2024 NR 546 EXAM WITH
CORRECT ANSWERS
The etiology of AD - CORRECT-ANSWERSGenes appear to play a strong role,
with late-onset AD showing heritability of 58-79% and early-onset AD
showing over 90%
The etiology of AD - CORRECT-ANSWERSNeurons in the brains of clients who
develop AD may also have genetic coding abnormalities associated with
amyloid precursor protein, while mutations of at least three different
chromosomes, 21, 14, and 1, are associated with early-onset AD
Neuroanatomy of AD - CORRECT-ANSWERSTwo hallmarks of AD are amyloid
plaques and neurofibrillary tangles. Toxic amyloid plaques are believed to
form in the brain of clients with AD due to the abnormal processing of
amyloid precursor protein
Neuroanatomy of AD - CORRECT-ANSWERSCell death leads to the atrophy of
brain tissue, which affects the areas responsible for memory and higher-level
thinking, such as the hippocampus and cerebral cortex.
Neural Networks of AD - CORRECT-ANSWERSIn addition to the development
of amyloid plaques and neurofibrillary tangles, multiple cellular changes are
associated with AD, including damage to synapses, mitochondrial
abnormalities, and inflammatory processes. These changes are associated
with neurotransmitter failure and neuronal death.
Neural Signaling in AD - CORRECT-ANSWERSAcetylcholine (ACh) is a
neurotransmitter necessary for processing memory and learning. AD leads to
decreased acetylcholinesterase activity and a permanent loss of cholinergic
neurons.
Neural Signaling in AD - CORRECT-ANSWERSDecreased cholinergic function
is linked to memory dysfunction, particularly short-term memory. Neuronal
damage may also occur due to abnormal activation of N-methyl-d-aspartate
(NMDA) receptors by glutamate
Diagnosis of AD - CORRECT-ANSWERSAD is currently diagnosed through the
exclusion of other causes of dementia, such as vascular disease, Lewy body
dementia, Parkinson's disease, and Creutzfeldt-Jacob disease.
,Early symptoms of AD - CORRECT-ANSWERSEarly AD may include anxiety,
irritability, and sleep disruption, which could be the presenting symptoms
that bring clients to providers for treatment.
Stages of AD - CORRECT-ANSWERSPreclinical (asymptomatic but brain
amyloid is increased)
Mild cognitive impairment (neurodegeneration due to elevated tau and brain
volume loss)
Severe cognitive deficits-(dementia)
Treatment of dementia begins in what stage? - CORRECT-ANSWERSMild
stage. Pharmacologic treatment focusing on helping the client manage
symptoms and behavioral issues that may present.
Medications for Alzheimer's Disease - CORRECT-ANSWERSTreatment for AD
includes cholinesterase inhibitors (ChEIs) and memantine.
First-line treatment of AD - CORRECT-ANSWERSUse of a cholinesterase
inhibitor, which increases the availability of acetylcholine, and may help
maintain functional ability, and slow cognitive decline.
First-line treatment of AD - CORRECT-ANSWERSChEIs are likely to be most
effective in the early stages of AD when postsynaptic cholinergic receptors
are still available; however, once neurons are destroyed by the disease,
ChEIs are no longer effective
Cholinesterase Inhibitors (ChEIs) function - CORRECT-ANSWERSChEIs
increase levels of the neurotransmitter acetylcholine
ChEIs do not change the progression of AD; they provide some alleviation of
symptoms
Aricept Mechanism of Action - CORRECT-ANSWERSInhibits centrally active
acetylcholinesterase
Aricept Common Side Effects - CORRECT-ANSWERS· gastrointestinal
symptoms (nausea and diarrhea)
· headache
· dizziness
· muscle weakness
Aricept Precautions - CORRECT-ANSWERS· sick sinus syndrome
· seizure disorder
· Cholinesterase inhibitors are not recommended in pregnancy and lactation.
,Aricept Prescribing Pearls - CORRECT-ANSWERS· Taper to avoid withdrawal
effects.
· donepezil (Aricept) is approved to treat moderate to severe AD at 23
mg/day dose, but there is minimal improvement in cognitive functioning
when compared to a 10 mg/day dose. At the higher dose, donepezil has a
higher incidence of adverse effects.
