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Clinical 2 (Part B) > 11 - Alzheimer's > Flashcards

11 - Alzheimer's Flashcards

1
Q

Alzheimer’s is a neurogenerative, describe that.

A

Affecting neurons and synaptic connections in the brain. One of the major causes of morbidity and mortality in the aging population.

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2
Q

Alzheimer’s is the primary cause of _____

A

dementia

dementia is a symptom

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3
Q

What is dementia?

A

a decline in mental ability severe enough to interfere with daily activities

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4
Q

Alzheimer’s disease is characterized by 3 hallmark brain changes, what are they?

A

1) Diffuse (widespread) neuritic plaques
2) Plaques display marked amyloid beta deposition
3) Neurofibillary tangles (NFTs) made up of phosphorylated tau (p-tau) protein

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5
Q

What is usually the first symptom to present?

A

memory impairment

*followed by others (to be discussed)

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6
Q

Alzheimer’s is a ____ disease

A

progressive

meaning it will inexorably get worse

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7
Q

Is there currently a treatment for the underlying disease?

A

Nope

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8
Q

Brain changes usually start in ______. Which accounts for early symptoms of memory loss; primary sensory and motor function is usually preserved until later in the disease when other areas in the brain are affected.

A

hippocampus

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9
Q

Alzheimer’s has a global concern in what 3 areas?

A
  • Mortality
  • Caregiver burden
  • Cost
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10
Q

Alzheimer’s makes up about ____% of dementia cases. The aging population is one of the major contributors to the increased rate of diagnosis and predicted spike in cases by mid-century.

A

60-70

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11
Q

Risk Factors:

Age?

A

Risk doubles every 10 years after 65 yo

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12
Q

Risk Factors:

Genetic factors?

A

More likely associated with rare “early-onset” AD (onset < 65 years old can be as early as 30 yo)

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13
Q

Risk Factors:

List some other risk factors

A
  • Hyperlipidemia
  • Hypertension (long term affects blood vessels in brain)
  • Cerebrovascular disease
  • Physical inactivity

-obesity, DM, brain trauma, some medications (benzos, anticholinergics, PPis), reduced brain capacity (low education, reduced mental activity)

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14
Q

Compare normal aging to dementia

A

Normal aging:

  • Details of an event that took place a year ago
  • Acquaintance name/face
  • Occasionally forget things
  • Worried about your memory but relatives are not

Dementia:

  • Details of recent events
  • Family member name/face
  • Frequently forget things
  • Relatives are worried about memory but you are unaware
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15
Q

To stay healthy, what must neurons do?

A

Neurons must communicate with each other, carry out metabolism, and repair themselves.

*Alzheimer’s disease disrupts all three of these essential jobs

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16
Q

Describe a normal frontal lobe and one with Alzheimer’s Disease (AD)

A

Normal:

  • plan and initiates activity
  • judgement/behavior

AD:

  • apathetic
  • withdrawn
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17
Q

Describe a normal parietal lobe and one with Alzheimer’s Disease (AD)

A

Normal:

  • puts activities in sequence
  • spatial information

AD:
-using words incorrectly, getting lots easily, dressed

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18
Q

Describe a normal limbic system and one with Alzheimer’s Disease (AD)

A

Normal:

  • emotions
  • basic needs (sleep/eat)

AD:
-suspiciousness, irritability, mood/anxiety

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19
Q

Describe a normal hippocampus/temporal lobe and one with Alzheimer’s Disease (AD)

A

Normal:
-short-term memories are converted to long-term memories

AD:
-inability to retain memory of recent past, recognize objects

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20
Q

How are caregivers affected?

A

psychological and physical toll

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21
Q

Neuropathologic changes of AD are ______ and _______, meaning they get worse over time. Ultimately fatal.

A

chronic and progressive

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22
Q

What is neurodegeneration due to ??

A

accumulation of neurofibrillary tangles (NFTs, “tau tangles”) and amyloid plaques

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23
Q

Pathological processes likely begin ______ before symptoms present (can we diagnose earlier?)

A

decades

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24
Q

What brain changes are included in Alzheimer’s?

A
  • NFT & amyloid plaque accumulation
  • decrease in functioning synapses
  • reduction in certain neurotransmitters (acylchaline)
  • cell death
  • brain atrophy
  • reduced metabolic and repair functioning
  • vascular dysfunction (reduced oxygenation)
  • breakdown of BBB
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25
Q

Does the severity of disease correlate with plaque burden ?

