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Yr 4 - Psychiatry > Dementia & Old Age Psychiatry > Flashcards

Dementia & Old Age Psychiatry Flashcards

1
Q

For a patient to be treated under the Mental Health Act (MHA), what 3 criteria must they meet?

A

1) They must have a mental disorder
2) There must be a risk to their health/safety or the safety of others
3) There must be a treatment (however this can include nursing care, not just drugs)

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2
Q

Does MHA permit the treatment of physical problems?

A

MHA only permits the treatment of mental health problems, UNLESS a patient’s physical problem is a result of or a cause of their mental disorder (e.g. refeeding in anorexia).

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3
Q

When is the Mental Capacity Act used?

A

When a person lacks capacity

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4
Q

What does the MCA allow?

A

It allows doctors (or less commonly, those with Lasting Power of Attorney) to make decisions in the best interests of their patient.

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5
Q

What are the 5 key principles of the MCA?

A

1) A person is assumed to have capacity unless proven otherwise
2) Steps must be taken to help a person have capacity
3) An unwise decision does not mean a person lacks capacity
4) Any decisions made under the MCA must be in the person’s best interests
5) Any decisions made should be the least restrictive to a person’s rights and freedoms

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6
Q

What 4 criteria must a person meet to have capacity?

A
  • Understand relevant information
  • Retain the relevant information
  • Weigh up the relevant information
  • Communicate a decision
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7
Q

Definition of dementia?

A

Syndrome that involves chronic impairment of multiple higher cortical functions e.g. memory, thinking, orientation, comprehension, and language.

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8
Q

What is the most common type of dementia?

A

Alzheimer’s

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9
Q

What is the 2nd most common type of dementia?

A

Vascular

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10
Q

What is a tauopathy?

A

A neurodegenerative disorder characterised by the deposition of abnormal tau protein in the brain.

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11
Q

Give a type of dementia that is a tauopathy with Beta-Amyloid

A

Alzheimer’s

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12
Q

Give 3 types of dementia that are a tauopathy without Beta-Amyloid

A
  1. Fronto-temporal Dementia
  2. Corticobasal degeneration
  3. Progressive supranuclear palsy
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13
Q

What is a Synucleinopathy

A

A group of neurodegenerative disorders characterised by the accumulation of the protein alpha-synuclein to form inclusions in the cell bodies or axons of neurons or oligodendrocytes.

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14
Q

Give 3 examples of alpha-Synucleinopathies

A
  1. Lewy body dementia
  2. Parkinson’s disease
  3. Multiple System’s Atrophy
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15
Q

What is a polyglutamine disorder?

A

Caused by expansion of CAG (cytosine-adenine-guanine) leading to a large polyglutamine tract.

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16
Q

Give an example of a polyglutamine disorder?

A

Huntington’s disease

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17
Q

What is vascular dementia caused by?

A

Reduced blood flow to brain

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18
Q

Name the 1ary neurodegenerative disorders

A

Alzheimer’s Disease
Fronto-temporal Dementia
Corticobasal degeneration
Progressive supranuclear palsy
Lewy Body Dementia
Parkinson’s Disease
Multiple System’s Atrophy
Huntington’s Disease

(N.B. vascular is 2ary)

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19
Q

Give the 10 subtypes of 2ary dementias

A
  1. Infectious
  2. Trauma
  3. Post-ictal state
  4. Toxic
  5. Autoimmune
  6. Metabolic
  7. Neoplastic
  8. Congenital
  9. Endocrine
  10. Functional
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20
Q

Examples of infectious causes of dementia

A

o Von Economo
o Whipple’s disease
o Encephalitis/meningitis
o Progressive Spongiform Encephalopathies
o AIDS-Dementia Complex
o Subacute Sclerosing Panencephalitis
o Progressive multifocal leukoencephalopathy (JC polyoma Virus in AIDS)

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21
Q

Examples of trauma causes of dementia

A

o Chronic sub-dural haematoma
o Punch-drunk syndrome (dementia pugilistica)
o Normal pressure hydrocephalus

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22
Q

What triad is seen in normal pressure hydrocephalus?

