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PHAR 350 > Dementia > Flashcards

Dementia Flashcards

1
Q

Define dementia

A

A clinical syndrome characterized by progressive cognitive decline that interferes with the individual’s ability to function independently

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2
Q

What is mild cognitive impairment?
How does it compare to dementia?

A

Modest decline in cognition from previous
- May be subjective or may be observable on cognitive testing
- This decline does NOT interfere with the ability to function independently
- Greater effort of compensatory strategies may be necessary to maintain function
- May or may not progress to dementia

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3
Q

How are delirium and dementia linked? (2)

A
  1. Individuals with dementia are particularly vulnerable to developing delirium
  2. Individuals that have experienced delirium are at higher risk of developing subsequent dementia
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4
Q

Dementia is a diagnosis of _________

A

exclusion

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5
Q

A helpful mnemonic for dementia when it comes to potentially reversible contributors to cognitive dementia is DEMENTIA. Should know it

A

Drugs (including alcohol)
Emotional (depression)
Metabolic, electrolytes, endocrine (hypothyroidism, hyponatremia, uremia)
Eyes and ears declining
Nutritional (e.g., vitamin B12 deficiency)
Tumor or other space-occupying lesion
Infection (neurosyphillus, HIV)
Anemia

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6
Q

Anticholinergics may impact cognitive function in three ways:

A
  1. May cause or contribute to delirium
  2. May cause cognitive impairment that is reversible upon discontinuing the anticholinergic agent(s)
  3. There is evidence that cumulative anticholinergic exposure increases risk for subsequent dementia
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7
Q

What are 5 types of dementia?

A
  1. Alzheimer’s disease
  2. Vascular dementia
  3. Frontotemporal dementia
  4. Parkinson disease dementia
  5. Lewy body dementia
    First 3 listed are the most common
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8
Q

Alzheimer’s disease is the most common form of dementia. What is it characterized by? (progression, and physically)

A
  1. Slow and progressive
    - Short-term memory –> all areas of functioning
  2. Associated with characteristic beta-amyloid plaques and neurofibrillary tangles on autopsy
    - Head CT: cerebral atrophy
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9
Q

Although the etiology of alzheimer’s is unclear, what are some risk factors? (6)

A
  1. Increased age
  2. Family history/genetics (APOE4 increases risk)
  3. Rare genetic mutations –> early onset-Alzheimer’s disease (<1%)
  4. History of severe head trauma
  5. Mild cognitive impairment
  6. Lifestyle - decreased exercise, smoking, obesity, HTN, poorly controlled diabetes, dyslipidemia
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10
Q

What are some protective measures against alzheimer’s disease? (3)

A
  1. Educational attainment
  2. Social engagement
  3. Lifelong learning
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11
Q

The main difference between dementia and mild cognitive impairment is:
a. Mild cognitive impairment develops quickly (hours-days)
b. With dementia, scores on cognitive tests are impaired (testing is normal in MCI)
c. Dementia impairs ability to perform functional activities
d. Mild cognitive impairment is the same as early dementia

A

c.

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12
Q

Which of the following medications would you be concerned about in a patient complaining of cognitive decline?
a. Sertraline 100mg daily
b. Dimenhydrinate 25mg daily
c. Aspirin 81 mg daily
d. A and B
e. All of the above

A

b.

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13
Q

What is vascular dementia?

A

Results from interrupted blood flow in parts of brain
- May or may not have a history of overt strokes - vascular damage usually visible on MRI and CT + CV risk factors

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14
Q

What are CV risk factors associated with vascular dementia? (5)

A
  1. HTN
  2. High cholesterol
  3. Smoking
  4. Diabetes
  5. Heart disease
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15
Q

Describe onset of vascular dementia

A

May be abrupt (after an event) OR gradual
- May have periods of relative stability interspersed with periods of more rapid decline (“stepwise” decline)

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16
Q

How do symptoms of vascular dementia compare to alzheimer’s disease? (2)

A
  1. Complex thinking and planning, personality changes, agitation, and moodiness are more common early on that in AD
  2. Insight into deficits may be more preserved in vascular dementia vs. AD
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17
Q

What is unique about frontotemporal dementia? (2)

A
  1. Strong genetic component
  2. Earlier onset (40-50 years) and no increased prevalence with age
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18
Q

In frontotemporal dementia, damage is initially limited to the frontal and temporal lobes…hence the name. What are the characteristics symptoms (3)

A
  1. Changes in speech, language, personality occur BEFORE memory changes
  2. Speech is more unusual, choppy, repetitive
  3. Poor judgement, disinhibited behaviour
    - Over time, progresses to global impairment
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19
Q

What is the main diagnostic criteria for parkinson’s dementia?

