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PHAR350 > Dementia > Flashcards

Dementia Flashcards

1
Q

What is the relationship between age and dementia?

A

prevalence of dementia increases with age
-6-10% of individuals > 65

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2
Q

What is the key takeaway regarding the presentation of dementia?

A

highly variable disease
-cant make generalizations

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3
Q

What is dementia?

A

a clinical syndrome characterized by progressive cognitive decline that interferes with the individuals ability to function independently

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4
Q

What is cognition?

A

all of the mental processes involved in learning, remembering, and using knowledge

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5
Q

What are the 6 cognitive domains that may be affected in dementia?

A

complex attention
executive function
learning and memory
language
perceptual-motor function
social cognition

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6
Q

What is mild cognitive impairment?

A

modest decline in cognition from previous
-may be subjective or may be observable on cognition testing
-does NOT interfere with ability to function independently
-greater effort or compensatory strategies may be required to maintain independence
may or may not progress to dementia

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7
Q

Differentiate delirium and dementia.

A

delirium develops quickly
key cognitive feature of delirium is inattention
symptoms of delirium fluctuate
delirium is reversible if cause is identified and treated

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8
Q

What is the relationship between delirium and dementia?

A

individuals with dementia are vulnerable to developing delirium
individuals who have experienced delirium are at increased risk of dementia

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9
Q

What are the potentially reversible contributors to cognitive impairment?

A

acronym: DEMENTIA
drugs (including alcohol)
emotional (depression)
metabolic, electrolyte, anemia
eyes and ears declining
nutritional (e.g. B12 def)
tumor or other lesion
infection (neurosyphilis, HIV)
anemia

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10
Q

What are examples of medications that can contribute to cognitive impairment?

A

anticholinergics
psychoactives
-anticonvulsants
-antidepressants (SSRI, SNRI, TCA)
-antiparkinsons
-antipsychotics
-hypnotics/sedatives
-opioids
non-psychoactives
-antibiotics
-class 1A antiarrhythmics
-corticosteroids
-digoxin
-H2RAs
-NSAIDs

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11
Q

What are the different types of dementia?

A

Alzheimers disease
vascular dementia
frontotemporal dementia
Parkinson disease dementia
Lew body dementia

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12
Q

What is the most common form of dementia?

A

Alzheimers disease

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13
Q

What does the typical course look like for Alzheimers?

A

slow and progressive
-short term memory –>–> all areas of functioning

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14
Q

What is seen on autopsy for Alzheimers?

A

B-amyloid plaques
neurofibrillary tangles

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15
Q

What is seen on CT scan for Alzheimers?

A

cerebral atrophy

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16
Q

What is the etiology of Alzheimers?

A

unclear
likely a mix of genetics, environment, lifestyle

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17
Q

What are the risk factors for Alzheimers?

A

age
family history/genetics
rare genetic mutations
history of severe head trauma
mild cognitive impairment
lifestyle: low exercise,obesity,smoking,HTN,DM,lipids

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18
Q

What are protective factors against Alzheimers?

A

educational attainment
social engagement
lifelong learning

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19
Q

What causes vascular dementia?

A

interrupted blood flow to parts of the brain
-may or may not have history of overt strokes
-vascular damage usually visible on imaging + CV risk factors

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20
Q

What are CV risk factors for vascular dementia?

A

HTN
dyslipidemia
smoking
diabetes
heart disease

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21
Q

What are the symptoms of vascular dementia?

A

depends of part of brain affected
-complex thinking and planning, personality changes, agitation, and moodiness usually more common early than AD

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22
Q

What does the typical course of vascular dementia look like?

A

onset may be abrupt (after an event) or gradual
-may have periods of relative stability interspersed with periods of more rapid decline

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23
Q

What is the major driver in the development of frontotemporal dementia?

A

genetics
-earlier onset (40-50yo) and no increased prevalence with age

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24
Q

Which area of the brain is impacted by frontotemporal dementia?

A

frontal and temporal lobes
-changes in speech, language, and personality occur before changes in memory
-over time, progresses to global impairment

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25
Q

What is Parkinson’s dementia?

A

dementia that develops after a clinical diagnosis of Parkinsons
-increased prevalence of PD dementia in older ppl with PD

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26
Q

What is the problem with dopaminergic treatments for Parkinsons in Parkinsons dementia?

A

dopaminergic treatments for Parkinsons may exacerbate behavioral and psychological symptoms of dementia

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27
Q

What are Lewy bodies?

A

abnormal deposits of alpha-synuclein protein in neurons

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28
Q

What is the typical presentation of Lewy Body dementia?

A

Parkinson disease in reverse
-present with cognitive impairment and visual hallucinations FIRST or CONCURRENLTY with PD motor symptoms

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29
Q

What are the distinctive clinical features of Lewy Body dementia?

A

early postural instability and repeated falls are common
detailed, recurrent hallucinations
pronounced fluctuations in cognition
extremely sensitive to antipsychotics

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30
Q

Describe some key points about the diagnosis of dementia.

