Dementia, Delerium & Depression Flashcards

1
Q

Memory - what is it?

A

Mental ability to retain,
recognize & recall:
- Facts
- Events
- Impressions
- Prior experiences

The process in which information is encoded,
stored, & retrieved

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2
Q

Delirium

A

Cerebral dysfunction that is:
● Transient
● Reversible (usually)
● Found in many neuropsychiatric
abnormalities
● Most common in the elderly
● May occur in addition to
underlying dementia
● Sometimes the only sign of a
serious underlying medical
condition

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3
Q

____% develop delirium near death

A

80

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4
Q

Delirium etiology

A
  • Multifactorial
  • Hypoxia
  • Hypoglycemia
  • Hyperthermia
  • Alcohol withdrawal
  • Medications
  • Infection
  • Structural lesions of brain
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5
Q

Delirium risk factors

A
  • > 80 yo
  • Male > Female
  • Pre-existing dementia
  • Fracture
  • Infection***
  • Malnutrition
  • Addition of > three medications
  • Use of neuroleptics & narcotics
  • Use of restraints
  • Bladder catheters
  • Iatrogenic event
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6
Q

Delirium pathogenesis

A
  • Not fully understood
  • Reversible impairment of cerebral metabolism & neurotransmitter abnormalities
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7
Q

Delirium clinical presentation

A
  • Confusion
  • New onset or acute deterioration
  • Cognitive changes
  • Inattention
  • Disorganized thinking
  • Altered LOC
  • Psychomotor agitation
  • Hallucinations
  • Paranoid/persecutory delusions
  • Grandiose delusions
  • Emotional lability
  • Sleep-wake cycle disturbances
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8
Q

Hypoactive delirium

A

Flat affect & apathy
* Hepatic
encephalopathy
& hypercapnia

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9
Q

Mixed delirium

A

Daytime sedation with
nocturnal agitation &
behavioral problems

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10
Q

Hyperreactive delirium

A

Agitation in a state of
withdrawal or intoxication
* Alcohol, PCP,
amphetamine, &/or LSD

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11
Q

Delirium diagnosis

A
  • Baseline mental status assessment
  • No specific lab test
  • CBC c diff
  • CMP
  • TSH, T3, T4, TPO
  • B1 & B12
  • UA
  • Drug screen
  • Tests for bacteriological & viral
    etiologies
  • Imaging
  • prn
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12
Q

Review delirium DSM criteria

A

Slide 14

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13
Q

Delirium
Management

A
  • Treat the underlying cause
  • Fluid & nutrition
  • ETOH toxicity or withdrawal, tx
    should include MVT & Thiamine
  • Reorientation techniques
  • Constant observation
  • Delirium that causes injury to the
    pt or others should be tx with
    meds

Environment should be
* Stable
* Quiet
* Well-lighted

Correct sensory deficits
* Eyeglasses, hearing aids

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14
Q

Delirium that causes injury to the
pt or others should be tx with these
meds:

A
  • Haloperidol
  • Risperidone
  • Lorazepam
  • Reserved for delirium
    resulting from seizures or
    withdrawal from alcohol or
    sedative hypnotics
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15
Q

Delirium complications

A
  • ↑ hospital stay
  • ↑ complications
  • ↑ cost
  • ↓ survival
  • Long-term disability
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16
Q

_____ = Most severe cognitive impairment

A

Dementia

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17
Q

NeuroCognitive Disorders (Dementia)

A
  • Sustained loss of intellectual functions (thinking) & memory
  • Gradual
  • Severity sufficient to cause dysfunction in daily living
  • ↓ ADLs
  • ↓ IADLs
  • Loss of functional ability due to impaired cognition
  • May be reversible or irreversible
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18
Q

NeuroCognitive Disorders (Dementia) epidemiology

A
  • Incidence doubles every 5 years after age 60
  • Community elders > 85 yo = 25%
  • SNF elders > 85 you = > 50%
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19
Q

Most common types of dementia

A
  • Alzheimer’s
  • 60-70%
  • Lewy body dementia
  • Vascular dementia
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20
Q

Reversible causes of neurocognitive disorders

A

Adverse medication effects
Recurrent hypoglycemia
Lyme disease
Delirium
Thyroid diseases
HIV-associated neurocognitive disorders (HAND)
Acute alcohol intoxication Other metabolic-endocrine
disorders
Chronic meningitis/encephalitis
Substance use disorders
Vitamins B 1 (thiamine), B 12, &/or D
deficiencies
Neurosyphilis
Obstructive sleep apnea
Uremia
Depression
Other sleep disorders

