Dementia Flashcards

1
Q

Definition of Dementia

A
  • category of degenerative brain diseases:
  • deteriorate cognition/affect/behavioural functions
  • severe enough to impede daily functioning
  • represent a decline from previous function
  • worse than expected from normal aging
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2
Q

Major Neurocognitive Disorder

A
  • DSM5, psych equivalent of dementia
  1. significant cognitive decline in one or more domains, based on concerns and impairment on testing
  2. interferes with independence and social functioning
  3. not exclusively in the context of delirium
  4. not better explained by another disorder
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3
Q

What are the six cognitive domains?
- how to test
- areas of brain

A
  1. Complex attention –> focus on task despite distraction, working memory, processing speed
    - test with serial 7s
    - mainly frontal lobes, also parietal
  2. Executive Functioning –> planning, correcting, inhibition, mental flexibility, goal-oriented tasks
    - test by copying shapes
    - mainly frontal lobes
  3. Learning and Memory –> visual and verbal memory, semantic and episodic memory, short and longterm
    - test with recall and recounting events
    - mainly temporal lobes
  4. Language –> motor (syntax, fluency, word-finding, writing) is dominant frontal lobe
    –> sensory (comprehension, reading) is dominant temporal and parietal lobes
    - test with yes/no questions, commands, complex syntax
  5. Perceptual-Motor –> gnosis (recognizing), copying drawings is occipital-temporal lobes
    –> praxis (gestures, using tools), construction is frontal-parietal lobes
    - test with clock drawing
  6. Social Cognition –> appropriate behaviour, consistent decisions, understanding emotions
    - frontal lobes
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4
Q

Gold standard for assessing dementia?

A
  • Neuropsychological assessment, but this is often difficult to access so MMSE, MoCA
  • Substantial impairment is considered at least 2SD below average
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5
Q

MMSE

A
  • widely used and understood
  • not well balanced (no executive functioning, tests lower end of functioning)
  • really only for alzheimer’s
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6
Q

ADLs vs IADLs

A

ADLs –> Dressing, Eating, Ambulating, Toileting, Hygiene (DEATH)

IADLs –> Shopping, Housekeeping, Accounting, Food Prep, Transport/Telephone, Medications (SHAFT-M)

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7
Q

How to determine functional impairment?

A
  • collateral information
  • questionnaires (disability assessment for dementia)
  • make house calls, OT/nursing
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8
Q

Mild Neurocognitive Disorder (mild cognitive impairment)

A
  • symptoms of dementia are present but no functional impairment
  • often precursor of major neurocognitive disorder
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9
Q

Delirium

A
  • usually an underlying cause
  • symptoms develop and fluctuate rapidly
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10
Q

Alzheimer’s

A
  • meets dementia criteria AND:
  • insidious (gradual onset)
  • clear cut history of worsening condition
  • initial and most prominent deficits are amnesia, impaired learning and recall
  • evidence of dysfunction in at least one other domain
  • can be atypical (language, visuospatial, executive)
  • most common cause of dementia in older adults
  • rare before 50
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11
Q

Physical Changes Seen in Alzheimer’s

A
  • neuritic senile amyloid plaques (amyloid beta specific to AD, deposits of fibrillar protein aggregates), central amyloid core surrounded by dystrophic neurites, affects neocortex the most
  • neurofibrillary tangles (hyperphosphorylated tau protein) - can be seen in other diseases
  • neuropil threads
  • mesial temporal lobes (memory) have greatest tangle pathology (hippocampus)
  • cortical atrophy most pronounced in frontal/temporal/ parietal on MRI
  • medial temporal lobe and limbic system affected early and severely (memory)
  • nucleus basalis of Meynert affected –> main cholinergic nucleus in the CNS, thought to modulate attention/learning/longterm memory
  • relative preservation of grey matter and the brainstem (motor issues are rare)
  • amyloid beta can also deposit in leptomeningeal and superficial cortical vessels (not specific to AD, can cause hemorrhages in elderly)
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12
Q

Vascular Dementia

A
  • clinical and imaging features suggest vascular contribution –> onset of deficits correlate with cerebrovascular events and/or a decline in complex attention and executive function
  • rare by itself
  • i.e. frontal subcortical dementia (frontal lobe and basal ganglia infarcts)
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13
Q

What are dementias associated with Parkinson’s? What are typical symptoms?

