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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
management of AD
* Care support (OT, community services) * Pharmacological * Cholinesterase inhibitors * Antidepressants * Antipsychotics (controversial)
26
pharmacological management of AD
***Newly diagnosed: Mild to moderate dementia:*** ***AChE Inhibitors monotherapy*** * [**Donepezil**](https://www.google.com/search?rlz=1C5CHFA_enGB881GB881&sxsrf=ALiCzsbWT45ghbGAAkvd8XIeBeqtVi7YgA:1661447840603&q=Donepezil+Rivastigmine+Galantamine-+licensed+for+the+treatment+of+mild+to+moderate+probable+AD&spell=1&sa=X&ved=2ahUKEwjliOjCv-L5AhX1oVwKHSC3BRcQkeECKAB6BAgBEDc) * [**Rivastigmine**](https://www.google.com/search?rlz=1C5CHFA_enGB881GB881&sxsrf=ALiCzsbWT45ghbGAAkvd8XIeBeqtVi7YgA:1661447840603&q=Donepezil+Rivastigmine+Galantamine-+licensed+for+the+treatment+of+mild+to+moderate+probable+AD&spell=1&sa=X&ved=2ahUKEwjliOjCv-L5AhX1oVwKHSC3BRcQkeECKAB6BAgBEDc) * [**Galantamine**](https://www.google.com/search?rlz=1C5CHFA_enGB881GB881&sxsrf=ALiCzsbWT45ghbGAAkvd8XIeBeqtVi7YgA:1661447840603&q=Donepezil+Rivastigmine+Galantamine-+licensed+for+the+treatment+of+mild+to+moderate+probable+AD&spell=1&sa=X&ved=2ahUKEwjliOjCv-L5AhX1oVwKHSC3BRcQkeECKAB6BAgBEDc) **People with intolerance to AChE inhitors** * Memantine monotherapy **People already taking AChE inhibitors** * add memantine **Newly diagnosed: severe dementia** * Memantine monotherapy
27
pathophysiology of vascular ementia
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
clinical features of vasculat demtnia
* stepwise progression * periods of stable symptoms, with sudden decrease in cognition * apathy * disinhibition * memory deficit * poor attention * slow processing
29
Risk factor for VD
same as IHD * smoking * obesity * high cholesterol
30
management of VD
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
Pathophysiology of lewy body dementia
* Spherical **Lewy body proteins** (alpha-synuclein) are deposited in the brain. * substantia nigra * temporal lobe * frontal lobe * cingulate gyrus
32
Parkinsons or LBD
These Lewy bodies are also present in [_Parkinson’s disease_](https://geekymedics.com/parkinsons-disease-examination-osce-guide/). 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
clinical features of LBD
* rapidly progressive * **visual hallucinations** * vivid dreams * depression * Parkinsonian features * repeated falls * urinary incontiennce/ constipation
34
RF for LBD
old age
35
management of LBD
similar to alzheimers +- carbidopa/ levodopa if motor symptoms severe
36
pathophysiology of frontotemporal dementia
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
RF of FTD
younger patients \<65
38
clincial features of FTD
**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
Management of FTD
\*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
pathophysiology of AIDs dementia complex
* 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
clinical features of AIDs dementia complex
Insidious onset, but rapid progression once established * Cognitive impairment * Psychomotor retardation (slow thoughts and movements, also seen in depression) * Tremor Ataxia Dysarthria Incontinence
42
prognosis of dementia
43
Define delirium
an **acute** , fluctuating syndrome of disturbed consciousness, attention, cognition and perception
44
classic features of delirium
* Acute onset * Symptoms/consciousness fluctuate and worse at night * Hallucinations and delusions * Usually visual * Transient *symptoms should resolve once underlying cause treated*
45
types of delirium
* **Hyperactive** – easier to spot * Agitated * Restless * Inappropriate behaviour * **Hypoactive** * Lethargy * Reduced conc * Increased appetite * **Mixed-** hyperactive and hypoactive
46
causes of delirium
**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
DRUG INDUCED DELIRIUM
* Antidepressants * Antipsychotics * Benzodiazepines * Antiparkinsonian drugs * Anticholinergic drugs * Opiates * Steroids * Diuretics * Recreational drug intoxication and withdrawal * Psychotropic drugs
48
screening tool for delirium
CAM
49
CAM
Confusion assessment method
50
**Investigations for delirium**
* Bloods * FBC * CRP * U nd E/cCa2+. LFT, B12/folate, TSH * ABG * Lumbar puncture * Toxicology * CT head
51
**General management of delirium**
* 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
immediate action
53
pharmacological management of delirium
* Haloperidol * Olanzapine (atypical antipsychotic for patients with parkinsons- think dopamine)
54
DoLs and delirium
55
prognosis and delirium
*‘Reversible cause of confusion’* can take up to a month to resolve- most resolves after 1 week
56
Dementia vis delirium

OPIC (Y4) (20 decks)

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