Psychopathopharmacology 1 MSN 671 quiz 3

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Free Psychopathopharmacology 1 MSN 671 quiz 3 Questions

1.

After being arrested for cocaine possession, a 26-year-old patient with ADHD recently checked himself into a drug rehabilitation facility. Because cocaine blocks the dopamine transporter (albeit it is not itself taken up into the neuron by the transporter), it may be an attempt by the patient to self-medicate for symptoms of ADHD. Thus, cocaine has the same action at the dopamine transporter as:

  • Cocaine has the same actions at the dopamine transporter as amphetamine

  • Cocaine has the same actions at the dopamine transporter as methylphenidate

  • A and B

  • Neither A nor B

Explanation

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.


2.

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

  • Presynaptic

  • Ligand

  • Voltage

  • 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.


3.

Which of the following are involved in regulating neurotransmission via excitation-secretion coupling?

  • Voltage-sensitive sodium channels

  • Voltage-sensitive calcium channels

  • Both A and B

  • Neither A nor B

Explanation

Correct Answer:

C. Both A and B

Explanation:

Excitation-secretion coupling in neurotransmission is the process that links an action potential to the release of neurotransmitters at the synaptic cleft.

Voltage-sensitive sodium channels are critical for generating and propagating the action potential along the axon.

Voltage-sensitive calcium channels open when the action potential reaches the presynaptic terminal, allowing calcium influx. This calcium entry triggers synaptic vesicle fusion and neurotransmitter release.

Thus, both sodium and calcium channels are required for efficient excitation-secretion coupling.

Why Other Options Are Wrong:

A. Voltage-sensitive sodium channels

This is incorrect alone because sodium channels propagate the action potential but do not directly cause neurotransmitter release without calcium entry.

B. Voltage-sensitive calcium channels

This is incorrect alone because calcium influx is essential for vesicle release, but without sodium channel–mediated action potential propagation, the depolarization would not reach the terminal.

D. Neither A nor B

This is incorrect because both channel types are central to the process of excitation-secretion coupling.


4.

What type of signaling molecules require carrier proteins due to their inability to freely float in the extracellular space?

  • Autocrine signals

  • Hydrophobic signaling molecules

  • Hydrophilic signaling molecules

  • Endocrine signals

Explanation

Correct Answer:

B. Hydrophobic signaling molecules

Explanation:

Hydrophobic signaling molecules (such as steroid hormones, thyroid hormones, and some lipids) are poorly soluble in the aqueous extracellular environment. To travel in blood or extracellular fluid, they require carrier proteins (e.g., albumin or hormone-specific binding proteins). These carriers protect the molecules, prolong their half-life, and ensure delivery to their target tissues.

Why Other Options Are Wrong:

A. Autocrine signals

This is incorrect because “autocrine” refers to the type of signaling (cells signaling to themselves), not the solubility of molecules. These signals can be either hydrophilic or hydrophobic.

C. Hydrophilic signaling molecules

This is incorrect because hydrophilic molecules (e.g., peptides, proteins, neurotransmitters) are water-soluble and can freely float in the extracellular space without carrier proteins.

D. Endocrine signals

This is incorrect because endocrine refers to signals (like hormones) released into the bloodstream to act on distant targets. While some endocrine hormones are hydrophobic and require carriers, not all endocrine signals need carrier proteins. The correct distinction is hydrophobicity, not the signaling route.


5.

What is the term for the process of adding methyl groups to histones or DNA to either activate or silence gene expression?

  • Acetylation

  • Transcription

  • Methylation

  • Epigenetic Modifications

Explanation

Correct Answer:

C. Methylation

Explanation:

Methylation refers to the addition of methyl groups (–CH₃) to DNA (commonly at cytosine bases in CpG islands) or histone proteins. This process can silence or activate gene expression depending on the location and context. DNA methylation usually represses transcription by blocking transcription factor binding or recruiting repressor proteins, making it a key regulator in epigenetics.

Why Other Options Are Wrong:

A. Acetylation

This is incorrect because acetylation involves adding acetyl groups to histone tails, which typically loosens chromatin and activates gene expression, not methyl groups.

B. Transcription

This is incorrect because transcription is the process of synthesizing RNA from DNA, not a chemical modification of DNA or histones.

D. Epigenetic Modifications

This is incorrect because epigenetic modifications is a broad category that includes both methylation and acetylation (among others). The specific process of adding methyl groups is called methylation.


6.

Which ethnic group is more susceptible to carbamazepine-induced Steven Johnson Syndrome, and why?

  • Han Chinese and HLA-B15:02

  • African American and HLA-B15:02

  • White American and HLA-B15:02

  • 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.


7.

What does the term 'Therapeutic Index' refer to in pharmacology?

