Psychopathopharmacology 1 MSN 671 quiz 3
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Free Psychopathopharmacology 1 MSN 671 quiz 3 Questions
A 44-year-old patient has schizophrenia and comorbid alcohol abuse disorder. Alcohol has what effect on GABA and glutamate in the ventral tegmental area?
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Increases GABA and decreases glutamate
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Increases both GABA and glutamate
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Decreases GABA and increases glutamate
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Decreases both GABA and glutamate
Explanation
Correct Answer:
C. Decreases GABA and increases glutamate
Explanation:
Alcohol enhances GABA-A receptor activity in many brain regions, but in the ventral tegmental area (VTA), its net effect is to reduce GABAergic inhibition of dopamine neurons. This disinhibition allows dopamine neurons to fire more readily. Alcohol also increases glutamatergic excitation onto these dopamine neurons. Together, decreased GABA and increased glutamate in the VTA lead to enhanced dopamine release in the nucleus accumbens, reinforcing alcohol’s rewarding effects.
Why Other Options Are Wrong:
A. Increases GABA and decreases glutamate
This is incorrect because increasing GABA and reducing glutamate would suppress dopamine neuron firing, opposite to alcohol’s rewarding effects.
B. Increases both GABA and glutamate
This is incorrect because while alcohol increases glutamate drive, its main effect on GABA in the VTA is a reduction in inhibition of dopamine neurons, not an increase.
D. Decreases both GABA and glutamate
This is incorrect because alcohol does decrease GABA inhibition but simultaneously increases glutamate excitation, not decrease it.
A 17-year-old boy presents with 3 hours of depersonalization, blurry vision, slurred speech, an ataxic gait, and hallucinations. The patient was at a party shortly before his symptoms began. Vital signs are blood pressure 170/92 mmHg, heart rate 120 bpm, and temperature 99.9 °F (37.7 °C). On physical examination, the patient is aggressive, combative, and poorly cooperative. His skin is diffusely erythematous, pupils are 8 mm bilaterally, and bilateral nystagmus is present. Urine toxicology confirms the diagnosis. The patient is also likely to experience which of the following symptoms?
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Homicidal impulses
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Increased appetite
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Nosebleed
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Decreased respiratory rate
Explanation
Correct Answer:
A. Homicidal impulses
Explanation:
This presentation is classic for phencyclidine (PCP) intoxication. Key features include violent behavior, psychosis (hallucinations, depersonalization), severe hypertension, tachycardia, nystagmus (especially vertical or rotary), ataxia, dysarthria, and muscle rigidity. PCP intoxication is notorious for producing impulsive violence, agitation, and homicidal impulses.
Why Other Options Are Wrong:
B. Increased appetite
This is incorrect because increased appetite is characteristic of cannabis intoxication, not PCP.
C. Nosebleed
This is incorrect because nosebleeds are more commonly associated with intranasal cocaine use, not PCP.
D. Decreased respiratory rate
This is incorrect because decreased respiratory drive is seen in opioid intoxication (eg, heroin, morphine, fentanyl), not PCP. PCP usually causes hyperactivity and autonomic stimulation.
An example of volume neurotransmission is:
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Dopamine in the prefrontal cortex
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Dopamine in the striatum
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Norepinephrine in the prefrontal cortex
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Norepinephrine in the striatum
Explanation
Correct Answer:
A. Dopamine in the prefrontal cortex
Explanation:
Volume neurotransmission refers to neurotransmitter release that is not restricted to the synaptic cleft but instead diffuses over a wider area, influencing multiple neurons. In the prefrontal cortex, dopamine terminals often lack classic synaptic specializations. Instead, dopamine is released into the extracellular space, where it diffuses and binds to receptors located away from release sites. This is a prime example of volume transmission.
Why Other Options Are Wrong:
B. Dopamine in the striatum
This is incorrect because dopamine release in the striatum occurs primarily at well-defined synaptic junctions with precise wiring, making it a clear case of wired transmission rather than volume transmission.
C. Norepinephrine in the prefrontal cortex
This is incorrect because norepinephrine in the prefrontal cortex can have modulatory effects, but it is dopamine that is specifically recognized in the literature as the classic example of volume transmission in this region.
D. Norepinephrine in the striatum
This is incorrect because norepinephrine projections to the striatum are sparse, and where present, they do not serve as the hallmark example of volume transmission.
What anesthetic agent is sometimes used to treat resistant depression and suicidal thoughts?
