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Dementia and delirium Flashcards

1
Q

What is dementia?

A
  • major neurocognitive disorder
  • term used to describe a cluster of sxs including:
    forgetfulness (progressive)
    difficulty doing familiar tasks
    confusion
    poor judgement
    decline in intellectual fxning

*dementia isn’t part of normal aging

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2
Q

Dx criteria for dementia?

A

sig cognitive impairment in at least one of the following cognitive domains:

  • learning and memory
  • language
  • executive fxn
  • complex attention
  • perceptual motor fxn
  • social cognition
  • the impairment must be acquired and represent a significant decline from a previous level of fxning
  • cognitive deficits must interfere with independence in everday activities
  • cog. deficits result in fxnl impairment (social/occupational)
  • cognitive deficits don’t occur exclusively solely during a delirium
  • not due to other medical or psychiatric conditions
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3
Q

Causes of dementia?

A
  • alzhemier’s disease (approx 70%)
  • vascular dementia (strokes, TIAs)
  • parkinson’s
  • frontotemporal dementia (FTD)
  • normal pressure hydrocephalus (NPH)
  • dementia with lewy bodies
  • delirium/depression
  • other, less common causes
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4
Q

What are modifiable causes of dementia?

A
  • meds (anticholinergics): link b/t long-term use of otc anticholinergics like diphenhydramine and dementia
  • alcohol
  • metabolic (B12, thyroid, hyponatremia, hypercalcemia, hepatic and renal dysfxn)
  • depression - severe
  • CNS neoplasms, chronic subdural hematoma
  • NPH
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5
Q

What is Alzheimer’s disease?

A
  • progressive neuro disorder that results in memory loss, personality changes, global cognitive dysfunction, and fxnl impairments
  • loss of short term memory most prominent early***
  • most common form of dementia in elderly (60-80% of cases)
  • est to affect more than 4 mill Americans
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6
Q

Dx of alzheimers?

A
  • dx of exclusion
    sxs and behaviors:
  • short term memory loss (early)
  • long term memory loss preserved until late
  • poor judgement and indecisiveness (early)
  • disorientation/inability to adapt new environments
  • personality change and disinhibition
  • communication disorders: comprehension and expression
  • demanding and repetitive behaviors (early to mid)
  • behavior changes with aggression, delusions, and hallucinations
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7
Q

AD dx?

A

clinical dx:

  • thorough detailed hx
  • mental status eval
  • depression screen
  • physical exam, underlying vision and hearing screen
  • limited lab testing
  • neuroimaging
  • more extensive neuropsychological testing
  • an MRI finding of hippocampal atrophy suggest AD, but not specific or sensitive
  • lab testing includes CBC, CMP, serum B12, and TSH
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8
Q

Assessment of AD - MMSE score, what do these scores mean? What score is suggestive of dementia?

A
  • 20-26 mild fxnl dependence
  • 10-20 moderate, more immediate dependence
  • score: less than 10 - severe, total dependence
  • 24/30 suggestive of dementia, not sensitive for mild cognitive impairment
  • results affected by educational level, low SES, language skills, literacy, impaired vision/hearing
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9
Q

Addition eval of AD?

A
  • short assessments with good validity: 3 items recall and clock face
  • neuro exam (focality, frontal release signs such as grasp, apraxia, cogwheeling, eye movements)
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10
Q

pathology of AD? Hallmarks?

A
  • 3 consistent neuropathological hallmarks:
    amyloid-rich senile plaques
    neurofibrillary tangles
    neuronal degeneration
  • these changes eventually lead to clinical sxs, but they begin years b/f the onset of sxs
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11
Q

Dx AD - possible AD?

A
  • deficit in only 1 area of cognition
  • atypical course
  • other dementia causes present
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12
Q

Dx AD - probable AD?

A
  • deficits in 2 or more areas of cognition
  • onset 40-90 (usually older than 65), progressive course
  • other causes excluded
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13
Q

Dx AD - definite AD?

A
  • histopathological evidence (requires autopsy)

- course and exam characterist of AD

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14
Q

Dx Ad - unlikely AD?

A
  • sudden onset
  • focal signs
  • seizures or gait disturbances early in course
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15
Q

7 stages of AD - stage 1?

A
  • normal:
    pt may potentially be free of objective or subjective sxs of cognition and fxnl decline and also free of assocd behavioral and mood changes
  • pathology has already begun
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16
Q

Stage 2 of AD?

A
  • normal aged forgetfulness
  • half or more pop over 65 - experience subjective complaints of cog and/or fxnl difficulties. Nature of these subjective complaints is characteristic
  • elderly persons with these sxs believe they can no longer recall names as well as they could 5-10 yrs previously
  • Also intermittently experience difficulties in concentration and in finding correct word when speaking
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17
Q

Stage 3 of AD?

