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OPIC (Y4) > 1- OPMH: Dementia and delirium > Flashcards

1- OPMH: Dementia and delirium Flashcards

1
Q

define dementia

A

is the loss of cognitive functioning — thinking, remembering, and reasoning — to such an extent that it interferes with a person’s daily life and activities

  • >6 months of symptoms
  • cognitive impairment
  • a syndrome: sets of signs and symptoms
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2
Q

cognitive impairment

A

disturbance of higher cortical functions including memory, thinking, judgement, language, perception and awareness

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3
Q

Types of dementia

A
  • Alzheimer’s most common (50-70%)
    • Women>men
  • Vascular dementia (25%)
  • Lewy body (15%)
  • Frontotemporal dementia
  • AIDS-dementia complex
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4
Q

what does BPSD stand for

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5
Q

4 key symptoms of BPSD

A
  1. Affective
  2. Apathetic
  3. Psychotic
  4. Hyperactive
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6
Q

BPSD management

A

Primary aim: reduce patient distress enough to engage with other around them and minimise risk to others

  • keep ABC chart
  • investigate and treat precipitating physical illness
  • Non-pharmacological e.g. music therapy
  • Pharmacological e.g. antipsychotics (caution with LBD)
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7
Q

ABC charts in acute hospitals

A

The ABC approach is a way of characterising events and resultant behaviours.

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8
Q

early signs and symptoms of dementia

A
  • poor memory
  • subtle mood and behaviour changes
  • still able to do most ADL
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9
Q

Mid stage signs and symptoms of dementia

A
  • more prominent memory problems
  • cognitive difficulties e.g. language and executive function
  • marked changes in behaviour
  • disability- trouble with ADL
    • finance
    • planning
  • frequent but not continuous support
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10
Q

Late stage signs and symptoms of dementia

A
  • Severe and pervasive memory problems accompany other major cognitive disabilities e.g. severe disorientation, failure to recognise familiar people, significant speech difficulties.
  • Marked (positive and negative) changes in behaviour e.g. agitation or restlessness, irritability, disinhibition, severe apathy.
  • Disability is severe, even basic aspects of personal functioning are failing and people require more or less continuous supervision.
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11
Q

inverse care law and dementia

A

those who are most dependent and vulnerable often have the least awareness of their disabilities

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12
Q

When concerned about a patients memory, what is key?

A

ALWAYS GET A COLLATERAL HISTORY

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13
Q

Collateral history taking

A

involves using family/friend/witness to complete a history that is struggling with information given just by the patient alone

e.g. poor memory or after a fall

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14
Q

investigations for dementia

A
  • History
  • Examination: Dementia screen
    • MMSE
    • AMT
    • 6-CIT
    • MOCA
    • GPCOG
  • Dementia blood screen:
    • Full blood count→anaemia
    • U&E→deranged sodium, calcium, glucose
    • TSH→hyper/hypothyroidism
    • Serum Vitamin B12
  • Urine drug screen
  • CT head
  • MRI brain
  • ECG in vascular dementia
  • Routine syphilis testing is not necessary but should be done if a risk is identified in the history
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15
Q

The GPCOG, mini-mental state examination , 6-CIT, AMT

A

are a common assessment used to test patients cognitive function. Usually used when patient/relation are concerned about a deterioration of patient memory

→ if patients test positive → refer to memory clinic for further testing

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16
Q

MMSE

A
  • Ask which hand they right with
  • Ask permission to do the test
  • I’m going to ask you some questions and give you some problems to solve answer them as best as you can
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17
Q

GPCOG

A

designed to be used in the time constraints of GP

  • involves a collateral history
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18
Q

MMSE scoring

A
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19
Q

6-CIT

A

6CIT uses an inverse score and questions are weighted to produce a total out of 28. Scores of 0-7 are considered normal and 8 or more significant.

