant distress
Memantine is an NMDA (N-methyl-D-aspartate) receptor antagonist and is an option for
Alzheimer’s disease in the following circumstances:
Moderate Alzheimer’s disease in those who are intolerant of or have a contraindication
to AChE inhibitors.
Severe Alzheimer’s disease.
For behaviour that challenges, if non-pharmacological strategies have proved ineffective, a
short course of an antipsychotic (e.g. risperidone) can be used. For low mood,
antidepressants (e.g. sertraline) can be initiated.

85
Q

Key facts of Acetylcholinesterase inhibitors

A

Acetylcholinesterase inhibitors are centrally acting agents that work by compensating for
the depletion of acetylcholine in the cerebral cortex and hippocampus in AD.
They are cautioned in arrhythmias (sick sinus syndrome and other supraventricular
conduction abnormalities), peptic ulcer disease and asthma/COPD. Galantamine is
contraindicated in severe renal or hepatic impairment.
Side effects include gastrointestinal disturbances, bradycardia and muscle spasms.
Rivastigmine may cause extrapyramidal side effects.
Doses: donepezil (5–10 mg OD), rivastigmine (1.5–6 mg BD), galantamine (4–12 mg BD).

86
Q

What is Mild cognitive impairment?

A

Cognitive impairment without functional impairment

Aetiology similar to dementia

Prognosis
1/3 will improve
1/3 will remain stable
1/3 will progress to dementia

87
Q

What is pseudodementia?

A

Cognitive Impairment secondary to mental illness
Most commonly depression
“Don’t know” answers

Impairments in executive functioning and attention

Frontal lobe changes
White matter hyperintensities on MRI

88
Q

Belinda Burrows
BG: T2DM, OA, CKD3

No history from patient currently

Clerking:
Found by daughter and son, drowsy at home and in ED.
Tender lower abdomen, suspected UTI.
Up on the ward, left her zimmer from by her bedside, poured her jug of water over the patient in the bed next to her, then attempted to throw her table at the support worker who attempted to help.

Fragmented speech, claiming she is fed up of all of the animals wandering around the ward, as she “never liked cats” and can’t believe they’ve been allowed in hospital
Blood tests
Significantly raised WCC and CRP
AKI on CKD
CT Head – no acute changes

Ring daughter (1st contact)
Normally cognitively intact – no confusion or memory problems
Struggles with mobility
Last seen one week previously – fit and well
Short period of lucidity on FAU last night
WCC 18 CRP 280
Urine MC+S on the system (only microscopy back so far, but 4+ White cells

What are the DDs and most likely diagnosis

A

Alzheimer’s Dementia

Lewy Body Dementia

Hyperactive Delirium

Delirium Tremens

89
Q

Charles Crown
88 year old man
BG: Osteoarthritis, HTN,
Hypercholesterolaemia

“I don’t know”

Clerking notes
Brought by son, reduced eating/drinking for weeks
Not getting out of bed
“I don’t know why I’m here”. Giving either shrugs or “don’t know” to most questions.

Brought by son – not eating or drinking for last few days. Appears tired and dehydrated. Called ambulance as he was so worried.
Bloods – normal
CT Head – no acute changes

Has been seeing GP for low mood for 3 years
Feels tired and exhausted
“I should have noticed her illness”
Appetite very poor

No hope for the future and wants to join his wife
Low mood for three years since his wife died, slowly getting worse
Tired and exhausted for weeks, but recently can’t get the energy to get out of bed
Waking up early in the morning, but staying in bed all day
Feels that he should have noticed her illness and notified GP sooner – blaming himself for her death

Losing appetite and recently can’t be bothered to get any food or drink, so has just stopped. Was drinking whisky as main calorific intake, but ran out a few days ago.

No eye contact, lots of psychomotor retardation. Looks dehydrated. Clothes look too big for him. Minimal speech.
Tearful when mentioning his wife’s death.

What are the DDs

A

Alzheimer’s Dementia

Depression

Delirium

Delirium Tremens

90
Q

Depression and Old Age

A

23% lifetime risk of developing by 75years

Prevalence ~3-15% in OA population
Higher in care homes/hospital

Higher rates of suicide in older adults

Approx 1/3 comorbid harmful drinking
Suicide tend to use more drastic measures in OA population.

