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PHAR350 > Dementia > Flashcards

Dementia Flashcards

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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
What is Parkinson's dementia?
dementia that develops after a clinical diagnosis of Parkinsons -increased prevalence of PD dementia in older ppl with PD
26
What is the problem with dopaminergic treatments for Parkinsons in Parkinsons dementia?
dopaminergic treatments for Parkinsons may exacerbate behavioral and psychological symptoms of dementia
27
What are Lewy bodies?
abnormal deposits of alpha-synuclein protein in neurons
28
What is the typical presentation of Lewy Body dementia?
Parkinson disease in reverse -present with cognitive impairment and visual hallucinations FIRST or CONCURRENLTY with PD motor symptoms
29
What are the distinctive clinical features of Lewy Body dementia?
early postural instability and repeated falls are common detailed, recurrent hallucinations pronounced fluctuations in cognition extremely sensitive to antipsychotics
30
Describe some key points about the diagnosis of dementia.
diagnosis of exclusion/clinical diagnosis -neuroimaging is supportive but not diagnostic -rule out reversible causes of cognitive impairment (meds!) -detailed history (need collateral information)
31
Describe the MMSE.
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)
32
Describe the FAQ.
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
33
What are behavioral and psychological symptoms of dementia?
non-cognitive symptoms of disturbed thoughts, perceptions, mood or behaviors that may occur with dementia -may pose safety concerns -frustrating or distressing to caregivers
34
What are examples of BPSD?
behavioral: -agitation -aggression -wandering -disinhibition -repetitive behaviors -hoarding -vocalizations -nocturnal restlessness psychological: -apathy -emotional lability -paranoia -hallucinations -delusions -involuntary laughing or crying -depression
35
What are triggers for BPSD?
psychological environmental medical medications
36
What are some medications that can trigger BPSD?
anticholinergics opioids benzos, sedatives, hypnotics cannabinoids anticonvulsants psychoactive NSAIDs some antibiotics (FQs, clarithromycin)
37
Describe the approach to the management of dementia.
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
What are the two categories of pharmacological treatment for dementia?
dementia treatment -cholinesterase inhibitors -NMDA antagonists -? emerging treatments management of BPSD -antipsychotics -other drugs as indicated
39
What is the goal of treatment for pharmacotherapy with dementia?
to improve QoL for the individual and caregivers, maintain optimal function and provide maximum comfort
40
What are examples of cholinesterase inhibitors?
rivastigmine galantamine donepezil
41
What is the MOA of cholinesterase inhibitors?
prevent breakdown of acetylcholine -acetylcholine is the main neurotransmitter involved in learning and memory
42
Describe the potential benefits of cholinesterase inhibitors.
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
What is the indication for cholinesterase inhibitors?
mild --> severe ALZHEIMERS -prefer earlier on when we can preserve function
44
What are the adverse effects of cholinesterase inhibitors?
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
What is the effect of dose on the AE's of cholinesterase inhibitors?
dose-related -may be minimized by slow titration, taking with food, maybe anti-emetic
46
What are contraindications to cholinesterase inhibitors?
uncontrolled/severe asthma or COPD conduction abnormalities, bradycardia
47
What are precautions to cholinesterase inhibitors?
PUD or uncontrolled GERD urinary incontinence seizure history concurrent anticholinergics
48
What is the MOA of NMDA antagonists?
block glutamate (excitatory amino acid) at NMDA receptor -theory: persistent activation of NMDA receptor contributes to sx -no effect on acetylcholine
49
How are NMDA antagonists used?
alone or in combination with cholinesterase inhibitors -conflicting evidence regarding benefit
50
What is the benefit of NMDA antagonists?
some evidence of benefit on cognitive testing, minimal clinical benefit in most cases
51
What is an example of an NMDA antagonist?
memantine
52
How are NMDA antagonists eliminated?
renally (dosage adjustments)
53
What is the indication for memantine?
moderate --> severe ALZHEIMERS
54
What is a benefit of NMDA antagonists compared to cholinesterase inhibitors?
better tolerated than cholinesterase inhibitors
55
What are the side effects of NMDA antagonists?
dizziness, constipation, confusion, insomnia, HA, HTN, restlessness, akathisia, nausea QT prolongation (<1%) caution with CV disease or seizures
56
Describe the risks vs benefits of drugs for dementia.
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
What are some examples where risk > benefit for dementia drugs?
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
What are some examples of benefit > risk for dementia drugs?
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
What are some examples of where we should discontinue treatment for dementia drugs?
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
How should dementia drugs be discontinued?
taper carefully over 2-4 weeks -monitor for worsening of cognitive symptoms and behavioral/psychological symptoms
61
How can dementia be prevented?
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
How were the new mab drugs designed?
to be disease-modifying
63
What is the MOA of the new "mab" drugs?
increase clearance of beta-amyloid
64
What are the new "mab" drugs for dementia?
lecanemab donanemab
65
What is the indication for lecanemab?
mild cognitive impairment or Alzheimer's disease at the mild stage
66
What is the potential benefit of lecanemab?
improvements in cognition and function
67
What are the risks of lecanemab?
significant risk of AE and monitoring burden
68
Provide a summary of the new "mab" drugs for dementia.
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
What are the steps in treating BPSD?
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
Which BPSD are amendable to pharmacotherapy?
aggression paranoia hallucinations delusions depression
71
Describe step 1 in treating BPSD.
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
Describe step 2 in treating BPSD.
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
Which antidepressants should be avoided in treating BPSD?
TCAs paroxetine fluoxetine
74
When are antidepressants used for BPSD?
when depression or anxiety is root trigger for behavior -daily use if for depression or chronic anxiety
75
Which medications can be considered for BPSD if sleep is a significant issue with depression/anxiety?
trazodone or mirtazapine
76
Which medications should be avoided for anxiety or sedation in BPSD?
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
When are antipsychotics used for BPSD?
if behavior is causing harm and/or has not responded to non-pharmacological methods
78
Which antipsychotics are preferred for BPSD?
atypicals
79
What are the risks with antipsychotics for BPSD?
black box warning: increased risk of mortality AEs: wt. gain, orthostasis, anticholinergic, sedation, falls, EPS, TD, UR *start low, go slow*
80
Can we use multiple antipsychotics for BPSD?
no evidence to support using > 1
81
Which antipsychotic is used to manage acute delirium?
haloperidol -prn only
82
What is a contraindication of haloperidol?
in Parkinsons patients due to risk of EPS
83
Describe stimulant use in BPSD.
MPH occasionally used to treat apathy and loss of motivation external activity and environment stimulation is more effective stimulant AE > benefit
84
Describe sedative use in BPSD.
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
Describe the role of analgesics in BPSD.
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 (17 decks)

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