A

Dementia that develops AFTER a clinical diagnosis of Parkinson disease
- Increased prevalance of PD dementia in older people with PD

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20
Q

What are the early symptoms of parkinson’s dementia?

A

Impairment in attention, visuospatial skills, and planning and completing complex tasks

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21
Q

What are the problems with parkinson’s disease treatment and parkinson’s dementia?

A

Dopaminergic treatments for PD may exacerbate behavioural and psychological symptoms of dementia

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22
Q

What are Lewy bodies?

A

Abnormal deposits of alpha-synuclein protein in neurons

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23
Q

What is lewy body dementia?

A

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

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24
Q

What are the 4 distinctive clinical features of lewy body dementia?

A
  1. Early postural instability and repeated falls are common
  2. Detailed, recurrent visual hallucinations
  3. Pronounced fluctuations in cognition
  4. Extremely sensitive to antipsychotics
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25
Q

While dementia is a diagnosis of exclusion, what should be assessed during the process of diagnosis? (4)

A
  1. Neuroimaging (MRI or CT) may be supportive but is not diagnostic
  2. Rule out reversible causes for cognitive changes, including medications
  3. Detailed history
    - Collateral information is very important to assess functional status
  4. Cognitive assessment
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26
Q

What is the most commonly used cognitive assessment tool used in diagnosing dementia?

A

Mini-Mental Status Examination (MMSE)

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27
Q

What does the mini-mental status exam assess?
What score are we looking for?

A
  1. Multiple cognitive domains: orientation, attention, language, recall, calculation, visual reconstruction
  2. Highly sensitive and specific to dementia (≤26/30 considered abnormal)
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28
Q

What does the functional activity questionnaire asses?
What does a higher score equal?
Who does it?

A
  1. Developed to assess functional impairment
  2. Higher score = poorer function
  3. Designed to be completed by a caregiver or close support
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29
Q

Define BPSD (behavioural and psychological symptoms of dementia)

A

Non-cognitive symptoms of disturbed thoughts, preceptions, mood, or behaviour that may occur with dementia (particularly in the later stages)
- May be frustrating or distressing to caregivers
- Also may pose safety concerns

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30
Q

Remember - all behaviour has meaning. Responsive behaviours are _____________ _________

A

communicating something

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31
Q

What are some of the behavioural aspects of BPSD? (8)

A
  1. Agitation
  2. Aggression (may be verbal or physical)
  3. Wandering
  4. Disinhibition
  5. Repetitive behaviours
  6. Hoarding
  7. Vocalizations
  8. Nocturnal restlessness
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32
Q

What are some of the psychological aspects of BPSD? (7)

A
  1. Apathy
  2. Emotional lability
  3. Paranoia
  4. Hallucinations
  5. Delusions
  6. Involuntary laughing or crying
  7. Depression
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33
Q

What are the 4 classes of triggers for BPSD?

A
  1. Psychological
  2. Environmental
  3. Medical
  4. Medication
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34
Q

What are some psychological triggers of BPSD? (5)

A
  1. Fear of danger or being abandoned
  2. Distress
  3. Loss of autonomy/control
  4. Paranoia
  5. Misinterpretation
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35
Q

What are some environmental triggers of BPSD? (7)

A
  1. Not liking who is around
  2. Boredom
  3. Confusing surroundings
  4. Change in routine
  5. Loneliness
  6. Noise/sounds
  7. Low lighting
36
Q

What are some medical triggers of BPSD? (8)

A
  1. Pain
  2. Constipation
  3. Dehydration
  4. Hunger
  5. Hypothyroidism
  6. Infection
  7. Urinary retention
  8. Metabolic or electrolyte disturbances
37
Q

What are some medication groups that can trigger BPSD? (7)

A
  1. Anticholinergics
  2. Benzos, sedatives, hypnotics
  3. Opioids
  4. Cannabinoids
  5. Anticonvulsants
  6. Some antibiotics (fluoroquinolones, clarithromycin)
  7. Psychoactive NSAIDs (indomethacin, diclofenac)
38
Q

How should we approach dementia management? (6)

A
  1. Optimize management of co-morbid conditions
  2. Attempt to decrease/stop meds that may be contributing to cognitive impairment
  3. Refer to Alzheimer Society of Saskatchewan (or local)
  4. Encourage regular exercise and a healthy diet
  5. Encourage cognitive and social activity
  6. Caregiver support
39
Q

What are the 2 categories of pharmacological treatment of dementia?

A
  1. Treatment of dementia
    - Cholinesterase inhibitors
    - N-methyl-D-aspartate (NMDA) antagonist
    - ? emerging treatments
  2. Management of BPSD
    - Antipsychotics
    - Other meds as indicated e.g., antidepressants, pain meds
40
Q

What is the goal of treatment in dementia? (3)

A
  1. To improve the QoL for the individual and caregivers
  2. Maintain optimal function
  3. Provide maximum comfort
41
Q

What are 3 examples of cholinesterase inhibitors?