A
  • mild cognitive impairment
  • persons at this stage manifest deficits which are subtle, but which are noted by persons who are in close contact such as:
    repeated questions,
    showing compromise in their ability to perform executive fxns, job performance may decline, hard to master new job skills
  • ex: grandma has hard time hosting family christmas
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18
Q

Stage 4 of AD?

A
  • mild alzheimer’s disease
  • dx of probable alzheimers disease can be made with considerable accuracy in this stage. The most common fxning deficit in these pts is a decreased ability to manage instrumental (complex) activities of daily life (hard to manage finances)
  • mean duration: 2 years
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19
Q

Stage 5 of AD?

A

moderate alzheimers disease:
deficits are of sufficient magnitude as to prevent catastrophe free, independent community survival
- Deficits in basic ADLs: inable to choose proper clothing for weather or just wear same outfit every day
- Can’t recall such major events and aspects of their current lives: presidnet, weather for that day, correct current address
- May not recall names of some of schools which they attended, hard to count backward from 20 by 2s

  • stage lasts: 1.5 years
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20
Q

stage 6 of AD?

A
  • moderately severe alzheimer’s disease:
    ability to perform basic ADLs becomes compromised Require assistance dressing
  • cognitive deficits: not be able to maintain living at home
  • lasts 2.5 years
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21
Q

stage 7 of AD?

A
  • severe AD
  • speech ability is limited to only few words, later all intelligible speech is essentially lost/ Ambulatory ability is lost, pt requires assistance
  • can’t even sit up
  • lasts 1 year, pts who surive subsequently lose ability to smile
  • only grimacing facial movements are observed in places of smiles. Will also lose ability to hold up their head
  • with approp care - pts can survvie in final stage for period of years
  • physical rigidity occurs due to immobility. Reflex changes become evident
  • Emergence of infantile or primitive reflexes (babinski)
  • Commonly die during this stage
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22
Q

Most common cause of death in AD?

A
  • aspiration pneumonia
  • also; infected decubital ulcerations
  • pts in 7th stage more vulnerable to stroke, heart disease, cancer
  • some pts just succumb to AD
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23
Q

AD tx?

A
  • no cure
  • pharm therapy to maintain and max. pt fxn
  • behavioral therapy: option to deal with behavioral issues that aren’t tx with medication
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24
Q

MOA of cholinesterase inhibitors?

A
  • curb breakdown of acetylcholine
  • help increase levels of acetylcholine in brain, this may slow progression of sxs for about 1/2 people taking them for about 6-12 months
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25
Q

Donepezil (Aricept)?

A
  • cholinesterase inhibitor
  • only tx approved by FDA for all stages of AD
  • well tolerated
  • qid dosing - hs
  • can improve neuropsychiatric sxs
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26
Q

Rivastigmine (Exelon)? Cholinesterase inhibitors

A
  • approved for use in mild to mod ADs and is available in skin patch, capsules, and liquid form
  • BID dosing for capsules and liquid, give with food
  • slow titration up of drug to help with SEs
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27
Q

Galantamine (Reminyl), Razadyne?
CIs?
SEs?
Cholinesterase inhibitors

A
  • approved for mild to mod AD and available as extended release capsule, immed release tablet, and liquid forms
  • BID dosing
  • CIs: severe renal and hepatic impairment
  • common SEs: usually mild, N/V/D, fatigue insomina, loss of appetite and wt loss
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28
Q

NMDA receptor antagonists - memantine (Namenda)?

SEs?

A
  • approved to tx mod-severe AD
  • may play protective role in brain by regulating activity of glutamate. GLutamate also plays role in learning and memory
  • brain cells in people with AD release too much glutamate. Namenda helps regulate glutamate activity
  • SEs: dizziness, confusion, hallucinations
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29
Q

Selegiline (Eldepryl)?

A
  • prevents breakdown of dopamine
  • not clearly shown to be helpful and has many SEs (dizziness, dry mouth, difficulty falling or staying asleep, muscle pain, rash, nausea, and constipation, severe HA, tachycardia, arrhythmia, hallucinations, chorea
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30
Q

Vitamin E?

SEs?

A
  • antioxidant properties
  • 1000 IU BID
  • SEs: weakness, hypercholesterolemia, bleeding
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31
Q

Use of antidepressants?What meds are recommended?