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21
Q

Irreversible causes of neurocognitive dysfunction

A

Corticobasal degeneration
Chronic traumatic encephalopathy
Alzheimer disease
Mass lesions (neoplasms, benign
tumors, hematomas)
Prion-related diseases (Creutzfeldt-
Jakob, bovine spongiform
encephalopathy)
Lewy body dementia
CNS, rheumatologic, autoimmune
disorders (SLC, sarcoidosis, vasculitis, MS) Normal pressure hydrocephalus
Vascular dementia/vascular
cognitive impairment
Huntington’s disease
Paraneoplastic syndromes
Frontotemporal dementia
Alcohol-related dementia

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22
Q

Subtle early signs of dementia:

A
  • Frequent repetition of the same
    questions or stories
  • ↓ participation in former hobbies
  • ↑ accidents
  • Missed appointments
  • Poorly controlled chronic
    conditions
  • Lack of adherence to Rx med 2 ◦
    memory problems
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23
Q

______ is the most commonly affected
cognitive domain in dementia

24
Q

Typical course of vascular dementia

A

Acute onset of cognitive impairment with some
stabilization (if only one vascular event) &/or stepwise
deterioration (if multiple infarcts)

25
Cognitive symptoms of vascular dementia
Various cognitive domains may be affected depending on the location of the clinical stroke(s) &/or severe subcortical cerebrovascular disease
26
Dementia with lewy bodies typical course
Progressive cognitive decline with fluctuating cognition, attention, & alertness
27
Cognitive symptoms Dementia with Lewy bodies
Cognitive symptoms may fluctuate May have prominent impairment in visuospatial ability, attention, &/or executive function
28
Dementia with Lewy bodies other associated symptoms/signs
May have recurrent well-formed visual hallucinations (usually people or animals), parkinsonism (including tremor, rigidity, & postural instability), recurrent falls & syncope, rapid eye movement (REM) sleep behavior disorder, neuroleptic sensitivity, &/or delusions
29
Dr. Alois Alzheimer first observed the symptoms in 1901 & discovered _____ in the same patient postmortem in 1906
amyloid plaques
30
Alzheimer’s Disease epidemiology
* Most prevalent = pts 60 + years * Familial early-onset can appear as early as the late 20’s
31
Alzheimer’s Disease risk factors
Advancing age * Family history * Obesity * Insulin resistance * Inflammatory markers * Down syndrome * Traumatic brain injury * Hypertension * Vascular factors * Dyslipidemia
32
Alzheimer’s Disease etiology
* Exact cause of amyloid plaques is unknown * Likely multifactorial * Brain nerve cells stop working * lose connections with other nerve cells, & die * Consequences → memory failure, personality changes, problems in carrying out daily activities, & other features of Alzheimer’s
33
Alzheimer’s Disease pathophysiology
* Microtubules (supportive structures) * Guide nutrients & molecules to the ends of the axon & back * Tau proteins bind & stabilize * In Alzheimer’s, tau is chemically altered & binds into neurofibrillary tangles (NFTs) * Microtubules disintegrate, collapsing the neuron’s transport system * Communication malfunctions → cell death
34
What are Beta-amyloid plaques
Arise from protein in the fatty membrane surrounding nerve cells * Beta-amyloid is chemically "sticky" & gradually builds up * Blocks cell-to-cell signaling * Might activate immune system cells → trigger * Inflammation * Devour disabled cells
35
Mutations for early-onset autosomal dominant Alzheimer’s
* Amyloid precursor protein ( APP) gene, chromosome 21 * Presenilin-1 ( PS1) gene, chromosome 14 * Presenilin-2 ( PS2) gene, chromosome 1
36
Alzheimer’s Disease clinical presentation
*Progressive memory impairment *Difficulty learning & recalling information (esp. new information) *Visuospatial problems *Language impairment *Classically, Alzheimer’s patients have little or no insight into their deficits, which may be a result of their compromised executive functioning (ie planning, insight, & judgment)
37
Alzheimer’s Disease screening tools
* Mini-Mental State Exam (MMSE) * No longer free: https://www.parinc.com/products/pkey/237 * Montreal Cognitive Assessment (MoCA) * Free: http://www.mocatest.org/ * Mini-Cog * Free: https://mini-cog.com/ * Mental Status Exam