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Ketamine
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Propofol
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Hydroxyzine
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Valium
Explanation
Correct Answer:
A. Ketamine
Explanation:
Ketamine, an NMDA receptor antagonist originally used as an anesthetic, has been found effective in treating treatment-resistant depression and rapidly reducing suicidal thoughts. Unlike traditional antidepressants that may take weeks to work, ketamine produces effects within hours. It is often administered intravenously in specialized clinics, and a related formulation, esketamine (Spravato®), is FDA-approved as a nasal spray for treatment-resistant depression.
Why Other Options Are Wrong:
B. Propofol
This is incorrect because propofol is an intravenous anesthetic used for induction and maintenance of anesthesia. It is not used in psychiatric treatment for depression or suicidality.
C. Hydroxyzine
This is incorrect because hydroxyzine is an antihistamine with sedative and anxiolytic properties. It may reduce anxiety but is not indicated for resistant depression or suicidal ideation.
D. Valium
This is incorrect because Valium (diazepam) is a benzodiazepine used for anxiety, muscle spasms, and seizures. It does not treat depression or suicidal thoughts and carries risks of dependence.
When considering prescribing Clozapine, what genetic factor for African Americans may hinder the initiation of this medication by a prescriber?
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Low plasma dimension
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Low Seizure Threshold
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Benign Neutropenia
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None
Explanation
Correct Answer:
C. Benign Neutropenia
Explanation:
Clozapine carries a risk of agranulocytosis, so prescribers monitor the absolute neutrophil count (ANC) before and during treatment. Some African American patients may have benign ethnic neutropenia (BEN) — a genetic variation leading to lower baseline neutrophil counts without an increased risk of infection. This can hinder initiation of clozapine because standard ANC cutoffs may falsely exclude these patients. Adjusted guidelines now allow for BEN, but prescribers must be aware of this factor before ruling out clozapine.
Why Other Options Are Wrong:
A. Low plasma dimension
This is incorrect because there is no recognized genetic factor called "low plasma dimension" influencing clozapine use.
B. Low Seizure Threshold
This is incorrect because clozapine does lower the seizure threshold at high doses, but this effect is not a specific genetic factor tied to African Americans.
D. None
This is incorrect because benign neutropenia is a real genetic factor in African Americans that impacts clozapine initiation.
A 35-year-old cigarette smoker would like to quit but is nervous because she typically craves a cigarette approximately every 2 hrs. The craving and withdrawal are due to:
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Desensitization of nicotinic receptors
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Resensitization of nicotinic receptors
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Desensitization of muscarinic receptors
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Resensitization of muscarinic receptors
Explanation
Correct Answer:
B. Resensitization of nicotinic receptors
Explanation:
Nicotine binds to nicotinic acetylcholine receptors (nAChRs) in the brain, causing receptor activation and dopamine release, which produces reinforcement. After nicotine exposure, nAChRs become desensitized and stop responding despite nicotine being present. Over time (about every 1–2 hours), the receptors resensitize, becoming responsive again. This resensitization drives craving and withdrawal because the brain seeks nicotine to re-activate the now-sensitive receptors, creating the cycle of dependence.
Why Other Options Are Wrong:
A. Desensitization of nicotinic receptors
This is incorrect because desensitization occurs right after smoking, not when cravings emerge. Cravings arise when receptors resensitize.
C. Desensitization of muscarinic receptors
This is incorrect because muscarinic acetylcholine receptors are not the primary target of nicotine in addiction. Nicotine acts on nicotinic receptors, not muscarinic ones.
D. Resensitization of muscarinic receptors
This is incorrect because muscarinic receptors are not central to nicotine craving and withdrawal. The addiction mechanism involves nicotinic receptor cycles, not muscarinic receptor activity.
The activation of N-methyl-D-aspartate (NMDA) receptors requires the presence of:
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Glutamate only
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Glutamate and glycine
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Glutamate, glycine, and magnesium
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Glutamate and magnesium
Explanation
Correct Answer:
B. Glutamate and glycine
Explanation:
NMDA receptors are a subtype of glutamate receptors that require co-activation by two ligands: glutamate (the main excitatory neurotransmitter) and glycine (or D-serine, acting as a co-agonist). Once both bind, the receptor channel can open, but only if the magnesium block is relieved by depolarization.
Why Other Options Are Wrong:
A. Glutamate only
This is incorrect because glutamate alone cannot open NMDA receptors; the co-agonist glycine (or D-serine) is also required.
C. Glutamate, glycine, and magnesium
This is incorrect because magnesium actually blocks the NMDA receptor channel at resting potential. For the channel to function, magnesium must be displaced by depolarization, not bound.
D. Glutamate and magnesium
This is incorrect because magnesium is not required for activation; instead, it is an inhibitor at resting membrane potential.