A

not generally

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26
Q

The brain in Alzheimer’s disease has ____ nerve cells and synapses than a healthy brain.

A

fewer

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27
Q

What are the 2 hallmarks of Alzheimer’s disease ?

A

1) Neuritic plaques

2) Neurofibrillary tangles

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28
Q

What is the net result of AD pathophysiology?

A

decrease in multiple neurotransmitters

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29
Q

The _____ system appears most significantly affected

A

cholinergic

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30
Q

What are the plaques formed from?

A

Protein pieces (called beta-amyloid) that “stick” together.

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31
Q

What do the plaques do?

A

Block cell-to-cell signalling at synapse

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32
Q

What are tangles?

A

They are collapsed and twisted fibres of protein (called tau) that build up inside the nerve cell.

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33
Q

What does Tau normally do?

A

Helps stabilizes the cell transport system that allows nutrients, cell parts, and other essential materials to move through the cells.

*Without this system, the nerve cell eventually dies.

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34
Q

List 3 neurotransmitter changes in AD

A

1) Reduced activity of choline acetyltransferase
2) Selective loss of certain nicotinic receptors subtypes
3) Reduced number of cholinergic neurons

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35
Q

Theory behind amyloid plaques?

A

Lesions found in brain and cerebral vasculature; possibly due to imbalance between production/clearance of AB

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36
Q

Theory behind neurofibrillary tangles?

A

Composed of hyperphosphorylated tau protein; causes eventual neuronal death; burden correlates to disease severity

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37
Q

Theory behind inflammatory mediators ?

A

Increased immune response (macrophage, cytokine release, etc.) may be in response to clear out AB, but may contribute to neuronal cell death

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38
Q

Theory behind loss of cholinergic activity ?

A

One of many neuronal pathways destroyed in AD; thought to be one of contributors to memory/cognition dysfunction but not the complete picture

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39
Q

Theory behind dysfunction of other NTs ?

A

In addition to acetylcholine, Its such as 5-HT, NE and Flu are depleted

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40
Q

Theory behind vascular dysfunction ?

A

Dysfunctional cerebral blood vessels may decrease nutrient delivery to brain and clearance of AB.

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41
Q

Usually onset of AD is very gradual and progresses _____

A

slowly

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42
Q

Who brings it up?

A

Usually family members, not the person themselves

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43
Q

List symptoms of AD

A

1) Memory dysfunction
2) Executive functioning problems
3) Behaviour/Psych
4) Other symptoms

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44
Q

Symptoms:

Describe memory dysfunction

A
  • usually first symptom to present
  • poor recall/losing items
  • aphasia, agnosia
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45
Q

Symptoms:

Describe executive functioning problems

A
  • includes dysfunction with problem-solving ability and judgement; impairment varies in early AD
  • decreased organization, decreased motivation, decreased ability to multitask
  • anosognosia (reduced self awareness; is less aware of deficits)
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46
Q

Symptoms:

Describe behavior/psych

A
  • Often present mid to late disease
  • Apathy, irritability, social disengagement
  • Agitation, aggressioin, wandering
  • Psychosis, hallucinations
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47
Q

What are some other symptoms?

A
  • Apraxia, motor disturbances
  • Sleep disturbances
  • Seizures (late)
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48
Q

Alzheimer’s:

What are the top early signs?

A
  • memory loss
  • changes in mood
  • misplacing belongings
  • hard to complete familiar task
  • confusion of time and place
  • changes in vision
  • struggling to communicate
  • poor judgement
  • social withdrawal
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49
Q

Describe Preclinical AD

A
  • Individuals do not demonstrate clinical signs of cognitive decline, but have underlying AD pathology, as shown on screening tests (CSF or PET)
  • Individuals may or may not progress to clinical AD
50
Q

Describe Prodromal AD

A

Also referred to as:

  • Mild cognitive impairment (MCI)
  • Amnestic MCI due to AD
  • Symptomatic pre-dementia of AD

-Evidence of clinical decline manifested by minor change in cognition and short-term memory loss

51
Q

Describe AD Dementia

A

-Full clinical dementia that includes the symptoms typically associated with AD, including memory loss, cognitive impairment, behavioural changes, motor and speech dysfunction, etc.

