MSN 672 Psychopathopharmacology II at Northern Kentucky University
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Free MSN 672 Psychopathopharmacology II at Northern Kentucky University Questions
The PMHNP does patient education with a 24-year-old female who is prescribed a mood stabilizer. The PMHNP informed the patient that she could experience the following side effects: weight gain, hair loss, acne, tremor, sedation, decrease in kidney function, and hypothyroidism. What medication is the PMHNP most likely prescribing that is congruent with this side-effect profile?
- Olanzapine
- Lithium
- Valproate
- Fluoxetine
Explanation
B. Lithium
This side-effect profile matches lithium more closely than any other option. Lithium commonly
causes weight gain, acne, hair loss (alopecia), tremor, and sedation. It can also lead to
decreased kidney function (nephrogenic diabetes insipidus) and hypothyroidism, both
hallmark long-term adverse effects requiring routine monitoring of renal and thyroid labs. These
combined features distinctly point toward lithium therapy.
The nurse practitioner is assessing a 28-year-old female patient diagnosed with bipolar I disorder. The nurse practitioner determines the patient is experiencing rapid mood cycling and decides to order valproate. Which of the following questions should the nurse practitioner ask the patient first before prescribing valproate?
- When was your last menstrual period
- How much do you weigh
- Do you experience migraine headaches or seizures
- None of the above
Explanation
A. When was your last menstrual period
Valproate is highly teratogenic and associated with severe fetal neural tube defects, decreased
IQ, and developmental disorders. For any patient who can become pregnant—especially a
28-year-old woman—the first priority is assessing pregnancy status. Providers must confirm that
the patient is not pregnant and discuss reliable contraception before prescribing valproate.
A 35-year-old man Army veteran presents with a chief complaint of excessive crying, which he notes is often triggered by thoughts of dying prior to seeing his family again. His wife reports that he is often tense and “flies off the handle,” followed by episodes of difficulty breathing and increased heart rate. The patient’s symptom of difficulty breathing is related to activation of what part of the brain?
- Hippocampus
- Hypothalamus
- Parabrachial nucleus
- Periaqueductal gray
Explanation
The parabrachial nucleus, located in the pons, plays a key role in autonomic and respiratory
regulation. It integrates input from emotional centers such as the amygdala and hypothalamus
and translates those emotional signals into physiological responses—including changes in
breathing and heart rate. In emotionally charged states such as anxiety or panic, activation of
this area can cause the sensation of difficulty breathing and hyperventilation.
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.)
- Norepinephrine
- Hypocretin
- Orexin
- 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?
- 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
- Methadone and Buprenorphine are both full antagonists. Buprenorphine is a weaker antagonist than Methadone. Both can be taken outpatient daily
- 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
- 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
Binge Eating Disorder (BED) is a condition that is part of the addictive disorders and is amongst the impulsive-compulsive disorders as well. BED is hypothesized to be linked to abnormalities in what part of the brain (where impulsivity leads to compulsivity)?
- Arachnoid membrane
- Cerebral cortex circuitry
- Cortical striatal circuitry
- Corpus callosum circuitry
Explanation
Cortical–striatal circuitry plays a central role in the transition from impulsivity to compulsivity, which is a hallmark of Binge Eating Disorder (BED). This brain pathway connects the prefrontal cortex with the striatum and is responsible for reward processing, impulse control, habit formation, and compulsive behaviors. Dysregulation in this circuit can impair inhibitory control and increase repetitive, compulsive eating patterns seen in BED.
Correct Answer Is:
C. Cortical striatal circuitry
------ 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.
- Gabapentin and Pregabalin
- Serotonin and Norepinephrine reuptake inhibitors (SNRIs)
- Histamine and Serotonin
- 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.
A 42-year-old police officer presents to the clinic with complaints of "sleep disturbances." After sufficient consultation, you prescribe the patient eszopiclone. Which receptors are primarily being targeted by this treatment, producing the desired effect of sedation?
- GABAA receptors that contain the α1 subunit/subtype
- Serotonin receptor that contains the β1 subtype/subunit
- Histamine1 receptor that contains an α2 subunit/subtype
- Histamine2 receptor that contains β2 subunits/subtypes
Explanation
Eszopiclone, a non-benzodiazepine hypnotic (commonly known as a “Z-drug”), selectively
binds to the GABAA receptor complex containing the α1 subunit. This subunit is primarily
responsible for the sedative and hypnotic effects of GABAergic medications. When eszopiclone
enhances GABA’s action at these receptors, it increases chloride ion flow, hyperpolarizing
neurons and inducing sleep without significant muscle relaxation or anticonvulsant properties.
This selective binding explains its efficacy in treating insomnia with minimal next-day sedation.
Which of the following medications is a D2 antagonist and is approved for bipolar depression?
- Risperidone
- Valproate
- Quetiapine
- Clonazepam
Explanation
C. Quetiapine
Quetiapine is an atypical antipsychotic that acts as a D2 antagonist and 5-HT2A antagonist. It
is FDA-approved for bipolar depression, bipolar mania, and maintenance therapy. Its
antidepressant effects come from its serotonergic actions, while its D2 blockade helps stabilize
mood and reduce agitation.
Histamine neurons all arise from a single small area of the hypothalamus known as the __________________.
- Laterodorsal Tegmental Nuclei
- Raphe Nuclei
- Tuberomammillary nucleus
- Locus Coeruleus
Explanation
All histaminergic neurons in the brain originate from the tuberomammillary nucleus of the
posterior hypothalamus. These neurons project widely throughout the central nervous system
and play a crucial role in maintaining wakefulness, attention, and arousal. The histamine
system is a key component of the ascending reticular activating system (ARAS). Inhibition of
these neurons—such as by sedating antihistamines—leads to drowsiness and reduced
alertness.
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