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Year 4 Psych > Dementia & Delirium > Flashcards

Dementia & Delirium Flashcards

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1
Q

What is dementia?

A

A generalised decline of intellect, memory and personality without impairment of consciousness, leading to functional impairment

= Clinical syndrome caused by multiple pathologies

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2
Q

What is presenile dementia?

A

Onset <65yr

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3
Q

List the clinical features of dementia (6 areas)

A

1) Cognition
- Poor memory
- Impaired attention
- Aphasia, agnosia, apraxia
- Disorientation
- ‘Personality change’

2) Behaviour
- Odd and disorganised
- Restless, wandering
- Self-neglect
- Disinhibition
- Social withdrawal

3) Mood
- Anxiety
- Depression

4) Thinking
- Slow, impoverished
- Delusions

5) Perception
- Illusions
- Hallucinations

6) Insight
- Impaired

= minimum duration 6 months

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4
Q

What is usually the presentation of dementia?

A

Poor memory / forgetfulness

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5
Q

Describe the onset of dementia

A

Usually insidious but can come to notice after an acute deterioration

May be triggered by a change in social circumstance or intercurrent illness

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6
Q

What is apraxia?

A

Neurological disorder characterised by loss of ability to carry out skilled movements and gestures (despite having the desire and physical ability to do so)

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7
Q

What is agnosia?

A

Inability to recognise objects / people / sounds / shapes

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8
Q

What % of people have dementia:

1) 75-80yr
2) 80-85yr
3) >85yr

A

1) 75-80yr = 4%
2) 80-85yr = 10%
3) >85yr = 40%

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9
Q

Is dementia more common in F or M?

A

4 x more common in M

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10
Q

List some primary degenerative conditions causing dementia (7)

A

1) Alzheimer’s disease
2) Lewy body dementia
3) Frontotemperoal dementia = Pick’s disease
4) Huntington’s disease
5) Wilson’s disease
6) Multiple sclerosis
7) Motor neron disease

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11
Q

List other irreversible causes of dementia (6)

A

1) Traumatic head injury
2) Infections: HIV, encephalitis, CJD
3) Vascular: multi-infarct dementia
4) Toxins: alcohol
5) Anoxia: cardia arrest, CO poisoning
6) Metabolic: hepatic encephalopathy, DM

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12
Q

List some potentially reversible causes of dementia (9)

A

Neurological:

  • Normal pressure hydrocephalus
  • Intracranial tumour
  • Chronic subdural haematoma

Vit deficiencies:

  • Vit B12
  • Folic acid
  • Thiamine

Endocrine:

  • Hypothyroidism
  • Cushing’s
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13
Q

What are the 5A’s of dementia?

A 
Amnesia
Aphasia
Agnosia
Apraxia
Associated behaviours = BPSD (Behavioural and psychological symptoms of dementia)
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14
Q

Outline mild dementia

A

Memory loss sufficient to interfere with everyday activities

Able to live independently

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15
Q

Outline moderate dementia

A

Memory loss is a serious handicap to independent living

Only highly learned / very familiar material retained

Individual unable to function without assistance of another in daily living

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16
Q

Outline severe dementia

A

Complete inability to retain new information

Virtual absence of intelligible ideation

The mind can no longer tell the body what to do

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17
Q

How should dementia be assessed?

A

1) Detailed hx
- Inc collateral

2) Physical exam
- Inc neuro

3) Cognitive testing
- MMSE

4) Laboratory investigations

5) Imaging
- CT / MRI

(EEG to rule out CJD)

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18
Q

What laboratory investigations can be done for dementia?

A 
FBC
LFTs
Thyroid function
Vit B12
Thiamine
Calcium
Glucose
Urinalysis

If indicated: HIV / syphilis testing

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19
Q

What is the management of dementia?

A

General:

  • Education / support / respite care
  • Written care plan

Psychological:

  • Structured group cognitive stimulation programme
  • For agitation - aromatherapy, dance/music therapy, animal therapy
  • Support for carers

Pharmacological:

  • ACh inhibitors
  • Memantine
  • For agitation - antipsychotics and benzodiazepines
  • For depression - antidepressants
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20
Q

What should be included in a written care plan?

A

Views on residential accommodation, end-of-life care, resuscitation

Input from OT, physio, dietician

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21
Q

Give 3 examples of ACh inhibitors

A

1) Donepizil
2) Galantamine
3) Rivastigmine

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22
Q

How do ACh inhibitors work?

