MSN 672 Psychopathopharmacology II at Northern Kentucky University
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Free MSN 672 Psychopathopharmacology II at Northern Kentucky University Questions
------ and --------------, also known as α2δ ligands since they bind to the α2δ subunit of presynaptic N- and P/Q-type VSCCs, block the release of excitatory neurotransmitters such as glutamate that occurs when neurotransmission is excessive, as postulated in the amygdala to cause fear.
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Gabapentin and Pregabalin
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Serotonin and Norepinephrine reuptake inhibitors (SNRIs)
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Histamine and Serotonin
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Pregabalin and Histamine
Explanation
Gabapentin and Pregabalin are α2δ (alpha-2-delta) ligands that bind to the α2δ subunit of
presynaptic voltage-sensitive calcium channels (VSCCs), specifically the N-type and P/Q-type.
This binding reduces calcium influx and inhibits the excessive release of excitatory
neurotransmitters like glutamate. By dampening overactive neurotransmission in regions such as
the amygdala, these drugs help reduce symptoms of anxiety and fear, making them effective in
conditions like generalized anxiety disorder and neuropathic pain.
The PMHNP decides to prescribe carbamazepine for a patient diagnosed with bipolar disorder. What is the initial intervention needed prior to prescribing carbamazepine?
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Screen for HLA-B*1502 allele
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Screen for GM2 gangliosidosis
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Screen for CFTR allele
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Screen for Variation AQA2 allele
Explanation
A. Screen for HLA-B1502 allele
Carbamazepine can trigger Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis
(TEN) in individuals who carry the HLA-B1502 genetic variant. This allele is found primarily in
people of Asian descent, but screening is recommended for any patient whose ancestry places
them at risk. Testing must occur before starting carbamazepine to prevent life-threatening
reactions.
Which medications listed below are considered "off-label" treatments of panic attacks in anxiety disorders? (Select all that apply.)
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Trazodone
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Mirtazapine
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Risperidone
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Haloperidol
Explanation
While SSRIs, SNRIs, and benzodiazepines are first-line treatments for panic disorder, several
other medications have been used off-label when standard therapies are ineffective or poorly
tolerated:
A. Trazodone
Although primarily prescribed for depression and insomnia, trazodone’s serotonergic
modulation can help reduce anxiety and panic symptoms in some patients.
B. Mirtazapine
An atypical antidepressant that enhances serotonergic and noradrenergic transmission,
mirtazapine has been shown in studies to reduce panic frequency and anxiety intensity,
making it an off-label option.
C. Risperidone
An atypical antipsychotic, risperidone has been used off-label in refractory anxiety and panic
disorders due to its serotonin 5-HT₂ and dopamine D₂ receptor blockade, which can stabilize
mood and reduce panic severity.
A 29-year-old male presents with complaints of not being able to stay awake in the daytime. He falls asleep during exams and conversations with others. The patient was previously diagnosed with narcolepsy. The nurse practitioner understands that narcolepsy is due to the hypothalamic degeneration of what neurons? (Select all that apply.)
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Norepinephrine
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Hypocretin
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Orexin
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Acetylcholine
Explanation
B. Hypocretin:
Hypocretin, also known as orexin, is a neuropeptide produced in the lateral hypothalamus. It
plays a vital role in promoting wakefulness and maintaining stable sleep-wake transitions. The
loss or degeneration of hypocretin-producing neurons disrupts normal sleep regulation, leading
to the hallmark symptoms of narcolepsy such as excessive daytime sleepiness, cataplexy, and
sudden REM sleep episodes. Low levels of hypocretin are often found in the cerebrospinal fluid
of individuals with narcolepsy.
C. Orexin:
Orexin is the same neuropeptide as hypocretin but is named differently depending on its
discovery context. It helps sustain wakefulness, energy metabolism, and arousal by activating
multiple brain regions responsible for alertness. Degeneration of orexin neurons in the
hypothalamus removes this stabilizing influence, causing inappropriate REM sleep transitions
and uncontrollable sleep attacks. Both hypocretin and orexin systems are central to preventing
sudden sleep onset during active periods.
Which statement below best describes the difference between methadone or buprenorphine?