A
  • Lewy Body dementia, PD dementia, other rare syndromes
  • extrapyramidal symptoms –> tremor, bradykinesia, rigidity, gait shuffle/ stoop, postural instability
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14
Q

Lewy Body Dementia
- including physical brain changes

A
  • 2 of:
  • one or more features of PD
  • visual hallucinations
  • REM sleep behaviour disorder
  • fluctuating cognition with variation in attention and alertness
  • Supportive: falls, ANS dysfunction, hypersomnia, anosmia, delusions, sensitivity to antipsychotics, apathy
  • substantia nigra degeneration
  • classical LBs (brainstem) and cortical LBs, lewy neurites
  • variable atrophy
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15
Q

PD Dementia

A
  • most patients with PD eventually develop dementia
  • basically identical to Lewy Body dementia, but the PD motor symptoms start at least 1 year before the onset of cognitive impairment
  • some have more frontal-subcortical symptoms (complex attention, processing speed, executive functioning) –> less hallucinations and no fluctuations
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16
Q

Behavioural Variant Frontotemporal Dementia

A
  • dysfunction of salience network –> social cognitive function
  • atrophy of frontal lobe seen on imaging
  • mostly TDP-43 and tau
  • progressive decline in behaviour/cognition and at least 3 of:
  • behavioural disinhibition
  • apathy or inertia
  • loss of sympathy/ empathy
  • perseverative, stereotyped, compulsive, ritualistic behaviour
  • hyperorality, dietary changes
  • decline in executive function with relative sparing of memory and visuospatial functions
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17
Q

Primary Progressive Aphasia (Frontotemporal Dementia)
- 3 subtypes

A
  • dysfunction of language networks
  • atrophy of frontal and temporal regions on MRI
  • mostly TDP-43 and tau
  • all 3 of:
  • most prominent decline is language
  • deficits are main cause of decline in ADLs
  • aphasia is most prominent early on
  • cannot have ANY of:
  • prominent initial memory/ visuospatial/behavioural disturbances
  • agrammatic/nonfluent –> halting, errors, effortful, inconsistent
  • semantic –> no comprehension of single words, trouble naming objects
  • logopenic –> word-finding, repetition (often a language variant of alzheimer’s)
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18
Q

Neurodegenerative Disease

A
  • slowly progressive dementia
  • unknown cause, can be sporadic or inherited
  • atrophy, neuron loss, gliosis, microglial activation, degeneration of white matter tracts, protein deposits, cellular inclusions
  • classified by the type of abnormal protein
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19
Q

Amyloid beta Hypothesis of AD

A
  • is the primary cause of dementia accumulation of abeta or tau?
  • some tau pathologies without ab don’t lead to AD
  • ab needed for tangles to spread to the cortex
  • ApoE4 increases ab
  • ab is neurotoxic, cause inflammation from microglia and astrocytes
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20
Q

ApoE

A
  • ApoE on Ch.19 increases risk of AD
  • E4 specifically increases risk and lowers age of onset
  • increases abeta but also exacerbates tau neurodegeneration
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21
Q

Specific Tests for AD

A
  • decreased AB42/AB40 in CSF
  • increased tau/p-tau in CSF
  • increased p-tau181 in plasma
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22
Q

Treatments for AD

A
  • cholinesterase inhibitors
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23
Q

Most common dementia presentation?

A
  • AD + vascular + other degenerative cause
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24
Q

What is normal sleep?