A
  • high incidence of depression in AD
  • sometimes diff to dx
  • SSRI’s recommended:
  • sertraline (zoloft) - max 200 mg/day
  • paroxetine (paxil) max 50 mg
  • citalopram (celexa) max 40 mg
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32
Q

Why are antipsychotics used in Dementia? Agents? SEs?

A
  • for hallucinations, delusions, aggression, hostility, and uncooperativeness
  • newer “atypical” agents:
    aripiprazole (abilify), olanzapine (zyprexa), quetiapine (seroquel)
  • atypical antipsych: sown an increased risk of sudden death, should only be used after discussion with pt’s internist or neurologist
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33
Q

Antiepileptics used in dementia?

A
  • depakote and gabapentin have limited roel in tx neuropsych sxs of dementia, and have no substantial studies
  • can be helpful in FTD
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34
Q

What drugs should be avoided in dementia pts?

A
  • benzodiazepines
  • antihistamines (can worsen sxs)
  • anticholinergics (worsen sxs)
  • all have limited value in pts with dementia
  • not recommended for management of neuropsych sxs of dementia, an can actually worsen sxs
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35
Q

Behavioral interventions in dementia pts?

A
  • steps to managing behaviors:
    1 - ID the behavior
    2 - understand the cause
    3 - adapt the pt’s enviro to remedy the situation
  • correctly ID what has triggered the sxs can help with selecting an approach
  • often triggers are: change in caregiver/living situations, travel, hospitalization, presence of houseguests, being asked to change
  • Rdirect pesron’s attention, rather than arguing, disagreeing or being confrontational. additional strategies:
    simplify environment, task, routine
  • allow adeq rest, use labesl to cue or remind person, use safety locks on doors, remove any dangerous object, control access to stove, use lighting to reduce confusion and restlessness at night
36
Q

What is vascular dementia?

A
  • onset of cognitives deficits assoc with CVA
  • abrupt onset of sxs followed by stepwise deterioration
  • findings on neuro exam consistent with prior strokes
  • infarcts on cerebral imaging
  • Cerebrovascular disease evident on hx, exam and or imaging along with onset of dementia within 3 months or abrupt, fluctuating or stepwise progression in dementia
37
Q

Overlap of dementia?

A
  • a lot of pts previously dx with alzheimers or vascular type dementia probably have both
  • Likelihood of both sig increases with age
  • vascular RFs to AD
38
Q

What is frontotemporal dementia?
Subtype?
Pathophys?

A
  • charactized by focal atrophy of the frontal and temporal lobes in absence of alzheimer pathology
  • subtype: pick’s disease first recog subtype
  • pathophys: by presence of pick bodies (silver staining intracytoplasmic inclusions) in the neocortex and hippocampus
39
Q

FTD occurence?

A
  • occurs b/t 35-75, only rarely after 75, mean: 60s
  • both sexes are equally affected
  • familial occurrence occurs in 20-40% of cases and may be assoc with variety of ID mutations in the tau gene on xsome 17
40
Q

Core features of FTD?

Supportive features?

A
  • insidious onset and gradual progression
  • early decline in social/interpersonal conduct
  • early impairment in personal conduct
  • early loss of insight
  • early emotional blunting
  • supportive:
    behavior disorder: hygiene, grooming, mental rigidity, dietary changes, persverative behavior
    speech and language: perseveration, mutism, economy of speech
    physical signs: akinesis, restlessness, rigidity, tremor, labile BP
41
Q

What is normal pressure hydropcephalus? Triad?

Tx?

A
  • condition of pathologically enlarged ventricular size with normal opening pressures on lumbar puncture
  • triad:
    dementia, gait disturbance, and urinary incontinence (wacky, wobbly, and wet)
  • tx: reversible with placement of ventriculoperitoneal shunt
42
Q

Dx NPH?

A
  • initially on neuroimaging, MRI better than CT

- miller fisher test: objective gait assessment before and after removal of 30 cc CSF

43
Q

Dementia with lewy bodies? (DLB)

A
  • most common dementia assoc with parkinsonism
  • 2nd most common form of neurodegen. dementia after AD
  • characterized by dementia accompanied by delirium, visual hallucinations, and parkinsonism. Other sxs include syncope, falls, sleep disorders and depression
44
Q

Dx DLB?

A
  • clinical dx:
    Main feature reqd: progressive cognitive decline of sufficient magnitude to interfere with normal social or occupational fxn
  • 2 of the following core features are essential for dx of probable DLB and one is essential for possible DLB:
    • fluctuating cognition with pronounced variations in attention and alertness
    • recurrent visual hallucinations that are typically well formed and detailed
    • spontaneous motor features of parkinsonism
45
Q

Supportive features for clinical dx of DLB?