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20
Q

AMT

A

abbreviated memory test

  • used in hospitals
  • quick and easy to use
  • validity isnt very high
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21
Q

Dementia subtypes comparison

A
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22
Q

Pathophysiology of Alzheimers dementia

A
  • Global atrophy of brain lobes (frontal, parietal and temporal)
    • Sulcus widening
  • Histological features
    • amyloid plaques (clumps of beta-amyloid)
    • neurofibrillary tangles (bundles of filaments within neurons, mostly made from tau protein).
    • The accumulation of these leads to a reduction in information transmission, and eventually to the death of brain cells, with abnormal depositions remaining post-mortem.
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23
Q

Risk factors for AD

A
  • Head injury
  • High serum cholesterol and fats
  • Lifestyle factors: smoking, midlife obesity and diet high in sat fats
24
Q

Clinical features of AF

A
  • > 60 (though there are early-onset cases)
  • family history
  • gradual deterioration
  • most common presenting symptom is memory loss, with evidence of varying changes in planning, reasoning, speech and orientation
  • apathy
  • decline in ADLs
  • personality/mood change
25
Q

management of AD

A
  • Care support (OT, community services)
  • Pharmacological
    • Cholinesterase inhibitors
    • Antidepressants
    • Antipsychotics (controversial)
26
Q

pharmacological management of AD

A

Newly diagnosed: Mild to moderate dementia:

AChE Inhibitors monotherapy

People with intolerance to AChE inhitors

  • Memantine monotherapy

People already taking AChE inhibitors

  • add memantine

Newly diagnosed: severe dementia

  • Memantine monotherapy
27
Q

pathophysiology of vascular ementia

A

Common endpoint of many vascular pathologies intracranially

  • Infarction
  • Haemorrhage
  • Leukaoraisois → disease of white matter also called subcortical leukoencephalopathy
  • Alzheimer’s disease → although not classified as a vascular pathology, AD has a strong vascular risk- factor spectrum
28
Q

clinical features of vasculat demtnia

A
  • stepwise progression
    • periods of stable symptoms, with sudden decrease in cognition
  • apathy
  • disinhibition
  • memory deficit
  • poor attention
  • slow processing
29
Q

Risk factor for VD

A

same as IHD

  • smoking
  • obesity
  • high cholesterol
30
Q

management of VD

A

Reducing risk of further sclerotic/embolic effects

  • Lifestyle modification
  • Antiplatelet therapy/Anticoagulation
  • BP control if HTN
  • Statin therapy if elevated LDL cholesterol
  • Optimisation of glycaemic control if diabetic
  • Carotid endarterectomy if carotid stenosis >70%
  • Cholinesterase inhibitors or memantine if concomitant AD
31
Q

Pathophysiology of lewy body dementia

A
  • Spherical Lewy body proteins (alpha-synuclein) are deposited in the brain.
    • substantia nigra
    • temporal lobe
    • frontal lobe
    • cingulate gyrus
32
Q

Parkinsons or LBD

A

These Lewy bodies are also present in Parkinson’s disease. In Parkinson’s they are mainly deposited in the substantia nigra, whereas they are more widespread in Lewy body dementia.

→ essentially the same disease: if movement disorder followed by dementia then we call this parkinsons disease, if dementia precedes movement disorder then we call it dementia with lewy bodies

33
Q

clinical features of LBD

A
  • rapidly progressive
  • visual hallucinations
  • vivid dreams
  • depression
  • Parkinsonian features
  • repeated falls
  • urinary incontiennce/ constipation
34
Q

RF for LBD

A

old age

35
Q

management of LBD

A

similar to alzheimers

+- carbidopa/ levodopa if motor symptoms severe

36
Q

pathophysiology of frontotemporal dementia

A

Neuron damage and death occurs in the frontal and temporal lobes.

Atrophy occurs due to deposition of abnormal proteins (often tau protein) within the lobes. There is thought to be a genetic component in about a quarter of cases.