Aricept Metabolism - CORRECT-ANSWERSWhen donepezil (Aricept) is added
to CYP2D6 or CYP3A4, there is a possibility of peripheral side effects, and
inducers of CYP2D6 and CYP3A4 may increase the rate of elimination
Rivastigmine (Exelon) Mechanism of Action - CORRECT-ANSWERS·
rivastigmine (Exelon) acts centrally for both acetylcholinesterase and
butyrylcholinesterase, thereby potentially increasing its efficacy.
Rivastigmine (Exelon) Common Side Effects - CORRECT-ANSWERS·
gastrointestinal symptoms (anorexia, nausea, vomiting, or diarrhea)
· weakness
· dizziness
· tremor
Rivastigmine (Exelon) Precautions - CORRECT-ANSWERS· asthma or chronic
obstructive pulmonary disorder (COPD)
· sick sinus syndrome
· gastrointestinal (GI) Bleeding
· weight < 50 kg
· asthma or chronic obstructive pulmonary disorder (COPD)
· sick sinus syndrome
· gastrointestinal (GI) Bleeding
· weight < 50 kg
· Cholinesterase inhibitors are not recommended in pregnancy and lactation.
Rivastigmine (Exelon) Prescribing Pearls - CORRECT-ANSWERS· rivastigmine
(Exelon) is administered orally or topically (transdermal patch).
· The transdermal patch is used for dementia associated with Parkinson's
disease.
Rivastigmine (Exelon) Metabolism - CORRECT-ANSWERSMedications that
induce or inhibit CYP450 metabolism will not modify rivastigmine (Exelon)
metabolism
Galantamine (Razadyne, Razadyne ER) Mechanism of Action - CORRECT-
ANSWERSgalantamine (Razadyne, Razadyne ER) acts by elevating
acetylcholine (Ach) in the cerebral cortex, modulating the nicotinic Ach
receptors to increase Ach release from existing presynaptic nerve terminals.
, It also increases glutamate and serotonin levels; however, the benefits of
this action are unknown
Galantamine (Razadyne, Razadyne ER) Side Effects - CORRECT-ANSWERS·
gastrointestinal symptoms (nausea, vomiting, diarrhea, anorexia, and weight
loss)
· headache
· dizziness
· fatigue
Galantamine (Razadyne, Razadyne ER) Precautions - CORRECT-ANSWERS·
nonsteroidal anti-inflammatory drug (NSAID) use
· GI bleed
· asthma or COPD
· concurrent use with medications that slow or decrease heart rate
Galantamine (Razadyne, Razadyne ER) Contraindications - CORRECT-
ANSWERS· severe hepatic impairment
· severe renal impairment
Galantamine (Razadyne, Razadyne ER) Metabolism - CORRECT-
ANSWERSThere are two major metabolizing enzymes CYP3A4 and CYP2D6
that increase galantamine (Razadyne, Razadyne ER) concentrations or
reductions in clearance and anticholinergic side effects when given
concurrently with inhibitors of these enzymes
Medications that induce or inhibit CYP450 metabolism will not modify
rivastigmine metabolism
N-Methyl-D-Aspartate NMDA receptor antagonist - CORRECT-
ANSWERSMemantine is the only NMDA approved to manage moderate to
severe AD. Based on clinical trials, improvement is modest
Memantine (Namenda) Mechanism of Action - CORRECT-ANSWERSThis drug
prevents glutamate, an excitatory neurotransmitter, from binding at the
receptor site. NMDA receptors control activity throughout the brain by
regulating how much calcium enters the nerve cell
Memantine (Namenda) Mechanism of Action - CORRECT-ANSWERSAn
overproduction of the NMDA receptor and excess glutamate can lead to
excessive calcium entering the cell and disrupting information processing.
