MSN 627 Psychopathopharmacology II
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Free MSN 627 Psychopathopharmacology II Questions
Histamine neurons all arise from a single small area of the hypothalamus known as the __________________.
- A. Laterodorsal Tegmental Nuclei
- B. Raphe Nuclei
- C. Tuberomammillary nucleus
- D. 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.
Which of the following neurotransmitters are considered part of the ascending reticular activating system in the brain that works together to regulate arousal? (Select all that apply.)
- A. Histamine
- B. Dopamine
- C. Orexin
- D. Methylation
Explanation
The ascending reticular activating system (ARAS) is responsible for regulating arousal,
wakefulness, and attention. Several neurotransmitters play a central role in this process:
A. Histamine
Histamine is produced in the tuberomammillary nucleus of the hypothalamus and promotes
alertness and wakefulness. Antihistamine medications that cross the blood-brain barrier often
cause drowsiness due to histamine inhibition.
B. Dopamine
Dopamine, released from the ventral tegmental area (VTA) and other midbrain regions, is
essential for maintaining arousal, motivation, and cognitive alertness. It supports the brain’s
reward and activation pathways that sustain wakefulness.
C. Orexin
Orexin (also known as hypocretin), produced in the lateral hypothalamus, stabilizes
wakefulness by stimulating other arousal-promoting systems. Deficiency in orexin is associated
with narcolepsy.
You have a 29-year-old patient with a history of Bipolar Disorder who comes in for a routine check-up. She is currently taking Lithium ER 450 mg PO at HS. The patient’s lithium level is 0.9. What is your next action as a nurse practitioner?
- A. Discontinue lithium and start valproate
- B. Give the medication as ordered and monitor lithium levels
- C. Hold lithium x72 hours and draw lithium level after 72 hours
- D. Hold lithium and notify medical for intervention
Explanation
A lithium level of 0.9 mEq/L is therapeutic (normal range: 0.6–1.2 mEq/L for maintenance).
The patient is stable, and there is no indication of toxicity or side effects requiring dose
adjustment. The appropriate action is to continue lithium as prescribed and maintain routine
monitoring. No medication changes or holds are required.
This particular mood stabilizer has a profound immediate suppressant effect upon the bone marrow, requiring initial monitoring of blood counts and notable induction of the cytochrome P450 enzyme. Which mood stabilizer is this?
- A. Lithium
- B. Carbamazepine
- C. Valproate
- D. Topiramate
Explanation
B. Carbamazepine
Carbamazepine can cause bone marrow suppression, including leukopenia, anemia, and, in
severe cases, aplastic anemia or agranulocytosis. Therefore, baseline and ongoing CBC
monitoring is required. Additionally, carbamazepine is a strong inducer of cytochrome P450
(CYP3A4), which can significantly lower serum levels of many medications by speeding their
metabolism. This combination—bone marrow suppression plus CYP450 induction—uniquely
fits carbamazepine.
Which symptoms should be reported immediately due to severity in a 15-year-old patient prescribed valproate? Select all that apply.
- A. Vomiting
- B. Severe abdominal pain
- C. Oily, smelly stools
- D. Weight gain
Explanation
A. Vomiting
Vomiting can be an early sign of valproate-induced hepatotoxicity or pancreatitis, both of
which are medical emergencies. Any sudden or severe vomiting in a patient taking valproate
requires immediate evaluation.
B. Severe abdominal pain
Severe or persistent abdominal pain is a classic warning sign of acute pancreatitis, a life-threatening adverse reaction to valproate. This symptom must be reported immediately for
emergency assessment.
C. Oily, smelly stools
Oily, foul-smelling stools (steatorrhea) may indicate pancreatic dysfunction, which can occur
in valproate-induced pancreatitis. This is a red-flag symptom requiring urgent medical attention.
A 28-year-old male returns to the clinic and reports worsening of nightmares after taking Trazodone for one month. The PMHNP reviewed the patient’s records and notices the patient has a chronic history of PTSD and alcoholism. What is likely the most appropriate alternative treatment for this patient?
- A. Switch to a Benzodiazepine
- B. Switch to Aripiprazole
- C. Switch to Wellbutrin
- D. Switch to α1 antagonists
Explanation
α1 antagonists, such as Prazosin, are effective in treating PTSD-related nightmares and sleep disturbances. Prazosin works by blocking adrenergic activity, reducing the excessive
noradrenergic response during sleep that contributes to vivid dreams and nightmares. Unlike
benzodiazepines or antidepressants, it has minimal risk for dependency—making it particularly
appropriate for a patient with a history of alcoholism. It improves sleep quality and decreases the
frequency and severity of trauma-related nightmares.
The PMHNP understands that anxiety can be triggered internally from traumatic memories stored in the ______________ and activated by connections with the ______________, especially in conditions such as PTSD.
- A. Hippocampus and Amygdala
- B. Parietal Lobe and Basal Forebrain
- C. Nucleus Caudate and Prefrontal Cortex
- D. Periaqueductal Gray and Nucleus Accumbens
Explanation
In post-traumatic stress disorder (PTSD), traumatic memories are stored in the hippocampus, the brain region responsible for memory formation and contextual processing.
When these memories are recalled or triggered, they activate the amygdala, which governs fear,
emotional response, and threat detection. This hippocampus–amygdala connection explains
why certain cues or internal thoughts can evoke intense anxiety, hyperarousal, or flashbacks in
PTSD patients.
Which medications listed below are considered "off-label" treatments of panic attacks in anxiety disorders? (Select all that apply.)
- A. Trazodone
- B. Mirtazapine
- C. Risperidone
- D. 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 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?
- A. GABAA receptors that contain the α1 subunit/subtype
- B. Serotonin receptor that contains the β1 subtype/subunit
- C. Histamine1 receptor that contains an α2 subunit/subtype
- D. 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.
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?
- A. 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
- B. The potential anxiolytic actions of buspirone could theoretically be due to an initial increase in serotonin/social anxiety disorder
- C. The potential anxiolytic actions of buspirone could theoretically be due to a decreased glutamate release/panic disorder
- D. 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.
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