Wilkes University NSG 552 Psychopharmacology - Exam 1
1. Serotonin (5-HT) is synthesized from which amino acid precursor?
A. Tryptophan
B. Tyrosine
C. Glutamine
D. Phenylalanine
Correct Answer: A. Tryptophan
Rationale: Serotonin is made from tryptophan via tryptophan hydroxylase. Tyrosine
is the precursor for dopamine and norepinephrine.
2. Which enzyme is the rate-limiting step in catecholamine (dopamine and
norepinephrine) synthesis?
A. Catechol-O-methyltransferase (COMT)
B. DOPA decarboxylase
C. Monoamine oxidase
D. Tyrosine hydroxylase
Correct Answer: D. Tyrosine hydroxylase
Rationale: Tyrosine hydroxylase converts tyrosine to L-DOPA and limits the pace of
catecholamine synthesis. COMT and MAO are degradative enzymes.
3. What is the major inhibitory neurotransmitter in the central nervous
system?
A. Glutamate
B. GABA
C. Dopamine
D. Acetylcholine
Correct Answer: B. GABA
Rationale: GABA opens chloride channels at the GABA-A receptor, hyperpolarizing
neurons. Benzodiazepines, barbiturates and many sedative-hypnotics enhance
GABA activity.
,4. What is the major excitatory neurotransmitter in the central nervous
system?
A. GABA
B. Glutamate
C. Serotonin
D. Norepinephrine
Correct Answer: B. Glutamate
Rationale: Glutamate acts on NMDA, AMPA and kainate receptors. Excess
glutamate activity is excitotoxic; memantine and ketamine act on the NMDA
receptor.
5. Hyperactivity of dopamine in the mesolimbic pathway is associated with
which clinical feature of schizophrenia?
A. Negative symptoms
B. Extrapyramidal symptoms
C. Positive symptoms (hallucinations, delusions)
D. Hyperprolactinemia
Correct Answer: C. Positive symptoms (hallucinations, delusions)
Rationale: Excess mesolimbic dopamine produces positive symptoms. D2 blockade
in this pathway is the basis of antipsychotic efficacy against them.
6. Reduced dopamine activity in the mesocortical pathway is most associated
with which symptoms?
A. Hallucinations
B. Akathisia
C. Negative and cognitive symptoms
D. Galactorrhea
Correct Answer: C. Negative and cognitive symptoms
Rationale: Mesocortical hypoactivity is linked to negative (flat affect, avolition,
alogia) and cognitive symptoms. D2 blockade here can worsen them (secondary
negative symptoms).
,7. Blockade of D2 receptors in the nigrostriatal pathway is responsible for
which adverse effect?
A. Extrapyramidal symptoms (dystonia, parkinsonism, akathisia)
B. Hyperprolactinemia
C. Improvement in positive symptoms
D. Weight gain
Correct Answer: A. Extrapyramidal symptoms (dystonia, parkinsonism,
akathisia)
Rationale: The nigrostriatal pathway controls voluntary movement. Blocking D2
receptors there causes EPS, especially with high-potency first-generation
antipsychotics.
8. Blockade of D2 receptors in the tuberoinfundibular pathway results in:
A. Parkinsonism
B. Worsening psychosis
C. Sedation
D. Hyperprolactinemia
Correct Answer: D. Hyperprolactinemia
Rationale: Dopamine normally inhibits prolactin release from the anterior pituitary.
Blockade raises prolactin, causing galactorrhea, amenorrhea, gynecomastia and
sexual dysfunction.
9. Which enzyme, located on the outer mitochondrial membrane, degrades
serotonin, norepinephrine and dopamine?
A. Tyrosine hydroxylase
B. Tryptophan hydroxylase
C. Acetylcholinesterase
D. Monoamine oxidase (MAO)
Correct Answer: D. Monoamine oxidase (MAO)
Rationale: MAO-A and MAO-B metabolize monoamines. MAOI antidepressants
inhibit this enzyme, raising monoamine levels and creating dietary and
drug-interaction risks.
, 10. What is the primary mechanism of action of SSRIs?
A. Blockade of postsynaptic 5-HT2A receptors
B. Inhibition of presynaptic serotonin reuptake via the serotonin transporter
(SERT)
C. Inhibition of monoamine oxidase
D. Stimulation of vesicular serotonin release
Correct Answer: B. Inhibition of presynaptic serotonin reuptake via the
serotonin transporter (SERT)
Rationale: SSRIs block SERT, increasing synaptic serotonin. Therapeutic effect
follows downstream receptor adaptations, not the immediate rise in serotonin.
11. The 2 to 4 week delay in the therapeutic effect of SSRIs is best explained
by:
A. Slow hepatic metabolism of the drug
B. Delayed absorption from the gut
C. Gradual desensitization of 5-HT1A somatodendritic autoreceptors
D. Slow passage across the blood-brain barrier
Correct Answer: C. Gradual desensitization of 5-HT1A somatodendritic
autoreceptors
Rationale: Initial serotonin increase activates autoreceptors that dampen firing.
Their desensitization over weeks allows increased serotonergic neurotransmission
and clinical benefit.
12. Blockade of which receptor is primarily responsible for sedation and
weight gain with mirtazapine, olanzapine and quetiapine?
A. Muscarinic M1
B. Alpha-1 adrenergic
C. Histamine H1
D. Dopamine D2
Correct Answer: C. Histamine H1
Rationale: H1 antagonism causes sedation and increased appetite. M1 blockade
causes anticholinergic effects and alpha-1 blockade causes orthostasis.
