Basics of Delirium, Dementia, and Depression Flashcards
Basic Activities of Daily Living (BADLs)
DEAT2H: Dressing, Eating, Ambulating, Transferring, Toileting, Hygeine
The things that keep you out of the nursing home
Instrumental Activities of Daily Living (IADLs)
SHAFTT: Shopping, Housekeeping, Accounting, Food prep/meds, Transportation, Telephone
Delirium or “Acute Brain Failure”
Acute (doesn’t come on slowly) disorder of attention & cognitive function
Usually secondary to other illness (infection, CNS disease, withdrawal, etc.)
Significant morbidity and mortality
Potentially preventable
Initiates downward spiral
Inc need for institutionalization/rehab
Unrecognized up to 70% of the time
Most common in ICU, inpatient units etc
1 year mortality after hospitalization with delirium 35-40%
May be caused by medications
DeliRIUM = changes in sensoRIUM
Reversible
Can be differentiated by diffuse slowing of EEG (although this is also sometimes shown with dementia)
Can last days, weeks, or long term. Poor prognosis in first year
CAM Criteria
Used for diagnosis of delirium 1: Acute onset and fluctuating course 2: Inattention 3: Disorganized thinking OR 4: Altered consciousness
Symptoms of Delirium
Disorganized thinking Hallucinations Illusions Misperceptions Disturbance in sleep/wake cycle Cognitive dysfunction
Etiology of Delirium
Possible cholinergic deficiency
Dysfunction of multiple brain regions and neurotransmitter systems
Older adults more vulnerable because of age related changes in central neurotransmission, stress mgmt, hormonal regulation, immune response
Predisposing factors for Delirium (Vulnerability)
Severe dementia, Severe illness, Major depression, Sensory impairment, Older age, History of delirium, Functional impairment
Precipitating factors for Delirium (Insults)
Major surgery/anesthesia, ICU stay, physical restraints, multiple psychoactive meds, metabolic derangement or infection, sleep deprivation, sleep meds
Treatment of Delirium
- Nonpharmacologic: reorientation, family involvement, eyeglasses/hearing aids, sleep protocol, encourage mobility/self care, ensure hydration, quiet room at night
- Pharmacologic: use ONLY when severely agitated patient at risk of 1. interruption of essential medical care, or 2. posing as safety hazard for themselves/staff
Meds: Haloperidol .25-1mg
AVOID benzodiazepines (except with alcohol withdrawal) and psychoactives
Dementia
Progressive
Cognitive/behavioral symptoms must: interfere with function (vs normal aging does not)
Cannot be explained by delirium or another psych disorder
Can lead to delirium (esp. when leads to illness first) Irreversible (if truly dementia)
DeMEMentia = MEMory loss
EEG usually normal
Terminal
Etiology of Dementia
Irreversible causes: AD, Lewy body dementia, Huntington disease, Pick disease, cerebral infarct, Wilson disease, Creutzfeldt-Jakob disease, chronic substance abuse (neurotoxicity of drugs), HIV
Reversible causes: Hypothyroidism, depression, vitamin deficiency (b1, b3, b12), normal pressure hydrocephalus, neurosyphilis
Symptoms of Dementia
Memory deficits (can’t learn new info well)
Problem-solving & judgement
Loss of abstract thought
Loss of semantic processing (listing animals)
Apraxia (motor speech disorder)
Aphasia (comprehend/formulate language, finding “right” words for thoughts)
Agnosia (inability to process sensory info)
Visuospatial (driving)
Behavioral (poor awareness, emotional lability)
Alzheimer Disease
Most common cause of dementia in elderly
Affects 5-10% of population over age 65
Amnesia (ST then LT memory loss) + language presentation, visuospatial presentation, or executive dysfunction
Changes in behavior and personality
Patients become bedridden and mute (infection is a common cause of death)
Focal neurologic deficits (affect a certain area of body) not seen in early disease
Decrease in ACh
Early onset AD
Seen in familial cases (associated with presenilin 1 and presenilin 2 mutations), APP
Down syndrome (commonly occurs by 40 years of age); APP is located on chromosome 21
Presenilin-1
One of four proteins considered to play an important role in generation of AB (beta amyloid) and Amyloid Precursor Proteins (APP)
Sporadicalness of AD
95% chance of being sporadic (non-inherited)
ApoE2: Decreased risk of being sporadic
ApoE4: Increased risk of sporadic form
Although sporadic does not run in families, one is at increased risk if one’s family has history of sporadic AD.
