Psychopathopharmacology 1 MSN 671 quiz 3

Correct Answer:

A. 5HT2C antagonism

Explanation:

While fluoxetine is primarily an SSRI (serotonin reuptake inhibitor), its early energizing effects are largely attributed to 5HT2C antagonism. The 5HT2C receptor normally inhibits dopamine and norepinephrine release in the prefrontal cortex. By blocking this receptor, fluoxetine disinhibits dopamine and norepinephrine release, leading to improvements in energy, attention, and cognition within days—much faster than the delayed mood-elevating effects from serotonin reuptake inhibition.

Why Other Options Are Wrong:

B. Norepi reuptake inhibition

This is incorrect because fluoxetine is not a norepinephrine reuptake inhibitor. Other antidepressants (e.g., SNRIs, TCAs) provide this effect, but fluoxetine does not significantly block norepinephrine transporters.

C. Serotonin reuptake inhibition

This is incorrect as the explanation for the rapid energizing effect. While fluoxetine does inhibit serotonin reuptake, those changes take weeks to translate into clinical mood improvement. The patient’s immediate boost in energy and cognition is better explained by 5HT2C antagonism.

Correct Answer:

B. Bipolar mania, Parkinson's disease

Explanation:

In bipolar disorder (mania) and Parkinson’s disease, psychosis can occur but is not required for the diagnosis. In mania, the defining feature is elevated, expansive, or irritable mood with increased energy/activity; psychotic features may appear in severe episodes but are not essential. In Parkinson’s disease, psychosis can emerge as a complication of the illness or treatment (e.g., dopamine agonists), but it is not a core diagnostic feature.

Why Other Options Are Wrong:

A. Parkinson's disease, schizophreniform disorder

This is incorrect because while psychosis is not core to Parkinson’s disease, it is core to schizophreniform disorder, where hallucinations, delusions, or disorganized thinking/behavior are defining diagnostic features.

C. Delusional disorder, Alzheimer disease

This is incorrect because psychosis (delusions) is a defining feature of delusional disorder. In Alzheimer disease, psychosis may appear, but since one of the pair (delusional disorder) makes psychosis defining, the set does not fit.

Correct Answer:

C: Both inside and outside the channel

Explanation:

Ligand-gated ion channels (LGICs), such as GABA-A, nicotinic acetylcholine, and NMDA receptors, are membrane-spanning proteins with primary ligand-binding sites located extracellularly. These external sites allow neurotransmitters to initiate rapid synaptic signaling. However, many LGICs also possess additional modulatory binding sites located within the ion channel pore (e.g., picrotoxin binding inside the GABA-A channel) or on intracellular regions (e.g., phosphorylation sites, binding sites for intracellular modulators). Thus, LGICs can indeed have receptor sites both outside and inside the channel, making option C the most comprehensive answer.

Why Other Options Are Wrong:

A: Inside the channel

This is incomplete. While some modulators bind within the channel pore, the primary neurotransmitter binding sites are extracellular.

B: Outside the channel

This is partially correct, as neurotransmitters like GABA and acetylcholine bind extracellularly. However, it ignores the important modulatory sites inside or intracellularly.

D: Ligand-gated ion channels do not have receptor sites

This is incorrect because their defining property is the presence of receptor sites that bind ligands to open or modulate the channel.

Correct Answer:

D. Transcription

Explanation:

Transcription is the process in which RNA polymerase reads the DNA template strand and synthesizes a complementary mRNA strand. This mRNA carries the genetic code from the nucleus to the ribosomes, where proteins are made. Transcription occurs in three stages: initiation, elongation, and termination.

Why Other Options Are Wrong:

A. Splicing

This is incorrect because splicing occurs after transcription in eukaryotes, where introns are removed and exons joined to form mature mRNA.

B. Replication

This is incorrect because replication refers to the copying of the entire DNA molecule before cell division, not the synthesis of RNA.

C. Translation

This is incorrect because translation is the process where the ribosome reads mRNA and builds a polypeptide (protein), not where RNA is made.

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.

Correct Answer:

A. Han Chinese and HLA-B*15:02

Explanation:

Han Chinese and several other Southeast Asian populations have a high prevalence of the HLA-B*15:02 allele, which is strongly associated with carbamazepine-induced Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN). Because of this genetic risk, guidelines recommend genetic testing for HLA-B*15:02 before prescribing carbamazepine in patients of Han Chinese, Thai, or related ancestry.

Why Other Options Are Wrong:

B. African American and HLA-B*15:02

This is incorrect because HLA-B*15:02 is extremely rare in African Americans, so their risk of carbamazepine-induced SJS/TEN is not significantly elevated.

C. White American and HLA-B*15:02

This is incorrect because the prevalence of HLA-B*15:02 is also very low in White Americans, making this population less vulnerable to carbamazepine-induced SJS/TEN.

D. Hispanic American and HLA-B*15:02

This is incorrect because Hispanic populations also have a very low frequency of HLA-B*15:02, so the genetic risk does not typically apply here.

Correct Answer:

B. Cocaine has the same actions at the dopamine transporter as methylphenidate

Explanation:

Cocaine and methylphenidate both block the dopamine transporter (DAT), preventing dopamine reuptake and increasing extracellular dopamine. Neither drug is transported into the presynaptic neuron via DAT; they act from the extracellular side to inhibit transporter function. This mechanism aligns with the acute “energizing” and attention-enhancing effects some users seek, paralleling therapeutic DAT blockade seen with methylphenidate in ADHD.

Why Other Options Are Wrong:

A. Cocaine has the same actions at the dopamine transporter as amphetamine

Amphetamine is taken up via DAT, enters the neuron, disrupts vesicular storage via VMAT2, and reverses DAT to promote dopamine efflux—distinct from simple blockade.

C. A and B

Incorrect because cocaine’s mechanism matches methylphenidate (blockade), not amphetamine (substrate/reverse transporter).

D. Neither A nor B

Incorrect because cocaine clearly shares DAT-blocking action with methylphenidate.

Correct Answer:

B: Synaptic backward transmission from postsynaptic neuron B to presynaptic neuron A

Explanation:

Retrograde transmission occurs when chemical messengers travel from the postsynaptic neuron back to the presynaptic neuron, reversing the usual direction of synaptic communication. Retrograde messengers include nitric oxide, endocannabinoids, and certain peptides. These signals modulate presynaptic activity, often regulating neurotransmitter release or synaptic plasticity. This process plays a crucial role in feedback mechanisms such as long-term potentiation (LTP) and long-term depression (LTD).

Why Other Options Are Wrong:

A: Synaptic forward transmission from presynaptic neuron A to a postsynaptic neuron B

This is incorrect because it describes the normal, forward direction of synaptic communication, not retrograde signaling.

C: Non-synaptic transmission from Neuron A back to Neuron A

This is incorrect because it describes autocrine signaling, where a cell releases signals that act on itself, not retrograde synaptic signaling.

D: Non-synaptic transmission from Neuron B to neighboring neuron B1 or B2

This is incorrect because it refers to paracrine or volume transmission, not retrograde transmission. Retrograde signaling specifically involves communication from the postsynaptic neuron back to its presynaptic partner.

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.