Psychopathopharmacology 1 MSN 671 quiz 3
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Free Psychopathopharmacology 1 MSN 671 quiz 3 Questions
Which ethnic group is more susceptible to carbamazepine-induced Steven Johnson Syndrome, 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 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.
When a neurotransmitter such as GABA binds to a gatekeeper receptor on an ion channel, that particular neurotransmitter causes a conformational change in the receptor that opens the ion channel. A neurotransmitter, drug, or hormone that binds to a receptor is sometimes called a
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Presynaptic
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Ligand
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Voltage
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Isomer
Explanation
Correct Answer:
B. Ligand
Explanation:
A ligand is any molecule, such as a neurotransmitter, drug, or hormone, that binds specifically to a receptor. When the ligand binds, it induces a conformational change in the receptor, which may open ion channels or activate intracellular signaling pathways. For example, GABA acts as a ligand for GABA receptors, opening chloride channels to inhibit neuronal activity.
Why Other Options Are Wrong:
Presynaptic
This is incorrect because "presynaptic" refers to the neuron releasing the neurotransmitter, not the molecule binding to a receptor.
Voltage
This is incorrect because "voltage" refers to electrical potential differences across the membrane, not the binding molecule.
Isomer
This is incorrect because an isomer is a molecule with the same chemical formula as another but with a different structure. It is unrelated to receptor binding.
What is the term for the process in which ligand binding to a receptor triggers the activation of intracellular molecules leading to a cellular response?
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Transduction
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Translation
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Response
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Reception
Explanation
Correct Answer:
A. Transduction
Explanation:
Signal transduction is the process in which a ligand (such as a hormone or neurotransmitter) binds to a receptor and activates intracellular molecules, ultimately leading to a specific cellular response. It acts as the “middle step” between reception of the signal and the actual cellular outcome.
Why Other Options Are Wrong:
B. Translation
This is incorrect because translation refers to the synthesis of proteins from mRNA on ribosomes, not receptor-mediated signaling.
C. Response
This is incorrect because the response is the final step of cell signaling (such as gene expression, secretion, or metabolic change), not the process of activating molecules inside the cell.
D. Reception
This is incorrect because reception is the first step, when the ligand binds to the receptor. Transduction follows this step.
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.
Receptor with four transmembrane regions changes conformation as GABA binds. Which system is this process describing?
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Presynaptic transporter
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Ligand-gated ion channel
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Voltage-sensitive ion channel
Explanation
Correct Answer:
B. Ligand-gated ion channel
Explanation:
GABA receptors, particularly the GABA-A receptor, are classic examples of ligand-gated ion channels. These receptors have multiple transmembrane domains, and when GABA binds to them, the receptor undergoes a conformational change that opens a central ion pore. This allows chloride ions to flow into the neuron, leading to hyperpolarization and inhibition of neuronal firing. This mechanism is rapid and directly links neurotransmitter binding to ion flow.
Why Other Options Are Wrong:
A. Presynaptic transporter
This is incorrect because presynaptic transporters are proteins that reuptake neurotransmitters from the synaptic cleft back into presynaptic neurons. They do not directly mediate ion flow in response to ligand binding.
C. Voltage-sensitive ion channel
This is incorrect because voltage-sensitive ion channels open or close in response to changes in membrane potential, not neurotransmitter binding. GABA binding specifically describes a ligand-gated mechanism, not a voltage-gated one.
Transport of monoamines requires energy, which is supplied by a:
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Calcium pump
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Potassium pump
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Sodium pump
Explanation
Correct Answer:
C. Sodium pump
Explanation:
The reuptake of monoamines (such as dopamine, norepinephrine, and serotonin) into presynaptic terminals is driven by secondary active transport. Monoamine transporters use the sodium gradient established by the Na⁺/K⁺-ATPase pump (sodium pump). The pump maintains high extracellular sodium and low intracellular sodium, providing the electrochemical gradient that powers monoamine reuptake. This process ensures efficient clearance of neurotransmitters from the synaptic cleft and recycling back into presynaptic neurons.
Why Other Options Are Wrong:
A. Calcium pump
This is incorrect because calcium pumps primarily regulate intracellular calcium concentrations, important for processes like neurotransmitter release, but they do not supply the driving force for monoamine reuptake.
B. Potassium pump
This is incorrect because there is no dedicated “potassium pump” responsible for powering monoamine transport. Potassium participates in the Na⁺/K⁺-ATPase cycle, but it is the sodium gradient created by this pump, not potassium itself, that drives neurotransmitter reuptake.
What is the term for the control of gene expression at the transcription stage involving transcription factors, promoters, and enhancers?
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Translational Regulation
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Epigenetic Modifications
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Transcriptional Regulation
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Regulation
Explanation
Correct Answer:
C. Transcriptional Regulation
Explanation:
Transcriptional regulation refers to the control of gene expression at the stage where DNA is transcribed into RNA. This involves transcription factors binding to promoters, enhancers, and silencers to either activate or repress RNA polymerase activity. It is a critical step because it determines whether a gene is turned “on” or “off,” thus controlling protein production.
Why Other Options Are Wrong:
A. Translational Regulation
This is incorrect because translational regulation controls gene expression at the level of mRNA translation into protein, not at transcription.
B. Epigenetic Modifications
This is incorrect because epigenetic modifications (e.g., DNA methylation, histone acetylation) regulate gene accessibility broadly, not specifically through promoters and transcription factors.
D. Regulation
This is incorrect because “regulation” is too vague a term. The precise term for control at the transcription stage is transcriptional regulation.
A 48 year old patient with depression was recently started on 20 mg/day fluoxetine to combat his presenting symptoms of apathy, fatigue, problems concentrating, and hypersomnia. The patient reports that he is feeling much energized and can see improvements in his cognition and attention within a day or two of starting fluoxetine. Which properties of fluoxetine are likely responsible for this positive response?
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5HT2C antagonism
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Norepi reuptake inhibition
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Serotonin reuptake inhibition
Explanation
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.
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.
The following are some instances of neurotransmitters that are made expressly as retrograde neurotransmitters, or those that travel from postsynaptic neurons to presynaptic neurons:
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GABA
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Galanin
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Histamine
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Nitric oxide
Explanation
Correct Answer:
D. Nitric oxide
Explanation:
Retrograde neurotransmitters are signaling molecules produced by the postsynaptic neuron that travel back to the presynaptic terminal to regulate neurotransmitter release. Nitric oxide (NO) is the classic example: it is synthesized on demand in the postsynaptic neuron and diffuses rapidly across membranes to modulate presynaptic activity. Endocannabinoids (e.g., anandamide, 2-AG) are also important retrograde messengers, but nitric oxide is the prototypical gaseous retrograde neurotransmitter.
Why Other Options Are Wrong:
A. GABA
This is incorrect because GABA is a classical inhibitory neurotransmitter released from presynaptic neurons, not a retrograde signal.
B. Galanin
This is incorrect because galanin is a neuropeptide that acts as a conventional transmitter/modulator, not a retrograde messenger.
C. Histamine
This is incorrect because histamine functions as a neuromodulator in arousal, attention, and immune responses but does not serve as a retrograde neurotransmitter.
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