A

Increase concentration and duration of action of acetylcholine in CNS

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23
Q

When are ACh used?

A

Alzheimers disease

  • MMSE 10-20 points OR
  • agitation not controlled by non-drug measures or antipsychotics

Evidence they can improve cognitive function and behaviour for up to a year (but do not halt or delay progression of disease)

Stop after 6 months if no benefit

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24
Q

What is memantine?

A

A glutamine NMDA antagonist

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25
Q

When is memantine used?

A

Improves cognition, mood and behaviour in moderate to severe Alzheimer’s

Not licensed in UK as little evidence and ?cost effective

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26
Q

What antipsychotics are used in dementia? When are they used?

A

Haloperidol
Olanzapine

Only use if severely distressed / agitated, after other methods eg low-stimulation environment, have been unsuccessful

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27
Q

What is the risk of using antipsychotics?

A

Inc risk of cerebrovascular events

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28
Q

What benzodiazepines are used in dementia? When are they used?

A

IM lorzepam - used as an alternative to an antipsychotic for extreme agitation

Avoid wherever possible esp in day

Use when antipsychotics fail

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29
Q

What is the most common form of dementia?

A

Alzheimer’s disease - 55%

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30
Q

After AD, what are the most common two causes of dementia?

A

Vascular dementia = 20%

Lewy body dementia = 15%

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31
Q

Describe the pathological findings in AD

A

Smaller aged matched brain:

  • Widened sulci
  • Enlarged ventricles
  • Cell loss
  • Shrinkage of dendritic tree
  • Proliferation of astrocytes
  • Increased gliosis
  • Loss of neurons and synapses

Amyloid plaques

Neurofibrillary tangles

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32
Q

What are amyloid plaques?

A

Areas of dense, insoluble beta-amyloid peptide surrounded by abnormal neuritis filled with highly phosphorylated tau protein

insoluble beta-amyloid peptide deposits as beta-pleated sheets in hippocampus, amygdala, and cerebral cortex

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33
Q

What are neurofibrillary tangles?

A

Made up of helical filaments of microtubule-associated protein, tau, in a highly phosphorylated state

Found throughout cortical and subcortical grey matter = cortex, hippocampus and substantia nigra

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34
Q

What genetics are implicated alzheimers disease?

A

Amyloid precursor protein:
- Long arm of Chr 21

Implicated in beta-amyloid peptide:

  • Presenilin 1 = Chr 13
  • Presenilin 2 = Chr 1

Apo E4 (risk not causative) = Chr 19

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35
Q

What is the ‘cholinergic hypothesis’?

A

Neurons (by plaques and tangles) lost tend to be primarily cholinergic suggesting that cognitive impairment in AD is due to a deficit of cholinergic neurotransmission

= development of Ach inhibitors

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36
Q

List some risk factors for AD (9)

A

1) Age
2) FH
3) APP, presenilin or apoE4 gene mutation carrier
4) Previous head injury
5) Down’s syndrome
6) Hypothyroidism
7) Parkinson’s disease
8) CV disease inc HTN
9) Low level of education or lower IQ

(M=F)

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37
Q

Which Chr codes for the amyloid precursor protein?

A

Chr 21

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38
Q

What mutations can lead to AD?

A

Mutations in APP

Mutations in presenilin = encode proteins involved in cleavage of APP to beta-amyloid
- Lead to autosomal dominant form of AD

Mutations in ApoE4

  • Inherited autosomal dominant forms of disease
39
Q

Describe the course of AD

A

Progressive decline (may not be steady)

Incidental physical illness may cause superimposed delirium resulting in a sudden deterioration in cognitive function from which they may not fully recover

40
Q

How long does someone typically live after the first signs of dementia? What is the most common cause of death?

A

5-8 years

Bronchopneumonia

41
Q

Outline the DSM-IV classification of AD

A

1) Multiple cognitive deficits manifested by both memory impairment and at least one of aphasia, apraxia, agnosia, or a disturbance in executive functioning

2) The cognitive deficits cause significant impairment
in social or occupational functioning and represent a significant decline from a previous level of functioning

3) Course: gradual onset and continuing cognitive decline
4) Cognitive defects not due to any CNS / systemic / substances which could affect memory or cognition
5) Deficits do not occur exclusively during the course of a delirium
6) Disturbance is not better accounted by another Axis I disorder

42
Q

What are possible protective factors of AD?