A
  1. Donepezil
  2. Galantamine
  3. Rivastigmine
42
Q

What is the MOA of cholinesterase inhibitors?

A

Prevent breakdown of ACh
- ACh is the main NT involved in memory and learning

43
Q

How effective are cholinesterase inhibitors? (2)

A
  1. May show small improvements in measures of cognition
    - Less frequently see improvements in functional abilities
  2. May slow progression (by months, not years) (~1 in 12)
44
Q

How long to see any benefits in cholinesterase inhibitors?
Long-term benefits?

A
  1. If benefit, seen in 3-6 months
  2. Long-term clinical benefit not clear
45
Q

What are the common adverse effects of cholinesterase inhibitors? (6)

A
  1. Nausea
  2. Loss of appetite
  3. Vomiting
  4. Diarrhea
  5. Insomnia
  6. Urinary urgency/frequency +/- incontinence
46
Q

What are the less common ADEs of cholinesterase inhibitors? (7)

A
  1. Weight loss
  2. Agitation
  3. Bradycardia
  4. Syncope
  5. GI bleed
  6. Behaviour disturbances
  7. Nightmares
47
Q

Cholinesterase inhibitors ADEs are ____-________

A

dose-related

48
Q

What are 2 contraindications to cholinesterase inhibitors?

A
  1. Uncontrolled/severe asthma or severe COPD
  2. Cardiac conduction abnormalities, bradycardia (HR < 55 bpm)
49
Q

What are 4 precautions to using cholinesterase inhibitors?

A
  1. Peptic ulcer disease or uncontrolled GERD
  2. Urinary incontinence
  3. Seizure history
  4. Concurrent anticholinergics
50
Q

What are the cardiovascular specific ADEs seen with cholinesterase inhibitors? (3)

A
  1. ↓ Heart rate and velocity of conduction
  2. ↓ Blood pressure
  3. Vasodilation of arterioles
51
Q

What is the respiratory specific ADE seen with cholinesterase inhibitors?

A

Increased bronchoconstriction

52
Q

What is the GI tract specific ADE seen with cholinesterase inhibitors?

A

Increased GI motility and peristalsis

53
Q

What is the urinary specific ADE seen with cholinesterase inhibitors?

A

↑ Contraction of ureter and bladder smooth muscle relaxation of sphincter

54
Q

What is the eye specific ADE seen with cholinesterase inhibitors?

A

Increased contractility of ciliary muscle and iris

55
Q

What are the secretions specific ADEs seen with cholinesterase inhibitors? (5)

A
  1. ↑ Salivation
  2. ↑ Lacrimation
  3. ↑ GI secretions
  4. ↑ Bronchial secretions
  5. ↑ Sweating
56
Q

True or False? Cholinesterase inhibitors are EDS

A

True
- Must NOT be taking concurrent anticholinergic meds at any time

57
Q

What is the NMDA antagonist medication?

A

Memantine (Ebixa)

58
Q

What is the MOA of memantine?

A

Block glutamate at NMDA receptor (Theory: persistent activation of NMDA contributes to symptoms)
- No effect on ACh

59
Q

True or False? NMDA antagonists are less tolerated than cholinesterase inhibitors?

A

False - better tolerated

60
Q

What are the ADEs of NMDA antagonist? (10)

A
  1. Dizziness
  2. Constipation
  3. Confusion
  4. Insomnia
  5. Headache
  6. Hypertension
  7. Restlessness
  8. Akathisia
  9. Nausea
  10. QT prolongation (<1%)
61
Q

When might we discontinue dementia pharmacological treatment?

A

General consensus - loss of ability to perform ADLs independently
- Dementia has progressed to a stage where there would be no meaningful benefit remaining

62
Q

True or False? There are no meds, vitamins, herbals etc. to help prevent cognitive decline or dementia

A

True - well, no evidence of anything at the moment

63
Q

What are some non-pharmacological ways to prevent dementia? (6)

A
  1. Usual CV risk reduction strategies
  2. Educational attainment/ongoing cognitive challenges
  3. Social engagement
  4. Exercise
  5. Healthy Diet
  6. Hearing/vision checks and use of aids as needed
64
Q

What is the basic MOA of new dementia -mab drugs?