A
  1. Gait disturbance (gait apraxia)
  2. Dementia
  3. Urinary incontinence
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23
Q

What can be seen on imaging in normal pressure hydrocephalus?

A

Ventricular enlargement (removal of CSF via repeated taps/shunts may help)

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24
Q

What is believed cause of normal pressure hydrocephalus?

A

impaired absorption of CSF at level of the arachnoid villi, possibly triggered by a bleed or head injury

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25
Q

Give 2 causes of toxic caused dementia

A
  1. Alcohol
  2. Solvent, metals including lead, carbon monoxide, barbiturates
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26
Q

Give 3 types of autoimmune dementia

A

o Sarcoidosis
o Late-stage MS
o Vasculitis

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27
Q

Examples of metabolic causes of dementia

A

o Hepatic/uremic encephalopathy
o B1 deficiency (thiamine) i.e. Wernicke-Korsakoff’s’
o B12 deficiency (cobalamin)
o B9 deficiency (folate)
o Pellagra (niacin aka nicotinamide/B3 deficiency –> triad of dermatitis, dementia, & diarrhoea)
o Electrolyte derangement (sodium)
o Glucose derangement

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28
Q

What is B1?

A

Thiamine

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29
Q

What is deficiency in B1 called?

A

Wernicke-Korsakoff’s’

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30
Q

What is B12?

A

Cobalamin

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31
Q

What is B9?

A

Folate

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32
Q

What is B3?

A

Niacin/nicotinamide

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33
Q

What is a deficiency in B3 called?

A

Pellagra

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34
Q

What triad is seen in Pellagra?

A

The three D’s:

dermatitis, dementia, & diarrhoea

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35
Q

What electrolyte derangement can cause metanolic induced dementia?

A

Sodium

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36
Q

Give 3 neoplastic causes of dementia

A

o Tumours
o Hydrocephalus due to posterior fossa tumours
o Paraneoplastic syndromes

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37
Q

Give 2 congenital causes of dementia

A

o Myotonic dystrophy
o Wilson’s disease

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38
Q

Give 2 endocrine causes of dementia

A

o Hypothyroidism
o Hyperparathyroidism

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39
Q

Give a functional cause of dementia

A

Pseudo-dementia in schizophrenia and depression

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40
Q

What is Alzheimer’s caused by?

A

Caused by characteristic neuropathological features such as amyloid plaques and tau proteins that build up in brain.

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41
Q

What are the 4 key features of Alzheimer’s (mnemonic 4A’s)

A
  1. Amnesia
  2. Aphasia
  3. Agnosia
  4. Apraxia
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42
Q

What is amnesia?

A

Memory loss - recent memories lost first

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43
Q

What memories are lost first in amnesia in Alzheimer’s?

A

Recent memories

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44
Q

What is aphasia?

A

word-finding problems, speech muddled and disjointed

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45
Q

What is agnosia?

A

recognition problems

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46
Q

What is apraxia?

A

inability to carry out skilled tasks despite normal motor function

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47
Q

What drugs can temporality reduce the symptoms in Alzheimer’s?

A
  • Acetylcholinesterase (AChE) inhibitors – e.g. Donepezil, galantamine, rivastigamine (in mild to moderate)
  • NMDA inhibitor - memantine (in severe) –> blocks excessive amounts of glutamate
  • Antidepressants
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48
Q

What are the characteristic histological features of Alzheimer’s?

A

Amyloid plaques (clumps of beta amyloid) and neurofibrillary tangles (bundles of filaments with neurons, mostly made from tau protein).

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49
Q

What is the hallmark of vascular dementia?

A

Progresses in step-wise fashion –> often shows a period of stability at one level of functioning, before an acute decline progression, followed by another period of stability

This typically occurs over a span of several months to years.

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49
Q

Is vascular dementia more common in males or females?

