dementia Flashcards
what is dementia
- Not specific disease, umbrella term
- Affects ≥2 domains of cognition
- Memory, language, attention, problem solving
- Many causes
- Endocrine, AD, hypothyroidism
- Static or progressive
- Occur at any age
- Need occur ≥ 6mnths
- Otherwise is just delirium
AD
- Specific disease
- Progressive disease
- Sx:
- Dementia + neuropsychiatric sx
- Old age (predominantly)
DSM5 dementia definition
major & minor
- Evidence of sig/ modest cognitive decline from prior level of performance in one or more cognitive domains
* Complex attention, executive function, learning & memory, language, perceptual-motor, social cognition
* Concern of the indiv, a knowledgeable informant or clinician there has been a significant/ mild decline in cognitive function
* A substantial/ modest impairment in cognitive performance preferably documented by standardised neuropsychological testing or in its absence other quantified clinical assessment - Cognitive deficits interfere with independence in everyday activities
- Cognitive deficits do not occur exclusively in the context of delirium
- Cognitive deficits are not better explained by another mental disorder
types of dementia
- Alzheimer’s disease (Slow gradual onset)
○ Brain atrophy (mesial temporal lobe)
○ Neuritic plaques (b-amyloid)
○ Neurofibrillary tangles (phospho TAU) - Vascular dementia
○ Cognitive impairment after vascular impairment (stroke)
○ Small, chronic infarcts/ large infarct (hemorrhage) - Lewy body dementia
○ Brain atrophy. Generalised (PD: substantia nigra) - Frontotemporal dementia
○ Focal brain atrophy affecting frontal/ anterior temporal lobes - Mixed type
manifestation of dementia
cognitive
(memory, attention, language, problem solving)
EARLY
* ST memory loss
* Word-finding difficulty
LATER
* Memory loss, unable to process and store info
* Loss of language, comprehension (aphasia)
manifestation of dementia
psychological
EARLY
* Apathy
* Depressive sx
LATER
* Delusions
* Anosognosia
manifestation of dementia
behavioural
EARLY
* Withdrawal from social engagement
* disinhibition
LATER
* agression
* hallucination
* wandering
manifestation of dementia
sleep
EARLY
* REM behavioural disorder
LATER
* altered sleep-wake cycle
manifestation of dementia
physical
EARLY
* gait impairment
* falls
LATER
* repititve, purposeless movements
* parkinson
* seizure
risk factors of AD
- Age >85yo
- Female
- Ethnicity: black, Hispanic
- Genetics: apoliprotein E (APOE4) gene
non-modifiable
* Hypertension
* DM
* Binge drinking
* Smoking
* Limited physical activities
* Obesity
* Hearing loss
* Depression
AD pathological characteristics
1) senile plaques
2) neurofibrillary tangles
senile plaque
- Aggregates AB-amyloid peptide
- APP (amyloid precursor protein) cleaved by:
- B- secretases (longer amino peptide length, more sticky)
◊ Forms plaque
◊ Very inflammatory, fibrosis - Y-secretases (soluble fragments)
neurofibrillary tangles
- TAU: tubulin associated protein (needed for microtubule stabilisation and intracellular transport)
□ Hyper-phosphorylated TAU protein aggregates
□ form paired helical filaments (PHF)
□ Less intracell transport = NEURON DEATH
loss of microtubules
AD brain atrophy
- Areas critical to cognition (neocortex, hippocampus)
- neurodegeneration
* involve neurons of multiple neurotransmitters (cholinergic, 5HT, glutamatergic, DA)
* neurochemical deficits and alterations
neurochemical deficit
- Eg: tryptophan hydroxylase immunoreactive (serotonergic) neurons
* Reduced in dorsal raphe nucleus (DRN) of AD - Mainly cholinergic systems in AD
* Central cholinergic neurons project to widespread areas of cortex
◊ Role: learning, attentional processes
* Degeneration in central cholinergic system in AD (nucleus basalis –> neocortex)
presentation of AD from neurochemical deficits & alterations
- psychiatric: behavioural abnormality
- neuropsychiatric: psychiatric behaviour that occur due to struc abnormality
* AD primary cause
impact of AD
- Caregiver distress – neuropsychiatric sx of AD
- Progressive loss of cognitive functions
* Memory, learning, thinking, personality, self
Brief cognitive screening tools
- Mini mental state examination (MMSE)
- Orientation
- Registration
- Attention and calculation
- Recall
- Language
- Copying
- montreal cognitive assessment (MoCA)
AD stage score
- MMSE (out of 30)
- Mild: 20-24
- Mod: 10-19
- Severe: <10
- MoCA (montreal cognitive assessment)
- Mild: 18-25
- Mod: 10-17
- Severe: <10
what tests to dx of AD
- PMH (pt, fam)
- Cognitive deficits
* Mini mental state examination (MMSE), neuropsychological test
* Functional deficits (ADL) - physical exam
