Deck 12: Antidepressant Drugs

Question 1

Tricyclic antidepressants (TCAs):

A) produce euphoria.
B) cause a number of side effects.
C) are known teratogens.
D) are advantageous for treatment because of the rapid onset of action.

Answer 1

B

Question 2

In depressed patients,tricyclic antidepressants _____ and are _____ in resistant patients.

A) elevate mood; effective
B) elevate mood; ineffective
C) do not affect mood; effective
D) do not affect mood; ineffective

Answer 2

A

Question 3

The major side effect associated with use of MAOIs is:

A) heart arrhythmias.
B) memory impairment.
C) cardiac toxicity.
D) hypertension.

Answer 3

D

Question 4

Compared to SSRIs,TCAs are:

A) more effective and less expensive.
B) no more effective and more expensive.
C) more effective and more expensive.
D) no more effective but less expensive.

Question 5

Availability of newer antidepressants has:

A) decreased the number of treatment-resistant people with major depression.
B) increased the efficacy of antidepressants.
C) accelerated the onset of action of antidepressants.
D) improved the side-effect profile.

Question 6

Dangerous interactions with aged cheese and other food products containing tyramine is associated with:

A) TCAs.
B) SSRIs.
C) atypical second-generation antidepressants.
D) MAOIs.

Question 7

The tricyclic antidepressants differ from SSRIs in that they also have major effects on the following neurotransmitter:

A) glutamate.
B) norepinephrine.
C) serotonin.
D) GABA.

Question 8

Imipramine (Tofranil)and desipramine (Norpramin)are examples of:

A) MAOIs.
B) SSRIs.
C) second-generation antidepressants.
D) TCAs.

Question 9

The first-generation antidepressants consist of:

A) TCAs only.
B) MAOIs only.
C) atypical antidepressants.
D) TCAs and MAOIs.

Question 10

First-generation tricyclic antidepressants are defined by a commonality in basic:

A) effect.
B) mechanism of action.
C) structure.
D) site of action.

Question 11

The mechanism of action of the MAOIs is:

A) blockade of postsynaptic receptors.
B) inhibition of degradation by enzymes.
C) inhibition of neurotransmitter reuptake.
D) inhibition of neurotransmitter release.

Question 12

Significant sedation is a side effect of the:

A) MAOIs.
B) SSRIs.
C) second-generation antidepressants.
D) TCAs.

Question 13

Cardiac toxicity is an effect most clearly associated with overdose of:

A) TCAs.
B) SSRIs.
C) second-generation antidepressants.
D) MAOIs.

Question 14

The therapeutic mechanism of action of the tricyclic antidepressants is:

A) blockade of postsynaptic receptors.
B) inhibition of degradation by enzymes.
C) inhibition of neurotransmitter reuptake.
D) inhibition of neurotransmitter release.

Question 15

Today,anxiety disorders may be treated with:

A) anxiolytics.
B) antidepressants.
C) antipsychotics.
D) barbiturates.

Question 16

The "neurogenic theory of depression" stems from recent findings that in the mature brain,nurons:

A) are incapable of repairing themselves.
B) are incapable of being newly produced.
C) can neither be repaired nor produced.
D) are capable of being repaired and produced.

Question 17

The dry mouth,memory impairment,and confusion associated with use of tricyclic antidepressants are a result of action on the following neurotransmitter:

A) norepinephrine.
B) serotonin.
C) histamine.
D) acetylcholine.

Question 18

Tricyclic antidepressants have all of the following actions,EXCEPT blocking:

A) glutamate receptors.
B) histamine receptors.
C) acetylcholine receptors.
D) norepinephrine reuptake.

Question 19

Tricyclic antidepressants (TCAs)exert which of the following pharmacological actions?