A
  • latency under 30m
  • brief arousals under 10s
  • brief awakenings under 30m total
  • total time 6-8h (less with age)
  • no daytime sleepiness

*sleep good for GH secretion, preventing infection, restoration via glymphatic system

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25
Q

Sleep Stages

A

1 –> 5% total sleep time, light sleep, transitional, if too much it can lead to sleep disruption

2 –> 50% total sleep time, medium sleep

3 –> 15-20% total sleep time, deep sleep, hard to awaken and sleep inertia when done so, NREM parasomnias (sleep walking/talking/terrors/confusional arousals)
- most restorative
- impaired by benzos, maintained by zopiclone and zolpidem

REM –> dreams, tonic (voluntary muscle atonia) and phasic stages (REM, twitching of voluntary muscles)

*measured by a hypnogram

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26
Q

Level 1 Sleep Study

A
  • EEG, EOG, ECG, EMG, airflow (nasal), respiratory effort (chest and abdo belts), digital oximetry
  • useful for diagnosing sleep apnea, NREM/REM parasomnias, periodic limb movement disorder
  • gives info on arousals and time in each stage
  • muscle tone (EMG) should decrease with sleep depth and be mostly absent in REM
27
Q

Level 3 (Home) Sleep Study

A
  • only useful for sleep apnea, no info on sleep stages
  • airflow, respiratory effort, digital oximetry, body position
28
Q

Changes in sleep with age

A
  • rarely get past stage II
  • shorter time asleep, shorter cycles
  • exercise less, longer periods in quiet rest
  • relative advance of sleep phase, more brief awakenings, more insomnia, unpleasant dreams
29
Q

Insomnia
- criteria
- tx

A
  • chronic in 10% of adults
  • associated with alcoholism, smoking, depression
  • daytime effects –> anticipatory anxiety –> hyperarousal –> stressors, etc.
  • increases risk of MVCs
  • dissatisfaction with sleep quantity or quality and at least one of:
  • difficulty initiating sleep
  • difficulty maintaining sleep
  • early-morning awakening
  • occurs at least 3 nights a week, present for 3 months
  • occurs despite adequate opportunity for sleep
  • causes distress and impairment
  • CBT* is best treatment, meds, herbals, hypnosis
    *wind down an hour before, don’t go to bed until sleepy, use bed only for sleep and sex, consistent wake time, decrease time in bed by 15m (sleep compression)
30
Q

Sedative and Hypnotic use for sleep
- alternatives?

A
  • concerns with carry-over effects, drug-drug interactions, dependence and tolerance (increases with dose and duration), falls, memory
  • use lowest dose for shortest period of time
  • take PRN, not nightly
  • treatment should not exceed 7-10 consecutive days
  • Z drugs (zopiclone and zolpidem) can cause anterograde amnesia and somnambulance
  • hypnotics are generally contraindicated in the elderly
  • low dose doxepin is well-tolerated, under 6mg can be appropriate for elderly but only helpful in 50% of pts
  • lemborexant another option
31
Q

Obstructive Sleep Apnea

A
  • unintentional sleep episodes, daytime sleepiness, unrefreshing sleep, fatigue, insomnia AND/OR
  • waking with breath holding, gasping, choking AND/OR
  • snoring, breathing interruptions
  • polysomnography shows 5+ respiratory events per hour and respiratory effort during each events OR
  • polysomnography shows 15+ respiratory events and respiratory effort during each event
  • will still have gauge strain (respiratory efforts persist)
  • apnea –> cessation of airflow for at least 10 seconds
  • hypopnea –> decrease in airflow for at least 10 seconds

*get evaluated (level 1 or 3) if symptomatic

32
Q

Central Sleep Apnea
-tx

A
  • apneas and hypopneas occur, but without respiratory effort
  • similar day time sx of OSA
  • usually a history of heart disease, stroke, opioid use
  • treat the underlying cause, BiPAP when necessary
33
Q

General Sleep Apnea Symptoms

A
  • Night –> snoring, pauses in breathing, choking, restlessness, frequent urination, sweating, acid reflux
  • Day –> fatigue, morning headaches, poor concentration, decreased libido and attention, irritability
  • scalloped tongue
  • Mallampati score –> how open airway is (IV is high risk)
34
Q

Features that increase risk of obstructive sleep apnea

A
  • overweight
  • neck circumference over 16/17 inches
  • macroglossia
  • dental overjet, retrognathia (recessed chin)
  • high and narrow hard palate
  • elongated and low lying uvula
  • enlarged tonsils and adenoids
35
Q