A

More common in males (may be due to their increased risk of vascular disease)

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50
Q

Risk factors for vascular dementia?

A
  1. Male
  2. Previous stroke (9x higher)
  3. Hypertension
  4. Other general vascular risk factors e.g. smoking, diabetes, hyperlipidaemia, obesity, hypoercholesterolaemia, AF
  5. Risk increases with age (rare before 65, but significantly increases after)
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51
Q

There are several subtypes of vascular dementia. What is the most common?

A

cerebrovascular infarcts

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52
Q

What are the most affected areas of the brain in vascular dementia?

A

The white matter of both cerebral hemispheres, grey nuclei, thalamus, and striatum

53
Q

Aetiology of vascular dementia?

A

Ischemic or hemorrhagic cerebrovascular disease, which leads to brain damage.

54
Q

Signs and symptoms of vascular dementia?

A

Hallmark of stepwise progression.

  • Single infarct disease –> classically presents with cognitive impairment (acutely or subacutely), following the event
  • Mood disturbances & mood disorders
  • Psychosis, hallucinations & paranoia (especially in later stages)
  • Depression – patients should be screened for this
  • Psychomotor retardation (this is the slowing down of your mental or psychical activities e.g. slow thinking, slow body movements)
  • Emotional lability – rapid, exaggerated changes in mood (e.g. uncontrollable laughing or crying, heightened irritability or temper)

N.B. –> Patients may present with a history of strokes, which may be accompanied by stepwise cognitive decline or sudden changes in cognitive function.

55
Q

How would you differentiate VaD from Alzheimer’s?

A

Alzheimer’s –> Predominant memory impairment, slower and continuous decline, usually lack of significant vascular risk factors or neuroimaging evidence of cerebrovascular disease.

56
Q

How would you differentiate VaD from Lewy Body Dementia?

A

LBD –> Fluctuating cognition, visual hallucinations, Parkinsonism, and REM sleep behavior disorder are the core features.

57
Q

How would you differentiate VaD from frontotemporal dementia?

A

Frontotemporal –> Prominent changes in personality and behavior or language difficulties with relative sparing of memory.

58
Q

How would you differentiate VaD from normal pressure hydrocephalus?

A

Normal pressure hydrocephalus –> Gait disturbance, urinary incontinence, and cognitive impairment (triad of Hakim-Adams).

59
Q

Investigations for VaD?

A
  1. Comprehensive history and examination.
  2. Formal cognition screening, such as MMSE (Mini-Mental State Examination) or MoCA (Montreal Cognitive Assessment).
  3. Medication review to exclude medication-induced cognitive impairment.
  4. Exclusion of reversible organic causes such as vitamin B12 or folic acid deficiency, hypothyroidism, or normal pressure hydrocephalus.
  5. Neuroimaging, preferably an MRI Head, to identify vascular changes, infarcts, or white matter hyperintensities indicative of cerebrovascular disease.
60
Q

Management of VaD?

A
  1. Symptomatic treatment –> cognitive enhancers such as cholinesterase inhibitors or memantine, and management of neuropsychiatric symptoms.
  2. Detection and address of cardiovascular risk factors such as hypertension, diabetes, hyperlipidemia, and smoking to slow disease progression.
  3. Advanced care planning to prepare for progressive cognitive and physical decline.
61
Q

What is the role of cholinesterase inhibitors in dementia?

A

Cholinesterase inhibitors function to decrease the breakdown of acetylcholine by cholinesterase.

Higher concentrations of acetylcholine leads to increased communication between nerve cells which may temporarily improve or stabilise the symptoms of dementia.

62
Q

What is Lewy Body Dementia characterised by?

A

The presence of Lewy bodies, abnormal protein deposits, within brain cells, particularly in the substantia nigra, paralimbic, and neocortical areas.

63
Q

Lewy bodies are also present in Parkinson’s disease. How does the location of these lewy bodies differ between DLB and Parkinson’s disease?

A

Parkinson’s –> deposited in substantia nigra
DLB –> widespread

64
Q

What are the 3 core features of DLB?