A

diagnosis of exclusion/clinical diagnosis
-neuroimaging is supportive but not diagnostic
-rule out reversible causes of cognitive impairment (meds!)
-detailed history (need collateral information)

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31
Q

Describe the MMSE.

A

requires minimal training, takes ~10 minutes
highly sensitive and specific to dementia
not very sensitive to mild cognitive impairment
scores affected by level of educational attainment
assess multiple cognitive domains (orientation, language, attention, recall, calculation, visual reconstruction)

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32
Q

Describe the FAQ.

A

developed to assess functional impairment
-higher score = poorer function
-needs to be correlated to baseline function
designed to be completed by a caregiver or close support
sometimes used to monitor response to pharmacotherapy

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33
Q

What are behavioral and psychological symptoms of dementia?

A

non-cognitive symptoms of disturbed thoughts, perceptions, mood or behaviors that may occur with dementia
-may pose safety concerns
-frustrating or distressing to caregivers

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34
Q

What are examples of BPSD?

A

behavioral:
-agitation
-aggression
-wandering
-disinhibition
-repetitive behaviors
-hoarding
-vocalizations
-nocturnal restlessness
psychological:
-apathy
-emotional lability
-paranoia
-hallucinations
-delusions
-involuntary laughing or crying
-depression

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35
Q

What are triggers for BPSD?

A

psychological
environmental
medical
medications

36
Q

What are some medications that can trigger BPSD?

A

anticholinergics
opioids
benzos, sedatives, hypnotics
cannabinoids
anticonvulsants
psychoactive NSAIDs
some antibiotics (FQs, clarithromycin)

37
Q

Describe the approach to the management of dementia.

A

optimize management of comorbidities
stop meds that contribute to cognitive impairment
refer to Alzheimer Society Saskatchewan
encourage regular exercise and a healthy diet
encourage cognitive and social activity
caregiver support

38
Q

What are the two categories of pharmacological treatment for dementia?

A

dementia treatment
-cholinesterase inhibitors
-NMDA antagonists
-? emerging treatments
management of BPSD
-antipsychotics
-other drugs as indicated

39
Q

What is the goal of treatment for pharmacotherapy with dementia?

A

to improve QoL for the individual and caregivers, maintain optimal function and provide maximum comfort

40
Q

What are examples of cholinesterase inhibitors?

A

rivastigmine
galantamine
donepezil

41
Q

What is the MOA of cholinesterase inhibitors?

A

prevent breakdown of acetylcholine
-acetylcholine is the main neurotransmitter involved in learning and memory

42
Q

Describe the potential benefits of cholinesterase inhibitors.

A

may show small improvements in measures of cognition
-less frequently see improvements in functional abilities
may slow progression (by months, not years)
if benefit is seen, it will be seen in 3-6 months
long-term clinical benefit not clear

43
Q

What is the indication for cholinesterase inhibitors?

A

mild –> severe ALZHEIMERS
-prefer earlier on when we can preserve function

44
Q

What are the adverse effects of cholinesterase inhibitors?

A

common:
-NVD, appetite loss, insomnia, urinary urge/frequency
less common:
-GI bleeds, agitation, weight loss, bradycardia, syncope, nightmares, behavior disturbances
QT prolongation (<1%): donepezil and galantamine
post-marketing: NMS and rhabdo

45
Q

What is the effect of dose on the AE’s of cholinesterase inhibitors?

A

dose-related
-may be minimized by slow titration, taking with food, maybe anti-emetic

46
Q

What are contraindications to cholinesterase inhibitors?

A

uncontrolled/severe asthma or COPD
conduction abnormalities, bradycardia

47
Q

What are precautions to cholinesterase inhibitors?

A

PUD or uncontrolled GERD
urinary incontinence
seizure history
concurrent anticholinergics

48
Q

What is the MOA of NMDA antagonists?

A

block glutamate (excitatory amino acid) at NMDA receptor
-theory: persistent activation of NMDA receptor contributes to sx
-no effect on acetylcholine

49
Q

How are NMDA antagonists used?

A

alone or in combination with cholinesterase inhibitors
-conflicting evidence regarding benefit

50
Q

What is the benefit of NMDA antagonists?

A

some evidence of benefit on cognitive testing, minimal clinical benefit in most cases

51
Q

What is an example of an NMDA antagonist?

A

memantine

52
Q

How are NMDA antagonists eliminated?

A

renally (dosage adjustments)

53
Q

What is the indication for memantine?

A

moderate –> severe ALZHEIMERS

54
Q

What is a benefit of NMDA antagonists compared to cholinesterase inhibitors?

A

better tolerated than cholinesterase inhibitors

55
Q

What are the side effects of NMDA antagonists?

A

dizziness, constipation, confusion, insomnia, HA, HTN, restlessness, akathisia, nausea
QT prolongation (<1%)
caution with CV disease or seizures

56
Q

Describe the risks vs benefits of drugs for dementia.

A

small potential improvements (both classes) with high risk of AE’s (cholinesterase inhibitors)
trials are done in healthy patients with no comorbidities
AEs worth a few months of slowed progression?
even a small side effect can drastically decrease QoL

57
Q

What are some examples where risk > benefit for dementia drugs?

