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MI Internal Medicine > Dementia > Flashcards

Dementia Flashcards

1
Q

Definition (4)

A

Acquired
General
Progressive impairment of cognitive function
Impaired activity of daily living

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2
Q

Cognitive functions impaired

A 
Memory
Recall
Orientation
Language
Abstraction
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3
Q

Prevalence at 60yo and doubling time

A

1% at 60, doubles every 5 years

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4
Q

Prevalence at 85yo

A

30-50%

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5
Q

Categories of dementia (Vitamin D Vest)

A 
Primary degenerative
Vascular
Infectious
Trauma
Rheumatological
Neoplastic
Vitamin, Intracranial tumor, Trauma, Anoxia, Metabolic, Infection, NPH, Degenerative, Huntingtons, Vascular, Endocrine, SOL, Toxic
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6
Q

Reversible causes of dementia

A 
Alcohol (withdrawal, intoxication)
Medications (benzodiazepines, anticholinergics)
Heavy metal toxicity
Hepatic/renal failure
Wilsons
Vit B12
Hypo/hyperglycemia
Cortisol
Thyroid
Normal pressure encephalus
Depression
Intracranial tumor
Subdural hematoma
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7
Q

Common differentials

A 
MCI
Delirium
Depression 
Alzheimers
Vascular dementia
Lewy body dementia
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8
Q

Uncommon differentials

A 
Amnesia
Aphasia
FTD
Parkinsons
Huntingtons
Brain tumors
Cushings
Hypothyroid
\+PTH
SLE
Syphillis
Wilsons
TB
Lyme disease
CJD
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9
Q

Primary neurodegenerative causes (4) with key clinical features

A

Alzheimers- Anterograde amnesia, aphasia, apraxia, agnosia, disturbance in executive function
Dementia with lewy body- visual halluncinations, parkinsonism, fluctuating cognition
Frontotemporal dementia- behavioural / language presentation
Huntingtons disease- chorea

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10
Q

Vascular causes of dementia with key clinical features

A

Multi-infarct dementia->acute onset, stepwise, focal neurological signs, dysexecutive
Vasculitis->systemic S&S of vasculitis

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11
Q

Infectious causes (6) with key clinical features

A

HIV
Syphillis->ataxia, myoclonu, tabes dorsalis
Chronic encephalitis
Chronic meningitis->F,H,N, meningismus, localising neurological defects
Abscess->+ICP, localising neuro signs
CJD->rapidly progressive, myoclonus

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12
Q

Traumatic causes

A

DAI, subdural, epidural hematoma->history, +ICP, papilloedema, localising neuro signs

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13
Q

Neoplastic causes

A

Mass effect, edema, hemorrhage, seizure->+ICP, localising signs, systemic symptoms of cancer

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14
Q

Emergency consideration for suspected dementia

A

Delirium

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15
Q

Initial test to order when delirium not ruled out

A

FBC, UEC, fasting blood glucose, urinalysis MCS, UDS

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16
Q

Importance of herpes simplex

A

Most common cause of sporadic encephalitis

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17
Q

How does HSV encephalitis present

A

Acute febrile illness
Altered mental status
Headache, seizure, focal neurology

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18
Q

What to give in all cases of suspected HSV encephalitis

A

Aciclovir

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19
Q

History

A

Psychiatric evaluation
Premorbid function
Geriatric giants
Changes in cognition, function, personality, language, skills, behaviour
Abrupt, step wise, gradual->vascular
Acute->infection, metabolic, lesion, medication, stroke, hydrocephalus
Rapid decline->delirium
Gait abnormalities, urinary incontinence
Change in ability to manage ADLs, and instrumental activities
Family history
Drug and alcohol
Past medical history
Stroke risk factors->hx, TIA, hypertension, cholesterol, diabetes, CAD, AF
Parkinson’s disease inquiry
Transient neurological->gait, incontinence

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20
Q

What are the activities of daily living (6)

A 
Eating
Bathing
Dressing
Toileting
Transferring
Continence
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21
Q

What are the instrumental activities of daily living (8)

A 
Housework
Cooking
Cleaning
Shopping
Finances
Telephone
Transport
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22
Q

Cognitive assessment tool and score when indicates an abnormal result

A

MMSE

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23
Q

Components of MMSE

A 
Orientation
Registration
Attention and calculation
Recall
Language
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24
Q

Components of language assessment (6)