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Buprenorphine is a full agonist at μ-opioid receptors and can suppress withdrawal symptoms completely given orally and usually administered daily at a clinic. Methadone is a μ-opioid partial agonist that has less powerful agonist effects and taken as an outpatient instead of returning daily to a clinic
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Methadone and Buprenorphine are both full antagonists. Buprenorphine is a weaker antagonist than Methadone. Both can be taken outpatient daily
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Methadone is a full antagonist at μ-opioid receptors and can suppress withdrawal symptoms completely given orally and usually administered daily at a clinic. Buprenorphine is a μ-opioid partial antagonist that has less powerful antagonist effects and taken as an outpatient instead of returning daily to a clinic
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Methadone is a full agonist at μ-opioid receptors and can suppress withdrawal symptoms completely given orally and usually administered daily at a clinic. Buprenorphine is a μ-opioid partial agonist that has less powerful agonist effects and taken as an outpatient instead of returning daily to a clinic
Explanation
Methadone is a full μ-opioid agonist, meaning it fully activates opioid receptors and can completely suppress withdrawal and cravings. Because of overdose risk and regulation, methadone is typically administered daily in a specialized clinic. Buprenorphine is a partial μ-opioid agonist, producing a ceiling effect that lowers overdose risk. Its pharmacology allows it to be prescribed for outpatient use, making it more flexible while still treating withdrawal and cravings effectively.
Correct Answer Is:
D. Methadone is a full agonist at μ-opioid receptors and can suppress withdrawal symptoms completely given orally and usually administered daily at a clinic. Buprenorphine is a μ-opioid partial agonist that has less powerful agonist effects and taken as an outpatient instead of returning daily to a clinic
Sam is a 73-year-old patient with Alzheimer's disease. Sam has been on donepezil, 10 mg/day for approximately 8 months to aid in improving his cognitive functioning. Sam's wife has begun to notice a loss of effectiveness over the past months of donepezil. Sam's wife is requesting an intervention. The PMHNP decides to augment the donepezil with memantine 5 mg/day at hs. Which of the following properties of memantine listed below may be useful in treating Alzheimer's disease?
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Serotonin 3 (5HT3) antagonism
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Sigma antagonism
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N-methyl-D-aspartate (NMDA) antagonism at the PCP site
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N-methyl-D-aspartate (NMDA) antagonism at the magnesium site
Explanation
Memantine works by blocking excessive activation of NMDA receptors at the PCP (phencyclidine) binding site, which reduces glutamate-mediated excitotoxicity in the brain. In Alzheimer's disease, chronic overstimulation of NMDA receptors contributes to neuronal damage and cognitive decline. By modulating this pathway, memantine helps protect neurons and can improve or stabilize cognitive functioning, especially when used together with cholinesterase inhibitors like donepezil.
Correct Answer Is:
C. N-methyl-D-aspartate (NMDA) antagonism at the PCP site
A 55-year-old female patient taking buspirone for generalized anxiety disorder for the past year returns to the clinic for a refill. She gladly notes that recently she has begun to experience an increased ability to concentrate and is more interested in participating in volleyball, which she used to enjoy. "I'm not afraid to enjoy myself anymore." The patient reports to the PMHNP that her anxiety symptoms have improved tremendously. What may be the underlying mechanism of this patient's positive response to buspirone? Additionally, what subtype of anxiety does buspirone treat?
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The potential anxiolytic actions of buspirone could theoretically be due to 5HT1A partial agonist actions at both presynaptic and postsynaptic 5HT1A receptors/generalized anxiety disorder
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The potential anxiolytic actions of buspirone could theoretically be due to an initial increase in serotonin/social anxiety disorder
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The potential anxiolytic actions of buspirone could theoretically be due to a decreased glutamate release/panic disorder
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The potential anxiolytic actions of buspirone could theoretically be due to an increase in antihistamine release/post-traumatic stress disorder
Explanation
Buspirone exerts its anxiolytic effects primarily through partial agonist activity at 5HT1A
serotonin receptors located both presynaptically (inhibiting serotonin release) and
postsynaptically (enhancing serotonergic transmission). This modulation balances serotonin
levels in the brain, leading to reduced anxiety without sedation or dependency. Buspirone is
specifically indicated for generalized anxiety disorder (GAD) and helps improve focus, mood,
and engagement in daily activities. Its slow onset of action makes it ideal for long-term
management rather than acute anxiety relief.
