Dementia Flashcards
Dementia Prevalence
- As the population age increases, the prevalence of dementia increases
Define Dementia
clinical syndrome characterized by progressive cognitive decline that interferes with the individual’s ability to function independently
Define Cognition
all of the mental processes involved in learning, remembering, and using knowledge
Define Mild COgnitive Impairment
Modest decline in cognition from previous. This decline does not interfere with ability to function independently. May or may not progress to dementia.
Describe relationship between demntia and delirium
o Individuals with dementia are particularly vulnerable to developing delirium
o Individuals that have experienced delirium are at increased risk of developing dementia
What must occur first for dementia management?
- Reversible causes of cognitive impairment (DEMENTIA): need to be ruled out or managed before diagnosis of dementia
What are some reversibale causes of demntia
o Drugs (including alcohol)
Anticholinergics: cumulative anticholinergic exposure increases risk for subsequent dementia!
Otherwise, pretty much the same as delirium
o Emotional (depression)
o Metabolic, electrolytes, endocrine
o Eyes and Ears declining
o Nutritional (B12 deficiency)
o Tumor or other space-occupying lesion
o Infection (neurosyphilis, HIV)
o Anemia
Describe alzheimer DIsease
o Most common
o Usually starts with short-term memory loss and slowly progresses to all areas of functioning
o Associated with characteristic beta-amyloid plaques and neurofibrillary tangles. Can see cerebral atrophy upon head CT.
Etyiology, Risk FActors and Prevention of AD
Etiology unclear; likely a mix of genetic, environmental, and social factors
o Risk factors: increased age, family history, genetic mutations, history of severe head trauma, mild cognitive impairment, and lifestyle (lack of exercise, obesity, smoking, etc.)
o Education, social engagement, and lifelong learning is protective
Describe VAcular Dementia
o Results from interrupted blood flow in parts of the brain. Damage is usually visible on MRI and CT and there are usually CV risk factors
o Onset may be abrupt OR gradual. May be stepwise (stable then sharp decline)
SX VAcular Dementia
Symptoms are based on the part of brain affected.
Complex thinking and planning, personality changes, agitation, and moodiness are more common early on than in AD
Insight into deficits may be more preserved in vascular dementia vs. AD
Describe Frontotemporal Dementia
o Strong genetic component and is earlier onset (40-50s)
o Damage is initially limited to frontal and temporal lobes. Over time, progresses to global impairment
Changes in speech and personality occur before memory changes
Describe PArkinson’s Dementia
o Dementia that develops after a clinical diagnosis of Parkinson disease
o Impairment in attention, visuospatial skills, and planning and completing complex tasks occurs early on
o Dopaminergic treatments for PD may exacerbate behavioural and psychological symptoms of dementia
Describe LEWY Body Dementoa
o Lewy bodies: abnormal deposits of alpha-synuclein protein in neurons
o “Parkinson disease in reverse:” present with cognitive impairment and visual hallucinations first, or concurrently with PD motor symptoms
Early postural instability and repeated falls are common
Pronounced fluctuations
Extremely sensitive to antipsychotics
Diagnosis of Dementia
- Diagnoses: based on diagnosis of exclusion
o Neuroimaging may be supportive
o Rule out reversible causes for cognitive changes
o Detailed history to assess functional status (individuals may or may not have insight)
o Cognitive assessment
Cognitive Assesments
Mini-Mental Status Examination (MMSE): assesses multiple cognitive domains in ~ 10 minutes. Highly sensitive and specific to dementia, but not to mild cognitive impairment. Scores are affected by level of educational attainment. Lower score = more impairment.
Functional Activities Questionnaire (FAQ): developed to assess functional impairment, therefore needs to correlate with baseline function. Developed to be completed by a caregiver or close support. Higher score = poorer function.
