200 Multiple Choice Questions with Bold Italic
Answers and Italic Explanations |2026/2027 |
( 100% correct answers ) upgrade
1. During assessment a patient states “Why are you asking me about my heart, I am here for my
head”, the PMHNP’s best response is:
A) "Your heart has nothing to do with your mental health."
B) "Anxiety can cause cortisol levels to increase and when this happens frequently it puts you at risk
for comorbidities such as type 2 diabetes."
C) "I am required to ask these questions by hospital policy."
D) "Your head and heart are connected through the nervous system."
This response provides psychoeducation about the physiological impact of chronic anxiety. Elevated
cortisol from chronic stress contributes to metabolic syndrome and type 2 diabetes, making this a
clinically appropriate and therapeutic response .
2. During gene expression, what must occur prior to a gene being expressed?
A) Transcription factor must bind to the regulatory region within the cell's nucleus.
B) The cell must divide.
C) The gene must be methylated.
D) The protein must be translated.
Transcription factors are proteins that bind to specific DNA sequences to regulate gene transcription.
Before a gene can be expressed, transcription factors must bind to regulatory regions (promoters or
enhancers) to initiate the transcription process .
3. The PMHNP is assessing a 29-year-old client who takes antipsychotics that block D2 receptors. This
client has begun to develop a common side effect of this medication. What is this side effect?
A) Weight gain
B) Sedation
C) Agranulocytosis
D) Tardive dyskinesia
,Chronic D2 receptor blockade in the nigrostriatal pathway leads to dopamine receptor supersensitivity,
which manifests as tardive dyskinesia—involuntary choreiform movements of the face, tongue, and
extremities. This is a well-known long-term side effect of typical antipsychotics .
4. After ordering flumazenil (Romazicon) the PMHNP cautions the staff to monitor for which possible
effect?
A) Hypotension
B) Tachycardia
C) Seizures
D) Respiratory depression
Flumazenil, a benzodiazepine antagonist, can precipitate seizures, particularly in patients with chronic
benzodiazepine dependence or those who have co-ingested proconvulsant drugs such as tricyclic
antidepressants. Seizures are the most significant adverse effect to monitor .
5. A patient is prescribed 50 mg of desvenlafaxine to take every other day for major depressive
disorder. What does the PMHNP understand about this patient?
A) The patient has hepatic impairment.
B) The patient is elderly.
C) The patient has severe renal impairment.
D) The patient has a history of seizures.
Desvenlafaxine is primarily renally excreted. In patients with severe renal impairment (CrCl <30 mL/min),
the recommended dose is reduced to 50 mg every other day. This dosing adjustment prevents drug
accumulation and toxicity .
6. A patient is prescribed sertraline to treat panic disorder. Knowing that sertraline can initially cause
anxiety or insomnia, what should the PMHNP do?
A) Start sertraline at a high dose.
B) Prescribe a short-acting benzodiazepine for 2 weeks, then discontinue.
C) Discontinue sertraline and try a different medication.
D) Increase the sertraline dose to overcome the side effect.
SSRIs can cause initial activation (anxiety, insomnia) before therapeutic benefits appear. A short-term
benzodiazepine (2 weeks) can bridge this period, then be tapered and discontinued. This strategy
improves adherence while waiting for the SSRI to become effective .
7. Though medications have the ability to target neurotransmitter release into the synapse by the
presynaptic neuron it is not always necessary. The PMHNP understands that this is because:
,A) Medications can directly enter the postsynaptic neuron.
B) Neurotransmitters can spread by diffusion.
C) Receptors can produce their own neurotransmitters.
D) The synapse is not important for neurotransmission.
Neurotransmitters can diffuse across the synaptic cleft and act on receptors without requiring
presynaptic release modulation. This diffusion-based neurotransmission (volume transmission) allows
neurotransmitters to affect distant receptors, making direct presynaptic modulation less critical for some
medications .
8. A patient is diagnosed with schizophrenia. What increases the patient's potential to mediate the
cognitive symptoms of the disease?
A) Achieving underactivity of the mesocorticol projections to the prefrontal cortex
B) Achieving overactivity of the mesolimbic pathway
C) Blocking all dopamine receptors
D) Increasing serotonin in the prefrontal cortex
Cognitive symptoms of schizophrenia (working memory, executive function) are associated with
hypofrontality—underactivity of dopamine projections to the prefrontal cortex. Achieving underactivity
in the mesocorticol pathway helps mediate cognitive symptoms by balancing dopamine levels in this
region .
9. The PMHNP spends a session with a client and notices behaviors correlating with a potential manic
episode. All of the following are possible manic symptoms the PMHNP could observe except:
A) Grandiosity
B) Decreased need for sleep
C) Pressured speech
D) Low self-esteem
Low self-esteem is a depressive symptom, not a manic symptom. Manic episodes are characterized by
grandiosity, decreased need for sleep, pressured speech, racing thoughts, distractibility, increased goal-
directed activity, and excessive involvement in risky activities .
10. A patient who is prescribed MAO inhibitors asks about whether he can continue taking
pseudoephedrine to relieve his congestion. Which response by the PMHNP indicates proper
understanding of drug-drug interactions?
A) "Pseudoephedrine is safe to take with MAOIs."
B) "You can take pseudoephedrine if you monitor your blood pressure."
C) "Pseudoephedrine may reduce the effectiveness of MAOIs."
D) "Decongestants should be avoided due to risk of hypertensive crisis."
, MAOIs inhibit the breakdown of tyramine and other sympathomimetic amines. Pseudoephedrine, a
sympathomimetic decongestant, can cause a hypertensive crisis when combined with MAOIs due to
excessive norepinephrine release. This combination is contraindicated .
11. Fluoxetine (Prozac) has been prescribed for a client with depression. Which of the following
statements is true regarding the action of this medication?
A) Fluoxetine blocks dopamine receptors.
B) Fluoxetine inhibits the serotonin transporter (SERT).
C) Fluoxetine increases norepinephrine reuptake.
D) Fluoxetine works on GABA receptors.
Fluoxetine is a selective serotonin reuptake inhibitor (SSRI) that works by inhibiting the serotonin
transporter (SERT), preventing serotonin reuptake into the presynaptic neuron. This increases serotonin
availability in the synaptic cleft .
12. A patient was diagnosed with GAD 4 weeks ago and was placed on Clonazepam (Klonopin) twice a
day and Citalopram (Celexa) once daily. When he asks the PMHNP why it is necessary to wean him off
of the Clonazepam, the best response is:
A) Benzodiazepines can lead to tolerance and dependence, and should be used short-term.
B) Citalopram is more effective than Clonazepam.
C) Clonazepam has too many side effects.
D) The patient no longer needs the Clonazepam.
Benzodiazepines are effective for short-term anxiety relief but carry risks of tolerance, dependence, and
withdrawal. For GAD, SSRIs like citalopram are first-line maintenance treatment. The benzodiazepine is
used as a bridge during the SSRI's initial 2-4 week lag period .
13. A patient with schizophrenia is given an inverse agonist that acts on the receptor 5HT and
neurotransmitter serotonin. What is the rationale for prescribing a medication such as this?
A) To promote the availability of serotonin
B) To block serotonin completely
C) To increase dopamine release
D) To stabilize mood
Inverse agonists at 5HT2A receptors (such as atypical antipsychotics) can promote serotonin availability
by modulating receptor activity. This action helps reduce negative symptoms and extrapyramidal side
effects while improving cognitive function in schizophrenia .
14. A patient is diagnosed with schizophrenia. What increases the patient's potential to mediate the
cognitive symptoms of the disease?