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alzheimer's Flashcards

1
Q

describe mechanisms of drug action that leads to (i) agonistic drug effects and (ii) antagonistic drug effects

A

agonistic drug effects
- increase synthesis of NT (eg. by increasing precursor)
- increase number of NT by destroying degrading enzymes
- increase release of NT from terminal buttons
- bind to autoreceptor and block inhibitory effect on NT release
- bind to postsynaptic receptors and either activate them or increase effect on them of NT molecules
- block deactivation of NT by blocking reuptake or degeneration

antagonistic drug effects
- block synthesis of NT (eg. by destroying synthesising enzymes)
- causes NT molecules to leak from vesicles and be destroyed by degrading enzymes
- block release of NT from terminal buttons
- activates autoreceptors and inhibits NT release
- postsynaptic receptor blocker

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2
Q

what is the presentation and diagnostic criteria of dementia

A
  • significant cognitive decline from prior level in one or more cognitive domains (complex attention, executive functioning, learning and memory, language, perceptual-motor or social cognition)
  • interfere with independence in everyday activities
  • cognitive deficits do not occur exclusively in the context of delirium
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3
Q

what are the manifestations of dementia

A

early-stage
cognition
- poor short term memory
- word finding difficulties

psychological
- apathy
- depressive

behavioral
- social withdrawal
- disinhibition

sleep
- rapid eye movement behavior disorder

physical
- gait impairment

later-stage
cognition
- memory loss in working memory
- more marked expressive difficulties

psychological
- delusions
- anosognosia (lack of awareness of own condition)

behavior
- aggression
- hallucination
- wandering

sleep
- altered sleep-wake cycle

physical
- repetitive purposeless movements
- parkinsonism (stooped posture, short stride, unsteady gait, rigidity)
- seizures

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4
Q

what are the types of dementia and how would you differentiate them based on pathologic characteristics, onset and course, and history, examination and cognitive features in early stage

A
  1. alzheimer’s disease
    - brain atrophy
    - senile plaques of beta-amyloid protein
    - neurofibrillary tangles of phosphorylated tau proteins
    - slow onset, gradual progression over months or years
    - often first presented as short term memory loss
    - presence of episodic memory impairment accompanied by other subtle cognitive deficits such as anomia and visuospatial problems
  2. vascular dementia
    - vascular lesions
    - temporal r/s between acute vascular event and onset of cognitive impairment, within mins or days, stepwise course
    - presents with vascular risk factors or prior stroke/ vascular event
    - focal neurologic deficits consistent with stroke
    - neuroimaging shows evidence of cerebrovascular disease such as infarcts or significant white matter changes
  3. lewy body dementia
    - brain atrophy
    - interneuronal lewy body inclusions containing alpha-synuclein, including in the neocortex
    - slow onset, gradual progressive over months or years, fluctuations in levels of alertness and cognition
    - RBD for years preceding cognitive impairment, visual and other hallucinations
    - marked visuospatial problems with relative preservation of memory, parkinsonism
  4. frontotemporal dementia
  5. mixed type
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5
Q

what are the risk factors of dementia

A

non-modifiable
- age
- female
- ethinicity: black, hispanic
- genetics: APOE4 gene

modifiable
- HTN
- DM
- binge drinking
- smoking
- limited physical activities
- obesity
- hearing loss
- depression

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6
Q

how is dementia clinically evaluated

A
  • medical hx (neuro, general, family)
  • physical exam (neuro signs - cognitive impairment, parkinsonism, focal signs; pertinent systemic - for vascular and metabolic diseases)
  • neuropsychological testing (MMSE, MoCA)
  • lab testing (thyroid, vitB12, others as indicated for metabolic, infectious, autoimmune etc)
  • structural brain imaging
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7
Q

what is the pathophysiology of alzheimer’s

A
  1. senile plaques of beta amyloid proteins
    - extracellular deposits
    - involves proteolytic cleavage of larger amyloid precursor protein via action of beta and gamma secretases resulting in fragments that gather together which some are large and insoluble, accumulating to form these plaques (5%)
    - alternative pathway precludes formation of Abeta (>95%)
  2. neurofibrillary tangles
    - tau proteins that become hyperphosphorylated leading to aggregation and formation of insoluble paired helical filaments
    - tau is a tubulin associated protein needed for microtuble stabilization and intracellular transport
    - insoluble filaments twist to form tangles
    - located within cell body of neurons, particularly in hippocampus and cortex
  3. brain atrophy
    - in areas critical to cognition (hippocampus, neocortex)
  4. neuronal death
    - results in neurochemical deficits and alterations
    - lead to cognitive decline and neuropsychiatric behaviors
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8
Q

what are the goals of therapy for alzheimer’s disease

A
  • slowing progression
  • delay the need to institutionalize
  • improve QoL for patients and caregivers
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9
Q

what is the pharmacological management of alzheimer’s disease

A

acetylcholinesterase inhibitors (AI)
- donepazil (avail 5,10mg; start 5mg OD x6w f/b 10mg OD)
- rivastigmine (avail as capsules and 4.6,9.5,13.3mg/24hr patches; start 4.6mg/24hrs x4w f/b 9.5mg/24hrs for at least 4w)
- galantamine (avail as 8,16,24mg; start 8mg OD x4w f/b 16mg OD for at least 4w)

