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17 Cards in this Set
- Front
- Back
Dementia:
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broad term encompassing disorders that involve cognitive decline (without mind)
Very debilitating |
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Forms of dementia
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Many different forms exist
** Insult to the brain: * Neurodegeneration: |
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Dementia insult to the brain
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traumatic brain injury (chronic traumatic encephalopathy), stroke (vascular dementia), infection (meningitis, AIDS, syphilis)
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nuerodegenration
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* Korsakoff’s Syndrome (vitamin B deficiency, seen in alcoholics),
* Huntington’s Disease, * Dementia with Lewy Bodies (related to Parkinson’s Disease), * Frontotemporal Dementia, * Alzheimer’s Disease (most common form of dementia) * internal/metabolic cause |
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Alzheimer's Features
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* Most common form of dementia
* Late Onset > 70 years (sporadic Alzheimer’s) * “Early onset” <65 years tends to be more severe and progress more quickly, has a larger genetic component then late onset * 2x as common in women as in men * Alzheimer’s numbers are on the rise, expected to more then double by 2050 burden on our healthcare system * Aging population increases incidence, obesity, stroke, HD also increase which increase risk for Alzheimer’s |
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Alzheimer's Symptoms (7)
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Cognitive Deficits:
* Severe memory loss (both reterograde and anterograde amnesia) * Language Impairments (become anomic cannot think of names, empty speech) * Visuospatial impairments (difficulties navigating space) Behavioural Deficits: * Anosognosia: not aware of own impairment, seen as * disorder progresses * Confusion * Wandering * Aggression * Psychosis -> due to chemical imbalance in the brain Sleep Disturbances |
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stages of alzheimer's disease
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* mild cognitive impairment
* Mild Alzheimer’s Disease * Moderate Alzheimer’s Disease * Severe Alzheimer’s Disease |
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Mild Cognitive Impairment
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* Transitionary stage: transitioning from someone who has normal decline w/ aging to Alzheimer’s disease
* Difficult to diagnose difficult to tell you who has declined more, overlap w/ symptoms b/w other forms of dementia Not everyone progresses to AD |
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Mild Alzheimer’s Disease
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people begin to seek out healthcare
* Memory loss for recent events anterograde amnesia * Getting lost, misplacing things * Difficulties performing tasks, problem solving, decision making * Conversation becomes difficult * Can become withdrawn or aggressive |
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Moderate Alzheimer’s Disease
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begin to have trouble w/ daily life
* Problems continue to intensify, people begin to need help with activities of daily living (difficult for caregivers) * Memory loss worsens, includes autobiographical memory (retrograde amnesia) Confusion deepens ( Easily overwhelmed by sensory stimulation ) * May become combative, suspicious, or hostile -> results from anosagnosia Possible psychosis |
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Severe Alzheimer’s Disease
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*Decline continues, basic activities of life now severely affected
* Loss of language/communication * Require intensive help with daily living |
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Neuropathology of alzheimer's
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* Widespread cortical atrophy (shrinkage)
* Cholinergic Disruption * Abnormal protein deposits * |
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Widespread cortical atrophy
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(shrinkage) particularly in language centers in temporal lobes and hippocampus (memory)
Not homogenous cerebral atrophy |
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Cholinergic Disruption
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* Projections (Acetylcholine) of the basal forebrain degenerate
* Loss of acetylcholine -> acetylcholinesterase inhibitors used (increase levels of acetylcholine b/c of less breakdown of Ach) * Stop working after 2-4 years b/c Ach is no longer produced |
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Abnormal protein deposits (Amyloid plaque)
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-> most likely cause
* Extracellular accumulation of beta-amyloid protein (Aβ plaques) -> accumulate on outside of neural cells * Toxic to neurons (cause neurons to die) * Have APO E4 gene -> higher risk of developing sporadic Alzheimer’s disease, also respond better to drugs for disease * Occurs in first in default network (opposite of paying attention in the world) -> first area affected in Alzheimer’s disease * These deposits are also seen in healthy individuals |
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Abnormal protein deposits: (Tau Protein)
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* rarely seen in healthy brains, key to Alzheimer’s
Intracellular accumulation of tau protein (neurofibrillary tangles) * Tau: microtubule integrity in neurons (allows cell body to perform basic functions) * Tau becomes pathologically altered, accumulates in neurons, walls begin to collapse and neuron cannot perform functions and dies |
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Bio marks of AD
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Biomarkers:
Hippocampal volume (hippocampus degenerates early in the disease) CSF markers: Tau (higher in people w/ Alzheimer’s) and Aβ (lower in people w/ Alzheimer’s) in CSF (lumbar puncture) -> most promising diagnostic tool |