Dementia, Delerium & Depression Flashcards
Memory - what is it?
Mental ability to retain,
recognize & recall:
- Facts
- Events
- Impressions
- Prior experiences
The process in which information is encoded,
stored, & retrieved
Delirium
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
____% develop delirium near death
80
Delirium etiology
- Multifactorial
- Hypoxia
- Hypoglycemia
- Hyperthermia
- Alcohol withdrawal
- Medications
- Infection
- Structural lesions of brain
Delirium risk factors
- > 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
Delirium pathogenesis
- Not fully understood
- Reversible impairment of cerebral metabolism & neurotransmitter abnormalities
Delirium clinical presentation
- 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
Hypoactive delirium
Flat affect & apathy
* Hepatic
encephalopathy
& hypercapnia
Mixed delirium
Daytime sedation with
nocturnal agitation &
behavioral problems
Hyperreactive delirium
Agitation in a state of
withdrawal or intoxication
* Alcohol, PCP,
amphetamine, &/or LSD
Delirium diagnosis
- 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
Review delirium DSM criteria
Slide 14
Delirium
Management
- 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
Delirium that causes injury to the
pt or others should be tx with these
meds:
- Haloperidol
- Risperidone
- Lorazepam
- Reserved for delirium
resulting from seizures or
withdrawal from alcohol or
sedative hypnotics
Delirium complications
- ↑ hospital stay
- ↑ complications
- ↑ cost
- ↓ survival
- Long-term disability
_____ = Most severe cognitive impairment
Dementia
NeuroCognitive Disorders (Dementia)
- 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
NeuroCognitive Disorders (Dementia) epidemiology
- Incidence doubles every 5 years after age 60
- Community elders > 85 yo = 25%
- SNF elders > 85 you = > 50%
Most common types of dementia
- Alzheimer’s
- 60-70%
- Lewy body dementia
- Vascular dementia
Reversible causes of neurocognitive disorders
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
Irreversible causes of neurocognitive dysfunction
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
Subtle early signs of dementia:
- 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
______ is the most commonly affected
cognitive domain in dementia
Memory
Typical course of vascular dementia
Acute onset of cognitive impairment with some
stabilization (if only one vascular event) &/or stepwise
deterioration (if multiple infarcts)
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
Dementia with lewy bodies typical course
Progressive cognitive decline with fluctuating
cognition, attention, & alertness
Cognitive symptoms Dementia with Lewy bodies
Cognitive symptoms may fluctuate
May have prominent impairment in visuospatial ability,
attention, &/or executive function
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
Dr. Alois Alzheimer first observed the symptoms in 1901
& discovered _____ in the same patient
postmortem in 1906
amyloid plaques
Alzheimer’s Disease epidemiology
- Most prevalent = pts 60 + years
- Familial early-onset can appear as early as the late 20’s
Alzheimer’s Disease risk factors
Advancing age
* Family history
* Obesity
* Insulin resistance
* Inflammatory markers
* Down syndrome
* Traumatic brain injury
* Hypertension
* Vascular factors
* Dyslipidemia
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
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
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
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
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)
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
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
Numerous consensus statements recommend against using _____
genotyping for predicting Alzheimer’s risk
APOE
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
- Fam hx of autosomal dominant dementia with 1+ cases of
- In relatives with a mutation consistent with early-onset
Alzheimer’s (ie, PS-1, PS-2,APP)
Alzheimer’s Disease imaging
- 1st line = MRI
- Single-photon emission computed tomography (SPECT)
- Positron Emission Tomography (PET)
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)
Donepezil MOA
- Cholinesterase Inhibitor — reversibly binds to & inactivates
acetylcholinesterase
Rivastigmine MOA
- Cholinesterase Inhibitor — reversibly binds to & inactivates
acetylcholinesterase
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
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
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
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
Alzheimer’s Disease: time from diagnosis to death
~ 3-10 years
Patients with early-onset Alzheimer’s = ____
more aggressive, rapid course
Primary cause of death in alzheimers is ____
concomitant illness (i.e. pneumonia)
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
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
Depression atypical signs in males vs. females
Males ♂
* Aggression
* Anger
* Substance abuse
* Risky behaviors
Females ♀
* Headaches
* Myalgias
* GI issues
* Emotional signs (ie. stress, crying)
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
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