What ethnic group is at higher risk for developing Steven Johnson Syndrome induced by carbamazepine and why?
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Han Chinese and HLA-B15:02
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African American and HLA-B15:02
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White American and HLA-B15:02
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Hispanic American and HLA-B15:02
Explanation
Correct Answer:
A. Han Chinese and HLA-B*15:02
Explanation:
Han Chinese individuals have a significantly increased risk of developing Stevens-Johnson Syndrome (SJS) or toxic epidermal necrolysis (TEN) when treated with carbamazepine if they carry the HLA-B*15:02 allele. This allele is strongly associated with severe cutaneous adverse reactions to carbamazepine, and screening is recommended before initiating therapy in populations with high prevalence, such as Han Chinese, Thai, and other Southeast Asian groups.
Why Other Options Are Wrong:
B. African American and HLA-B15:02
This is incorrect because while African Americans may carry other HLA risk alleles, **HLA-B15:02 is rare in this population**, making the risk much lower than in Han Chinese or Southeast Asians.
C. White American and HLA-B15:02
This is incorrect because the prevalence of **HLA-B15:02 in White Americans is extremely low**, so carbamazepine-induced SJS/TEN is not strongly linked to this allele in this population.
D. Hispanic American and HLA-B15:02
This is incorrect because Hispanic populations also have a low frequency of HLA-B15:02, so the genetic risk is not comparable to Han Chinese or other Asian groups.
According to Stahl, approximately one-fifth of psychotropic drugs currently utilized in clinical practice are known to act at the ionotropic receptors and have the potential to take immediate effects through processes of drug-induced modifications in signaling transduction. Using the options below, select the medications that are known to act on ionotropic receptors by way of this process.
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Benzodiazepines
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Ionic compounds
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Antipsychotic
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Antidepressants
Explanation
Correct Answer:
A. Benzodiazepines
Explanation:
Benzodiazepines are well known to act on ionotropic receptors, specifically the GABA-A receptor, which is a chloride ion channel. By binding allosterically, benzodiazepines increase the frequency of chloride channel opening in response to GABA, leading to enhanced inhibitory signaling. This ionotropic mechanism allows benzodiazepines to take immediate clinical effects, such as sedation, anxiolysis, or anticonvulsant action, compared to drugs that act via slower metabotropic pathways.
Why Other Options Are Wrong:
B. Ionic compounds
This is incorrect because "ionic compounds" is not a drug class in psychopharmacology. It is a chemistry term referring to substances made of ions, not medications that act on receptors.
C. Antipsychotic
This is incorrect because most antipsychotics act on metabotropic G-protein-coupled receptors (GPCRs), such as dopamine D2 or serotonin 5-HT2A receptors. Their effects are slower and not mediated through ionotropic channels.
D. Antidepressants
This is incorrect because antidepressants, including SSRIs, SNRIs, and TCAs, primarily act by blocking neurotransmitter reuptake or influencing GPCR-mediated systems. They do not exert their main actions at ionotropic receptors and therefore do not produce immediate effects.
The PMHNP knows that clinicians should carefully consider a client's smoking status when determining a medication for psychosis.
The CYP1A2 enzyme is known to "speed up" the metabolism of some medications in the presence of smoking, causing medications to be less efficacious. Select all the medications below that are metabolized by the CYP1A2 enzyme and effectiveness is significantly reduced by smoking.
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Olanzapine
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Lamotrigine
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Fluphenazine
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Benztropine
Explanation
Correct Answer:
A. Olanzapine
Explanation:
Cigarette smoke (polycyclic aromatic hydrocarbons) induces CYP1A2, increasing the clearance of drugs that are CYP1A2 substrates. Olanzapine is primarily metabolized by CYP1A2 (with minor roles for UGT and CYP2D6), so smokers often have lower serum levels and reduced efficacy, frequently requiring higher doses compared with non-smokers. When patients start or stop smoking, olanzapine doses often need adjustment to maintain therapeutic effect and avoid side effects.
Why Other Options Are Wrong:
B. Lamotrigine
Incorrect. Lamotrigine is cleared mainly by UGT1A4 glucuronidation, not CYP1A2. Smoking does not meaningfully reduce lamotrigine effectiveness via CYP induction.
C. Fluphenazine
Incorrect. Fluphenazine is metabolized largely by CYP2D6 (and some CYP3A4). While smoking can have modest effects on various pathways, it’s not a CYP1A2 substrate of clinical concern like olanzapine (or clozapine).
D. Benztropine
Incorrect. Benztropine is not primarily metabolized by CYP1A2, and smoking is not known to significantly reduce its effectiveness through this mechanism.
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