A 
Smoking 
Oestrogen
NSAIDs
Vit E
Higher premorbid education
43
Q

What factors are associated with a worse prognosis with AD?

A

1) Greater severity at presentation
2) Male, <65yr
3) Parietal lobe damage
4) Prominent behavioural problems
5) Severe focal deficits
6) Depression
7) Absence of misidentification syndrome

44
Q

What is the management of AD?

A

AChEIs (2nd gen)

  • Donepezil: OD, CI in asthma, GI SE, liver metabolism but non-hepatotoxic
  • Rivastigimine: BD, GI SE
  • Galantamine: BD

AChEIs (1st gen)
- Tacrine: hepatotoxic, GI SE, QD

Memamtine

Others inc statins / antioxidants eg vit E

45
Q

What is vascular dementia?

A

aka multi-infarct dementia

Focal disease results from multiple thrombotic / embolic infarcts in the brain
- Infarcts in midbrain or thalamic region especially severe

46
Q

Describe findings of vascular dementia on neuroimaging

A
  • Multiple infarctions and ischaemic lesions in white matter
  • Atrophy of old infarcted areas
  • Infarcts tends to be bilateral
  • Lesions involve the full thickness of white matter
  • Changes in blood flow in unaffected areas
  • Entire brain is smaller and ventricles expanded
47
Q

Describe the onset of vascular dementia

A

Late 60s / early 70s

More sudden onset than AD

Pt often present after a stroke or due to a sudden unexplained loss of function

48
Q

How does vascular dementia often present?

A

1) Early personality changes (often before memory loss)
2) Fluctuating symptoms
3) Episodes of confusion common esp at night
4) Depression

+/- Fits (10%), TIA, other signs of cerebral ischaemia

49
Q

What may be found on examination of someone with vascular dementia?

A

Focal neurological deficits

Signs of CV elsewhere

50
Q

List clinical features of AD vs vascular dementia

A

AD:

  • Insidious decline
  • Poor memory
  • Progressive disorientation
  • Mood change
  • Restless activity
  • Insomnia
  • Decline in social behaviour
  • Personality change
  • Dysphasia / dyspraxia

Vascular dementia:

  • Stepwise progression
  • Patchy impairment of cognitive function
  • Poor memory
  • Episodes of confusion
  • Mood change
  • Personality change
  • Seizures
  • Neurological signs
51
Q

List some risk factors for vascular dementia

A

1) Male
2) CVD / HTN / high cholesterol
3) Smoking
4) FH of CVD / cerebrovascular disease
5) AF
6) DM
7) Coagulopathies
8) Polycythaemia
9) Sickle-cell anaemia
10) Carotid disease

52
Q

What is the life expectancy of vascular dementia following diagnosis? What is the usual cause of death?

A

4-5yrs

Approx half from IHD, others from cerebral infarction or renal complications

53
Q

What is Binswanger’s disease?

A

Small vessel vascular dementia = course may be gradual due to multiple microvascular infarcts

54
Q

What investigations may be useful in vascular dementia?

A

Bloods - cholesterol, clotting, ESR, CRP (vasculitis) etc

CVD - ECG, CXR, BP, Echo, Dopplers

55
Q

What is the management of vascular dementia?

A

Treat contributing disease

Aspirin OD may delay

General health interventions - diet, exercise, smoking etc

56
Q

What 3 conditions are ‘Lewy bodies’ seen in?

A

1) Parkinson’s disease
2) Dementia with Lewy bodies
3) Autonomic failure associated with degeneration of sympathetic neurons in the spinal cord

57
Q

What is the pathophysiology of dementia with lewy bodies?

A

Lewy bodies are abnormally phosphorylated neurofilament proteins aggregated with ubiquitin and alpha-synuclein (present in Parkinson’s). They are found in the cytoplasm of neurons in the basal ganglia (brainstem nuclei), paralimbic, and neocortical structures

There is associated neuronal loss leading to decreased ACh however there is minimal cortical atrophy

58
Q

What are the clinical features of Lewy body dementia?

A

1) Dementia - relative sparing of memory with fluctuating cognitive ability and level of consciousness

2) Parkinsonism (70%)
- Triad of limb rigidity, bradykinesia and gait disorder

3) Visual hallucinations
- Less commonly auditory

4) Recurrent falls / syncope
5) Depression (40%)
6) Sleep disorders - daytime somnolence

59
Q

Is Lewy body dementia more common in M or F?