A

frail with multiple comorbidities
problematic urinary incontinence
significant weight loss/anorexia/malnutrition
significant aggression or agitation
financial restrictions
severe dementia
if concerned about adherence

58
Q

What are some examples of benefit > risk for dementia drugs?

A

early-onset dementia in a relatively healthy individual
early on in disease progression
few comorbidities
no financial restrictions
few adverse effects once started
no concerns about adherence or AEs

59
Q

What are some examples of where we should discontinue treatment for dementia drugs?

A

progression to situation where risk > benefit
general consensus: loss of ability to perform ADLs independently
-dementia has progressed to a stage where there would be no meaningful benefit remaining

60
Q

How should dementia drugs be discontinued?

A

taper carefully over 2-4 weeks
-monitor for worsening of cognitive symptoms and behavioral/psychological symptoms

61
Q

How can dementia be prevented?

A

no drug/herbal/vitamin/supplement shown to prevent
non-pharm:
-CV risk reduction
-educational attainment/ongoing cognitive challenges
-social engagement
-exercise
-healthy diet
-hearing/vision checks and use of aids as needed

62
Q

How were the new mab drugs designed?

A

to be disease-modifying

63
Q

What is the MOA of the new “mab” drugs?

A

increase clearance of beta-amyloid

64
Q

What are the new “mab” drugs for dementia?

A

lecanemab
donanemab

65
Q

What is the indication for lecanemab?

A

mild cognitive impairment or Alzheimer’s disease at the mild stage

66
Q

What is the potential benefit of lecanemab?

A

improvements in cognition and function

67
Q

What are the risks of lecanemab?

A

significant risk of AE and monitoring burden

68
Q

Provide a summary of the new “mab” drugs for dementia.

A

first potentially disease-modifying tx’s for AD/MCI
slow progression of amyloid pathology in MCI/early AD
-unclear clinical significance
not indicated for other types of dementia
high cost
administration and monitoring challenges
associated with significant AE
not yet approved in Canada

69
Q

What are the steps in treating BPSD?

A
  1. assess for and treat any medical/medication causes or contributors
  2. explore and minimize psychological and environmental triggers
  3. pharmacotherapy ONLY if behavior is causing harm or significant distress to individual, caregivers, or others AND is persistent or recurrent
  4. re-evaluate drug regimen after 3 months
70
Q

Which BPSD are amendable to pharmacotherapy?

A

aggression
paranoia
hallucinations
delusions
depression

71
Q

Describe step 1 in treating BPSD.

A

assess for medical causes:
-taper/stop any contributing medications
-look for underlying medical issues (PAIN)
-offer food/drink often to prevent hunger/thirst
-manage constipation proactively

72
Q

Describe step 2 in treating BPSD.

A

assess for psychological causes:
-avoid social isolation
-allow individual to make choices whenever possible
-provide simple instructions
-show warm, kind, manner
-do not argue
assess for environmental causes:
-encourage use of glasses/hearing aids
-provide regular structured routine
-comfortable environment
-avoid overstimulation
-engaging activities

73
Q

Which antidepressants should be avoided in treating BPSD?

A

TCAs
paroxetine
fluoxetine

74
Q

When are antidepressants used for BPSD?

A

when depression or anxiety is root trigger for behavior
-daily use if for depression or chronic anxiety

75
Q

Which medications can be considered for BPSD if sleep is a significant issue?

A

trazodone or mirtazapine

76
Q

Which medications should be avoided for anxiety or sedation in BPSD?

A

benzos
-worsen cognitive impairment, increase fall risk, may worsen disinhibition
-occasionally used short term following a stressful event (low doses of short t1/2 benzo - lorazepam)

77
Q

When are antipsychotics used for BPSD?

A

if behavior is causing harm and/or has not responded to non-pharmacological methods

78
Q

Which antipsychotics are preferred for BPSD?

A

atypicals

79
Q

What are the risks with antipsychotics for BPSD?

A

black box warning: increased risk of mortality
AEs: wt. gain, orthostasis, anticholinergic, sedation, falls, EPS, TD, UR
start low, go slow

80
Q

Can we use multiple antipsychotics for BPSD?

A

no evidence to support using > 1

81
Q

Which antipsychotic is used to manage acute delirium?

A

haloperidol
-prn only

82
Q

What is a contraindication of haloperidol?

A

in Parkinsons patients due to risk of EPS

83
Q

Describe stimulant use in BPSD.

A

MPH occasionally used to treat apathy and loss of motivation
external activity and environment stimulation is more effective
stimulant AE > benefit

84
Q

Describe sedative use in BPSD.

A

considered when behavior is thought to be directly correlated with lack of sleep OR behaviors during night
avoid antihistamines, sedating OTCs
watch for dependence and tolerance
increase risk of delirium and falls

85
Q

Describe the role of analgesics in BPSD.

A

when pain is thought to be cause of behavior
a good trial of acet for pain is often overlooked
re-assess and increase dosage, or switch to opioids if necessary

PHAR350 (16 decks)

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