Consequences of Obstructive Sleep Apnea

A
  • increased MVC risk
  • hypertension
  • stroke
  • heart disease
  • DM control
  • fatigue, irritability
36
Q

Treatment for Obstructive Sleep Apnea

A
  • CPAP (continuous positive airway pressure) is most reliable, persistance and a fitted mask are key
  • mandibular advancement splint for mild/mod, less reliable and can shift teeth
  • tongue stabilizing device for mild/mod, difficult to fit but cheap and affordable
  • weight loss, don’t sleep on back, avoid alcohol/benzos/opioids near bed time
37
Q

Narcolepsy
- type 1 vs 2
- sx

A

type 1 –> cataplexy
type 2 –> without cataplexy (10-50%)
- onset between 15-25, cataplexy within a year

  • unwanted sleep episodes several times a day that can last minutes to hours
  • excessive daytime sleepiness
  • cataplexy –> muscle weakness associated with emotion, respiratory muscles not involved, usually a few seconds to minutes
  • sleep paralysis –> scary experience at sleep onset or awakening, unable to move or speak, regain muscle control in seconds to minutes
  • hypnagogic hallucinations –> visual hallucinations at sleep onset or awakening, sometimes auditory or tactile
  • sleep disruption –> repeated awakenings, scary dreams, periodic leg movements, REM sleep behaviour disorder is common
38
Q

Pathophysiology of narcolepsy

A
  • deficiency in hypothalamic peptide hypocretin (orexin)
  • can be assessed by CSF hypocretin-1 level
39
Q

Diagnosis and Treatment of Narcolepsy

A

Dx –> excessive daytime sleepiness for over 3 months
- cataplexy
- MSLT showing mean sleep latency under 8minutes and 2 or more sleep-onset REM periods (or REM onset under 15 min may replace one of these)

  • investigate with PSG followed by MSLT (4/5 20 min nap opportunities, if sleep begins give 15 minutes to reach REM)
  • some may have latency over 8 minutes so consider Hx

Tx –> modanifil and methylphenidate/ dextroamphetamine (increase NE/DA) for wakefulness
- antidepressants (venlafaxine) and stimulants (atomoxetine) for cataplexy
- sodium oxybate (GHB) for both (decreases DA, GABA-b agonist, VERYYYYYYY expensive, abuse potential)

40
Q

Restless Leg Syndrome
- causes
- dx
- tx

A
  • urge to move limbs due to dys/parasthesias
  • worse at rest and at night, temporary relief with activity
  • most also have periodic limb movement disorder, but the reverse is not true
  • genetic component
  • pregnancy, ESRD, iron deficiency (ferritin under 50), sedating antihistamines, DA antagonists, most antidepressants (except bupropion aka Wellbutrin)
  • clinical DX but can use Standardized Immobilization Test
  • treat underlying cause
  • gabapentin, pregabalin, DA agonists, clonazepam, opioids if refractory
41
Q

Periodic Limb Movement Disorders
- tx

A
  • EMG shows repetitive highly stereotyped limb movements
  • inter movement interval of 5-90 seconds, %+/hr for kids, 15+/hr for adults
  • daytime fatigue, sleep disturbance
  • treat only if affecting life, same treatment as RLS
42
Q

NREM Parasomnias

A
  • sleep walking, sleep terrors, confusional arousals, sexsomnia
  • confusion after arousal from slow wave sleep antero/retrograde amnesia, inappropriate or violent behaviour
  • genetics, shift work, stress, anxiety, mood disorders, other sleep disorders, not enough sleep, alcohol, psychotropics
  • treatment –> manage stress, consistent sleep schedule
  • melatonin, low dose clonazepam, maybe cannabis
43
Q

REM Sleep Behaviour Disorder

A
  • REM without atonia
  • injurious hazardous behaviours and abnormal behaviours documented during PSG
  • absence of EEG epileptiform activity in REM
  • dream enactment about 90 mins in, ends quickly upon awakening
  • sleepwalking is uncommon
  • mostly male, 50+, commonly develop PD, LBD, MSA

risks –> alpha-synucleopathies (PD, LBD, MSA), narcolepsy, stroke, SSRIs, mirtazapine, venlafaxine, med withdrawal

tx –> safety! sleeping bag, partner in other bed
- melatonin, clonazepam

44
Q

Emmetria
Myopia
Hyperopia
Astigmatism

A
  • normal
  • nearsightedness, treat with concave lens (minus)
  • farsightedness, treat with convex (magnify)
  • refractive powers in diff axes (football)
45
Q

