Dementia Flashcards
Define dementia
Severe impairment or loss of intellectual capacity and personality integration, due to the loss of or damage to neurons in the brain
Diagnosing dementia:
a) There must be a decline in what 2 things?
b) But preserved…?
c) Present for at least…?
d) May also have what emotional/ behavioural issues?
a) Cognition - memory, judgement, planning, organisation. And function (impairment of ADLs etc.)
b) Consciousness
c) 6 months
d) Apathy, agitation, lability, irritability, disinhibition
Mild Cognitive Impairment (MCI)
Evidence of cognitive deterioration without loss of functional impairment
- 10-15% develop dementia each year
- 50% eventually develop dementia
Classifying dementia
a) Primary or secondary
b) Cortical
c) Subcortical
a) Due to another disease process/injury or not
b) Cortical: memory, language, executive function, social skills.
c) Subcortical: emotions, movements, memory problems
Dementia: causes
a) Degenerative
b) Vascular
c) Trauma
d) Infection
e) Other intracranial
f) Metabolic/toxic
a) Alzheimer’s Disease, Frontotemporal dementia, Lewy Body Dementia, Parkinson’s Disease, Huntington’s disease, Progressive supranuclear palsy, CJD
b) Multi-infarct dementia, Cerebral infarcts, Binswanger’s disease, CADASIL, Vasculitis e.g. lupus
c) Head injury, repeated stress (boxer)
d) HIV, syphilis, PML
e) Neoplasia, chronic SDH, NPH
f) Alcoholic, Wilson’s, Hypothyroid, B12
AD: features
a) Early (mild)
b) Middle (moderate)
c) Late (severe)
a) Short term memory, difficulty with change, difficulty word finding, repetition of questions, occasional confusion, mislaying items and blaming others
b) Needs regular prompting, difficulty with ADLs, difficulty recognising people, disorientated, long-term memory relatively preserved
c) Final 1-2 years of life: increasing dependence and frailty, incontinence, aggression, agitation, dysphagia, weight loss, loss of speech, difficulty with mobility
Genetics in AD
a) 3 implicated genes in familial AD and their chromosomes (1 is the cause of increased risk in Downs)
b) Age of onset in familial AD
c) Gene that confers a risk of late-onset AD (> 65)
d) Genetic disease conferring risk of vascular dementia
e) Proteins implicated in FTD (genetic component)
f) What other dementias have a strong genetic component?
a) Amyloid precursor protein (APP) (chromosome 21), Presenilin gene 1 (PSEN-1) (chromosome 14), Presenilin gene 2 (PSEN-2). (chromosome 1)
b) < 65 (often 30 - 40 years)
c) APO-E4
d) CADASIL
e) Tau proteins, TDP43
f) Huntington’s (AD), Wilsons (AR)
AD pathophysiology:
a) Cortical
b) Histological
a) Gross atrophy of the affected regions:
- temporal lobe
- parietal lobe
- parts of the frontal cortex
- cingulate gyrus
- ventricular enlargement
b) B-amyloid plaques, neurofibrillary tangles (tau protein)
Diagnosing AD: (MEAGRE)
a) There should be an objective…? (M)
b) Plus one other cognitive function lost out of…? (E)
c) Interference with…? (A)
d) Onset and course (G)
e) Compared with previous functioning (R)
f) And must also…? (E)
M - Memory loss (amnesia)
E - Executive functions: aphasia, apraxia, agnosia or social impairment
A - ADLs, functional ability
G - Gradual onset and progressive course
R - Reduction in cognition from previous function
E - Exclude other causes
Vascular dementia
a) Causes
b) Subcortical vascular dementia is AKA…?
c) Features more suggestive of vascular vs other dementia (4 S)
d)
a) Post-stroke, multi-infarct, CVD,
b) Subcortical Vascular dementia: Binswanger’s disease
c) Features of VD:
- ‘Step wise’ progression with stable disease and then sudden deteriorations,
- Subcortical features (depression, emotional lability, behavioural change, early gait disturbance, unsteadiness and falls)
- Stroke disease signs and symptom (visual problems, weakness, seizures, etc.)