What is BPSD
- Behavioural and Psychological Symptoms of Dementia (BPSD): non-cognitive symptoms of disturbed thoughts, perception, mood, or behaviour, that may occur with dementia
Describe Sx of BPSD
o Behavioral: agitation, aggression, wandering, disinhibition, repetitive behaviours, hoarding, vocalizations, nocturnal restlessness
o Psychological: apathy, emotional lability, paranoia, hallucinations, delusions, involuntary laughing/crying, depression
Triggers of BPSD
Psychological (fear of danger or being abandoned)
Environmental (not liking who is around them)
Medical (pain, constipation, hunger)
Medication (anticholinergics, benzos, opioids, cannabinoids, anticonvulsants, fluoroquinolones, clarithromycin, psychoactive NSAIDs)
Cholinesterase Inhibitor Examples
- Cholinesterase inhibitors: donepezil, galantamine, rivastigmine
Cholinesterase MOA
o MOA: prevents the breakdown of acetylcholine
Cholinesterase Inhbitors Effecr
o May show small improvements in measures of cognitions, but less likely to see improvements in functional abilities (1 in 42)
o May slow progression (1 in 12)
Seen in 3-6 months if there is a benefit (EDS criteria – MMSE, FAQ)
Cholinesterase Indication
o Indication: mild to severe Alzheimer’s
Side Effects Cholinesterase Inhibitors
o Side effects: dose related
Common: N/V/D, loss of appetite, insomnia, urinary urgency +/- incontinence
Less common: weight loss, agitation, bradycardia, syncope, GI bleed, behaviour disturbances, nightmares, QT prolongation (donepezil and galantamine)
Cholinesterase CI and CAutions
o Contraindications: uncontrolled/severe asthma or COPD, cardiac conduction abnormalities, bradycardia (< 55 bpm)
o Precautions: ulcers, uncontrolled GERD, urinary incontinence, seizure history, current anticholinergics (EDS)
NDMA ANtgonist Examples
- NMDA antagonist: memantine
NDMA MOA
o MOA: blocks glutamate at NMDA receptor
NDMA Effect
o Can be combined with cholinesterase inhibitor, but unknown benefit
o Benefits seen in cognitive testing, but minimal clinical benefit in most cases
Indication NDMA
o Indication: moderate to severe Alzheimer’s
Side Effects NDMA and Cuation
o Side effects: better tolerated than cholinesterase inhibitors
Dizziness, constipation, confusion, insomnia, headache, hypertension, restlessness, akathisia, nausea, QT prolongation
o Precautions: cardiovascular disease or seizures
o Must renal adjust
TX Discontinuation Dementia
o When the situation progresses to risk>benefit (adverse effects)
o When loss of ability to perform ADLs independently i.e., no meaningful benefit remaining
o Taper at least over 2-4 weeks
Monoclonal ANtibodies Dementia
o Current drugs may decrease symptoms, but new “-mab” drugs were developed to be disease-modifying
o Unclear clinical significance: CLARITY-AD trial showed that Lecanemab slowed cognitive decline by 27% over placebo.
Monoclonal Antibodies Avilable Dementia
o Lecanemab
MOA: reduces beta-amyloid plaques in the brain
Indication: mild cognitive impairment or mild AD
Formulation: IV q2weeks
Significant risk for adverse effects: brain bleeding and/or swelling
Currently under review by Health Canada
o Donanemab
Formulation: IV monthly x 18 months
TX BPSD
What sx of bPSD are ammendable to pharmacotx?
Aggression (may be verbal or physical)*
Paranoia
Hallucinations
Delusions
Depression
Antidepressants BPSD
Citalopram, escitalopram, sertraline, venlafaxine, duloxetine, mirtazapine, bupropion
Avoid TCAs and paroxetine (anticholinergic)
Avoid fluoxetine (Drug interactions, longer t1/2)
When to use antidepressants in BPSD?
When depression or anxiety is root trigger of behaviour
Daily if for depression or chronic anxiety
If sleep is a significant issue – mirtazapine or trazodone may be preferred (avoid Z drugs)
AVOID benzodiazepines for anxiety or for sedation!
Why should BZD’s be avoided in BPSD?
Worsen cognitive impairment, ↑ fall risk, may also worsen disinhibition
Occasionally may be used short-term following a stressful event (e.g. change in residence, bereavement) OR preventatively before dental work, etc.
Low dose of short half-life benzodiazepine, e.g. lorazepam 0.5 mg as a single dose
Antipsychotics BPSD
Risperidone*, olanzapine, quetiapine, aripiprazole, clozapine, haloperidol (delirium)
Atypical preferred (decreased EPS, older adults more susceptible to developing EPS)
Given only if behaviour is causing harm and/or has not responded to non-pharmacological methods
Black box warning: ↑ risk of mortality (1.2-1.6x)
Try to taper and stop every 3 months
Risk of Antipsychotics
Watch for: weight gain, ↓BP (orthostatic hypotension), anticholinergic effects, sedation, falls, EPS, tardive dyskinesia, urinary retention
MUST be followed, monitored, and removed if necessary
START LOW, GO SLOW (↑ and ↓)
decision of which anti-psychotics
No atypical antipsychotics better than another –> Pick something based off of side effects profile
Olanzapine not used in older adults (anticholinergic effects)
Quetiapine and Risperidone are main ones used
Quetiapine less DA blocking effects (EPS), more sedation
Risperidone is the only one that has an on-label indication for BPSD
Haloperidol BPSD
Haloperidol to manage acute delirium – PRN only
Not recommended in Parkinson’s patients due to extra-pyramidal symptoms (EPS)
Apathy Management BPSD
Generally risk»_space; benefit!
Stimulants
Sedatives
Methylephenidate
Sedtaives
Analgesics