* neurologic sign (cognitive impair, focal signs, parkinsonism)
* pertinent systemic signs (vascular, metabolic) - Lab:
* CSF
* Blood biomarkers of AB and pTAU (not routine)
* TFT, vit B12
* metabolic, infectious, autoimmune, other tests - struc imaging:
* CT, MRI – exclude other brain pathologies
* Hippocampus, neocortex shrink
struc imaging differentials
- AD: generalised, focal cortical atrophy. Often asymmetrical (hippocampal atrophy)
- Shrinkage of cerebral cortex
- Shrinkage of hippocampus
- Enlarged ventricles
- Vascular: brain infarcts, white matter lesions
- Frontotemporal: frontal lobe or anterior temporal lobe atrophy
- Abnormalities: brain mass (tumor), hydrocephalus
AD management goals
- Slow progression (reduce cognitive decline and preserve function)
- Delay need to institutionalise
- Manage behavioural sx of AD
- Support & educate caregiver
- Unable to modify disease
ADLs vs IADLs
ADL: activities of daily living
more basic tasks that are essential to independent living. (bath, eat, toilet, hygiene)
IADLs= instrumental activities of daily living
more complex tasks that are still a necessary part of everyday life
Shopping, housekeeping, accounting, food prep, transportation
mild-mod tx plan
1) acetycholinesterase inhibitors (AChEIs) – 6mnths progression
2) non-competitive NMDA antagonist (memantine) – mod-severe
3) neuropsychiatric behavioural sx tx (off-label)
anticholinesterase inhibitors MOA
- inhibit Acetylcholinesterase enzyme
- Incr Ach at synaptic cleft for cholinergic neurotransmission
AChEi indications
- 6mnth of decline from natural hx of AD dementia (but condition continues for years)
- Modest improvement in ADL and behaviour
- More for early stages (maintain function for as long as possible)
- Eventually discontinue use, no longer effective
AChEi dose
- slow titration dosing regimen over 4-8wks
- reach target dose and minimise ADR
* ADR = Lower dose temporarily (days - wks) reescalate
* slowly and monitor for ADR recurrence - Discontinue and switch to another AI
AChEis eg and doses
- Donepezil (severe AD, PO disintegrating)
* 5mg OD (6wk) —> 10mg OD (max 23mg/d) - galantamine (mild-mod, PO, longer t1/2, LIVER)
* Act on nicotinic receptors in brain
* $$$ - Rivastigmine (mild-mod, PO, TD patch, shorter t1/2, KIDNEY)
* Ach bind to both muscarinic and nicotinic receptors
* 4mg/ 24hr (4wks) —> max 6mg BD
AChEi ADR
- cholinergic hyperactivation (incr parasympathetic, rest & digest)
- NVD, LOA, incr gastric juice secretion
- Muscle cramp, bradycardia
- NVD, LOA, incr gastric juice secretion
AChEi CI and caution
Bradycardia
Caution: PUD, seizure, UT obstruction
monitor AChEi
○ Good response (caregiver notice slight improvement in ADL, functions)
○ Routine cognitive tests (MoCA)
ADR: weight loss, GI bleed (more rest & digest)
NMDA antagonist (memantine)
MOA
(MAY) block NMDA receptor mediated excitotoxicity
- preserve neurons
indication for NMDA antagonist
- In pt with mod-severe dementia (switch therapy or 1st line in new diagnosis)
- Pt who cannot tolerate AChEi
NMDA antagonist ADR
hallucination, confusion, dizzy, headaches, constipation
dose and monitor for NMDA antagonist
- extended release capsule (Start) 7mg OD (1wk)–> 28mg OD
- Tab, solution 5mg OD (1wk) –> 10mg BD
- monitor: caregiver feedback (improvement) + routine cognitive test (MoCA) ADLs
caution use of NMDA antagonist
pt with CVD, seizure, hepatic, renal impairment
non pharm approach
- Cognitive stimulating activity (read, games)
- Physical exercise
- Social interaction
- Healthy diet (green leafy vege)
- Adequate sleep (suff hrs + uninterrupted)
- Proper personal hygiene
- Safety
- Medical and advanced care directives
- LT health care planning (living arrangements)
- Financial planning
- Effective communication (visual aids, language barrier, hearing loss)
- Psychological health
other considerations
- Reduce polypharmacy
- Review meds that may contribute to cognitive impairment
○ Anticholinergics
○ Antihistamines - Assist caregiver on med management issues
○ Simplify med regimen, arrange for med refill (home delivery etc) - Evaluate risk/ benefit of existing medications
○ Antithrombotic: anticoag have lots of SE
○ Acetylcholine: fall risk
BPSD - Behavioural and psychological sx of dementia
- Spectrum of non-cognitive and non-neurological sx of dementia
- 1st: Depression, anxiety
- Later: Agitation, aggression
○ Unable to communicate and understand environment - Psychosis, apathy
- Stressful for person and caregivers/ family
tx plan for BPSD
- Nonpharmacologic (person-centred)
a. Pt background (life story, culture, religion, job, interest, routine, family, sig life events) - Identify target behaviour