A
  1. Fluctuating cognition - changes in attention and alertness
  2. Parkinsonism
  3. Visual hallucinations
65
Q

Give some features of parkinsonism

A
  1. Bradykinesia (slow movement)
  2. Rigidity
  3. Postural instability
  4. Tremor
66
Q

What drugs are patients with DLB highly sensitive to?

A

Neuroleptics

67
Q

What is the effect of neuroleptics in DLB?

A

These drugs can induce or worsen parkinsonism. Can also potentially lead to neuroleptic malignant syndrome, a life-threatening neurological disorder.

68
Q

How would DLB differ from Alzheimer’s?

A

Characterised by gradual memory loss, difficulties with problem-solving, and changes in mood or behaviour. However, Alzheimer’s patients do not typically exhibit the severe sensitivity to neuroleptics seen in DLB.

69
Q

How would DLB differ from Parkinson’s disease dementia?

A

While it shares many symptoms with DLB, Parkinson’s disease dementia typically starts with motor symptoms before cognitive decline.

70
Q

How would DLB differ from vascular dementia?

A

This condition features stepwise cognitive decline and evidence of cerebrovascular disease. Parkinsonism and hallucinations are less common.

71
Q

What 3 invesitgations may be useful in DLB?

A
  1. Dopamine transporter (DaT) scan: This can help distinguish DLB from other types of dementia.
  2. Neuropsychological testing: To assess cognitive functioning and fluctuations.
  3. Electroencephalography (EEG): Although not diagnostic, a slowing background rhythm may be seen in DLB.
72
Q

Which dementia progresses the quickest: Alzheimer’s, VaD, DLB, or frontotemporal?

A

DLB

73
Q

What medications can be used in management of DLB?

A

Cholinesterase inhibitors to help manage cognitive symptoms

74
Q

Overall management of DLB?

A
  1. Medication
  2. Non-pharmacological interventions e.g. cognitive stimulation, physical therapy, and occupational therapy.
  3. Supportive care e.g. palliative and end-of-life care considerations are essential.
75
Q

How does the age group that frontotemporal dementia affects differ from other dementias?

A

It characteristically presents at a younger age compared to other forms of dementia

76
Q

What is frontotemporal dementia (FTD)?

A

A heterogeneous group of neurodegenerative disorders characterized by progressive atrophy of the frontal and/or temporal lobes of the brain.

77
Q

Typical age of onset of FTD?

A

during the sixth or seventh decade of life

78
Q

What causes atrophy in FTD?

A

Atrophy occurs due to deposition of abnormal proteins (often tau protein) within the lobes

79
Q

What protein is often deposited in FTD?

A

Tau protein

80
Q

What are 4 key clinical signs in FTD?

A
  1. Personality changes e.g. disinhibited behaviour, apathy
  2. Language impairments
  3. Cognitive decline
  4. Motor abnormalities e.g. muscle weakness, dysarthria
81
Q

Give 4 differentials for FTD

A
  1. Alzheimer’s
  2. VaD
  3. Creutzfeldt-Jakob disease
  4. Primary progressive aphasia
82
Q

How can pathology determine between Alzheimer’s and FTD?

A

Alzheimer’s pathology is defined by the presence of beta-amyloid plaques and neurofibrillary tangles

83
Q

How can you differentiate between VaD and FTD?

A

VaD - step-wise cognitive decline, focal neurological signs, and evidence of cerebrovascular disease on neuroimaging.

84
Q

What sign on an EEG can be used to differentiate between FTD and Creutzfeldt-Jakob disease?

A

In Creutzfeldt-Jakob disease, periodic sharp wave complexes on EEG are suggestive.

85
Q

How can you differentiate between primary progressive aphasia and FTD?

A

Primary progressive aphasia - characterised by gradual, insidious decline in language abilities with relative preservation of other cognitive functions, at least in the early stages.

86
Q

Investigations in FTD?