A 
Name two objects
Repeat "no ifs, ands, or buts"
Follow a three stage command
Read and obey the following
Write a sentence
Copy the design
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25
Q

Physical examination- what to test and what it may mean

A

General: vitals, BP, hearing and vision
CN->vascular may have visual field defects. Ataxia, nystagmus and lateral gaze palsy may suggest alcohol
Motor->vascular and hemiparesis
Sensory->peripheral neuropathy may indicate vitamin, toxic metabolic
Co-ordination and gait->vitamin B12, NPH, vascular
Reflexes-> may have primitive, asymetric in vascular, myoclonus in CJD
CV->hypertension, dysrhythmias, PVD, vascular disease, CHF

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26
Q

What are the geriatric giants in history

A

Confusion, incontinence, falls, polypharmacy
Memory and safety
Behavioural

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27
Q

Behaviour issues in dementia

A 
Mood
Anxiety
Psychosis
Suicide
Personality
Aggression
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28
Q

Safety issues in dementia

A

Wandering
Leaving electrical items on
Losing objects
Leaving doors unlocked

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29
Q

Laboratory investigations

A 
UEC, glucose
FBC w. differential
TSH
Vit B12
Folate
ESR
CRP
Urinalysis
Urine MCS
CXR
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30
Q

Other tests to consider based on history

A 
HIV
Urine toxicology
Collage vascular
Urinalysis for heavy metals
Syphyllis serology
CSF
FDG-PET
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31
Q

Imaging

A

CT or MRI

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32
Q

Definition of alzheimers

A

Progressive chronic neurocognitive decline

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33
Q

Define aphasia

A

Language disturbance

34
Q

Define apraxia

A

Inability to perform motor tasks despite normal motor function

35
Q

Define agnosia

A

Difficulty recognising objects despite intact sensory modality

36
Q

Epidemiology of AD

A

60-70% of all dementias
5% of 80
More common in women

37
Q

Gender preference in AD

A

More common in women

38
Q

How is early onset AD inherited, genes involved and how common

A

Autosomal dominant->APP, presenilin 1 and 2

39
Q

Pathophysiology of AD- two theories

A

Amyloid hypothesis->excess interneuronal amyloid (abeta) as overproduction/reduced clearance of beta amyloid->dense amyloid as plaques. Cause inflammation, microglial activation, complement cascade->neuritic plaques leading to cell death.
Tau-protein theory->tau protein accumulation as neurofibrillary tangles.

40
Q

Gross pathology of AD

A

Cortical atrophy +in frontal, parietal, temporal lobes

41
Q

Microscopic pathology of AD

A 
Senile plaques
Loss of synapses
Hyperphosphorylate tau
Neurofibrillary tangles
Loss of cholinergic neurons
42
Q

Biochemical pathology of AD

A

50-90% reduction in choline acetyltransferase

43
Q

Risk factors for AD (6)

A 
Age
Family history
Down syndrome
Genetics
Cerebrovascular disease
Hyperlipidemia
(Weak= brain injury, obesity, low IQ, female, depression, female, DM)
44
Q

Clinical presentation catgories (3)

A

Cognitive
Psychiatric
Motor

45
Q

Cognitive impairment in AD

A

Impaired memory, language, abstract, executive

46
Q

Psychiatric manifestations in AD

A

Mood
Psychosis
Apathy

47
Q

Motor manifestations in AD

A

Occurs late–>Parkinsonism

48
Q

Key diagnostic factors in AD (9)

A 
Presence of risk factors
Memory loss
Disorientation
Nominal aphasia
Misplacing/getting lost
Apathy
Decline in ADL, IADL
Personality change
Unremarkable physical examination
49
Q

Investigations for AD (9)

A 
Bedside cognitive assessment
FBC
ESR
Glucose
TSH
Vit B12 and folate
Metabolic panel
UDS
CT, MRI
50
Q

DSM 5 criteria for AD

A

Memory impairment + one >
aphasia, apraxia, agnosia, disturbed executive function
Gradual and progressive
Not due to general medical condition, psychiatric illness or other neurological illness or substance use

51
Q

Findings on MRI of AD (3)

A

Cortical atrophy, +in hipocampua
Dilitation of lateral ventricles
Widened cortical sulci

52
Q

Management overview of AD

A

Supportive
Environmental control
Cholinesterase inhibitors
Symptomatic management

