NR 546 FINAL EXAM (NR546 ACTUAL) WITH CORRECT
A+ GRADED ANSWERS
If an AD medication is discontinued: - ANSWER the medication may not be as
effective if restarted
Current gold standard of treatment for cognitive symptoms includes: - ANSWER
pharmacologic management with a cholinesterase inhibitor (ChEIs) and an N-
methyl-D-aspartate (NMDA) receptor antagonist.
Four Major causes of Dementia - ANSWER_-Alzheimer Disease (AD)
-vascular dementia
-Lewy body dementias (LBD)
-frontotemporal dementia (FTD)
three pathological hallmarks of AD seen in the brain at autopsy are: -
ANSWER_(1) amyloid-beta (Aβ), aggregated into plaques
(2) neurofibrillary tangles composed of hyperphosphorylated tau protein
(3) substantial neuronal cell loss
Differential diagnosis, clinical presentation: Vascular dementia - ANSWER_-
Impaired abstraction, mental flexibility, processing speed, and working memory
-Verbal memory is better preserved
-Slower cognitive decline
-Dementia occurs within several months of a stroke
Differential diagnosis, clinical presentation: Lewy body dementias (LBD) -
ANSWER_-Visual hallucinations
-Spontaneous parkinsonism
-Cognitive fluctuations
, NR 546 FINAL EXAM (NR546 ACTUAL) WITH CORRECT
A+ GRADED ANSWERS
-Visuospatial, attention, and executive function deficits are worse
-Memory impairment is not as severe
-Earlier presentation of psychosis and personality changes
-Rapid eye movement (REM) sleep disturbances
Differential diagnosis, clinical presentation: Frontotemporal degeneration (FTD) -
ANSWER_-Progressive behavioral and personality changes that impair social
conduct (apathy, disinhibition, etc.)
-Language impairment
-Possibly preserved episodic memory
Lewy Body Dementias (LBD) - ANSWER_Dementia with Lewy bodies (DLB)
and the related Parkinson's disease dementia (PDD)
-10-15% of all cases of dementia
-abnormal accumulation of a protein called α-synuclein
• aggregate to form oligomers, eventually turning into "Lewy bodies" & Lewy
neurites, as neurons degenerate
The Amyloid cascade Hypothesis - ANSWER_Alzheimer disease (AD) is caused
by the accumulation of toxic Aβ, which form into plaques, hyperphosphorylation
of tau, neurofibrillary tangle formation, synaptic dysfunction, and ultimately
neuron loss with memory loss and dementia
risk of developing AD - ANSWER_-inheritance of two copies of APOE4 leads to a
tenfold increased AD risk
-APOE2 gene appears to offer some protection from AD
-APOE3 gene (the most common form of the APOE gene) conveys a risk that falls
between APOE2 and APOE4
, NR 546 FINAL EXAM (NR546 ACTUAL) WITH CORRECT
A+ GRADED ANSWERS
Non-pharmacological options for behavioral symptoms in dementia - ANSWER_•
Address unmet needs (hunger, pain, thirst, boredom)
• Identify/modify environmental stressors
• Identify/modify daily routine stressors
• Caregiver support/training
• Behavior modification
• Group/individual therapy
• Problem solving
• Distraction
• Provide outlets for pent-up energy (exercise, activities)
• Avoid behavior triggers
• Increase social engagement
• Relaxation techniques
• Reminiscence therapy
• Music therapy
• Aromatherapy
• Pet therapy
Tx dementia-related psychosis – ANSWER Pimavanserin
-hypothetically reduces overactivity in the psychosis network caused by plaques,
tangles, Lewy bodies, or strokes, presumably by lowering the normal 5HT2A
stimulation to surviving glutamate neurons that have lost their GABA inhibition by
neurodegeneration
-approved for the treatment of Parkinson's disease psychosis & there are positive
trials in dementia-related psychosis
, NR 546 FINAL EXAM (NR546 ACTUAL) WITH CORRECT
A+ GRADED ANSWERS
Neuronal Networks of Agitation in Alzheimer Disease – ANSWER imbalance in
"top-down" cortical inhibition with "bottom-up" limbic and emotional drives
Targeting Multimodal Neurotransmitters (Norepinephrine, Serotonin, and
Dopamine) for the Symptomatic Treatment of Agitation in Alzheimer Disease –
ANSWER Brexpiprazole
-serotonin-dopamine-norepinephrine antagonist/partial agonist
-combines several simultaneous mechanisms to quell the excessive activity of the
agitation network in AD
-warning for increased mortality in dementia-related psychosis, using this agent for
agitation in AD and in doses lower than those generally used to treat psychosis in
schizophrenia may provide a greater safety margin
Targeting Glutamate for the Symptomatic Treatment of Agitation in Alzheimer
Disease – ANSWER dextromethorphan-bupropion
-The NMDA antagonist dextromethorphan (DXM), in combination with the
norepinephrine-dopamine reuptake inhibitor (NDRI) bupropion, is in testing as a
treatment for agitation
Apathy – ANSWER diminished motivation and reduced goal-directed behavior,
accompanied by decreased emotional responsiveness
-lack of motivation is at the core of apathy
-affects approximately 90% of patients with dementia
-one of the most persistent and frequent secondary behavioral symptoms of
dementia
-shown to predict disease-worsening
-if med needed for apathy: cholinesterase inhibitors are first-line in AD, FTD
patients may benefit mor
A+ GRADED ANSWERS
If an AD medication is discontinued: - ANSWER the medication may not be as
effective if restarted
Current gold standard of treatment for cognitive symptoms includes: - ANSWER
pharmacologic management with a cholinesterase inhibitor (ChEIs) and an N-
methyl-D-aspartate (NMDA) receptor antagonist.