AD Dementia can be classified as mild, moderate or severe

52
Q

Diagnosing:

Cognition

A

At least 2 of the following:

  • Decreased ability to acquire & remember new info
  • Decreased reasoning & handling of complex tasks
  • Change in personality, behaviour
  • Decreased visuospatial abilities
53
Q

Diagnosing:

Initial symptoms

A

Or most prominent is one of:

  • Amnestic presentation (impairment of learning & recall of recently learned info)
  • Non-amnestic presentation (word finding, visuospatial, reasoning, judgement)
54
Q

Diagnosing:

Symptom pattern

A
  • Insidious onset (not abrupt, gradual)
  • Clear history of worsening over time
  • Enough to interfere with work, usual activities
55
Q

Diagnosing:

Rule out differentials

A
  • Not due to another psych disorder

- Due to a drug side effect

56
Q

Diagnosing:

What additional testing needs to be done?

A
  • Brain imaging
  • CSF testing
  • AD biomarker assay
57
Q

What drugs can cause cognitive decline ?

A

sedative hypnotics, narcotics, anticholinergics (more on this later), polypharmacy, drug withdrawal, etc.

58
Q

What primary neurologic diseases can cause cognitive decline ?

A
  • stroke
  • intracranial hemorrhage
  • meningitis
  • encephalitis
  • hydrocephaly
59
Q

What other illnesses can cause cognitive decline ?

A
  • anemia
  • hypothyroidism
  • hypo/hyper-glycemia
  • electrolyte imbalances
60
Q

What are 2 other causes of cognitive decline ?

A
  • surgery
  • environment (admission to intensive care unit, use of physical restraints, bladder catheter, pain, emotional stress, prolonged sleep deprivation)
61
Q

What are some red flags (neuroimaging required) ?

A
  • < 60 years of age
  • new onset
  • rapid progression
  • post-head injury
  • focal or lateralizing signs
  • history of cancer
  • use of anticoagulants
  • early urinary incontinence and gait disorder
  • unusual cognitive symptoms
62
Q

What are we screening for?

A
  • Possible neoplasm
  • Subdural hematoma
  • Hydrocephalus
63
Q

What are some other diagnostics ?

A
  • Bloodwork
  • Biomarker Assay
  • Rule out drug-induced causes
  • Cognition Assessment Tools
64
Q

Describe bloodwork

A

Not useful in diagnosis but helps with exclusion (hypothyroidism, B12 deficiency, anemia, infectious causes, hypo/hyperglycemia, etc.)

65
Q

Describe biomarker assay

A

Not part of routine diagnosis … YET!

Includes specific measures to evaluate Ab deposition and tau burden

66
Q

What anticholinergic drugs contribute to cognitive decline?

A
  • antihistamines
  • antipsychotics
  • TCAs
  • antiemetics
  • oxybutinin
  • ranitidine

*B/c losing Ach and this is also against Ach transmission

67
Q

What psychoactive drugs contribute to cognitive decline ?

A
  • alcohol
  • anticonvulsants
  • antidepressants
  • antiparkinsons
  • antipsychotic
  • muscle relaxant
  • opioids
  • sedative hypnotics
  • anything that causes sedation

*Due to CNS depression

68
Q

What are some other drugs that cause cognitive decline?

A
  • ciprofloxacin
  • clarithromycin
  • antiarrhythmics
  • digoxin
  • NSAIDs
  • corticosteroids
69
Q

Cognitive tests may be difficult to interpret but are used, because ??

A
  • Required for drug benefit programs
  • Help inform clinical judgement (part of the diagnostic picture)
  • Provides an objective measure vs. qualitative assessments (ex. how do you feel he is doing?) can be used to measure change over time
70
Q

Describe MMSE (Mini-Mental State Exam)

A
  • Most widely used instrument to estimate severity and to monitor change in cognitive impairment during therapy
  • Repeat tests every 6 months
71
Q

MMSE:

What is an aggressive drop ?

A

> 3 points

*often a reason to stop the meds cause they aren’t working

72
Q

What is sundowning?

A
  • happens in the evening
  • starts to decline rapidly
  • happens at any stage
73
Q

Describe Stage 1: Pre-dementia

A
  • Short-term memory loss
  • Decline in attention span
  • Decreased awareness
74
Q

Describe Stage 2: Mild

A
  • More severe learning and memory impairment
  • Language difficulty (reduced vocabulary and word fluency)
  • Apraxia (inability to perform purposeful movements)

*this stage, aware of what’s coming

75
Q

Describe Stage 3: Moderate

A
  • Long-term memory loss
  • Inability to recognize close relatives
  • Aimless wandering
  • Emotional change
  • Urinary incontinence
76
Q

Describe Stage 4: Severe

A
  • Complete loss of speech
  • Severe apathy and exhaustion
  • Bedridden, ability to feed oneself
  • Death

*at this stage it is 5-10 years after diagnosis

77
Q

Can we prevent AD?

