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NR 546 / NR546 Final Exam Guide 2024/2025:
Chamberlain’s Verified Q&A for Psychopharmacology
(New!!!)
If an AD medication is discontinued: - ANSWER the medication may not be as
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effective if restarted
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Current gold standard of treatment for cognitive symptoms includes: -
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ANSWER pharmacologic management with a cholinesterase inhibitor
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(ChEIs) and an N- methyl-D-aspartate (NMDA) receptor antagonist.
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Four Major causes of Dementia - ANSWER_-Alzheimer Disease (AD)
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-vascular dementia HN
-Lewy body dementias (LBD)
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-frontotemporal dementia (FTD) HN HN
three pathological hallmarks of AD seen in the brain at autopsy are: -
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ANSWER_(1) amyloid-beta (Aβ), aggregated into plaques
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(2) neurofibrillary tangles composed of hyperphosphorylated tau protein
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(3) substantial neuronal cell loss HN HN HN
Differential diagnosis, clinical presentation: Vascular dementia - ANSWER_-
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Impaired abstraction, mental flexibility, processing speed, and working memory
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-Verbal memory is better preserved
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-Slower cognitive decline
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-Dementia occurs within several months of a stroke
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Differential diagnosis, clinical presentation: Lewy body dementias (LBD)
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- ANSWER_-Visual hallucinations
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-Spontaneous parkinsonism HN
-Cognitive fluctuations HN
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-Visuospatial, attention, and executive function deficits are worse
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-Memory impairment is not as severe HN HN HN HN HN
-Earlier presentation of psychosis and personality changes
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-Rapid eye movement (REM) sleep disturbances
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Differential diagnosis, clinical presentation: Frontotemporal degeneration (FTD)
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- ANSWER_-Progressive behavioral and personality changes that impair
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social conduct (apathy, disinhibition, etc.)
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-Language impairment HN
-Possibly preserved episodic memory HN HN HN
Lewy Body Dementias (LBD) - ANSWER_Dementia with Lewy bodies (DLB)
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and the related Parkinson's disease dementia (PDD)
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-10-15% of all cases of dementia
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-abnormal accumulation of a protein called α-synuclein
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• aggregate to form oligomers, eventually turning into "Lewy bodies" &
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Lewy neurites, as neurons degenerate
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The Amyloid cascade Hypothesis - ANSWER_Alzheimer disease (AD) is
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caused by the accumulation of toxic Aβ, which form into plaques,
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hyperphosphorylation of tau, neurofibrillary tangle formation, synaptic
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dysfunction, and ultimately neuron loss with memory loss and dementia
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risk of developing AD - ANSWER_-inheritance of two copies of APOE4 leads to a
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tenfold increased AD risk
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-APOE2 gene appears to offer some protection from AD
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-APOE3 gene (the most common form of the APOE gene) conveys a risk that falls
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between APOE2 and APOE4
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, NR 546 FINAL EXAM (NR546 ACTUAL) WITH CORRECT
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Non-pharmacological options for behavioral symptoms in dementia - HN HN HN HN HN HN HN
ANSWER_• Address unmet needs (hunger, pain, thirst, boredom)
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• Identify/modify environmental stressors HN HN
• Identify/modify daily routine stressors HN HN HN
• Caregiver support/training HN
• Behavior modification HN
• Group/individual therapy HN
• Problem solving HN
• Distraction
• Provide outlets for pent-up energy (exercise, activities)
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• Avoid behavior triggers
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• Increase social engagement
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• Relaxation techniques HN
• Reminiscence therapy HN
• Music therapy HN
• Aromatherapy
• Pet therapy
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Tx dementia-related psychosis – ANSWER Pimavanserin
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-hypothetically reduces overactivity in the psychosis network caused by plaques,
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tangles, Lewy bodies, or strokes, presumably by lowering the normal 5HT2A
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stimulation to surviving glutamate neurons that have lost their GABA inhibition by
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neurodegeneration
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-approved for the treatment of Parkinson's disease psychosis & there are
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positive trials in dementia-related psychosis
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