Four Major causes of Dementia - ANSWER_-Alzheimer Disease (AD)
-vascular dementia
-Lewy body dementias (LBD)
-frontotemporal dementia (FTD)
three pathological hallmarks of AD seen in the brain at autopsy are: -
ANSWER_(1) amyloid-beta (Aβ), aggregated into plaques
(2) neurofibrillary tangles composed of hyperphosphorylated tau protein
(3) substantial neuronal cell loss
Differential diagnosis, clinical presentation: Vascular dementia - ANSWER_-
Impaired abstraction, mental flexibility, processing speed, and working memory
-Verbal memory is better preserved
-Slower cognitive decline
-Dementia occurs within several months of a stroke
Differential diagnosis, clinical presentation: Lewy body dementias (LBD) -
ANSWER_-Visual hallucinations
-Spontaneous parkinsonism
-Cognitive fluctuations
, NR 546 FINAL EXAM (NR546 ACTUAL) WITH CORRECT
A+ GRADED ANSWERS
-Visuospatial, attention, and executive function deficits are worse
-Memory impairment is not as severe
-Earlier presentation of psychosis and personality changes
-Rapid eye movement (REM) sleep disturbances
Differential diagnosis, clinical presentation: Frontotemporal degeneration (FTD) -
ANSWER_-Progressive behavioral and personality changes that impair social
conduct (apathy, disinhibition, etc.)
-Language impairment
-Possibly preserved episodic memory
Lewy Body Dementias (LBD) - ANSWER_Dementia with Lewy bodies (DLB)
and the related Parkinson's disease dementia (PDD)
-10-15% of all cases of dementia
-abnormal accumulation of a protein called α-synuclein
• aggregate to form oligomers, eventually turning into "Lewy bodies" & Lewy
neurites, as neurons degenerate
The Amyloid cascade Hypothesis - ANSWER_Alzheimer disease (AD) is caused
by the accumulation of toxic Aβ, which form into plaques, hyperphosphorylation
of tau, neurofibrillary tangle formation, synaptic dysfunction, and ultimately
neuron loss with memory loss and dementia
risk of developing AD - ANSWER_-inheritance of two copies of APOE4 leads to a
tenfold increased AD risk
-APOE2 gene appears to offer some protection from AD
-APOE3 gene (the most common form of the APOE gene) conveys a risk that falls
between APOE2 and APOE4
, NR 546 FINAL EXAM (NR546 ACTUAL) WITH CORRECT
A+ GRADED ANSWERS
Non-pharmacological options for behavioral symptoms in dementia - ANSWER_•
Address unmet needs (hunger, pain, thirst, boredom)
• Identify/modify environmental stressors
• Identify/modify daily routine stressors
• Caregiver support/training
• Behavior modification
• Group/individual therapy
• Problem solving
• Distraction
• Provide outlets for pent-up energy (exercise, activities)
• Avoid behavior triggers
• Increase social engagement
• Relaxation techniques
• Reminiscence therapy
• Music therapy
• Aromatherapy
• Pet therapy
Tx dementia-related psychosis – ANSWER Pimavanserin
-hypothetically reduces overactivity in the psychosis network caused by plaques,
tangles, Lewy bodies, or strokes, presumably by lowering the normal 5HT2A
stimulation to surviving glutamate neurons that have lost their GABA inhibition by
neurodegeneration
-approved for the treatment of Parkinson's disease psychosis & there are positive
trials in dementia-related psychosis
, NR 546 FINAL EXAM (NR546 ACTUAL) WITH CORRECT
A+ GRADED ANSWERS
Neuronal Networks of Agitation in Alzheimer Disease – ANSWER imbalance in
"top-down" cortical inhibition with "bottom-up" limbic and emotional drives
Targeting Multimodal Neurotransmitters (Norepinephrine, Serotonin, and
Dopamine) for the Symptomatic Treatment of Agitation in Alzheimer Disease –
ANSWER Brexpiprazole
-serotonin-dopamine-norepinephrine antagonist/partial agonist
-combines several simultaneous mechanisms to quell the excessive activity of the
agitation network in AD
-warning for increased mortality in dementia-related psychosis, using this agent for
agitation in AD and in doses lower than those generally used to treat psychosis in
schizophrenia may provide a greater safety margin
Targeting Glutamate for the Symptomatic Treatment of Agitation in Alzheimer
Disease – ANSWER dextromethorphan-bupropion
-The NMDA antagonist dextromethorphan (DXM), in combination with the
norepinephrine-dopamine reuptake inhibitor (NDRI) bupropion, is in testing as a
treatment for agitation
Apathy – ANSWER diminished motivation and reduced goal-directed behavior,
accompanied by decreased emotional responsiveness
-lack of motivation is at the core of apathy
-affects approximately 90% of patients with dementia
-one of the most persistent and frequent secondary behavioral symptoms of
dementia
-shown to predict disease-worsening
-if med needed for apathy: cholinesterase inhibitors are first-line in AD, FTD
patients may benefit mor