A

F

60
Q

What is the management of Lewy body dementia?

A

Parkinsonisn treated with L-dopa

Anticholinergics should be avoided as they can increase confusion and visual hallucinations

Atypical antipsychotics should be used over typical:
- Lewy body dementia carries higher risk of neuroleptic malignant syndrome

Psychosocal

61
Q

What is neuroleptic malignant syndrome? How does it present? What is the management?

A

Life-threatening reaction to neuroleptic or antipsychotic medication

Symptoms include high fever, confusion, rigid muscles (high CK), variable BP

Raised CK can lead to renal failure

Stop antipsychotic
IV fluids
Dantrolene can be given to stop spasms
Bromocriptine can be given

62
Q

What is delirium?

A

aka acute confusional state

Acute impairment of consciousness producing a generalised cognitive impairment

63
Q

How common is delirium?

A

Common

15% pt in general medical / surgical wards

64
Q

List the clinical features of delirium (6 areas)

A

1) Impaired consciousness
- Disorientation
- Poor attention and concentration
- Loss of memory

2) Behaviour
- Overactive / underactive

3) Thinking
- Muddled
- Ideas of reference
- Delusions

4) Mood
- Anxious / irritable
- Depressed
- Perplexed

5) Perception
- Misinterpretations
- Hallucinations (mainly visual)

65
Q

Describe the course / onset of delirium?

A

Acute onset
Fluctuating course
Worse in evening

66
Q

List some causes of delirium?

A

1) Systemic infection - UTI, chest, cellulitis, IV lines
2) Neurological infection - meningitis or encephalitis
3) Stroke or MI
4) Trauma or head injury
5) Metabolic failure - cardiac, respiratory, renal or hepatic
6) Hypoglycaemia
7) Electrolyte abnormalities
8) Nutritional deficiencies - vit B12, thiamine, nicotinic acid
9) Drug intoxication or withdrawal
10) Alcohol withdrawal
11) Raised ICP or SOL
12) Postictal states / status epilepticus

67
Q

What investigations can be for delirium?

A

Bloods - FBC, U&Es, LFTS, TFTs, calcium, phosphate, magnesium, glucose, lactate, troponin, albumin, paracetamol and salicylate, haematinics

Blood and urine cultures

ABG
ECG
Urinalysis
CXR
Further tests eg CT head, LP, EEG
68
Q

What tests can be performed to quantify cognitive impairment?

A

Abbreviated mental test score (AMTS)

Mini mental state examination (MMSE)

69
Q

What is the AMTS?

A

1) What is your age? (1 point)
2) What is the time to the nearest hour? (1 point)
3) Give the patient an address, and ask him or her to repeat it at the end of the test. (1 point) e.g. 42 West Street
4) What is the year? (1 point)
5) What is the name of the hospital or number of the residence where the patient is situated? (1 point)
6) Can the patient recognise two persons (the doctor, nurse, carer, etc.)? (1 point)
7) What is your date of birth? (day and month sufficient) (1 point)
8) In what year did World War 2 begin? (1 point) (other dates can be used, with a preference for dates some time in the past)
9) Name the present monarch/dictator/prime minister/ president. (1 point)
10) Count backwards from 20 down to 1. (1 point)

Score <6 = delirium

70
Q

What scores of MMSE indicate delirium?

A

/ 30

25 or more = normal
21-25 = mild dementia
10-20 = moderate dementia
Less than 10 = severe

71
Q

What is the management of delirium?

A

Treat underlying cause

  • Oxygen
  • Fluids
  • Abx
  • Pain relief etc

Reassurance and reorientation

  • Clock visible at all times
  • Pt reminded of time, place regularly
  • Routines

Sleep
- Hypnotics eg zopiclone 3.75mg or benzodiazepine eg temazepam 10mg may be needed at night

May need sedatives
- Haloperidol 0.25-2mg every 4hrs or lorazepam

72
Q

What is the prognosis of delirium?

A

Usually gradual reduction of symptoms with effective treatment of cause

Often patchy amnesia following recovery

Approx 20% mortality around that admission, 50% at 1 year

May be a marker for subsequent development of dementia

73
Q

What cerebral lesions may have psychiatric symptoms?