Empathogens produce an altered state of consciousness described as experiences of emotional communion, oneness, relatedness, and emotional openness. Using the options below, please select the prototype empathogen.
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3,4-methylenedioxymethamphetamine (MDMA)
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Phencyclidine (PCP)
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Tropane Alkaloid (TK)
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Gamma-hydroxybutyrate (GHB)
Explanation
MDMA is the prototype empathogen, known for enhancing empathy, emotional closeness, and feelings of connection with others. It increases serotonin, dopamine, and oxytocin release, creating the emotional openness and interpersonal bonding characteristic of empathogens. PCP, tropane alkaloids, and GHB belong to different substance classes and do not produce the unique empathogenic effects seen with MDMA.
Correct Answer Is:
A. 3,4-methylenedioxymethamphetamine (MDMA)
Which of the following statements is true regarding first-line pharmacological treatment of agitation and aggression in a patient diagnosed with dementia?
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First-line pharmacological treatment of agitation and aggression in dementia is actually considered by many experts to be therapy with selective serotonin reuptake inhibitors (SSRIs) and serotonin–norepinephrine reuptake inhibitors (SNRIs), which can help some patients.
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First-line pharmacological treatment of agitation and aggression in dementia is actually considered by many experts to be therapy with selective second-generation antipsychotics which can help some patients.
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First-line pharmacological treatment of agitation and aggression in dementia is actually considered by many experts to be therapy with valproate which can help some patients.
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First-line pharmacological treatment of agitation and aggression in dementia is actually considered by many experts to be therapy with topiramate which can help some patients.
Explanation
SSRIs—especially citalopram and sertraline—are increasingly considered first-line pharmacologic options for agitation and aggression in dementia because they carry a far safer profile than antipsychotics. Antipsychotics, while effective, are not first-line due to their black box warning for increased mortality, risk of stroke, sedation, and extrapyramidal symptoms in elderly dementia patients. SSRIs target underlying affective symptoms such as irritability, anxiety, and depressive features that frequently drive behavioral disturbances, making them safer and often effective early options.
Correct Answer Is:
A. First-line pharmacological treatment of agitation and aggression in dementia is actually considered by many experts to be therapy with selective serotonin reuptake inhibitors (SSRIs) and serotonin–norepinephrine reuptake inhibitors (SNRIs), which can help some patients.
A 25-year-old patient comes into the clinic for treatment of alcoholism. The PMHNP decides to prescribe disulfiram for treatment of alcoholism. Which of the following statements best describes the action of disulfiram?
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When alcohol is ingested in the presence of disulfiram, alcohol metabolism is inhibited and the result is the build-up of toxic levels of acetaldehyde. This creates an aversive experience with flushing, nausea, vomiting, and hypotension
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When alcohol is ingested in the presence of disulfiram, alcohol metabolism is inhibited and the result is the build-up of toxic levels of acetanilide. This creates an aversive experience with flushing, nausea, vomiting, and hypertension
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When alcohol is ingested in the presence of disulfiram, alcohol metabolism is promoted and the result is the build-up of toxic levels of glutathione. This creates an aversive experience with flushing, nausea, vomiting, and hypertension
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When alcohol is ingested in the presence of disulfiram, alcohol metabolism is promoted and the result is the build-up of toxic levels of acetonitrile. This creates an aversive experience with flushing, nausea, vomiting, and hypotension
Explanation
Disulfiram works by inhibiting the enzyme aldehyde dehydrogenase, which is necessary for the breakdown of acetaldehyde, the toxic intermediate of alcohol metabolism. When alcohol is consumed while on disulfiram, acetaldehyde accumulates rapidly and produces an unpleasant reaction—flushing, severe nausea, vomiting, headache, chest pain, palpitations, and hypotension. This aversive reaction is intended to condition patients to avoid alcohol use.
Correct Answer Is:
A. When alcohol is ingested in the presence of disulfiram, alcohol metabolism is inhibited and the result is the build-up of toxic levels of acetaldehyde. This creates an aversive experience with flushing, nausea, vomiting, and hypotension
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