A 
- features supportive of dx:
repeated falls
syncope
transient LOC
neuroleptic sensitivity 
systematized delusions
hallucinations in other modalities
46
Q

Cardinal motor features of Parkinson’s?

A
  • brady and akinesia
  • rigidity
  • resting tremor
  • postural instability
  • dementia typically occurs in last half of clinical course of PD, whereas it is often one of the presenting features of DLB
47
Q

RFs of dementia w/ parkinsons?

A
  • 78% incidence of dementia in PD
  • RFs:
    age over 70
    depression
    confusion/psychosis on levodopa
    facial masking upon presentation
  • hallucinations and delusions: may be exacerbated by tx
48
Q

What is progressive supranuclear palsy? (PSP)

A
  • steele richardson Olszewski syndrome
  • rare syndrome that can mimic PD in early phase
  • characteristic features: restricted up and down eye movement (***vertical gaze palsy): hallmark
    postural instability with unexplained falls
  • pts with PSP usually stand straight or occasionally even tilt heads backward (fall backward), while those with parkinson’s bend forward
49
Q

What is Creutzfeldt-Jacob disease?

A
  • Mad Cow disease
  • progressive and fatal: caused by prion, humans can contract disease by consuming material from animals infected with the bovine form of the disease
  • characterized by:
    dementia with rapid onset and deterioration, motor deficits, and seizures
50
Q

Neurosyphilis?

A
  • final stage of syphilis, known as tertiary stage (occurs in 15-20% of people with untx syphilis), slow progressive, destructive infection of the brain and spinal cord
51
Q

HIV dementia?

A
  • common neuro disorder assoc with HIV and AIDs. Metabolic encephalopathy which typically occurs after years of HIV infection. It sometimes seen as first sign of onset of AIDS
52
Q

What is delirium?

A
  • sudden and sig decline in mental fxning not better accounted for by a preexisting or evolving dementia
  • disturbance of consciousness with reduced ability to focus, sustain, and shift attention
53
Q

4 major causes of delirium?

A
  • underlying medical condition (hypoglycemia)
  • substance intoxication
  • substance withdrawal
  • combo of any or all of these
54
Q

What pt groups are at high risk for delirium?

A
  • elderly: older than 80, hx of dementia, polypharmacy
  • post-cardiac surgery
  • burns
  • drug withdrawal
  • AIDs
55
Q

Prevalence of delirium?

A
  • in hosp medically ill: 10-30%
  • in hosp elderly: 10-40%
  • postop pts: up to 50%
  • near death terminal pts: up to 80%
56
Q

Clinical features of delirium?

A
  • prodrome: restlessness, anxiety, and sleep disturbances
  • fluctuating course
  • attention deficits
  • arousal/psychomotor disturbance
  • impaired cognition
  • sleep-wake disturbance
  • altered perceptions
  • affective disturbances
57
Q

Fluctuating course of delirium?

A
  • develops over short period (hrs to days)
  • sxs fluctuate during course of days with changes in:
    levels of consciousness
    orientation, short term memory
  • or occurrences of:
    agitation, hallucinations
58
Q

Attention deficits: delirium?

A
  • easily distracted by enviro

- may be able to focus initially but won’t be able to sustain or shift attention

59
Q

arousal/psychomotor disturbance of delirium?

A
  • hyperactive (agitated, hyperalert)
  • hypoactive (lethargic, hypoalert)
  • mixed
60
Q

Impaired cognition of delirium?

A
  • memory deficits
  • language disturbance
  • disorganized thinking
  • disorientation: time of day, date, place, situation, others, self
61
Q

Sleep-wake disturbances in delirium?

A
  • fragmented throughout 24 hr period

- reversal of normal cycle

62
Q

Altered perceptions in delirium?

A
  • illusions
  • hallucinations: visual (most common), auditory, tactile and olfactory
  • delusions
63
Q

Affective disturbance in delirium:

A
  • anxiety/fear
  • depression
  • irritability
  • apathy
  • euphoria
  • lability
64
Q

Duration of delirium sxs?

A
  • typically resolve in 10-12 days, may last up to 2 months

- dependent on underlying problem and management

65
Q

I WATCH DEATH causes of delirium?

A
  • I: infections
  • W: withdrawal
  • A: acute metabolic
  • T: trauma
  • C: CNS pathology
  • H: hypoxia
  • D: deficiencies
  • E: endocrinopathies
  • A: acute vascular
  • T: toxins or drugs
  • H: heavy metals
  • *44% est to have 2 or more etiologies
66
Q

Infections that cause delirium:

A
  • encephalitis
  • meningitis
  • sepsis
  • urosepsis
67
Q

Withdrawals that cause delirium?