- Scanning - CT/MRI infarcts
d)
Lewy Body Dementia (LBD)
a) Lewy bodies are made up of…?
b) Commonly deposited where?
c) Features: 3 core, 4 supporting
d) Imaging
e) Drugs to avoid
f) Possible drug to trial
a) Protein alpha synuclein
b) The substantia nig ra (classical Lewy bodies) - as seen in Parkinson’s disease and cortex (cortical Lewy bodies).
c) Features of LBD (2 core, or 1 core/1 supporting = probable LBD)
Core: Parkinsonism, Visual hallucinations, Fluctuating course.
Supporting: Falls, REM sleep behaviour disorder (move, jerk, speak), syncope (postural hypotension), sensitivity to neuroleptics, delusions, other psychiatric problems
d) DAT scan: Low dopamine uptake in basal ganglia
e) Neuroleptics - causes Parkinsonism, and possibly fatal NMS. Dopamine agonists/L-Dopa - may worsen psychosis
f) Rivastigmine - may help with cognition and behaviour
Frontotemporal dementia (FTD)
a) Usual age of onset
b) Earlier features (what is preserved usually?)
c) What are frontal release signs?
d) Diagnosis: LOSER (core early features)
e) Supporting features (language, behaviour)
a) Usual onset < 65
b) Behavioural/emotional changes (e.g. disinhibition, emotional lability, personality change, hyperphagia), and language difficulty (e.g. word finding)
c) Primitive reflexes (e.g. palmar grasp, rooting)
d) Core features:
L - Loss of insight early
O - Onset insidious and gradual progression
S - Social interpersonal conduct decline early
E - Emotional blunting early
R - Regulation of personal conduct impaired early
e) Supporting features:
Language - Echolalia, Perseveration, Mutism
Behaviour - Neglect, Mental rigidity & inflexibility, Distractibility, Hyperphagia, Incontinence,
FTD (continued)
f) O/E
g) Investigations
h) Variants of FTD (3)
i) May be overlap with what 3 conditions?
j) Drugs to avoid
k) Management
f) O/E: Primitive reflexes, Akinesia, Tremor, Low BP
g) Investigations: FAB (impaired frontal lobe function but preserved memory and orientation), MRI (frontotemporal atrophy)
h) bvFTD, semantic (fluent) and non-fluent
i) MND, PSP, CBD
j) Acetylcholineterase inhibitors - may worsen the condition
k) Incurable. Non-pharm (general, + SALT/psychology). Drugs for symptoms: antipsychotics, SSRIs, etc.
Parkinson’s disease dementia
a) vs. LBD
b) Prominent features
c) Drugs to avoid
d) If diagnosis not clinically obvious - imaging?
a) PD - unilateral onset, cognitive decline after 1 year. LBD - bilateral Parkinsonism within 1 year of cognitive decline
b) Marked forgetfulness, lethargy and executive dysfunction
c) Typical antipsychotics, also PD drugs may exacerbate dementia
d) DAT scan for dopamine uptake
Features of cortical dysfunction:
a) Frontal
b) Temporal
c) Parietal
a) Inhibition, initiating, reasoning, abstract thought
b) Memory, inattention, alexia, agnosia
c) Difficulty carrying out sequence of events, agnosia
Examinations for dementia
- Neurological - CN dysfunction (SOL), weakness (stroke), gait abnormalities (NPH, LBD, PD, Wernicke’s, etc.), chorea (HD), tremor (PD, LBD), myoclonus (CJD)
- CV - vascular risk factors, AF
- Abdo - hepatomegaly (alcohol, hepatic encephalopathy)
- Thyroid
Assessments of dementia
a) Test for fluency
b) Visuospatial function and multi-step task planning
a) Word generation tests
b) Clock drawing test (11:10 is the best time to get them to draw, sensitive to abnormal cognition)
Investigations for dementia
a) Bloods
b) Imaging (all patients with suspected dementia should have brain imaging!)
c) All patients should be referred to …?
a) FBC, ESR or CRP, MSU, U&E, LFT, glucose, Ca2+, TFT, B12 and folate
b) MRI to exclude intracranial pathology, SPECT if subtype not clinically obvious
c) MEMORY CLINIC
Communicating diagnosis:
a) Advantages of knowing
b) Disadvantages
a) Plan for the future, know what to expect, start medication, relief it’s not more sinister, eligible for benefits/ care etc.
b) Death sentence, stigma of the label, incurable
Classifying severity of dementia
Mild - independent living.