Blocking NMDA receptors protects neurons from the effects of too much
glutamate without affecting normal neurotransmission
Memantine (Namenda) Common Side Effects - CORRECT-ANSWERS·
gastrointestinal symptoms (constipation, diarrhea, and weight gain)
· urinary frequency
CORRECT ANSWERS
The etiology of AD - CORRECT-ANSWERSGenes appear to play a strong role,
with late-onset AD showing heritability of 58-79% and early-onset AD
showing over 90%
The etiology of AD - CORRECT-ANSWERSNeurons in the brains of clients who
develop AD may also have genetic coding abnormalities associated with
amyloid precursor protein, while mutations of at least three different
chromosomes, 21, 14, and 1, are associated with early-onset AD
Neuroanatomy of AD - CORRECT-ANSWERSTwo hallmarks of AD are amyloid
plaques and neurofibrillary tangles. Toxic amyloid plaques are believed to
form in the brain of clients with AD due to the abnormal processing of
amyloid precursor protein
Neuroanatomy of AD - CORRECT-ANSWERSCell death leads to the atrophy of
brain tissue, which affects the areas responsible for memory and higher-level
thinking, such as the hippocampus and cerebral cortex.
Neural Networks of AD - CORRECT-ANSWERSIn addition to the development
of amyloid plaques and neurofibrillary tangles, multiple cellular changes are
associated with AD, including damage to synapses, mitochondrial
abnormalities, and inflammatory processes. These changes are associated
with neurotransmitter failure and neuronal death.
Neural Signaling in AD - CORRECT-ANSWERSAcetylcholine (ACh) is a
neurotransmitter necessary for processing memory and learning. AD leads to
decreased acetylcholinesterase activity and a permanent loss of cholinergic
neurons.
Neural Signaling in AD - CORRECT-ANSWERSDecreased cholinergic function
is linked to memory dysfunction, particularly short-term memory. Neuronal
damage may also occur due to abnormal activation of N-methyl-d-aspartate
(NMDA) receptors by glutamate
Diagnosis of AD - CORRECT-ANSWERSAD is currently diagnosed through the
exclusion of other causes of dementia, such as vascular disease, Lewy body
dementia, Parkinson's disease, and Creutzfeldt-Jacob disease.
,Early symptoms of AD - CORRECT-ANSWERSEarly AD may include anxiety,
irritability, and sleep disruption, which could be the presenting symptoms
that bring clients to providers for treatment.
Stages of AD - CORRECT-ANSWERSPreclinical (asymptomatic but brain
amyloid is increased)
Mild cognitive impairment (neurodegeneration due to elevated tau and brain
volume loss)
Severe cognitive deficits-(dementia)
Treatment of dementia begins in what stage? - CORRECT-ANSWERSMild
stage. Pharmacologic treatment focusing on helping the client manage
symptoms and behavioral issues that may present.
Medications for Alzheimer's Disease - CORRECT-ANSWERSTreatment for AD
includes cholinesterase inhibitors (ChEIs) and memantine.
First-line treatment of AD - CORRECT-ANSWERSUse of a cholinesterase
inhibitor, which increases the availability of acetylcholine, and may help
maintain functional ability, and slow cognitive decline.
First-line treatment of AD - CORRECT-ANSWERSChEIs are likely to be most
effective in the early stages of AD when postsynaptic cholinergic receptors
are still available; however, once neurons are destroyed by the disease,
ChEIs are no longer effective
Cholinesterase Inhibitors (ChEIs) function - CORRECT-ANSWERSChEIs
increase levels of the neurotransmitter acetylcholine
ChEIs do not change the progression of AD; they provide some alleviation of
symptoms
Aricept Mechanism of Action - CORRECT-ANSWERSInhibits centrally active
acetylcholinesterase
Aricept Common Side Effects - CORRECT-ANSWERS· gastrointestinal
symptoms (nausea and diarrhea)
· headache
· dizziness
· muscle weakness
Aricept Precautions - CORRECT-ANSWERS· sick sinus syndrome
· seizure disorder
· Cholinesterase inhibitors are not recommended in pregnancy and lactation.
,Aricept Prescribing Pearls - CORRECT-ANSWERS· Taper to avoid withdrawal
effects.
· donepezil (Aricept) is approved to treat moderate to severe AD at 23
mg/day dose, but there is minimal improvement in cognitive functioning
when compared to a 10 mg/day dose. At the higher dose, donepezil has a
higher incidence of adverse effects.