A
  • substantial evidence to suggest that pathophysiological processes begin > a decade before any clinical symptoms present
  • data is still very early, and not one modification shown (yet) to be effective in prevention
  • intensive risk factor modification mid-life (45-65 years)&raquo_space;> delay or prevent ?
78
Q

Describe the management of AD

A
  • improve/maintain sleep
  • preserve patient function
  • treat symptoms of cognitive dysfunction
  • manage behavioural complications
  • patient/caregiver education (& caregiver care)
  • treat psychiatric complications (ex. depression due to the diagnosis and decreased serotonin)
79
Q

What considerations do we need to consider in the management of AD ?

A
  • compliance
  • support system (home care?)
  • other medical conditions
80
Q

What are areas involved in secondary prevention?

A
  • Diet (olive oil, fish, red wine)
  • Hyperlipidemia (statin treatment has interest but needs further study)
  • Hypertension (role of antihypertensives on risk reduction unclear, but enough reason to treat hypertension regardless)
  • Lifestyle and exercise (physical exercise, cognitive training, higher education = reduced risk of dementia)
81
Q

List some points to patient & caregiver counselling

A

1) Currently no cure for AD exists

2) Cholinesterase inhibitors (ChEI):
- modest benefit in stabilizing/slowing progression of AD
- may help with deficits in memory, language, and thinking ability; not all patients respond to treatment
- Side effects (GI, fall risk, urinary incontinence, stimulating - sleep?)

  • dose titration to minimize side effects
    3) Evaluate medications that can further compromise cognitive function (OTC and Rx)
82
Q

What are some treatment options for mild-moderate AD ?

A

Cholinesterase inhibitors:

  • Donepezil
  • Rivastigmine
  • Galantamine

*these block the breakdown of Ach

83
Q

What are some treatment options for moderate-severe AD?

A

Add anti-glutamatergic:
-Memantine

(Alternatively, use memantine or a cholinesterase inhibitor alone)

84
Q

How do Cholinesterase inhibitors help?

A

-They prevent the breakdown of Ach

1) Increase availability of ACh at synapse (AChE inhibition)
2) Increase release of Ash into synapse (allosteric modulation of presynaptic nicotinic receptors)

85
Q

read slide 37 comparing cholinesterase inhibitors

A

okay

86
Q

All three Cholinesterase inhibitors are indicated for initial mono therapy for mild-moderate AD, which one is also indicated for severe AD?

A

donepezil

87
Q

All ChEIs demonstrate similar benefit/stabilization of AD for ____ months, followed by gradual decline.

A

6-9

88
Q

Are ChEIs effective ?

A
  • Limited data on relevant outcomes (function, behaviour, caregiver burden, QOL)
  • No delay in institutionalization
89
Q

What are the choices of ChEI based on?

A

ease of use (oral vs patch), patient preference, cost, and safety issues, such as potential for drug interactions

90
Q

ChEI:

What is the most common SE?

A

Dose-dependent GI (anorexia, nausea, vomiting, diarrhea); worse if <55kg

  • most likely to occur at start of treatment or dose escalation
  • Longer & titration and administration with food will help (increase dose every 4 weeks or longer)
  • caution with antiemetics (increased anticholinergic effects)
91
Q

ChEI:
____ can be a problem, especially if taken later in the day (sleep is already compromised in AD); if insomnia, make sure patient takes in the am to lessen

A

Insomnia

*this can be a problem with BID dosing

92
Q

ChEI:

What are some relative CI based on conditions affected by increasing cholinergic tone?

A
  • Cardiac conduction abnormalities, bradycardia (monitor for syncope, HR, falls if on beta blocker)
  • Active PUD (PPI may be protective) - ChEIs may increase gastric acid secretion
  • Asthma/COPD (avoid in uncontrolled lung disease)
93
Q

What are some reasons for discontinuing ChEI’s?

A
  • poor adherence to therapy
  • persistent side effects
  • mutual agreement by HCP-caregiver
  • rapid progression of AD (no meaningful benefit)
  • symptoms deteriorate after 3-6 months of therapy
94
Q

How do we discontinue ChEI’s?

A

if discontinuing - taper by 25-50% Q1-2W to minimize risk of rebound constipation and other side effects

95
Q

How does Memantine work?

A

Memantine (NMDA receptor blocker) blocks the sustained activation of NMDA receptors caused by abnormal glutaminergic activity in AD

*Glutamine can have negative effect, it runs rampage causing neuronal death and damage synapses by blocking less glutamine allowed to do that.