Moderate - needing some help
Severe - dependent
Example features of:
- Apraxia
- Amnesia
- Agnosia
- Aphasia
Apraxias (struggling to get dressed)
Agnosia (not sure if the cup is for tea; not recognising faces)
Amnesia (forgetting names, appointments, misplacing)
Aphasia (difficulty word findings, require prompting)
Mrs Jones takes her 82 year old husband to the GP as she is concerned about his memory. During the consultation he answers “I don’t know” to most of the questions and appears to make little eye contact. What would be the next appropriate step?
Perform a Geriatric Depression Scale (GDS) test as this could be pseudodementia (caused by depression)
GDS-4:
- Give the 4 questions (CHEB)
- scoring?
- relevance in dementia?
C - Content - Are you basically satisfied with your life?
H - Happy - Do you feel happy most of the time?
E - Empty - Do you feel that your life is empty?
B - Bad - Are you afraid that something bad is going to happen to you?
2 - 4 = Depressed, 1 = uncertain, 0 = Not depressed
If positive, consider antidepressants and reassess cognition once depression has resolved
Memantine:
a) Class
b) How does this affect cognition?
c) Indications (2)
d) Side effects
a) NMDA antagonist
b) It works on NMDA glutamate receptors. At normal levels, glutamate aids in memory and learning, but if levels are too high, it leads to overstimulation of nerve cells resulting in degeneration
c) Moderate Alzheimer’s disease who are intolerant of or have a contraindication to AChE inhibitors or severe Alzheimer’s disease
d) Headaches, dizziness, drowsiness, constipation
AChEIs:
a) Name 3
b) Contraindications (give 4)
c) Licensed for what 2 dementias?
d) Should be commenced within __ weeks of diagnosis
e) Which drug has the best effect on behavioural symptoms in dementia?
f) Common side effects
a) Donepezil, galantamine, rivastigmine
b) Asthma, COPD, heart block, sick sinus syndrome
c) AD, LBD
d) 6 weeks
e) RIvastigmine
f) Nausea and vomiting, diarrhoea
Non-pharmacological dementia management
a) Vascular
b) General principles
c) Specific interventions
d) Self-help approaches
a) Reducing vascular risk (blood pressure, lipid profile, glycaemic control, etc) may slow the progression of vascular dementia.
b) Person-centred care, support for carers (including Admiral Nurses), written information and education (including medicolegal), Dementia Friends
c) Cognitive stimulation therapy, social prescribing (music therapy, art therapy, dance therapy)
d) Label items in house, clock and calendar, write things down/reminders, daily newspaper, healthy lifestyle and diet
Management of BPSD
a) What is BPSD? What might it be confused with?
b) Why is management of BPSD important?
c) Non-pharm
d) Pharm (depends on the cause, e.g. pain, constipation, depression, psychosis)
e) Why should TCAs generally not be used for depression in dementia?
a) Behavioural and psychological symptoms of dementia: symptoms of disturbed perception (hallucinations), thought content (delusions), mood (depression, anxiety) and behaviour (disinhibtion, apathy, agitation, wandering) that frequently occur in patients with dementia. May be confused with delirium
b) Reduce carer burden, reduce care costs, reduced chance of institutionalisation/hospitalisation, improve patient and carer QoL
c) Reduce precipitants (e.g. PINCH ME), environmental factors (as with delirium): family involvement, clear communication, orientation, sensory stimuli (including glasses, hearing aids), consistency, mobility
d) Painkillers, laxatives, SSRI, antipsychotic
e) Worsen cognition
Antipsychotics in dementia
a) Do not use/be cautious in what dementia?
b) Increase the risk of…?
c) Help with what symptoms?
a) LBD and PD dementia
b) Sedation, falls, stroke, EPSEs
c) Physical aggression, agitation and psychosis