A

1) Stroke
2) Cerebral tumours
3) Epilepsy
4) Head injury

74
Q

What psychiatric symptoms may someone who has had a stroke experience?

A 
Depression
Emotional liability
Personality changes
Behavioural problems
Dementia
  • High incidence of depression in first year
75
Q

What psychiatric symptoms may someone who with epilepsy experience?

A 
Auras
Hallucinations and other disorders of perception
Deja vu
Psychosis
Neurotic disorders

Can have complex partial seizures of temporal lobe epilepsy, schizophrenia-like psychosis and increased risk of suicide

76
Q

What may be the organic cause of:

  • Depression
  • Fatigue and low energy
  • Irritability
  • Cognitive slowing?
A

Hypercalcaemia

77
Q

What may be the organic cause of:

  • Emotional disturbance and lability
  • Delirium
  • Depression
  • Panic / anxiety episodes
  • Psychotic episodes?
A

Porphyria (acute intermittent type)

78
Q

What may be the organic cause of:

  • Weight gain
  • Depression
  • Insomnia
  • Loss of libido
A

Cushing’s disease

79
Q

What may be the organic cause of:

  • Anxiety
  • Panic

Associated with HTN

A

Phaeochromocytoma

80
Q

What may be the organic cause of:

  • Depression
  • Sleep disturbances
A

Hypokalaemia

81
Q

What may be the organic cause of:

  • Weight loss
  • Inc appetite
  • Anxiety
  • Psychosis
  • Irritability
  • Loss of libido
  • Restlessness
  • Weakness
A

Hyperthyroidism

82
Q

What may be the organic cause of:

  • Depression
  • Memory problems
  • Delirium (33%)
  • Psychosis

May present with hepatic or movement disorders, or psychiatric symptoms including dementia

A

Wilson’s disease

83
Q

What may be the organic cause of:

  • Altered consciousness
  • Confusion
  • Seizures
  • Dysphasia
  • Movement disorders
  • Sensory changes
  • Abnormal behaviour
  • Hallucinations
  • Nightmares
A

Viral encephalitis

Many causative organisms eg tick-borne viruses, measles, mumps, rubella, rabies, HS

84
Q

What may be the organic cause of:

  • Depression
  • Apathy
  • Tiredness
  • Weight loss
  • Anorexia
  • Mild cognitive impairment
A

Addison’s disease

= Primary adrenal insufficiency

85
Q

What may be the organic cause of:

  • Depression
  • Maina
  • Schizophrenic-like psychosis
  • Cognitive slowing
  • Dementia
  • Ataxia
  • Weight gain
  • Depressed mood or psychotic symptoms
  • Loss of libido
  • Poor memory
A

Hypothyroidism

“myxoedema madness”

86
Q

What is the DEMENTIA pneumonic?

A 
Drugs / delirium
Emotions / depression
Metabolic disorders
Eye and ear problems
Trauma / toxins / tumours
Infections
Alcohol / atherosclerosis
87
Q

What age is frontp-temporal dementia usually diagnosed?

A

45-65yr

88
Q

List 3 subtypes of fronto-temporal dementia (FTD)

A

1) Behavioural variant FTD
- Change in personality, behaviour and interpersonal skills

2) Progressive, non-fluent aphasia
- Loss of language skills

3) Semantic dementia
- Loss of semantic memory

89
Q

What investigations are performed for FTD?

A

To determine if there is FTD and what type

  • Fluency assessment
  • Abstract thinking and metaphor interpretation
  • Sorting tasks = Wisconsin sort task
  • Stroop tests (eg word ‘orange’ written in blue and you have to say what colour the word is not what the word says)
  • Hand-positoning test
  • Copying tasks
  • Rhythm tapping taska
  • Trail making tests
  • Cognitive assessments
90
Q

What does an MRI show in FTD?

A

Bilateral atrophy of frontal and temporal lobes

91
Q

What are the histologically different types of FTD?

A

1) Microvascular (60%)
2) Pick’s type (25%)
3) Combined (15%)

92
Q

What is Pick’s type FTD?

A

Presence of Pick’s bodies = intraneuronal masses of cytoskeletal elements

93
Q

What is the management of FTD?

A

Unknown aetiology of FTD makes it difficult to manage

  • Do not use ACHeis
  • Treat symptoms
  • ?SSRI beneficial

Year 4 Psych (10 decks)

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