37
Q

RF of FTD

A

younger patients <65

38
Q

clincial features of FTD

A

3 behavioural presentations of FTD

  • Apathetic
  • Disinhibited
  • Stereotypic

History

  • Coarsening of personality, social behaviour, and habits
  • Progressive loss of language fluency or comprehension
  • Development of memory impairment, disorientation, or apraxias
  • Progressive self-neglect and abandonment of work, activities, and social contacts
  • Age at onset peak in mid-50s
  • FHx
  • Altered eating habits
39
Q

Management of FTD

A

*not standard dementia medication*

Dependent on patient need:

  • Acute irritability, restlessness, agitation, or aggression → benzos
  • Home-assistance, respite care
  • Compulsions → SSRIs
  • Sleeping disturbance → Mirtazapine 1st line
  • Distractibility → amantadine
  • Gluttony → topiramate
40
Q

pathophysiology of AIDs dementia complex

A
  • As patients with HIV infection live longer thanks to modern treatments, their chance of developing AIDS associated dementia is increasing
  • HIV-infected macrophages enter the brain, causing indirect damage to neurones
41
Q

clinical features of AIDs dementia complex

A

Insidious onset, but rapid progression once established

  • Cognitive impairment
  • Psychomotor retardation (slow thoughts and movements, also seen in depression)
  • Tremor Ataxia Dysarthria Incontinence
42
Q

prognosis of dementia

A
43
Q

Define delirium

A

an acute , fluctuating syndrome of disturbed consciousness, attention, cognition and perception

44
Q

classic features of delirium

A
  • Acute onset
  • Symptoms/consciousness fluctuate and worse at night
  • Hallucinations and delusions
    • Usually visual
  • Transient

symptoms should resolve once underlying cause treated

45
Q

types of delirium

A
  • Hyperactive – easier to spot
    • Agitated
    • Restless
    • Inappropriate behaviour
  • Hypoactive
    • Lethargy
    • Reduced conc
    • Increased appetite
  • Mixed- hyperactive and hypoactive
46
Q

causes of delirium

A

THINK

  • Trauma (head injury, intracranial event)
  • Hypoxia (PE< CCF, MI, COPD, pneumonia)
  • Increasing age/frailty
  • Neck of femur fracture
  • SmoKer or alcohol withdrawal

DELIRIUM

  • Drugs (new stopped /started, side effects, drug interactions)
  • Environment- especially ward moves
  • Lack of sleep
  • Imbalanced electrolytes (renal failure, Na+, Ca2+, glucose, liver function)
  • Retention (urinary and constipation)
  • Infection/sepsis
  • Uncontrolled pain
  • Medial conditions (Dementia, Parkinson’s disease)
47
Q

DRUG INDUCED DELIRIUM

A
  • Antidepressants
  • Antipsychotics
  • Benzodiazepines
  • Antiparkinsonian drugs
  • Anticholinergic drugs
  • Opiates
  • Steroids
  • Diuretics
  • Recreational drug intoxication and withdrawal
  • Psychotropic drugs
48
Q

screening tool for delirium

A

CAM

49
Q

CAM

A

Confusion assessment method

50
Q

Investigations for delirium

A
  • Bloods
    • FBC
    • CRP
    • U nd E/cCa2+. LFT, B12/folate, TSH
  • ABG
  • Lumbar puncture
  • Toxicology
  • CT head
51
Q

General management of delirium

A
  • Treat underlying cause
    • environmental
    • sensory impairment
    • orientation in place/time
    • create familiar environment
    • allow wandering if safe
    • involve family and loved ones
  • Pharmacological
  • Deprivation of liberty safeguards (DoLs)
52
Q

immediate action

A
53
Q

pharmacological management of delirium

A
  • Haloperidol
  • Olanzapine (atypical antipsychotic for patients with parkinsons- think dopamine)
54
Q

DoLs and delirium

A
55
Q

prognosis and delirium

A

‘Reversible cause of confusion’

can take up to a month to resolve- most resolves after 1 week

56
Q

Dementia vis delirium

A

OPIC (Y4) (20 decks)

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