  • Ratio between absorption and distribution

  • Ratio between metabolism and excretion

  • Ratio between toxic dose and effective dose

  • Ratio between chemical and generic names

Explanation

Correct Answer:

C. Ratio between toxic dose and effective dose

Explanation:

The Therapeutic Index (TI) is a measure of a drug’s safety margin. It is calculated as the ratio between the toxic dose (TD₅₀ or LD₅₀) and the effective dose (ED₅₀). A higher TI means the drug is relatively safe because the toxic dose is much higher than the effective dose, while a low TI indicates a narrow safety margin, requiring close monitoring.

Why Other Options Are Wrong:

A. Ratio between absorption and distribution

This is incorrect because these are pharmacokinetic processes, not measures of drug safety.

B. Ratio between metabolism and excretion

This is incorrect because metabolism and excretion describe drug clearance, not the therapeutic safety margin.

D. Ratio between chemical and generic names

This is incorrect because therapeutic index has nothing to do with drug nomenclature.


8.

The leading hypothesis of schizophrenia is:

  • Hyperfunctioning NMDA receptors

  • Hypofunctioning NMDA receptors

  • Hyperdopaminergic activity in mesolimbic pathways

  • Hypodopaminergic activity in mesocortical pathways

Explanation

Correct Answer:

B: Hypofunctioning NMDA receptors

Explanation:

The glutamate hypothesis, specifically NMDA receptor hypofunction, is the leading explanation for schizophrenia today. NMDA antagonists like ketamine and PCP can mimic both positive and negative symptoms of the disorder. Hypofunction of NMDA receptors on inhibitory interneurons disrupts excitatory–inhibitory balance, contributing to abnormal dopamine signaling.

Why Other Options Are Wrong:

A: Hyperfunctioning NMDA receptors

This is incorrect because schizophrenia is linked to reduced, not increased, NMDA receptor activity.

C: Hyperdopaminergic activity in mesolimbic pathways


This describes the older dopamine hypothesis of schizophrenia, which explains positive symptoms well, but it does not fully account for negative and cognitive symptoms.

D: Hypodopaminergic activity in mesocortical pathways


This is partially true since mesocortical dopamine deficits are linked to negative symptoms and cognitive dysfunction. However, the broader unifying hypothesis is NMDA receptor hypofunction, which influences both dopamine pathways.


9.

A man maintained on clozapine now presents with depressive symptoms. His clinician is considering adding fluvoxamine. If fluvoxamine, a CYP1A2 inhibitor, is added to clozapine, a CYP1A2 substrate, which of the following lab test would you most likely expect for this patient?

  • decreased plasma levels of clozapine

  • increased plasma levels of clozapine

  • no effect of plasma levels of clozapine

Explanation

Correct Answer:

B: increased plasma levels of clozapine

Explanation:

Clozapine is primarily metabolized by the liver enzyme CYP1A2. Fluvoxamine is a strong inhibitor of CYP1A2. When fluvoxamine is added, it inhibits clozapine metabolism, reducing its clearance. As a result, plasma levels of clozapine increase, which may raise the risk of dose-related adverse effects such as seizures, sedation, or agranulocytosis. Therefore, monitoring clozapine levels and adjusting dosage becomes essential when combining these drugs.

Why Other Options Are Wrong:

A: decreased plasma levels of clozapine

This is incorrect because inhibition of CYP1A2 decreases metabolism, leading to higher, not lower, plasma concentrations.

C: no effect of plasma levels of clozapine


This is incorrect because fluvoxamine has a well-established inhibitory effect on CYP1A2, and the drug interaction consistently leads to elevated clozapine levels.


10.

Which of the following is considered the pleasure center of the brain?

  • Cortico-striatal-thalamic-cortical loop

  • Mesolimbic dopamine pathway

  • Mesocortical dopamine pathway

  • None of the above

Explanation

Correct Answer:

B. Mesolimbic dopamine pathway

Explanation:

The mesolimbic dopamine pathway, projecting from the ventral tegmental area (VTA) to the nucleus accumbens, is considered the brain’s pleasure and reward center. Activation of this pathway underlies the experience of reward, reinforcement, and motivation, and it plays a central role in addiction and reinforcement learning. Dopamine release in the nucleus accumbens is especially critical for the sensation of pleasure.

Why Other Options Are Wrong:

A. Cortico-striatal-thalamic-cortical loop

This is incorrect because this loop is more involved in motor control, habits, and obsessive-compulsive behaviors rather than direct mediation of pleasure.

C. Mesocortical dopamine pathway


This is incorrect because the mesocortical pathway projects from the VTA to the prefrontal cortex and is primarily involved in cognition, attention, and regulation of affect—not the sensation of pleasure.

D. None of the above


This is incorrect because the mesolimbic dopamine pathway is well established as the primary pleasure and reward pathway in the brain.


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