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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

____% develop delirium near death

A

80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Delirium etiology

A
  • Multifactorial
  • Hypoxia
  • Hypoglycemia
  • Hyperthermia
  • Alcohol withdrawal
  • Medications
  • Infection
  • Structural lesions of brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Delirium pathogenesis

A
  • Not fully understood
  • Reversible impairment of cerebral metabolism & neurotransmitter abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hypoactive delirium

A

Flat affect & apathy
* Hepatic
encephalopathy
& hypercapnia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Mixed delirium

A

Daytime sedation with
nocturnal agitation &
behavioral problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hyperreactive delirium

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Review delirium DSM criteria

A

Slide 14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Delirium complications

A
  • ↑ hospital stay
  • ↑ complications
  • ↑ cost
  • ↓ survival
  • Long-term disability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

_____ = Most severe cognitive impairment

A

Dementia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Most common types of dementia

A
  • Alzheimer’s
  • 60-70%
  • Lewy body dementia
  • Vascular dementia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

______ is the most commonly affected
cognitive domain in dementia

A

Memory

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
Q

Cognitive symptoms of vascular dementia

A

Various cognitive domains may be affected depending on the location of the clinical stroke(s) &/or severe subcortical cerebrovascular disease

26
Q

Dementia with lewy bodies typical course

A

Progressive cognitive decline with fluctuating
cognition, attention, & alertness

27
Q

Cognitive symptoms Dementia with Lewy bodies

A

Cognitive symptoms may fluctuate
May have prominent impairment in visuospatial ability,
attention, &/or executive function

28
Q

Dementia with Lewy bodies other associated symptoms/signs

A

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
Q

Dr. Alois Alzheimer first observed the symptoms in 1901
& discovered _____ in the same patient
postmortem in 1906

A

amyloid plaques

30
Q

Alzheimer’s Disease epidemiology

A
  • Most prevalent = pts 60 + years
  • Familial early-onset can appear as early as the late 20’s
31
Q

Alzheimer’s Disease risk factors

A

Advancing age
* Family history
* Obesity
* Insulin resistance
* Inflammatory markers
* Down syndrome
* Traumatic brain injury
* Hypertension
* Vascular factors
* Dyslipidemia

32
Q

Alzheimer’s Disease etiology

A
  • 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
Q

Alzheimer’s Disease pathophysiology

A
  • 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
Q

What are Beta-amyloid plaques

A

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
Q

Mutations for early-onset autosomal
dominant Alzheimer’s

A
  • Amyloid precursor protein ( APP) gene,
    chromosome 21
  • Presenilin-1 ( PS1) gene, chromosome 14
  • Presenilin-2 ( PS2) gene, chromosome 1
36
Q

Alzheimer’s Disease clinical presentation

A

*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
Q

Alzheimer’s Disease screening tools

A
  • 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
Q

Alzheimer’s Disease labs

A
  • 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
Q

Numerous consensus statements recommend against using _____
genotyping for predicting Alzheimer’s risk

A

APOE

40
Q

APP, PS1, PS2 testing in alzheimers disease

A
  • 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
Q

Alzheimer’s Disease imaging

A
  • 1st line = MRI
  • Single-photon emission computed tomography (SPECT)
  • Positron Emission Tomography (PET)
42
Q

Alzheimer’s Disease management

A
  • 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
Q

Donepezil MOA

A
  • Cholinesterase Inhibitor — reversibly binds to & inactivates
    acetylcholinesterase
44
Q

Rivastigmine MOA

A
  • Cholinesterase Inhibitor — reversibly binds to & inactivates
    acetylcholinesterase
45
Q

Memantine MOA

A
  • 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
Q

Aducanumab (Aduhelm®) MOA

A
  • 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
Q

lecanemab (Leqembi®) MOA

A
  • Humanized immunoglobulin gamma 1 (IgG1) monoclonal antibody directed against aggregated soluble and insoluble forms of amyloid beta
  • lecanemab reduces amyloid beta plaques
48
Q

Antidepressants/mood modulators for Alzheimers disease

A
  • 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
Q

Alzheimer’s Disease: time from diagnosis to death

A

~ 3-10 years

50
Q

Patients with early-onset Alzheimer’s = ____

A

more aggressive, rapid course

51
Q

Primary cause of death in alzheimers is ____

A

concomitant illness (i.e. pneumonia)

52
Q

Serotonin hypothesis for depression

A
  • 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
Q

Depression clinical presentation - SIG E CAPS

A
  • Sleep disorders ↑ ↓
  • interest deficit (anhedonia)
  • guilt (worthless/hopelessness, regret)
  • energy deficit
  • concentration deficit
  • appetite disorder ↑ ↓
  • psychomotor retardation or agitation
54
Q

Depression atypical signs in males vs. females

A

Males ♂
* Aggression
* Anger
* Substance abuse
* Risky behaviors

Females ♀
* Headaches
* Myalgias
* GI issues
* Emotional signs (ie. stress, crying)

55
Q

Challenges with diagnosis elderly adults with depression

A
  • 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
Q

Depression management in the elderly

A
  • 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