A
  1. Neuroimaging (MRI or CT)
  2. Genetic testing - may be used in cases where an inherited form of FTD is suspected, especially if there is a strong family history.
87
Q

What will neuroimaging in FTD show?

A

Structural imaging (MRI or CT) can show atrophy of the frontal and/or temporal lobes.

88
Q

Management of FTD?

A

No cure, management focuses on alleviating symptoms and providing support.

  1. Behavioural interventions e.g. behaviour modification strategies, caregiver support etc
  2. Pharmacotherapy
  3. Supportive care e.g. speech and language therapy, physiotherapy etc
89
Q

What medications can be used to help control behavioural symptoms in FTD?

A

Selective serotonin reuptake inhibitors (SSRIs) and antipsychotics (their use must be carefully balanced against side effects).

90
Q

What age group does ‘old age psychiatry’ refer to?

A

Aged 65 and over

91
Q

What % of older people people with depression receive no help from the NHS?

A

85%

92
Q

Give some differential diagnoses for dementia

A

D - Drugs/delirium
E - Emotions (e.g. depression)
M - Metabolic disorders
E - Eye/ear impairment
N - Nutritional disorders
T - Tumours/toxins/trauma
I - Infections
A - Alcohol

93
Q

What are the four pathological findings found in Alzheimer’s?

A
  1. Cerebral atrophy
  2. Amyloid plaques
  3. Neurofibrillary tangles
  4. Reduced levels of acetylcholine
94
Q

What area of the brain is most affected by cerebral atrophy in Alzheimer’s?

A

Medial temporal lobes (the part of the brain responsible for memory)

95
Q

4 diagnostic features for dementia?

A
  1. No clouding of consciousness
  2. Disturbance of higher cortical functions
  3. Deterioration in functioning
  4. > 6 months
96
Q

What are the 2 classes of drugs used in Alzheimer’s?

A
  1. Acetylcholinesterase inhibitors (1st line)
  2. NMDA (N-methyl-D-aspartate) receptor antagonists
97
Q

What is 1st line pharmacological management of Alzheimer’s?

A

Acetylcholinesterase inhibitors

98
Q

Give some examples of acetylcholinesterase inhibitors

A

Galantamine
Rivastigmine
Donepezil

99
Q

Give an example of an NMDA receptor antagonists

A

Memantine

100
Q

MOA of acetylcholinesterase inhibitors and NMDA receptor antagonists?

A

Both acetylcholinesterase inhibitors and NMDA receptorantagonists work by increasing levels of acetylcholine.

They don’t reverse the decline but can slow the rate of progression.

101
Q

What is pharmacolgocial treatment for vascular dementia?

A

No specific options (unlike Alzheimer’s)

BUT
1) Consider anticoagulants
2) Consider medications to modify risk factors

102
Q

Psychological management in dementia?

A
  • Emotional support
  • Cognitive rehabilitation /cognitive stimulation
  • Treatments for comorbid illness (e.g. CBT for anxiety)
103
Q

What are some characteristic features features of FTD?

A
  • Behavioural variant –> changes in personality, behaviour, interpersonal and executive skills
  • Progressive non-fluent aphasia (PNFA) –> loss of language skills (ability to produce or understand language)
  • Semantic dementia –> loss of semantic memory (knowledge)
104
Q

What is semantic memory?

A

a type of long-term memory involving the capacity to recall words, concepts, or numbers, which is essential for the use and understanding of language.

105
Q

Management for FTD?

A

 Treat symptoms (e.g. depression)
 Psychosocial interventions
 DON’T use AChEIs
 Can use SSRI (some evidence in improving disinhibition)

106
Q

What are 3 core features of lewy body dementia?

A

 Fluctuating presentation
 Features of Parkinson’s
 Visual hallucinations

107
Q

Give some other features of LBD

A

 REM sleep disorder
 Neuroleptic sensitivity
 Reduced DA on SPECT imaging (DaT scan)
 Delusions

108
Q

How does dementia in Parkinson’s differ from DLB?