A

Increase clearance of beta-amyloid, reducing beta-amyloid plaques in the brain
- Only indicated for alzheimer’s disease (early)

65
Q

Name the mab drugs being used for dementia

A

Lecanemab and donanemab - not yet approved in Canada but being reviewed

66
Q

Go through the steps of management of BPSD (4)

A
  1. Assess for and treat any medical/medication causes or contributors
  2. Explore and minimize psychological and environmental triggers
  3. Pharmacotherapy ONLY if behaviour is causing harm or significant distress to individual, caregivers, or others AND is persistent or recurrent
  4. Re-evaluate drug regimen after 3 months
67
Q

Which of the behavioural and psychological symptoms of BPSD may be amenable to pharmacotherapy? (5)

A
  1. Aggression
  2. Paranoia
  3. Hallucinations
  4. Delusions
  5. Depression
68
Q

When managing BPSD how do we assess and treat medical causes? (4)

A
  1. Taper/stop any medications that may be contributing
  2. Look for and manage any underlying medical issues
    - Infection
    - Endocrine (thyroid, diabetes, etc.)
    - Electrolyte abnormalities
    - Urinary retention
    - Assess for and treat pain**
  3. Offer food/drink often to prevent hunger and thirst
  4. Manage constipation proactively
69
Q

When managing BPSD, how do we assess for and manage psychological triggers? (5)

A
  1. Avoid social isolation; consider impact of environment/company on mood
  2. Allow individual to make decisions whenever possible
    - Give simple, clear choices
  3. Provide simple instructions
  4. Show a warm, kind, manner; do not infantilize or speak as if the individual is not present
  5. Do not argue; reassure and redirect
70
Q

When managing BPSD, how do we assess for and manage environmental triggers? (6)

A
  1. Encourage use of glasses/hearing aids
  2. Provide regular, structured daily routine
  3. Comfortable, familiar environment
  4. Avoid overstimulation (noises, crowds)
  5. Engaging activities, social opportunities
  6. Sun/bright light exposure during the day, dark at evening and nighttime
71
Q

What antidepressants do we want to be using in the management of BPSD? (3)

A
  1. SSRIs minus fluoxetine and paroxetine
  2. SNRIs
  3. Bupropion
72
Q

What classes of antidepressants do we want to avoid in the management of BPSD? (2)

A
  1. TCAs and paroxetine
  2. Fluoxetine
73
Q

Which class of antipsychotics is preferred in the management of BPSD?

A

Atypical
- Risperidone
- Olanzapine
- Quetiapine

74
Q

When do we give APs in the management of BPSD?

A

Given only if behaviour is causing harm and/or has not responded to non-pharmacological methods

75
Q

What are some ADEs to watch out for when using APs? (8)

A
  1. Weight gain
  2. ↓BP
  3. Anticholinergic effects
  4. Sedation
  5. Falls
  6. EPS
  7. Tardive dyskinesia
  8. Urinary retention
76
Q

Typically, in Saskatchewan, what AP is actually used in BPSD?

A

Quetiapine

77
Q

Using >1 antipsychotic at a time in BPSD. Yay or nay?

A

Nay - no evidence for it

78
Q

When is haloperidol specifically used in BPSD?

A

To manage acute delirium - PRN only
- Not recommended in Parkinson’s pts due to EPS

79
Q

When MIGHT stimulants (methylphenidate) be used in BPSD?
What would we prefer?

A
  1. Very occasionally used to treat apathy and loss of motivation
  2. External activity and environmental stimulation is
    more effective
80
Q

Why do we prefer not to use stimulants in BPSD? (2)

A
  1. Stimulant adverse effects usually outweigh any potential benefit
  2. ↑ blood pressure and heart rate, ↓ appetite, dizziness, insomnia, agitation
81
Q

When MIGHT sedatives be used in BPSD?

A

Considered when behaviour is thought to be directly correlated with lack of sleep OR behaviours are during night

82
Q

What sedatives should be avoided in BPSD? What to watch for? (3 item)

A
  1. Avoid antihistamines, sedating OTCs
  2. Watch for dependence and tolerance
  3. Increase risk of delirium and falls!!
83
Q

What is the pharmacist’s role in BPSD and dementia in general? (5)

A
  1. Communication is key
  2. Re-assessment of pharmacological treatments frequently as clinical status, function, goals of care change
  3. Advertise/refer to the Alzheimer Society; a support for both patient and caregiver(s)
  4. Recognize non-obvious presentations of other conditions in individuals with dementia
    - A change in behaviour could be due to many underlying factors (e.g. UTI, pain, change in routine, etc.)
  5. Be a calm, patient resource for both patient and caregiver for drug information, advice
    - Supplement with written information when possible
84
Q

What analgesics are appropriate to use in BPSD? (3)

A
  1. Acet
  2. NSAIDs
  3. Opioids
85
Q

Talk about analgesic use in BPSD (3)

A
  1. When pain is thought to be cause of behaviour
  2. A good trial of acetaminophen for pain is often overlooked
  3. Re-assess and increase dosage, or switch to opioids if necessary
    - Expect and manage constipation, sedation

PHAR 350 (6 decks)

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