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Year 3 - Clinical (Winter) > 11 - Alzheimer's Disease > Flashcards

11 - Alzheimer's Disease Flashcards

1
Q

Dementia

A
  • A group of disorders characterized by a progressive non-reversible loss of cognitive function
  • Memory loss, performing familiar tasks, language, etc.
  • Dementia types differ by:
    • Sx onset and type
    • Response to tx
  • Can have a mix of various dementias
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2
Q

What are some examples of normal aging memory loss?

A
  • Details of an event that took place a year ago
  • Acquaintance name/face
  • Occasionally forget things
  • Worried about your memory but relatives aren’t
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3
Q

What are some examples of dementia memory loss?

A
  • Details of recent events
  • Family member name/face
  • Frequently forget things
  • Relatives are worried about memory but you are unaware
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4
Q

Briefly describe the brain and Alzheimer’s disease

A
  • Most people undergo a gradual cognitive decline over their life span
  • 100 billion neurons and 100 trillion synapses
  • To stay healthy, neurons must communicate w/ each other, carry out metabolism, and repair themselves
  • Alzheimer’s disease disrupts all 3 of these essential jobs
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5
Q

Describe “three pounds, three parts”

A
  1. Cerebral hemispheres
    - Process sensory info
    - Voluntary movement
    - Regulates conscious thought
  2. Cerebellum
    - Balance and coordination
  3. Brain stem
    - Connects brain and spinal cord
    - Controls automatic functions (ex: HR, BP, breathing, digestion)
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6
Q

Compare and contrast normal function vs. Alzheimer’s in the frontal lobe

A
  • Normal = plan and initiate activity, judgement/ behaviour

- AD = apathetic, withdrawn

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7
Q

Compare and contrast normal function vs. Alzheimer’s in the limbic lobe

A
  • Normal = emotions, basic needs (sleep/ eat)

- AD = suspiciousness, irritability, mood/ anxiety

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8
Q

Compare and contrast normal function vs. Alzheimer’s in the hippocampus/ temporal lobe

A
  • Normal = short-term memories converted to long-term memories
  • AD = inability to retain memory of recent past, recognize objects
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9
Q

Compare and contrast normal function vs. Alzheimer’s in the parietal lobe

A
  • Normal = puts activities in sequence, spatial information

- AD = using words incorrectly, getting lost easily, dressed

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10
Q

Describe what occurs in the brain during Alzheimer’s dementia

A
  • The brain in Alzheimer’s disease has fewer nerve cells and synapses than a healthy brain
  • Hallmarks of Alzheimer’s disease = neuritic plaques and neurofibrillary tangles
  • Central atrophy (brain shrinkage)
  • Net result = decrease in multiple NTs (cholinergic system appears most significantly affected)
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11
Q

Neuritic plaques

A
  • Plaques are formed from protein pieces (called beta-amyloid) that “stick” together
  • Block cell-to-cell signaling at synapse
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12
Q

Neurofibrillary tangles

A
  • Tangles are collapsed and twisted fibers of protein (called tau) build up inside the nerve cell
  • Tau helps stabilize the cell transport system that allows nutrients, cell parts, and other essential materials to move through the cells
  • W/o this system, the nerve cells eventually die
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13
Q

NT changes in Alzheimer’s

A
  • Reduced activity of choline acetyltransferase
  • Selective loss of certain nicotinic receptor subtypes
  • Reduced # of cholinergic neurons
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14
Q

Diagnosing AD

A
  • Detailed pt hx w/ info from caregiver
    • Caregivers w/o pt present may allow for truthful hx
    • Include comorbid conditions and medications
  • Cognitive status (brief cognitive tests)
  • Physical & neurological exams and lab tests (to rule out other conditions)
  • Behavioural sx, daily functioning
  • Imaging (CT scan, MRI, PET) to rule out vascular disease
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15
Q

Precipitating factors for AD

A
  • Drugs (sedative hypnotics, narcotics, anticholinergics)
  • Primary neurologic disease (stroke, intracranial hemorrhage, meningitis)
  • Intercurrent illness
  • Surgery
  • Environment (admission to ICU, use of physical restraints, bladder catheter, pain, emotional stress, prolonged sleep deprivation)
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16
Q

Drugs that can cause/ contribute to cognitive impairment

A
  • Anticholinergics –> TCAs (paroxetine), anti-emetics, antihistamines (1st gen), antipsychotics, ranitidine
  • Psychoactive –> alcohol, anticonvulsants, antidepressants, antipsychotics, lithium, muscle relaxants, opioids
  • Other –> cipro, clarithro, corticosteroids, digoxin, NSAIDs
17
Q

Brief cognitive tests (MMSE or MoCA)

A
  • Lack of evidence to recommend one over the other
  • Not used to differentiate between dementia subtypes
  • Used because:
    • Required for drug benefit programs (part 3 EDS)
    • Help inform clinical judgement
    • Provides objective measure vs. qualitative assessments
18
Q

MMSE (mini-mental state exam)

A
  • Most widely used instrument to estimate severity and to monitor change in cognitive impairment during therapy
  • Score of 10-26 required for anticholinesterase drug coverage; score < 24 typically included in AD RCTs
  • Normal = 1-2 point drop/year
  • Untreated AD = 2-4 drop/year
  • Strengths –> quick to administer, easy to use, established validity
  • Limitations –> not sensitive for detecting mild dementia, score influenced by age, education, language, inattention, motor/ visual impairment
19
Q