Accomodation
Presbyopia

A
  • ability of the ciliary muscle to contract, making the lens more convex
  • with age the lens loses its ability to accomodate, decreases ability to see near objects but distance vision is unchanged
  • treat with plus lenses
46
Q

Cataracts
-dx
-tx

A
  • opacity or discolouration of the lens affecting vision, can be subcapsular, cortical, or nuclear
  • issues in dim/ bright light, halos and glare, monocular diplopia
  • increase in myopia (better near vision) due to increase in refractive power of denser lens nucleus
  • no pupillary signs
  • secondary to aging most commonly, congenital, trauma, systemic disease, meds , radiation
  • dx on eye exam
  • tx with correcting refractive error, cataract surgery if symptomatic and vision <20/50 or disabling
47
Q

Vitreous
- posterior detachment?
- dx
- tx

A
  • transparent CT in the posterior chamber
  • connections to posterior lens, optic nerve and retina
  • liquifies with age and can collapse and detach from these structures
  • gradual symptoms usually mild
  • if sudden can lead to tear, floaters/flashes, hemorrhage
  • vision should be preserved, no pupillary findings
  • risk if 60+, myopia, trauma, cataract surgery, inflammation

dx - dilated fundus exam to r/o tear/detachment
tx - should subside in months, follow up if worsening symptoms and repeat exam

48
Q

Glaucoma
- open
- closed
-treatment

A
  • umbrella term, progressive neuropathy and loss of visual fields, decrease in vision is irreversible but often preventable
  • damage to optic nerve, central usually preserved until late
  • open –>insidious, painless, slow progressing
  • constricted visual fields, cupping, hemorrhage, maybe RAPD or increased IOP
  • risks –> old, increased IOP most important
  • dx –> optic nerve and visual fields
  • closed –> sudden onset, painful, nausea, halos, decreased vision
  • very increased IOP, fixed mid-dilated pupil, low visual acuity, red conjunctiva, tearing, hazy cornea
  • risks –> inuit, asian, hyperopia, old, female
  • dx –> IOP, neuropathy, exam findings

Tx –> topical agents to decrease IOP (latanoprost - prostaglandin analogue that increases outflow)
- laser, surgeries

49
Q

Age Related Macular Degeneration
- dry
- wet

A
  • bilateral incurable acquired disease
  • # 1 cause of irreversible central vision loss in elderly
  • dry –> most common, slowly progressive, less visual impairment, drusen (lipid rich material), atrophic pigment changes
  • wet –> rapidly progressive, significant central vision loss, macular hemorrhage, macular edema, choroidal neovascular membrane

risks –> old, female, light coloured iris, smoking, hypertn, familial

sx –> blurred vision, distortion, metamorphosia, scotoma
dx –> macular exam, tomography scanning, IV fluorescin angiogram
tx –> dry –> no smoking, lower htn, leafy greens, uv protection, vitamin C/E/zinc/Cu/lutein, vision aids
–> wet –> same + introcular injections of anti-VEGF

50
Q

Driving Vision Standards

A

> 20/50 with both eyes open together
120 horizontal and 15+/- vertical fields
physicians must report if someone unsafe to drive

51
Q

Risk factors for dementia

A

early –> low education
mid –> hearing loss, TBI, HTN, EtOH, obesity
late –> smoking, depression, social isolation, physical inactivity, pollution, DM

  • see preserved and increased hippocampal volumes with exercise
52
Q

Cognitive Stimulation Therapy

A
  • reminiscence, stimulation, reality orientation, stimulating language, implicit teaching
  • helps maintain functioning, most benefit for mild/mod dementia
53
Q