38
Alzheimer’s Disease labs
* Labs * CBC c diff * CMP * B12 * TSH, T3, T4, TPO * RPR * Vitamin D* * Lumbar puncture * CSF levels of tau & phosphorylated tau are often elevated * CSF levels of amyloid levels are usually low
39
Numerous consensus statements recommend against using _____ genotyping for predicting Alzheimer’s risk
APOE
40
APP, PS1, PS2 testing in alzheimers disease
* Testing for the APP & presenilin genes for early-onset, autosomal dominant Alzheimer’s should be offered: * Pt’s w/ early-onset Alzheimer’s + family hx of dementia (or unknown fam hx) * + Fam hx of autosomal dominant dementia with 1+ cases of early-onset Alzheimer’s * In relatives with a mutation consistent with early-onset Alzheimer’s (ie, PS-1, PS-2,APP)
41
Alzheimer’s Disease imaging
* 1st line = MRI * Single-photon emission computed tomography (SPECT) * Positron Emission Tomography (PET)
42
Alzheimer’s Disease management
* No cure, only symptomatic therapies * If pt is a danger to him/herself or others: * Short-term hospitalization = r/o infxn & metabolic processes & adjusting psychotropic medications * Admission to a long-term care facility = Need for 24-hour supervision * Mental exercise/activities * Cholinesterase inhibitors (ChEIs) (Donepezil)
43
Donepezil MOA
* Cholinesterase Inhibitor — reversibly binds to & inactivates acetylcholinesterase
44
Rivastigmine MOA
* Cholinesterase Inhibitor — reversibly binds to & inactivates acetylcholinesterase
45
Memantine MOA
* NMDA receptor antagonist — binds N-methyl-D-aspartate receptors → slows Ca ++ influx/accumulation & subsequent nerve damage * memantine + ChEI significantly delays institutionalization in Alz patients
46
Aducanumab (Aduhelm®) MOA
* High affinity, fully human IgG1 monoclonal antibody that targets beta amyloid & binds to aggregated forms of beta-amyloid; preferentially binds to parenchymal over vascular amyloid; reduces plaque formation on neurons
47
lecanemab (Leqembi®) MOA
* Humanized immunoglobulin gamma 1 (IgG1) monoclonal antibody directed against aggregated soluble and insoluble forms of amyloid beta * lecanemab reduces amyloid beta plaques
48
Antidepressants/mood modulators for Alzheimers disease
* Citalopram * Older patients should not use doses > 20 mg * Can ↑ the QT interval * Trazodone * Pts sleep an average of 42.5 minutes longer per night * Valproic acid * Helpful in ↓ disruptive behaviors & outbursts of anger
49
Alzheimer’s Disease: time from diagnosis to death
~ 3-10 years
50
Patients with early-onset Alzheimer’s = ____
more aggressive, rapid course
51
Primary cause of death in alzheimers is ____
concomitant illness (i.e. pneumonia)
52
Serotonin hypothesis for depression
* Reduced 5-HT (serotonin) levels in the body increases the risk of being affected by depression * Other neurotransmitters may also influence risk (ie. Norepinephrine, dopamine) * Serotonin is also a precursor for melatonin, necessary for sleep & psychological function
53
Depression clinical presentation - SIG E CAPS
* Sleep disorders ↑ ↓ * interest deficit (anhedonia) * guilt (worthless/hopelessness, regret) * energy deficit * concentration deficit * appetite disorder ↑ ↓ * psychomotor retardation or agitation
54
Depression atypical signs in males vs. females
Males ♂ * Aggression * Anger * Substance abuse * Risky behaviors Females ♀ * Headaches * Myalgias * GI issues * Emotional signs (ie. stress, crying)
55
Challenges with diagnosis elderly adults with depression
* Concurrent medical illness or medication side effects with overlapping symptoms of depression * Impaired communication skills in the elderly * Patient presentation with multiple somatic complaints * Lack of time psychological problems in patients with complex medical issues * Lack of prioritization * Patient's reluctance 2°perceived stigma of mental illness
56
Depression management in the elderly
* Consider side effects of an agent * Monotherapy preferred * SSRIs = 1st line, not necessarily more effective * Response is typically delayed * Start with ½ doses to compensate for decreased drug clearance in the elderly * Non-pharmacological * Psychotherapy, exercise, & electroconvulsive therapy