A
  • ETOH, sedative-hypnotics, barbiturates
68
Q

Acute metabolic causes of delirium?

A
  • acid-base, electrolytes, liver or renal failure
69
Q

Trauma causes of delirium?

A
  • brain injury

- burns

70
Q

CNS pathologies of delirium?

A
  • hemorrhage, seizures, stroke, tumor (mets)
71
Q

Hypoxia causes of delirium?

A
  • CO poisoning, pulmonary or cardiac failure, severe anemia
72
Q

Deficiences that can cause delirium?

A
  • thiamine, niacin, B12
73
Q

Endocrinopathies that can cause delirium?

A
  • hyper or hypo-adrenocortisolism, hyper or hypoglycemia
74
Q

Acute vascular causes of delirium?

A
  • hypertensive encephalopathy and shock, MI
75
Q

Toxins and drugs that can dcuase delirium?

A
  • pesticides, solvents, meds,
    anticholinergics, narcotic anlagesics, sedatives
  • drugs of abuse: ETOH, amphetamines, cannabis, cocaine, hallucinogens, inhalants, opiates, PCP, sedatives, hypnotics
76
Q

Heavy metals that can cause delirium?

A
  • lead, manganese, and mercury
77
Q

Workup of delirium?

A
  • Hx
  • interview: also with family
  • physical, cognitive and neuro exam
  • vital signs, fluid status
  • review of medical record: anesthesia and medication record review
78
Q

MMSE?

A
  • tests orientation, short term memory, attention, concentration, constructional ability
  • 30 pts: perfect score
  • less than 24 suggestive of problem
  • not helpful w/o knowing baseline
79
Q

Workup of delirium?

A
  • electrolytes
  • CBC
  • EKG
  • CXR
  • EEG (not usually necessary)
  • ABGs or O2 sats
  • UA +/- culture and sensitivity
  • urine drug screen
  • blood alcohol
  • serum drug levels (digoxin, theophylline, phenobarbital, cyclosporin, lithium, etc)
  • rarely consider: heavy metals (urinary porphyrins)
    lupus workup
80
Q

Management of delirium?

A
  • ID and tx underlying etiology
  • increase observation and monitoring: VS’s, I&O, O2, safety
  • D/C or minimize dosing of nonessential meds
  • coord with other physicians and providers
  • monitor and assure safety of pt and staff: violence potential, fall and wandering risk, need for a sitter, remove potentially dangerous items from the environment, restrain when other means not effective
  • assess individual and family psychosocial characteristics, est and maintain an alliance with family, ask for their help, educate the family
  • provide post-delirium education and processing for the pt
81
Q

Environmental interventions in management of deliriuim?

A
  • correct sensory impairment (vision, hearing)
  • orientation cues
  • family members
  • frequent reorientation
  • nightlights
82
Q

Pharm management of agitation in delirium?

A
  • low doses of high potency neuroleptics (haloperidol)
  • atypical antipsychotics (risperidone)
  • inapsine (more sedating with more rapid onset than haloperidol - IM or IV only, monitor for hypotension)
83
Q

SEs of haloperidol and inapsine?

A
  • both have been assoc with torsades and sudden death by lengthening the QT interval, avoid or monitor by telemetry if corrected QT interval is greater than 450 msec or greater than 25% from previous EKG
84
Q

Use of benzodiazepines in delirium?

A
  • toc for delirium due to benzodiazepine or ETOH withdrawal
  • may worsen confusion in delirium
  • may cause behavioral disinhibition: amnesia, ataxia, respiratory depression
  • CI in hepatic failure pts
85
Q

Common cases of delirium?

A
  • homeless male, hx of ETOH abuse, 2 days post-op
  • 82 yo women with UTI
  • burn victim after mult med changes
  • mildly demented 71 yo after hip replacement (ICU psychosis)
86
Q

Outcome of delirium?

A
  • may progress to stupor, coma, seizures, or death, particularly if untx
  • increased risk for postop complications, longer postop recuperation, longer hop stays, and long term disability
  • elderly pts 22-76% chance of dying during hospitalization
  • 25% of all pts with delirium die w/in 6 months
87
Q

Diff in dementia and delirium?

A

dementia:
-slow, gradual onset
time of onset unclear, note changes over several months
- due to chronic disorders like AD
-progressive process attention not impaired until late stages
- no effect on consciousness until late stages
- loss of memory esp for recent events

delirium:
acute onset, cause is usually tx: infection, meds, pain, MI
- usually reversible
- attention impaired
- concsciousness ranges from lethargic to hyperalert
- effect on memory varies

Neuro (19 decks)

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