BPSD
- pharm and non pharm treatment

A
  • aggression, agitation, restlessness, anxiety, depression, psychosis, sleep disturbances, sundowning
  • symptoms, not a diagnosis
  • give structure, calming activities (massage, art, music, walks, pets, light therapy) TREAT WITHOUT MEDS FIRST, deflect, redirect, avoid triggers
  • may need to treat pain
  • path –> NT changes, environmental triggers, communication challenges
  • cognitive enhancers
  • antipsychotics (risperidone, quietiapine has decreased efficacy, sedation, may be safer) –> metabolic syndrome, extrapyramidal sx (only give quietia if PD/LBD), falls, sedation, INCREASED RISK OF STROKE AND DEATH)
  • antidepressants (SSRIs, SNRIs venlafaxine, NDRIs buproprion, mirtazapine/ trazodone good for sleep)
  • anticonvulsants –> no valproates, carbemazapine
54
Q

PIECES (things to consider for dementia? BPSD?)

A

Physical (delirium, disability)
Intellectual (amnesia, apathy)
Emotional (mood, adjustment disorder)
Capabilities (ADLs, IADLs)
Environment (stimulation, routine)
Social (network)

55
Q

Cholinergic Hypothesis of AD

A
  • cholinergic neurons affected early in AD (especially nucleus basalis of Meynert)
  • cholinergic projections involved in complex attention, working/episodic/spatial memory (affected in PD, LBD)
    -anti-cholinergic drugs impair cognition
56
Q

Cholinesterase Inhibitors

A
  • Donepizil
  • main AD treatment
  • consistent shorterm, small mean effect, doesn’t alter natural history
  • start 5mg, target is 10mg
  • some will respond others won’t, try for 6 months, s/e should show up early

S/E –> GI, anorexia, vivid dreams, cramps, BRADYCARDIA, SYNCOPE
CI –> severe COPD and asthma, PUD, severe bradycardia

  • covered if MMSE 10-26
57
Q

Memantine

A
  • non-competitive NMDA-R antagonist
  • blocks pathological activation of NMDA receptors that would otherwise lead to neurodegeneration and impair neurotransmission and the plastic process
  • ONLY for mod/severe
  • start 5mg, target is 10mg BID (20mg)

S/E –> headache, dizzy, constipation, confusion
- not covered

58
Q

Disease Modifying Therapies

A
  • none approved in Canada
  • acducanumab and lecanumab
  • expensive, lack of evidence, can cause hemorhhages
  • both anti-amyloid Abs
59
Q

Frailty Scale

A
  • 1 very fit
  • 4 vulnerable
  • 5 mild (high order IADLs)
  • 6 moderate (outside, housekeeping, bathing)
  • 7 severe (everything)
  • 8 very severe
  • 9 terminal
60
Q

Vaccines

A
  • herpes zoster (shingrix and zostavax)
  • pneumovax 23 free 65+ LTC (prevnar 13 given if HIV, transplant, routine in childhood)
  • flu vaccine free if 65+ in LTC
  • less effective in elderly in general
61
Q

Delirium

A
  • awareness and attention are disturbed
  • short development, acute change, fluctuating
  • additional disturbance (memoru, language, perception, etc.)
  • not better explained…
  • direct consequence of a specific etiology (DIMS, I WATCH DEATH)
  • only lasts hours/ weeks
  • neuroinflamm, oxidative stress, NT deficiency, neuroendocrine, diurnal dysregulation, network disconnection, neuronal aging
  • CXR, neuroimaging, EEG
  • common causes –> opiates (morphine worst, oxycodone best), benzos, z-drugs
  • treat environmentally –> re-orientation, cognitive stimualtion, sleep inducing stimuli, exercise, auditory and visual aids, treat dehydration
  • restraints as last resort, give both physical and chemical
  • ANTIPSYCHOTICS –> HALDOL (high d2, low sedation)
  • even gravol can cause
62
Q

Hyper vs hypoactive

A

hyper –> disorientation, agitation, hallucinations
hypo –> sleep wake distrubances, fluctuation, imapired attention, acute

  • similar to depression –> psychomotor poverty, amotivation, sleep disturbances, flat affect
63
Q

alcohol withdrawl

A
  • seizures, hallucinations, delirium tremors
  • can overtreat wiht benzos