A) presynaptic reuptake transporter for acetylcholine
B) blockade of postsynaptic receptors for serotonin (5-HT)
C) presynaptic reuptake transporter for norepinephrine
D) blockade of postsynaptic transporters for GABA

Question 20

Impairment of memory is a side effect clearly associated with the use of:

A) TCAs.
B) SSRIs.
C) second-generation antidepressants.
D) MAOIs.

Question 21

The mechanism of action of buspirone (BuSpar)involves:

A) 5-HT_1A receptors.
B) 5-HT₂ receptors.
C) D₂ receptors.
D) alterations in GABA levels.

Question 22

The mechanism of action of newer antidepressants like Prozac and Zoloft is:

A) blockade of postsynaptic receptors.
B) inhibition of degradation by enzymes.
C) inhibition of neurotransmitter reuptake.
D) inhibition of neurotransmitter release.

Question 23

The use of S-Adenosylmethionine (SAM-e):

A) is a frequent addition to SSRI treatment for depression.
B) may be helpful for mild depression.
C) is commonly used to treat major depression.
D) involves substance P antagonism.

Question 24

The dual-acting antidepressant Effexor EX (extended release)is FDA-approved for the treatment of:

A) bipolar disorder.
B) panic disorder.
C) decreased libido.
D) ADHD.

Question 25

The various SSRIs (Prozac,Zoloft,Paxil)differ in terms of:

A) efficacy but not mechanism of action.
B) mechanism of action but not efficacy.
C) neither efficacy nor mechanism of action.
D) both efficacy and mechanism of action.

Question 26

The dual-acting antidepressant Nefazodone (Serzone)blocks _______; however,its use has been associated with ______.

A) 5-HT₁; kidney failure
B) 5-HT₁; liver failure
C) 5-HT₂; kidney failure
D) 5-HT₂; liver failure

Question 27

The SSRI most associated with "serotonin syndrome" is:

A) sertraline (Zoloft).
B) fluoxetine (Prozac).
C) fluvoxamine (Luvox).
D) paroxetine (Paxil).

Question 28

The sensation of electric shocks is associated with discontinuation of:

A) tricyclic antidepressants.
B) SSRIs.
C) MAOIs.
D) atypical second-generation antidepressants.

Question 29

Some patients do not respond to SSRIs presumably because:

A) they lack serotonin receptors.
B) they are slow metabolizers resulting in accumulation of the drug.
C) they are rapid metabolizers resulting in inadequate blood levels.
D) of dietary issues resulting in poor absorption.

Question 30

MAO-B's mechanism of action involves:

A) norepinephrine
B) serotonin
C) dopamine
D) glutamate

Question 31

Selective norepinephrine reuptake inhibitors (SNRIs)are:

A) ineffective in treating depression.
B) ineffective in treating ADHD.
C) effective in treating depression,but not ADHD.
D) effective in treating depression and ADHD.

Question 32

When discontinuing an MAOI,patients may:

A) switch immediately to a new drug.
B) switch immediately to a new drug and ignore dietary restrictions.
C) discontinue use,but must continue to follow dietary restrictions for about 2 weeks.
D) discontinue use and take twice as much as prescribed on the new medication.

Question 33

Interest in the MAOIs as potential drugs to treat depression persists because they:

A) are safer than SSRIs.
B) are particularly good for treating major depression-better than SSRIs or TCAs.
C) are an excellent choice for patients with substance abuse issues.
D) work in patients who do not respond to TCAs and SSRIs.

Question 34

Of the following classes of antidepressant drugs,the one associated with the highest incidence (up to 80% of patients taking the drug)of sexual dysfunction is:

A) anxiolytic
B) anxiogenic
C) analgesic
D) sedating

Question 35

Use of Maprotiline (Ludiomil),an atypical antidepressants developed in the 1980s,is not a first choice antidepressant because it:

A) has a short half life.
B) blocks glutamate receptors.
C) makes people feel anxious.
D) can cause seizures.

