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3153 psych > dementia > Flashcards

dementia Flashcards

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1
Q

what is dementia

A
  • 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
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2
Q

AD

A
  • Specific disease
  • Progressive disease
  • Sx:
    • Dementia + neuropsychiatric sx
  • Old age (predominantly)
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3
Q

DSM5 dementia definition

major & minor

A
  1. 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
  2. Cognitive deficits interfere with independence in everyday activities
  3. Cognitive deficits do not occur exclusively in the context of delirium
  4. Cognitive deficits are not better explained by another mental disorder
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4
Q

types of dementia

A
  • 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
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5
Q

manifestation of dementia
cognitive
(memory, attention, language, problem solving)

A

EARLY
* ST memory loss
* Word-finding difficulty

LATER
* Memory loss, unable to process and store info
* Loss of language, comprehension (aphasia)

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6
Q

manifestation of dementia
psychological

A

EARLY
* Apathy
* Depressive sx

LATER
* Delusions
* Anosognosia

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7
Q

manifestation of dementia
behavioural

A

EARLY
* Withdrawal from social engagement
* disinhibition

LATER
* agression
* hallucination
* wandering

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8
Q

manifestation of dementia
sleep

A

EARLY
* REM behavioural disorder

LATER
* altered sleep-wake cycle

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9
Q

manifestation of dementia
physical

A

EARLY
* gait impairment
* falls

LATER
* repititve, purposeless movements
* parkinson
* seizure

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10
Q

risk factors of AD

A
  • 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

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11
Q

AD pathological characteristics

A

1) senile plaques
2) neurofibrillary tangles

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12
Q

senile plaque

A
  • 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)
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13
Q

neurofibrillary tangles

A
  • 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

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14
Q

AD brain atrophy

A
  • Areas critical to cognition (neocortex, hippocampus)
  • neurodegeneration
    * involve neurons of multiple neurotransmitters (cholinergic, 5HT, glutamatergic, DA)
    * neurochemical deficits and alterations
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15
Q

neurochemical deficit

A
  • 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)
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16
Q

presentation of AD from neurochemical deficits & alterations

A
  • psychiatric: behavioural abnormality
  • neuropsychiatric: psychiatric behaviour that occur due to struc abnormality
    * AD primary cause
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17
Q

impact of AD

A
  • Caregiver distress – neuropsychiatric sx of AD
  • Progressive loss of cognitive functions
    * Memory, learning, thinking, personality, self
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18
Q

Brief cognitive screening tools

A
  • Mini mental state examination (MMSE)
    • Orientation
    • Registration
    • Attention and calculation
    • Recall
    • Language
    • Copying
  • montreal cognitive assessment (MoCA)
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19
Q

AD stage score

A
  • MMSE (out of 30)
    • Mild: 20-24
    • Mod: 10-19
    • Severe: <10
  • MoCA (montreal cognitive assessment)
    • Mild: 18-25
    • Mod: 10-17
    • Severe: <10
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20
Q

what tests to dx of AD

A
  • 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
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21
Q

struc imaging differentials

A
  • 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
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22
Q

AD management goals

A
  • Slow progression (reduce cognitive decline and preserve function)
  • Delay need to institutionalise
    • Manage behavioural sx of AD
    • Support & educate caregiver
  • Unable to modify disease
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23
Q

ADLs vs IADLs

A

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

24
Q

mild-mod tx plan

A

1) acetycholinesterase inhibitors (AChEIs) – 6mnths progression
2) non-competitive NMDA antagonist (memantine) – mod-severe
3) neuropsychiatric behavioural sx tx (off-label)

25
Q

anticholinesterase inhibitors MOA

A
  • inhibit Acetylcholinesterase enzyme
  • Incr Ach at synaptic cleft for cholinergic neurotransmission
26
Q

AChEi indications

A
  • 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
27
Q

AChEi dose

A
  • 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
28
Q

AChEis eg and doses

A
  • 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
29
Q

AChEi ADR

A
  • cholinergic hyperactivation (incr parasympathetic, rest & digest)
    • NVD, LOA, incr gastric juice secretion
      • Muscle cramp, bradycardia
30
Q

AChEi CI and caution

A

Bradycardia

Caution: PUD, seizure, UT obstruction

31
Q

monitor AChEi

A

○ Good response (caregiver notice slight improvement in ADL, functions)
○ Routine cognitive tests (MoCA)

ADR: weight loss, GI bleed (more rest & digest)

32
Q

NMDA antagonist (memantine)
MOA

A

(MAY) block NMDA receptor mediated excitotoxicity

  • preserve neurons
33
Q

indication for NMDA antagonist

A
  • In pt with mod-severe dementia (switch therapy or 1st line in new diagnosis)
  • Pt who cannot tolerate AChEi
34
Q

NMDA antagonist ADR

A

hallucination, confusion, dizzy, headaches, constipation

35
Q

dose and monitor for NMDA antagonist

A
  • 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
36
Q

caution use of NMDA antagonist

A

pt with CVD, seizure, hepatic, renal impairment

37
Q

non pharm approach

A
  • 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
38
Q

other considerations

A
  • 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
39
Q

BPSD - Behavioural and psychological sx of dementia

A
  • 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
40
Q

tx plan for BPSD

A
  1. Nonpharmacologic (person-centred)
    a. Pt background (life story, culture, religion, job, interest, routine, family, sig life events)
  2. Identify target behaviour
  3. modify factors that may contribute to BPSD
  4. pharm (off label)
41
Q

depression presentation and management

A
  • Sadness, tearful, pessimistic thoughts, withdrawal, inactivity, fatigue

manage:
* Exercise, social connection, engaging activities
* Cognitive behavioural therapy – Early stages (still have cognition)

42
Q

ANX presentation and management

A
  • 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

43
Q

agitation, aggression presentation and management

A
  • 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

44
Q

apathy presentation and management

more for vascular, lewy body, frontotemporal dementia

A
  • 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

45
Q

psychosis presentation and management

A
  • 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

46
Q

wandering presentation and management

A
  • 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

47
Q

nocturnal disruptions presentation and management

  • esp in lewy
A
  • 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

48
Q
  1. modify factors that contribute to BPSD
A
  1. medical
  2. pharm
  3. environ, social
49
Q

medical comor to treat first

A

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

50
Q

(DDI) pharm considerations that can lead
to BPSD

A
  • 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
51
Q

environmental or social factors affecting BPSD

A
  • unfamiliar environ
  • separation from fam
  • noise, crowd, lack privacy
  • light, under/ over stimulation
  • w/d alc/ drug
  • loneliness
  • difficult r/s with caregiver
52
Q
  1. pharm tx role in BPSD

when can it be considered

A
  • 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
53
Q

monitor, review __ if tx used in BPSD

A

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

54
Q

eg off-label BPSD control
Behavioural and psychological sx of dementia (BPSD)

A
  • 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

55
Q

CI for BPSD tx in dementia

A

TCA, disrupts cognition further (Disorientation or confusion, seizure)

56
Q

SSRI uses

A
  • improve DEP, ANX, agitation, improve delusions
    * citalopram!
  • caution: QT prolongation, worsen cognition
57
Q

antipsychotics uses

A
  • 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

3153 psych (11 decks)

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