Non-sporadic/inherited AD is rare
Risk factors of Dementia
Delirium in past year Family history (either inherited or incidence of sporadic dementia) Substance abuse Age Co-morbidities
Cognitive testing
Mini-cog: 3 item recall, draw a clock
Mini Mental Status Exam (MMSE): Been around a while, very validated, research challenge, scored out of 30, check for dementia *think about ed level
St. Louis Mental Status Exam (SLUMS): Good for those in higher ed; for those expected to have dementia or AD; oral/written; more sensitive than MMSE
Montreal Cognitive Assessment MoCA: Good at detecting mild impairment and early AD
Depression in Elderly
High prevalence
Underdiagnosed
Risk factors: loss of social support, death of close ones, changing social role, physical limitations
Independent risk factor for neurodeg. disorders (w/ depression, more likely to have dementia)
More likely to be psychosomatic (issues with body caused by psych issues) than in younger patients
Weight loss, sadness, apathy
Evaluation of Depression in Elderly
Geriatric Depression Scale (GDS): 4+ suggests depression, doesn’t diagnose
Cornell Scale for Depression in Dementia: for patients with both depression and dementia
Treatment of Depression in Elderly
Gold: Medication, Cognitive Behavioral Therapy
Severe: ECT (Electric Convulsive Treatment)
Eval for suicide factors (age >80, caucasian, male, isolated, debilitating health, change in social roles, substance abuse, etc….#1 person to be successful at committing suicide)
Cognitive Behavioral Therapy
Short-term, goal-oriented
hands-on, practical approach to problem-solving
goal: change patterns of thinking or behavior that are behind people’s difficulties, and so change the way they feel.
Electric Convulsive Treatment
procedure
small electric currents are passed through the brain, intentionally triggering a brief seizure.
ECT seems to cause changes in brain chemistry that can quickly reverse symptoms of certain mental illnesses.
Diagnosis of Delirium (tests)
CBC (complete blood count) with diff.
CMP (complete metabolic panel)
Diagnosis of Dementia (tests)
Cognitive testing
B12 levels (deficiency)
TFT (Thyroid function test- symptoms can worsen)
GDS
Diagnosis of Depression (tests)
TFT
GDS
Treatment of Dementia
AchE Inhibitors
NMDA Antagonist
Quality of life focus
Ach and AchE in AD
In AD we see decreased Ach levels
AchE (acetylcholinesterase, breaks down Ach)
AchE inhibitors: allow Ach to exist longer
Acetylcholine
responsible for much of the stimulation of muscles, including the muscles of the gastro-intestinal system. It is also found in sensory neurons and in the autonomic nervous system, and has a part in scheduling REM (dream) sleep.
NMDA Antagonists
NMDA (N-methyl-D-aspartate) receptor antagonist (inhibits NMDA receptor)
Regulates the activity of glutamate, an important neurotransmitter in the brain involved in learning and memory.
In AD, we need to reduce the NMDA activity because it can lead to excitotoxicity
Symptoms of AD
Impairment of anterograde memory
Impairment of attention
Deterioration of language skills, visuospatial orientation, abstract thinking, judgement
Alterations of personality
Alterations of sleep pattern, mood, appetite, endocrine functions, motor activity
Hippocampus function
Establishing new memories
Basal ganglia and cerebellum function
Motor activities and acquisition and storage of procedural memories
Cerebral cortex function
Long-term declarative memory
Path of AD
Glutamate NMDA receptor mediated excitotoxicity
Loss of norepinephrine-producing neurons in the locus coeruleus (nucleus in pons of brain stem)
Excitotoxicity
pathological process by which neurons are damaged and killed by the overactivations of receptors for the excitatory neurotransmitter glutamate, such as the NMDA receptor and AMPA receptor.
Excitatory postsynaptic potential
Depolarization (loss of difference in charge) of membrane due to transient increase in Na+ or Ca2+ conductance
Inhibitory Postsynaptic potential
Hyperpolarization (makes it more negative) of membrane due to transient increase of K+ or Cl- conductance
Treatments for AD
NMDA antagonists (reduce activity of NMDAR)
Promote action of norepinephrine on adrenergic receptors