A

 For DPD there must have been PD symptoms for at least ONE YEAR before cognitive symptoms

 If cognitive symptoms and Parkinson’s features start within a year of each other (either being present first) then it’s LBD

109
Q

How is dopamine implicated in Parkinson’s disease, LBD, and psychosis?

A

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

110
Q

LBD and DPD are associated with hallucinations.

How does this implciate treatment?

A

Treatment is notoriously difficult and is a fine balance between PD and psychotic symptoms

111
Q

Which acetylcholinesterase inhibitor (AChEI) can help with hallucinations in LBD?

A

Rivastigmine

112
Q

Why should antipsychotics be used cautiously in LBD?

A

Can worsen PD symptoms

113
Q

What are the ‘5 A’s’ of dementia?

A
  1. Amenesia
  2. Aphasia
  3. Agnosia
  4. Apraxia
  5. Associated behaviours
114
Q

What is apraxia?

A

Apraxia is the loss of ability to execute or carry out skilled movement and gestures, despite having the physical ability and desire to perform them

115
Q

Give some behavioural symptoms of dementia

A

 Wandering
 Restlessness
 Pacing
 Agitation
 Disinhibition
 Screaming
 Physical aggression
 Swearing
 Apathy
 Repetitive

116
Q

Give some psychological symptoms of dementia

A

 Anxiety
 Misidentification
 Depressed
 Insomnia
 Delusions
 Hallucinations

117
Q

What can cause Behavioural + Psychological Symptoms of Dementia (BPSD)?

Acronym - PINCH ME

A

P - Pain
IN - Infection
C - Constipation
H - Hydration

M - Medication
E - Environment

118
Q

How do we assess BPSDs?

A

 Behavioural ABC Charts
 Look for causes (PINCH ME)
 Mental state examination
 Collateral history

119
Q

What is a behavioural ABC chart?

A

Antecedent –> What happened before thebehaviour?

Behaviour –> What was the behaviour?

Consequence –> What was the consequence?

120
Q

Management of BPSDs?

A

 Treat the cause
 If necessary refer to medics
 Environmental modification and practicalmanagement (e.g. education for family / staff)
 Medication as a last resort

121
Q

Which is the ONLY antipsychotic licensed for the management of agitation?

A

Risperidone

122
Q

Why should risperidone be avoided if possible? What are the associated risks?

A

 Parkinsonism
 Falls
 Stroke risk (2-3 times baseline risk)
 Cardiovascular risks
 Death

If it is used then the lowest possible dose should beprescribed for a time limited period

123
Q

What is a formal screening test for cognitive assessment?

A

AMTS

  1. How old are you?
  2. What is your date of birth?
  3. What is the year?
  4. What is the time to the nearest hour?(give the address 42 West Street)
  5. What is this building?
  6. Who is the monarch?
  7. What were the dates of WWI?
  8. Count from 20 to 1
  9. Tell me the roles of those 2 people
  10. Can you recall the address I gave you?
124
Q

Which cognitive test is the gold standard for screening and diagnosis?

A

ACE-III

125
Q

What 5 domains are tested in ACE-III?

A

1) Attention
2) Memory
3) Fluency
4) Language
5) Visuospatial

126
Q

What score in the ACE-III indicates likely dementia?

A

< 82/100

(88/100 high sensitivity, 82/100 high specificity)

127
Q

How long does the ACE-III take to administer?

A

15-20 mins

128
Q

What is the benefit of using MoCA cognitive test over ACE-III?

A

Quicker to administer (10 mins)

Can be useful in anxious/impaired concentration

BUT less diagnostic accuracy than ACE-III

129
Q

What is normal pressure hydrocephalus?

A

An abnormal buildup of CSF in the brain’s ventricles. It occurs if the normal flow of CSF throughout the brain and spinal cord is blocked in some way. This causes the ventricles to enlarge, putting pressure on the brain.

130
Q

How are ACh levels affected in Alzheimer’s?

A

Reduced

Yr 4 - Psychiatry (17 decks)

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