91
Q

Depression features in OA

A

Under-recognised and under-diagnosed
“Depression without sadness”
Biological symptoms thought of as physical illness
Less likely to seek help
Vague presentations

Relationship with physical health
Bidirectional relationship
Higher physical morbidity and mortality

Depression without sadness – more lethargy/apathy/physical complaints
Larger burden of physical illness in OA group, so biological symptoms are thought of as being more likely to be linked to physical problems
Don’t complain of symptoms or seek help for this
Non-specific and vague symptomatology

92
Q

Physical health relationship and OA depression

A

Depression increases risk of physical disease
Physical illness increases risk of depression
High physical morbidity/mortality in depression

93
Q

What is vascular depression?

A

hanges to cortical circulation

White matter hyperintensities on MRI

Presentation associated with:
Cognitive Impairment
Psychomotor retardation and apathy
Poor Insight

Poor response to antidepressants
Often considered to be “treatment resistant”
Commonly prodromal to dementia

94
Q

What are some reversible causes of depression

A

Drugs
Beta-blockers/nifedipine/clonidine
Opiods/antipsychotics/benzodiazepines
Methyldopa/anti-parkinsonian medications
Digoxin
Metabolic
Anaemia/B12 or folate deficiency
Hypercalcaemia/Hypothyroidism/
hyper- or hypo- kalaemia or natraemia
Infective
Post-viral/neurosyphillis
Intracranial
Post-stroke/subdural haematoma/Parkinson’s Disease/SOL/Dementia

95
Q

Treatment of depression in older age

A

Same as for younger adults

“Start low and go slow” with antidepressants

Psychological therapies/social inclusion

ECT
Max doses of antidepressants sometimes the same as for younger adults
Some specifics – sertraline in post-MI

ECT more commonly used in older adults age group

96
Q

Prognosis of depression

A

Cerebrovascular changes major risk factor

Good prognostic factors:
Onset <70y
Absence of physical illness
Good previous recovery
Religious beliefs

Two-fold increase in risk of Alzheimer’s Disease

97
Q

9 year old man
BG: HTN, depression,
Neuropathic pain

“I can’t take it any more”

Brought to ED by daughter after overdose
“Bizarre thoughts about his legs”
Daughter surprised him by coming to visit unexpectedly. Found him at home having just taken large overdose of stockpile of amitriptyline, gabapentin and sertraline.

Depression treated by GP for many years
Neuropathic leg pain with spinal nerve impingement after lower back injury at work many years previously

Undergoing treatment for his overdose

States his legs “aren’t there any more”
Recently realised that he doesn’t have any internal organs either

2nd person auditory hallucinations

Appears low in mood and tearful
No regrets about overdose

Reports his legs aren’t present and he lost them in an accident.
Neuropathic pain is “phantom limb syndrome”

2nd person auditory hallucinations – voices of unrecognised people talking at him telling him that he is dead and in hell. Telling him he needs to take an overdose to attempt to escape this hell.

DDs and which one?

A

Capgras – Delusion that a close friend/relative/pet has been replaced by an identical imposter
Fregoli – Delusion that a stranger is someone they know in disguise
Cotard – Nihilistic delusion that body parts are missing/person is dead/parts are rotting
De Clerambault – Erotomania (beliefs of another person being in love with the patient)

98
Q

Primary mental illnesses that could cause psychosis?

A

Secondary to delirium?

Primary mental illness
Schizophrenia
Late onset schizophrenia
Delusional disorder
Affective disorder
Dementia

99
Q

Features of psychotic department

A

Common psychotic elements include:
Nihilistic delusions
Hypochondriacal delusions
Delusions of poverty
Auditory hallucinations (second person derogatory)

Treat with antidepressants +/- antipsychotics

100
Q

Late onset schizophrenia

A

AKA Paraphrenia

Onset of symptoms >60 years old

F>M

Persecutory delusions classical
Negative symptoms and thought disorder uncommon

101
Q

Delusional disorders of old age

A

Persistent delusions without hallucinations

Often more distressing to other people than the patient

Patients often reluctant to seek or accept help

Common delusions include:
Persecutory (being targeted by someone)
Erotomania (someone is in love with them) – often dangerous!
Theft
Mistaken Identity

102
Q

What is Charles Bonnet Syndrome

A

Visual hallucinations
Simple repeated patterns
Complex images of people/landscapes/objects

Associated with visual impairment

No role for antipsychotics/treatment

Patient usually retains insight

103
Q

Management of psychosis includes

A

Do patients need treatment?
How much distress are symptoms causing?

Treat underlying cause
Dementia/Depression

Antipsychotics
Cardiovascular side-effects
EPSEs
Effect on cognition