NMDA receptor angtagonist
- memantine (avail as 10mg; start 5mg OD x1w f/b 5mg BD for at least 1w f/b 5mg OD 10mg ON for at least 1w f/b 10mg BD)

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10
Q

what are the indications for the each agent

A
  • donepazil for all stages
  • rivastigmine for mild to moderate
  • galantamine for mild to moderate
  • memantine for moderate to severe, and unable to tolerate AI
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11
Q

what is the moa of AI

A

inhibit acetylcholinesterase enzyme to promote a relative increase in acetylcholine abundance within the synaptic cleft for cholinergic neurotransmission

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12
Q

what is the moa of NMDA receptor antagonist

A

inhibit NMDA type of glutamate receptors to decrease excitoxicity and restore normal balance of neurotransmission and protect neurons from further damage (excessive glutamate activity can cause excitotoxicity that damages neurons)

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13
Q

what are the s/e, c/i and caution of AI

A

common s/e
- N/V, loss of appetite (counsel to take after food)
- insomnia
- vivid dreams
- increase frequency of bowel movements

c/i
- bradycardia

caution
- PUD
- seizure
- respiratory disease
- urinary tract obstruction

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14
Q

what are the s/e, c/i and caution of NMDA receptor antagonists

A

common s/e
- HA, constipation (common)
- dizziness
- confusion

caution
- CVD
- seizure
- severe R/H impairment

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15
Q

what are the non-pharmacological management of alzheimer’s

A
  • cognitively stimulating activities (eg. reading and games)
  • physical exercise
  • social interaction with others
  • proper personal hygiene
  • adequate sleep quality and quantity
  • healthy diet
  • safety inside the home and outside
  • financial planning
  • long term healthcare planning
  • medical and advanced care planning
  • effective communication (eg. visual aids)
  • psychological health (meaningful activities)
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16
Q

what is BPSD

A

behavioral and psychological symptoms (BPSD) is a spectrum of non-cognitive and non-neurological symptoms of dementia

is often the way patient is trying to communicate

17
Q

what are the types of BPSD

A

agitation and aggression
- verbal or physical
- may be due to unmet needs or perceived threat or violation of personal space, boredom or discomfort thus make environmental modifications
- music therapy

depression
- more common in early stages
- present as sadness, tearfulness, inactivity, fatigue, social withdrawal, pessimistic thoughts
- manage by exercise, social connection and engaging activities, CBT
- more severe depression requires clinician input

apathy
- more frequently in vascular, frontotemporal and lewy body
- present as lack of initiative, motivation and drive, aimlessness and reduced emotional response
- manage by reading to the person and encouraging them to ask small questions, music therapy, exercise and multi-sensory stimulation

anxiety
- may present as exaggerated response to separation from family or unable to make sense of environment especially in later stages of dementia
- focus on identifying and eliminating trigger
- maintain structure and routine and reduce the need for stressful decision making
- music and CBT

psychotic symptoms
- hallucinations reflecting memory loss or perception changes
- vivid visual hallucinations common esp in lewy body
- potentially reversible causes include delirium, sensory or vision loss, over-stimulation, substance misuse, initiation of new medication
- manage by confirming patient’s claim not occurring and use memory aids to cue the person back to reality or through distraction

wandering
- may be circular, between two points, random or direct to a location
- can have positive effects through exercise, leading to improved sleep, mood and general health and let the elderly feel less confined
- consider how to make wandering safe

nocturnal disruptions
- likely secondary to depression, anxiety, pain, agitation etc
- more frequently in lewy body
- address underlying cause and adopt proper sleep hygiene

18
Q

what are some factors that may be contributing to BPSD

A

medical
- depression
- anxiety
- delirium (due to infection, metabolic disturbances, medication toxicity, withdrawal)
- untreated pain
- infection
- dehydration or hyponatremia
- constipation or urinary retention
- fatigue
- hearing or visual impairment

pharmacological
- anticholinergic action
- ASM
- systemic corticosteroids
- sedatives (opioids, BZP, Z-drugs)
- antiPD

social or environment
- unfamiliar environment
- family separation
- noise
- crowding
- lack of privacy
- difficulty finding facilities
- difficulty accessing outdoors
- lack of space to move around
- perceived lack of security
- glare from sunlight or artificial lighting or poor lighting
- under or overstimulation
- withdrawal from alcohol or another drug
- loneliness
- difficult r/s with carer, family member or another resident in care

19
Q

what are the key concepts and the pharmacological management for BPSD

A

key concepts
- target behavior
- only if potentially reversible causes have been excluded and non-pharmacological management trialed, plus immediate risk to patient or others or patient is severely distressed
- review at least q3m and routinely withdrawn

pharmacological management
- SSRIs for depression and anxiety (citalopram but consider dose-dependent risk of QTc prolongation and worsening cognition)
- TCAs avoided as anticholinergic may further disrupt cognition
- antipsychotics can help for aggression, agitation or psychotic symptoms but note increased risk of mortality and stroke associated, and is not beneficial for wandering, calling out, social withdrawal

20
Q

what are the care coordination community resources

A
  • integrated northern dementia care system (yishun dementia-friendly community, CARTIAS network)
  • nursing homes and day care center (orange valley)
  • caregiver support services (dementia singapore)

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