- modify factors that may contribute to BPSD
- pharm (off label)
depression presentation and management
- Sadness, tearful, pessimistic thoughts, withdrawal, inactivity, fatigue
manage:
* Exercise, social connection, engaging activities
* Cognitive behavioural therapy – Early stages (still have cognition)
ANX presentation and management
- Worsens at later stages
- exaggerated response to separation, New environment
manage:
* Identify, eliminate trigger > sx control
* Structure, routine, reduce decision making
* Sensory overstimulation
* Music
* CBT
agitation, aggression presentation and management
- Verbal
- Complain, moan, angry statements
- Physical
- Resistance, spit, hit
- Due to:
- Depression, unmet needs, bored, discomfort, perceived threat, personal space
manage:
* Make environ modifications
* Management modifications
* Calm, positive exp
○ Music, touch therapy, massage
apathy presentation and management
more for vascular, lewy body, frontotemporal dementia
- Lack of initiative, motivation, drive, aimless, reduced emotional response
- Absence of sadness other psychological distress
manage:
* Read, encourage them to ask qns , small grp activities
* Music, exercise, multi-sensory stimulation (touch, smell, sound, spend time with pets)
* Enriched prompts and cues
psychosis presentation and management
- Delusions (memory loss or change in perception)
- Lewy (vivid visual)
manage:
* Reversible causes:
* Sensory or vision loss, over stimulation delirium, initiate new meds, sub misuse
* Confirm claims are not occurring
* Reassure
* Distraction
wandering presentation and management
- Related to agitation
- Circular, pacing b. 2 points
- Random, direct to location without diversion
- Safety concern
manage:
* Make wandering safe
* Supervised walks, secured space, exercise equipments, GPS watch
nocturnal disruptions presentation and management
- esp in lewy
- 2nd to DEP, ANX, AGITATION, PAIN (Sx exacerbated at night)
- Sundowning
- Incr agitation in late afternoon
- Sleep-wake reversal
manage:
* Underlying causes (thirst, hunger)
* Restrict caffeine, limit fluid intake before bed
* Night time routine
* Minimise light, noise
* Adequate daytime stimulating activities
- modify factors that contribute to BPSD
- medical
- pharm
- environ, social
medical comor to treat first
existing psychological conditions (ANX, DEP)
delirium (infection, metabolic disturbances, med toxicity, sub w/d)
untx pain
infection (UTI, pneumo)
dehydration, hypoNa
constipation, urinary retention
fatigue
hearing/ visual impairment
(DDI) pharm considerations that can lead
to BPSD
- anticholinergic action (amitriptyline, oxybutynin)
- anticonvulsants (CBP, PT)
- sys CS (high dose)
- sedative (opioid, BZP, anti-H1)
- anti-parkinsonian
- shift to OM/ reduce dose/ decr freq
environmental or social factors affecting BPSD
- unfamiliar environ
- separation from fam
- noise, crowd, lack privacy
- light, under/ over stimulation
- w/d alc/ drug
- loneliness
- difficult r/s with caregiver
- pharm tx role in BPSD
when can it be considered
- Limited role in BPSD management: ADR, indication for use
- Tx for target sx or behaviours (not for other indications/ difficult to manage)
□ Only if reversible causes excluded, non-pharm tried
□ Immediate danger to pt/ caregiver - Combi with non-pharm
monitor, review __ if tx used in BPSD
1) Review response to tx, dose, ADR (every 3mnths)
2) Routine withdrawn after 3mnths
* Improved sx
* Unless severe sx// comorbid psych disorder (MDD, bipolar)
3) Restart at lowest effective dose (if sx return after withdrawal)
* 3-6mnths review
eg off-label BPSD control
Behavioural and psychological sx of dementia (BPSD)
- Antidep (SSRI - citalopram, sertraline)
- Anxiolytics (BZP – diazepam, SSRI)
- Neuroleptics (2nd gen antipsyhotics - risperidone, quetiapine)
- Sleep medication (z-hypnotics)
start lowest dose possible, adj as necesary, ST use
“off-label” dose: as AD pt may face more SE
CI for BPSD tx in dementia
TCA, disrupts cognition further (Disorientation or confusion, seizure)
SSRI uses
- improve DEP, ANX, agitation, improve delusions
* citalopram! - caution: QT prolongation, worsen cognition
antipsychotics uses
- Aggression, agitation, psychotic sx (severe distress/ immediate harm to pt/ others), pt has co-morbidity for psychosis
- NOT FOR: Wandering, calling out, social withdrawal, inapp behaviours / Environ triggers
- Effectiveness: modest/ varies
- Caution: stroke, CVS events, mortality (in short time frame)
- Pneumonia (aspiration from sedation), stroke, cardiac arrest
- Assess every 6-12wks to discontinue
