Nurs 663: Unipolar
Depression (NEI) questions
and answers
A 26-year-old woman began treatment for a major depressive
episode 8 months ago. Two months into her treatment she began to
experience noticeable symptom improvement, and for the last 5
months, she has been mostly symptom-free, except for persistent
cognitive dysfunction. Which of the following statements regarding
cognitive dysfunction in depression is most accurate?
A. Cognitive dysfunction is one of the most common residual
symptoms following recovery
B. Cognitive dysfunction can be treated with serotonergic
modulation of glutamate transmission
C. Both A and B
C. Both A and B
Cognitive dysfunction is one of the most common residual
symptoms of major depressive disorder and can endure longer than
mood symptoms following recovery. Moreover, cognitive dysfunction
is strongly correlated with physical, mental, and functional
disability. Pharmacotherapies used to treat depression that have
action on glutamate signaling via serotonergic modulation also
show pro-cognitive effects. The prime example is vortioxetine,
which has agonist action at 5HT1A, weak partial agonist action at
5HT1B/D, and antagonist action at 5HT3, 5HT1D, 5HT7, and the
serotonin transporter. Antagonism of 5HT3 disinhibits glutamate
release, while antagonism of 5HT7 enhances release of glutamate
release in the prefrontal cortex. In addition, agonism of 5HT1A (full)
and 5HT1B (partial) may enhance or suppress glutamate
transmission based on neuronal localization.
Amir is a 19-year-old patient with depression. He requests
treatment with a serotonin norepinephrine reuptake inhibitor (SNRI)
because he heard they are more effective than selective serotonin
reuptake inhibitors (SSRI). Theoretically, what is the therapeutic
advantage of a SNRI over a SSRI?
, A. Increased norepinephrine via norepinephrine transporter
inhibition
B. Increased dopamine via norepinephrine transporter inhibition
C. Increased norepinephrine and dopamine via norepinephrine
transporter inhibition
C. Increased norepinephrine and dopamine via noreepinephrine
transporter inhibition
In addition to boosting serotonin like SSRIs (via inhibition of
serotonin reuptake by the serotonin transporter [SERT]), SNRIs can
boost norepinephrine by inhibiting reuptake by the norepinephrine
transporter (NET). Additionally, in the prefrontal cortex, SNRIs can
boost dopamine levels. In prefrontal cortex, SERTs and NETs are
present in abundance on serotonin and norepinephrine nerve
terminals, respectively, but there are very few dopamine
transporters (DATs) on dopamine nerve terminals. Therefore,
dopamine action is terminated either by enzymatic degradation or
NET. If NET is inhibited by an SNRI then it cannot terminate the
action of dopamine and dopamine levels increase in this brain
region.
A 36-year-old man with major depressive disorder is having lab work
done to assess his levels of inflammatory markers. Based on the
current evidence regarding inflammation in depression, which of the
following results would you most likely suspect for this patient?
A. Elevated levels of tumor necrosis factor-alpha (TNF-alpha)
B. Reduced levels of interleukin 6 (IL-6)
C. Reduced C-reactive protein (CRP)
D. Elevated interferon gamma (IFN?)
A. Elevated levels of tumor necrosis factor-alpha (TNF-alpha)
There is growing evidence that inflammation may play an important
role in the pathophysiology of major depression. Clinical studies
have shown that depressed patients have significantly higher
concentrations of several inflammatory central and peripheral
markers, including the pro-inflammatory cytokines TNF-alpha and
interleukin-6. Patients with depression also have higher
concentrations of C-reactive protein, which is synthesized by the
liver in response to pro-inflammatory cytokines, and reduced
interferon gamma, which is a proinflammatory cytokine.
Depression (NEI) questions
and answers
A 26-year-old woman began treatment for a major depressive
episode 8 months ago. Two months into her treatment she began to
experience noticeable symptom improvement, and for the last 5
months, she has been mostly symptom-free, except for persistent
cognitive dysfunction. Which of the following statements regarding
cognitive dysfunction in depression is most accurate?
A. Cognitive dysfunction is one of the most common residual
symptoms following recovery
B. Cognitive dysfunction can be treated with serotonergic
modulation of glutamate transmission
C. Both A and B
C. Both A and B
Cognitive dysfunction is one of the most common residual
symptoms of major depressive disorder and can endure longer than
mood symptoms following recovery. Moreover, cognitive dysfunction
is strongly correlated with physical, mental, and functional
disability. Pharmacotherapies used to treat depression that have
action on glutamate signaling via serotonergic modulation also
show pro-cognitive effects. The prime example is vortioxetine,
which has agonist action at 5HT1A, weak partial agonist action at
5HT1B/D, and antagonist action at 5HT3, 5HT1D, 5HT7, and the
serotonin transporter. Antagonism of 5HT3 disinhibits glutamate
release, while antagonism of 5HT7 enhances release of glutamate
release in the prefrontal cortex. In addition, agonism of 5HT1A (full)
and 5HT1B (partial) may enhance or suppress glutamate
transmission based on neuronal localization.
Amir is a 19-year-old patient with depression. He requests
treatment with a serotonin norepinephrine reuptake inhibitor (SNRI)
because he heard they are more effective than selective serotonin
reuptake inhibitors (SSRI). Theoretically, what is the therapeutic
advantage of a SNRI over a SSRI?
, A. Increased norepinephrine via norepinephrine transporter
inhibition
B. Increased dopamine via norepinephrine transporter inhibition
C. Increased norepinephrine and dopamine via norepinephrine
transporter inhibition
C. Increased norepinephrine and dopamine via noreepinephrine
transporter inhibition
In addition to boosting serotonin like SSRIs (via inhibition of
serotonin reuptake by the serotonin transporter [SERT]), SNRIs can
boost norepinephrine by inhibiting reuptake by the norepinephrine
transporter (NET). Additionally, in the prefrontal cortex, SNRIs can
boost dopamine levels. In prefrontal cortex, SERTs and NETs are
present in abundance on serotonin and norepinephrine nerve
terminals, respectively, but there are very few dopamine
transporters (DATs) on dopamine nerve terminals. Therefore,
dopamine action is terminated either by enzymatic degradation or
NET. If NET is inhibited by an SNRI then it cannot terminate the
action of dopamine and dopamine levels increase in this brain
region.
A 36-year-old man with major depressive disorder is having lab work
done to assess his levels of inflammatory markers. Based on the
current evidence regarding inflammation in depression, which of the
following results would you most likely suspect for this patient?
A. Elevated levels of tumor necrosis factor-alpha (TNF-alpha)
B. Reduced levels of interleukin 6 (IL-6)
C. Reduced C-reactive protein (CRP)
D. Elevated interferon gamma (IFN?)
A. Elevated levels of tumor necrosis factor-alpha (TNF-alpha)
There is growing evidence that inflammation may play an important
role in the pathophysiology of major depression. Clinical studies
have shown that depressed patients have significantly higher
concentrations of several inflammatory central and peripheral
markers, including the pro-inflammatory cytokines TNF-alpha and
interleukin-6. Patients with depression also have higher
concentrations of C-reactive protein, which is synthesized by the
liver in response to pro-inflammatory cytokines, and reduced
interferon gamma, which is a proinflammatory cytokine.