53
Q

Supportive management of AD

A 
Carer support
Home safety evaluation
OT assessment
Driving, shopping, finances
Self care
Written instructions and explanations for carers
Calenders, clocks, charts for orientation
Lighting
Exercise
AHD
54
Q

Environmental control measures for AD

A

Identification bracelets

Tagging devices with GPS

55
Q

Cholinesterase inhibitor goals, when to start, first line

A

To slow the decline
Begin when mild AD diagnosed
Donepezil 5mg OD or rivastigmine OR Galantaine

56
Q

Symptomatic management AD- mood, psychosis, insomnia, behavioural

A

Antidepressant->sertraline, citalopram, escitalopram
Agitation, wandering, psychosis->risperidone, olanzepine, quetiapine, aripiprazole
Insomnia->sleep hygeine
Behavioural->environmental and behavioural modification

57
Q

When should you consider mirtazepine

A

If poor appetite and insomnia

58
Q

When antipsychotics not to be used in dementia

A

Evidence of vascular dementia

59
Q

When antipsychottic treatment should be stopped

A

Evidence of worsening neurology

60
Q

What environmental factors should you consider with exacerbation of psychosis and confusion

A

Poor lighting
Disorientation
Isolation

61
Q

MOA of donepezil

A

Decrease breakdown of ACh- alleviating the relative deficiency

62
Q

Donepezil CI and cautions, pregnancy and breastfeeding

A

CI in active peptic ulcer and GI/ureteric obstruction

Caution in hx peptic ulcer, heart block/bradyA, parkinsons, asthma, COPD

63
Q

Common side effects of donepezil (10)

A

Nausea, abdominal pain
Urinary frequency, diarrhea
Insomnia, fatigue, depression, drowsy
Sweating, hypertension

64
Q

Counselling use of donepezil

A

Initial dose 5mg
May cause dizzy/drowsy, if it does do not use heavy machinery
Omit one or more if adverse effects
If interrupted treatment, start back at low dose to minimise risk of severe vomiting

65
Q

Key diagnostic factors in Lewy body dementia

A 
Presence of risk factors (old age, male)
Cognitive impariment
Fluctuations in mental state
Visual hallucinations
Depression
EPS
REM sleep disturbance
Severe antipsychotic sensitivity
Others- auditory, falls and syncope, delusions
66
Q

Etiology and pathogenesis of LBD

A

protein alpha-synuclein, a cytoplasmic protein associated with synaptic vesicles

67
Q

Epidemiology of LBD

A

15-25% of all dementias

68
Q

Treatment of lewy body dementia

A

Donepezil

69
Q

Prognosis of lewy body dementia

A

3-5 years

70
Q

Key diagnostic factors in FTD

A

Coarsening of personality, social behaviour and habits
Progressive loss of language fluency/comprehension
Memory impairment, disorientation, apraxias
Self neglect, abandonment of work, activity and social contacts

71
Q

Two variants of FTD

A

Behavioural

Language

72
Q

Which FTD variant is more common

A

Bahavioural

73
Q

Language variants of FTD

A

Progressive non fluent aphasia

Semantic dementia

74
Q

Features of progressive non-fluent aphasia

A

non fluent, laboured speech, anomia, preserved single word comprehentions, word finding deficit, impaired repetition

75
Q

Features of semantic dementia

A

fluent, normal rate, impaired single word comprehension, intact repetition, use of words of generalisation (things) or supraordinate categories (animal for dog)

76
Q

What are supraordinate categories

A

Use of animal for dog

77
Q

Two histology types of FTD

A

Frontal lobe degeneration with microvacuolar change

Pick type with astrocytic gliosis +/- ballooned cells and inclusion bodies

78
Q

Epidemiology of FTD

A

10% of all dementias

79
Q

Core features in FTD

A

Insidious decline and gradual
Early decline in social interpersonal conduct
Early impairment of regulation of personal conduct
Early emotional blunting
Early loss of insight

80
Q

Supportive features in FTD

A

Behavioural
Language
Motor

81
Q

Motor features of FTD

A 
Primitive reflexes
Incontinence
Akinesia
Rigid
Tremor
Low and labile blood pressure
82
Q

Management of FTD

A 
Supportive care
Treat irritability with benzodiazepine
Treat any concurrent illness
Home assistance, respite
Treat mania etc with valproate
Organise and manage end of life care

MI Internal Medicine (67 decks)

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