MoCA (montreal cognitive assessment)

A
  • Alternative instrument used in clinical practice validated in px 55-85 y/o
  • Average MoCA for mild cognitive impairment (MCI) = 22 (19-25)
  • Average MoCA for mild AD = 16 (11-21)
  • AD = cognitive impairment (MoCA < 10) + loss of autonomy
20
Q

Stages of dementia

A
  • Early/ mild (1-3 years from sx onset)
  • Moderate (2-8 years from sx onset)
  • Severe (6-12 years from sx onset)
21
Q

Drug tx for cognitive sx of AD

A
  • Cholinesterase inhibitors (donepezil, rivastigmine, or galantamine)
  • NMDA antagonist (memantine)
  • Mild to moderate = cholinesterase inhibitor; moderate to severe = add anti-glutamatergic (memantine)
22
Q

Goals of therapy for Alzheimer’s

A
  • Treat sx of cognitive difficulties
  • Preserve pt function
  • Treat psychiatric and behavioural sequelae
  • *Current tx have not been shown to prolong life, cure dementia, or stop/reverse the pathophysiologic processes of dementia
23
Q

Pt and caregiving counselling for Alzheimer’s

A
  • Currently no cure for AD exists
  • Cholinesterase inhibitors
    • Modest benefit in stabilizing/ slowing progression of AD
    • May help w/ deficits in memory, language, and thinking abilities; not all px respond
    • SE = GI, fall risk, urinary incontinence; titrate dose to minimize
  • Evaluate medications that can further compromise cognitive function
  • *Decision to initiate therapy should be made after a detailed discussion w/ pt & caregiver
24
Q

Cholinesterase inhibitors - MOA, indication, SE, choosing one over the other, contraindications

A
  • Donepezil, rivastigmine, galantamine
  • MOA –> increase availability of ACh at synapse
  • All 3 indicated as acceptable initial monotherapy for mild to moderate AD (donepezil also indicated for severe AD)
  • All 3 demonstrate similar benefit/ stabilization of AD for 6-9 months, followed by gradual decline
  • Limited data on relevant outcomes (ex: function, behaviour, caregiver burden, QOL); no delay in institutionalization
  • Choice based on ease of use, pt preference, cost, safety issues
  • Most common SE = dose-dependent GI (N/V, diarrhea) most likely to occur at start of tx or dose escalation; longer titration and administration w/ food will help
  • Relative contraindications based on conditions affected by increasing cholinergic tone
    • Cardiac conduction abnormalities, bradycardia
    • Active PUD (PPI may be protective)
    • Asthma/ COPD (avoid in uncontrolled lung disease)
  • If d/c, taper by 25-50% q1-2w to minimize risk of rebound constipation & other SE
25
Q

Memantine - MOA, indication, SE

A
  • NMDA antagonist
  • Not recommended for mild dementia
  • Option as monotherapy or combo tx w/ cholinesterase inhibitors for moderate to severe AD
  • Caution in seizures and CV disease
  • SE = dizziness, constipation, confusion, headache, HTN
26
Q

Behavioural and psychological sx of dementia (BPSD)

A
  • High prevalence in AD (70-90% of px)
  • Verbal abuse
  • Most common reason for placement
  • BPSD behaviours include depression, anxiety (caution w/ BZDs), psychosis, agitation (wandering, uncooperative, aggression, pacing)
  • Triggers = sensory deficits (poor eyesight/ hearing), SE of some meds, psychiatric illness, unfamiliar environment, physical conditions
27
Q

Non-drug approaches for Alzheimer’s

A
  • 1st line for non-threatening & stressful behaviours
  • Environment –> ABC charting, reduce noise, keep area well lit
    • ABC charting –> Antecedents (causes) = PIECES (physical, intellectual, emotional, cultural, environmental, social); behaviours; consequences
  • Activities –> schedule activities the pt enjoys throughout the day, discourage naps throughout the day, music therapy
  • Pt/caregiver interactions –> calm demeanor & well-paced, quiet tone, refocus & redirect the pt as needed, caregiver education critical
28
Q

Antipsychotics in dementia

A
  • Modest effect for BPSD
  • Serious adverse effects (death, stroke)
  • Avoid use; potentially appropriate in hallucinations, delusions, or aggressive behaviour
    • Appropriate if sx presents a danger to pt or others
29
Q

Delirium vs. dementia

A
  • Delirium = acute and abrupt onset, fluctuating course, possibly reversible, alertness and vitals are decreased/altered
  • Dementia = chronic onset, duration progressive and continuous, progressive decline, non-reversible, alertness and vitals are normal
30
Q

Other drugs for AD? (estrogen, NSAIDs, statins, NHPs)

A
  • Estrogen –> observational studies show lower incidence in AD w/ estrogen use; not recommended
  • NSAIDs –> not recommended b/c of SE & lack of evidence
  • Statins –> no evidence to prove they are helpful; only recommended for px who have other indications for statin use
    • Cognitive impairment recognized as a rare adverse event associated w/ statin in case reports
  • No NHPs are recommended (vitamin E, gingko biloba, polyphenol/ resveratrol)

Year 3 - Clinical (Winter) (30 decks)

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