1. Serotonin (5-HT) is synthesized from which amino acid precursor?
A. Tryptophan
B. Tyrosine
C. Glutamine
D. Phenylalanine
Correct Answer: A. Tryptophan
Rationale: Serotonin is made from tryptophan via tryptophan hydroxylase. Tyrosine
is the precursor for dopamine and norepinephrine.
2. Which enzyme is the rate-limiting step in catecholamine (dopamine and
norepinephrine) synthesis?
A. Catechol-O-methyltransferase (COMT)
B. DOPA decarboxylase
C. Monoamine oxidase
D. Tyrosine hydroxylase
Correct Answer: D. Tyrosine hydroxylase
Rationale: Tyrosine hydroxylase converts tyrosine to L-DOPA and limits the pace of
catecholamine synthesis. COMT and MAO are degradative enzymes.
3. What is the major inhibitory neurotransmitter in the central nervous
system?
A. Glutamate
B. GABA
C. Dopamine
D. Acetylcholine
Correct Answer: B. GABA
Rationale: GABA opens chloride channels at the GABA-A receptor, hyperpolarizing
neurons. Benzodiazepines, barbiturates and many sedative-hypnotics enhance
GABA activity.
,4. What is the major excitatory neurotransmitter in the central nervous
system?
A. GABA
B. Glutamate
C. Serotonin
D. Norepinephrine
Correct Answer: B. Glutamate
Rationale: Glutamate acts on NMDA, AMPA and kainate receptors. Excess
glutamate activity is excitotoxic; memantine and ketamine act on the NMDA
receptor.
5. Hyperactivity of dopamine in the mesolimbic pathway is associated with
which clinical feature of schizophrenia?
A. Negative symptoms
B. Extrapyramidal symptoms
C. Positive symptoms (hallucinations, delusions)
D. Hyperprolactinemia
Correct Answer: C. Positive symptoms (hallucinations, delusions)
Rationale: Excess mesolimbic dopamine produces positive symptoms. D2 blockade
in this pathway is the basis of antipsychotic efficacy against them.
6. Reduced dopamine activity in the mesocortical pathway is most associated
with which symptoms?
A. Hallucinations
B. Akathisia
C. Negative and cognitive symptoms
D. Galactorrhea
Correct Answer: C. Negative and cognitive symptoms
Rationale: Mesocortical hypoactivity is linked to negative (flat affect, avolition,
alogia) and cognitive symptoms. D2 blockade here can worsen them (secondary
negative symptoms).
,7. Blockade of D2 receptors in the nigrostriatal pathway is responsible for
which adverse effect?
A. Extrapyramidal symptoms (dystonia, parkinsonism, akathisia)
B. Hyperprolactinemia
C. Improvement in positive symptoms
D. Weight gain
Correct Answer: A. Extrapyramidal symptoms (dystonia, parkinsonism,
akathisia)
Rationale: The nigrostriatal pathway controls voluntary movement. Blocking D2
receptors there causes EPS, especially with high-potency first-generation
antipsychotics.
8. Blockade of D2 receptors in the tuberoinfundibular pathway results in:
A. Parkinsonism
B. Worsening psychosis
C. Sedation
D. Hyperprolactinemia
Correct Answer: D. Hyperprolactinemia
Rationale: Dopamine normally inhibits prolactin release from the anterior pituitary.
Blockade raises prolactin, causing galactorrhea, amenorrhea, gynecomastia and
sexual dysfunction.
9. Which enzyme, located on the outer mitochondrial membrane, degrades
serotonin, norepinephrine and dopamine?
A. Tyrosine hydroxylase
B. Tryptophan hydroxylase
C. Acetylcholinesterase
D. Monoamine oxidase (MAO)
Correct Answer: D. Monoamine oxidase (MAO)
Rationale: MAO-A and MAO-B metabolize monoamines. MAOI antidepressants
inhibit this enzyme, raising monoamine levels and creating dietary and
drug-interaction risks.
, 10. What is the primary mechanism of action of SSRIs?
A. Blockade of postsynaptic 5-HT2A receptors
B. Inhibition of presynaptic serotonin reuptake via the serotonin transporter
(SERT)
C. Inhibition of monoamine oxidase
D. Stimulation of vesicular serotonin release
Correct Answer: B. Inhibition of presynaptic serotonin reuptake via the
serotonin transporter (SERT)
Rationale: SSRIs block SERT, increasing synaptic serotonin. Therapeutic effect
follows downstream receptor adaptations, not the immediate rise in serotonin.
11. The 2 to 4 week delay in the therapeutic effect of SSRIs is best explained
by:
A. Slow hepatic metabolism of the drug
B. Delayed absorption from the gut
C. Gradual desensitization of 5-HT1A somatodendritic autoreceptors
D. Slow passage across the blood-brain barrier
Correct Answer: C. Gradual desensitization of 5-HT1A somatodendritic
autoreceptors
Rationale: Initial serotonin increase activates autoreceptors that dampen firing.
Their desensitization over weeks allows increased serotonergic neurotransmission
and clinical benefit.
12. Blockade of which receptor is primarily responsible for sedation and
weight gain with mirtazapine, olanzapine and quetiapine?
A. Muscarinic M1
B. Alpha-1 adrenergic
C. Histamine H1
D. Dopamine D2
Correct Answer: C. Histamine H1
Rationale: H1 antagonism causes sedation and increased appetite. M1 blockade
causes anticholinergic effects and alpha-1 blockade causes orthostasis.