Aricept Metabolism - CORRECT-ANSWERSWhen donepezil (Aricept) is added
to CYP2D6 or CYP3A4, there is a possibility of peripheral side effects, and
inducers of CYP2D6 and CYP3A4 may increase the rate of elimination
Rivastigmine (Exelon) Mechanism of Action - CORRECT-ANSWERS·
rivastigmine (Exelon) acts centrally for both acetylcholinesterase and
butyrylcholinesterase, thereby potentially increasing its efficacy.
Rivastigmine (Exelon) Common Side Effects - CORRECT-ANSWERS·
gastrointestinal symptoms (anorexia, nausea, vomiting, or diarrhea)
· weakness
· dizziness
· tremor
Rivastigmine (Exelon) Precautions - CORRECT-ANSWERS· asthma or chronic
obstructive pulmonary disorder (COPD)
· sick sinus syndrome
· gastrointestinal (GI) Bleeding
· weight < 50 kg
· asthma or chronic obstructive pulmonary disorder (COPD)
· sick sinus syndrome
· gastrointestinal (GI) Bleeding
· weight < 50 kg
· Cholinesterase inhibitors are not recommended in pregnancy and lactation.
Rivastigmine (Exelon) Prescribing Pearls - CORRECT-ANSWERS· rivastigmine
(Exelon) is administered orally or topically (transdermal patch).
· The transdermal patch is used for dementia associated with Parkinson's
disease.
Rivastigmine (Exelon) Metabolism - CORRECT-ANSWERSMedications that
induce or inhibit CYP450 metabolism will not modify rivastigmine (Exelon)
metabolism
Galantamine (Razadyne, Razadyne ER) Mechanism of Action - CORRECT-
ANSWERSgalantamine (Razadyne, Razadyne ER) acts by elevating
acetylcholine (Ach) in the cerebral cortex, modulating the nicotinic Ach
receptors to increase Ach release from existing presynaptic nerve terminals.
, It also increases glutamate and serotonin levels; however, the benefits of
this action are unknown
Galantamine (Razadyne, Razadyne ER) Side Effects - CORRECT-ANSWERS·
gastrointestinal symptoms (nausea, vomiting, diarrhea, anorexia, and weight
loss)
· headache
· dizziness
· fatigue
Galantamine (Razadyne, Razadyne ER) Precautions - CORRECT-ANSWERS·
nonsteroidal anti-inflammatory drug (NSAID) use
· GI bleed
· asthma or COPD
· concurrent use with medications that slow or decrease heart rate
Galantamine (Razadyne, Razadyne ER) Contraindications - CORRECT-
ANSWERS· severe hepatic impairment
· severe renal impairment
Galantamine (Razadyne, Razadyne ER) Metabolism - CORRECT-
ANSWERSThere are two major metabolizing enzymes CYP3A4 and CYP2D6
that increase galantamine (Razadyne, Razadyne ER) concentrations or
reductions in clearance and anticholinergic side effects when given
concurrently with inhibitors of these enzymes
Medications that induce or inhibit CYP450 metabolism will not modify
rivastigmine metabolism
N-Methyl-D-Aspartate NMDA receptor antagonist - CORRECT-
ANSWERSMemantine is the only NMDA approved to manage moderate to
severe AD. Based on clinical trials, improvement is modest
Memantine (Namenda) Mechanism of Action - CORRECT-ANSWERSThis drug
prevents glutamate, an excitatory neurotransmitter, from binding at the
receptor site. NMDA receptors control activity throughout the brain by
regulating how much calcium enters the nerve cell
Memantine (Namenda) Mechanism of Action - CORRECT-ANSWERSAn
overproduction of the NMDA receptor and excess glutamate can lead to
excessive calcium entering the cell and disrupting information processing.
Blocking NMDA receptors protects neurons from the effects of too much
glutamate without affecting normal neurotransmission
Memantine (Namenda) Common Side Effects - CORRECT-ANSWERS·
gastrointestinal symptoms (constipation, diarrhea, and weight gain)
· urinary frequency
