module 14 Flashcards
NCD’s result from
biological irregularities, not
aging/stress/trauma
What are some disorders often connected to aging?
depressive, anxiety, substance abuse disorders
What are the med risks for treatments for aging disorders?
may be metabolized differently; may cause cognitive impairment
disorders of cognition
delirium, major and mild NCDs, resulting from brain irregularities
Delirium
significant disturbance in attention and orientation to the environment
What is delirium often associated with?
hospitalization for medical
condition; or disease/infection, strokes, head injuries, stress,
incorrect meds
Neurocognitive Disorder (NCD)
a significant decline in at
least one area of cognitive functioning, e.g., memory,
attention, visual perception, planning/decision-making,
language ability, social awareness
major NCD
substantial decline, interferes significantly w/independence
Minor NCD
modest decline, does not interfere w/independence
Worldwide NCD prevalence
age 65, 1-2%; over 85, up to 50%
What is the most prevalent NCD
Alzheimer’s disease
Alzheimers prevalence
Some “early onset” cases –prior to 65
Most are “late onset” 65+ (5% prevalence)
marked increase in prevalence by late 70’s (13%); 85+ (33%)
Women 2:1 men
People of color (except Asian-Americans) higher than non-Hispanic whites
Identified in 1907 by German neurologist Alois Alzheimer
Seventh leading cause of death in US
Alzheimers disease progression
mild NCD due to Alzheimer’s disease, most prominent impairment is in memory; also attention, language, communication pblms
progressing to “major NCD due to Alzheimer’s disease” w/task completion
pblms, worsening memory, personality changes, e.g., aggressiveness.
Often become depressed/anxious/agitated; more withdrawn, confused,
wandering, poor judgment; eventually become fully dependent on others; as
physical heath declines,
Alzheimer’s disease brain cause
Formation of exceptionally high levels of senile plaques deposits of
beta-amyloid proteins in synapses in brain structures (incl
hippocampus) and blood vessels.
Formation of exceptionally high levels of neurofibrillary tangles—
twisted tau protein fibers within neurons in brain structures (incl
hippocampus)
Both plaques and tangles contribute to the death of neurons
Alzheimer’s disease genetic factor
early onset (before 65; fewer than 10% of cases): family transmission of
mutations in genes related to production of a plaque-related proteins
Late onset: inheritance of a specific gene related to production of a plaque-related protein. But not everyone with this gene develops the disease.
Other factors? Environment, lifestyle, stress?
Other brain factors: dysfunctional brain structures and/or brain circuits;
irregularities in chemicals, e.g., acetylcholine, glutamate, calcium
NCD due to Huntington’s disease:
inherited; memory pblms, personality and mood changes, twitching, spasms; progressive
NCD due to Parkinson’s disease
tremors, rigidity, unsteadiness; progressive
CTE (Chronic traumatic encephalopathy)
affecting many athletes, after
repeated blows (incl mild ones) to the head. Excessive formation of tangles
produced by tau proteins and other structural irregularities lead to
disorientation, memory loss, behavioral and personality changes, cognitive
decline, suicidal ideation, death. Diagnosable only by brain exam after death
NCD treatment
none stop the progression of the disease
those impacting acetylcholine and glutamate (memory).
CBT
Classes, calculations, reading aloud, computer-based simulations may
prevent or delay onset
Support for caregivers
Relatives care for more than 80% of Alzheimer’s patients.