96
Q

Memantine is not recommended for _____ dementia

A

mild

97
Q

Memantine:

Used for what type of AD?

A

moderate to severe

98
Q

Memantine:

What is it associated with?

A

lower aggression/agitation (evidence not rigorous)

99
Q

Memantine:

Caution in ?

A

seizures and CV disease

100
Q

Memantine:

What are some mild to moderate SE ?

A

-dizziness, constipation, confusion, headache, hypertension

101
Q

What is the problem with sleep in AD?

A

fragmented nocturnal sleep, multiple and prolonged awakenings, relative decrease in slow-wave sleep percentage and increased daytime napping

102
Q

What is the management for sleep problems in AD?

A

Start with non-pharms:

  • establish regular sleep/wake times (routine!)
  • limit daytime napping (keep individual engaged)
  • limit evening fluid intake
  • calming bedtime rituals (consistency; avoid “screen-induced sleep”)
  • keep mind and body active during the day
103
Q

What are some pharmacological interventions that can be used for sleep management in AD?

A
  • trazodone
  • non-benzo hypnotics
  • avoid benzos, especially triazolam
  • avoid OTC sleep aids
104
Q

What is BPSD?

A

Behavioural & psychosocial symptoms of dementia

  • Most commonly presents as verbal abuse
  • Most common reason for placement
105
Q

What do BPSD behaviours include ?

A
  • Depression (sleep disturbance, apathy, weight loss, tearful)
  • Anxiety (caution with benzos)
  • Psychosis (suspicious, paranoia, delusions, hallucinations)
  • Agitation (wandering, uncooperative, aggression, pacing)
106
Q

List a few common causes of BPSD (more on slide 47)

A
  • unfamiliar environment
  • physical conditions (fever, pain, infections, malnutrition)
  • unfamiliar caregivers
  • poor sleep
107
Q

Describe the non-drug approaches for BPSD

A
  • reduce noise
  • keep area well lit
  • avoid sudden changes in surrounding
  • lots of physical activity
  • schedule activities that they enjoy
  • discourage naps

Patient/Caregiver interactions:

  • calm demeanour and well paced, quiet tone
  • plan care when patient is functioning best
  • refocus and redirect the patient as needed
  • caregiver education critical
108
Q

When are antipsychotics in BPSD potentially appropriate ?

A
  • hallucinations
  • delusions
  • aggressive behaviour (esp. physical)
109
Q

When are antipsychotics in BPSD appropriate ?

A
  • If the symptom presents a danger to the patient or others
  • The patient is experiencing inconsolable or persistent distress
  • The patient is experiencing significant decline in function
  • The patient is experiencing substantial difficulty receiving needed care.
110
Q

When are antipsychotics in BPSD INappropriate ?

A
  • Wandering, uncooperativeness, nuisance behaviours, restlessness, hoarding (unlikely to respond well to drug therapy)
  • Unsociability, poor self-care, impaired memory, inattention/indifference to surroundings, mild anxiety
  • Verbal expression or behaviours that do not represent a danger to patient or others
111
Q

Antipsychotics have a ____ effect for BPSD

A

modest

112
Q

What are some serious adverse events of antipsychotics ?

A
  • death
  • stroke
  • weight gain, hyperlipidemia, hyperglycemia
  • sedation/lethargy/falls/postural hypotension
  • EPS, anticholinergic
  • urinary infection, pneumonia

*40% spontaneously resolve or respond to psychosocial interventions

113
Q

see slide 51 on delirium vs dementia

A

okay

114
Q

Causes of delirium:

What are some metabolic disorders ?

A
  • organ failure
  • DM
  • thyroid disorder
  • dehydration
115
Q

Causes of delirium:

What are some illnesses ?

A
  • infection, fever
  • head trauma
  • low blood oxygen
  • post-surgical complication
116
Q

Causes of delirium:

What are some drugs and drug withdrawal ?

A
  • anticholinergics
  • ethanol
  • anticonvulsants
  • corticosteroids
  • lithium
  • antibiotics
  • sedatives
117
Q

Causes of delirium:

What are some street drugs?

A

ethanol, marijuana, LSD, amphetamines, cocaine, opiates, heroin

118
Q

What are some other agents for AD?

A
  • estrogen
  • NSAIDs
  • statins
119
Q

Which one is recommended?

A

statins - only recommended for patients who have other indications for statin use

120
Q

Are dietary supplements recommended?

A

nope

Clinical 2 (Part B) (30 decks)

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