NR 546 PSYCHOPHARMACOLOGY FINAL Exam Latest Updated 2025 Questions With
Detailed Answers
patho of alzheimer's disease
progressive, neurodegenerative, irreversible, memory loss and decreasing brain function
most common type of dementia
70% of all dementia cases
no cure
treatment may alter disease progression and reduce symptoms
10 early warning signs of AD:
memory loss
challenges in planning or solving problems
trouble understanding visual and spatial relationships
difficulty completing familiar tasks
disorientation
problems with word finding
misplacing things
impaired judgment
social withdrawal
changes in mood
Cause of AD:
plaques: abnormal protein fragments between neurons
tangles: tau protein twisted and abnormal inside neurons
Genetics of AD:
late-onset AD showing heritability of 58-79%
early-onset AD showing over 90%
genetic coding abnormalities with amyloid precursor protein
mutations of at least three different chromosomes, 21, 14, and 1
Nueroanatomy of AD:
Toxic amyloid plaques - form in the brain due to the abnormal processing of amyloid
precursor protein
Amyloid plaques and neurofibrillary tangles - impair the function of neurons
lose connections with other brain cells and die
,Cell death leads to the atrophy of brain tissue
affects the areas responsible for memory and higher-level thinking
such as the hippocampus and cerebral cortex
Atrophy also leads to enlarged ventricles.
Neural Signaling of AD:
Acetylcholine (ACh) - neurotransmitter necessary for processing memory and learning.
AD leads to decreased acetylcholinesterase activity and a permanent loss of cholinergic
neurons.
Decreased cholinergic function is linked to memory dysfunction, particularly short-term
memory
Neuronal damage may also occur due to abnormal activation of NMDA receptors by
glutamate
early stage of AD
(1-3 years)
short term memory deficits
disoriented to date
diminished recall of recent events
mild language and decision-making deficits
mild problem copying figures (clock drawing)
social withdrawal
mood change
personality changes
problems with managing finances
middle stage of AD
(2-8 years)
disoriented to date and place
may get lost in familiar places
impaired learning new skills
agitation, aggression, restlessness, or anxiety
difficulty with activities of daily living (ADLs) such as cooking and grooming
late stage AD
(6-12 years)
disoriented to person, time, or place
non-verbal
, long term memory diminished
unable to groom or dress
progress to need for total care at end stage
incontinent
motor or verbal agitation
medical tests for diagnosing AD
medical history, physical exam, neurological exam, cognitive functional and behavior tests,
computerized cognitive tests and devices, depression screen and mood assessment, brain
imaging, cerebrospinal fluid tests, blood test (not FDA approved)
cholinesterase inhibitors
first line treatment
increases availability of acetylcholine!
may help maintain function ability and slow cognitive decline
most effective in early stages of AD when postsynaptic cholinergic receptors are still
available, and the neurons are not destroyed yet by the disease
they do not change progression, just alleviate some symptoms
NOT recommended in pregnancy and lactation.
donepezil
mild, moderate, severe AD
also treats psychological symptoms of AD such as anxiety, depression, apathy, delusions,
and pacing
MOA: inhibits centrally active acetylcholinesterase
Dose: 5 mg/day
adverse effects: GI s/s, headache, dizziness, muscle weakness
cautions: sick sinus syndrome, seizure disorder, increases gastric acid secretion,
bradycardia
taper to avoid withdrawals!
*donepezil at a higher dose has a higher incidence of adverse effects without increased
cognitive benefit
rivastigmine
mild-moderate AD & parkinsons disease dementia
MOA: inhibits both centrally active acetylcholinesterase and butyrylcholinesterase,
increasing its efficacy
dose: 1.5 mg twice daily OR transdermal patch 4.6 mg/24 hours
Detailed Answers
patho of alzheimer's disease
progressive, neurodegenerative, irreversible, memory loss and decreasing brain function
most common type of dementia
70% of all dementia cases
no cure
treatment may alter disease progression and reduce symptoms
10 early warning signs of AD:
memory loss
challenges in planning or solving problems
trouble understanding visual and spatial relationships
difficulty completing familiar tasks
disorientation
problems with word finding
misplacing things
impaired judgment
social withdrawal
changes in mood
Cause of AD:
plaques: abnormal protein fragments between neurons
tangles: tau protein twisted and abnormal inside neurons
Genetics of AD:
late-onset AD showing heritability of 58-79%
early-onset AD showing over 90%
genetic coding abnormalities with amyloid precursor protein
mutations of at least three different chromosomes, 21, 14, and 1
Nueroanatomy of AD:
Toxic amyloid plaques - form in the brain due to the abnormal processing of amyloid
precursor protein
Amyloid plaques and neurofibrillary tangles - impair the function of neurons
lose connections with other brain cells and die
,Cell death leads to the atrophy of brain tissue
affects the areas responsible for memory and higher-level thinking
such as the hippocampus and cerebral cortex
Atrophy also leads to enlarged ventricles.
Neural Signaling of AD:
Acetylcholine (ACh) - neurotransmitter necessary for processing memory and learning.
AD leads to decreased acetylcholinesterase activity and a permanent loss of cholinergic
neurons.
Decreased cholinergic function is linked to memory dysfunction, particularly short-term
memory
Neuronal damage may also occur due to abnormal activation of NMDA receptors by
glutamate
early stage of AD
(1-3 years)
short term memory deficits
disoriented to date
diminished recall of recent events
mild language and decision-making deficits
mild problem copying figures (clock drawing)
social withdrawal
mood change
personality changes
problems with managing finances
middle stage of AD
(2-8 years)
disoriented to date and place
may get lost in familiar places
impaired learning new skills
agitation, aggression, restlessness, or anxiety
difficulty with activities of daily living (ADLs) such as cooking and grooming
late stage AD
(6-12 years)
disoriented to person, time, or place
non-verbal
, long term memory diminished
unable to groom or dress
progress to need for total care at end stage
incontinent
motor or verbal agitation
medical tests for diagnosing AD
medical history, physical exam, neurological exam, cognitive functional and behavior tests,
computerized cognitive tests and devices, depression screen and mood assessment, brain
imaging, cerebrospinal fluid tests, blood test (not FDA approved)
cholinesterase inhibitors
first line treatment
increases availability of acetylcholine!
may help maintain function ability and slow cognitive decline
most effective in early stages of AD when postsynaptic cholinergic receptors are still
available, and the neurons are not destroyed yet by the disease
they do not change progression, just alleviate some symptoms
NOT recommended in pregnancy and lactation.
donepezil
mild, moderate, severe AD
also treats psychological symptoms of AD such as anxiety, depression, apathy, delusions,
and pacing
MOA: inhibits centrally active acetylcholinesterase
Dose: 5 mg/day
adverse effects: GI s/s, headache, dizziness, muscle weakness
cautions: sick sinus syndrome, seizure disorder, increases gastric acid secretion,
bradycardia
taper to avoid withdrawals!
*donepezil at a higher dose has a higher incidence of adverse effects without increased
cognitive benefit
rivastigmine
mild-moderate AD & parkinsons disease dementia
MOA: inhibits both centrally active acetylcholinesterase and butyrylcholinesterase,
increasing its efficacy
dose: 1.5 mg twice daily OR transdermal patch 4.6 mg/24 hours