Question 36

A deficiency of the B vitamin folate:

A) increases monoamine levels and the risk of depression.
B) decreases monoamine levels and the risk of depression.
C) increases monoamine levels and decreases the risk of depression.
D) decreases monoamine levels and increases the risk of depression.

Question 37

Which of the following statements is TRUE?

A) TCAs,but not SSRIs,are useful in treating clinical pain syndromes.
B) SSRIs,but not TCAs,are useful in treating anxiety disorders.
C) Both TCAs and SSRIs are useful in treating clinical pain syndromes.
D) Neither TCAs nor SSRIs are useful in treating anxiety disorders.

Question 38

Formulated as a short-acting immediate release medication,Trazodone (Desyrel)an atypical antidepressants developed in the 1980s:

A) has been used as an antidepressant anxiolytic.
B) causes drowsiness resulting in its use as a antidepressant hypnotic.
C) blocks D₂ receptors as well as 5HT_2A receptors.
D) stimulates acetylcholine function resulting in improved memory.

Question 39

Tianeptine is a unique antidepressant in that its mechanism of action is the:

A) blockade of presynaptic reuptake of norepinephrine.
B) facilitation of presynaptic reuptake of norepinephrine.
C) blockade of presynaptic reuptake of serotonin.
D) facilitation of presynaptic reuptake of serotonin.

Question 40

The atypical second-generation antidepressant Effexor (venlafaxine)differs most from the tricyclic antidepressants in its effect (or lack thereof)on the neurotransmitter:

A) dopamine.
B) serotonin.
C) norepinephrine.
D) acetylcholine.

Question 41

Antidepressant drugs can repair stress-induced neuronal damage.

Question 42

Selective serotonin reuptake inhibitors block some postsynaptic serotonin receptors.

Question 43

The birth of new neurons is called synaptogenesis.

Question 44

Second-generation antidepressants are similar in structure to the selective serotonin reuptake inhibitors (SSRIs).

Question 45

The neurogenic theory of depression suggests that memory and attention may be affected in depressed patients by impaired neurogenesis.

Question 46

The major side effects of tricyclic antidepressants result from effects on the neurotransmitters acetylcholine and histamine.

Question 47

Tricyclic antidepressants have little effect on the neurotransmitter dopamine.

Question 48

Monoamine oxidase regulates the amount of biogenic amine transmitters in the presynaptic nerve terminal.

Question 49

Monoamine oxidase inhibitors (MAOIs)may interact with specific foods and/or other medications with fatal results.

Question 50

Antidepressants may be prescribed to alleviate anxiety associated with depression.

Question 51

All the tricyclic antidepressants affect both the neurotransmitters norepinephrine and serotonin.

Question 52

The first-generation antidepressants have a more favorable profile of toxicity than SSRIs.

Question 53

The presence of cAMP response element-binding protein (CREB)activates genes that control levels of brain-derived neurotrophic factor (BDNF).

Question 54

Antidepressants may relieve depressed mood by increasing cAMP response element-binding protein (CREB).

Question 55

First-generation tricyclic antidepressants are defined by a commonality in basic mechanism.

Question 56

Depression can physically shrink the hippocampus.

Question 57

Tricyclic antidepressants have a rapid onset of action.

Question 58

Generally speaking,desipramine (Norpramin)is a good choice for newly diagnosed depressed patients.

Question 59

The SSRIs are more effective than older TCAs.

Question 60

Tricyclic antidepressants have a common chemical structure as opposed to second generation antidepressants that are defined by their mechanism of action.

Question 61

Long-term antidepressant use in children and adolescents appears to be associated with an increased risk of suicide.

Question 62

A person discontinuing the use of an SSRI,may experience flulike symptoms.

Question 63

Paroxetine (Paxil)is approved for the treatment of generalized anxiety disorder as well as major depression.

Question 64

Evidence suggests that _____ may be a final common target of antidepressant treatment.

A) cAMP-dependent protein kinase (PKA)
B) brain-derived neurotrophic factor (BDNF)
C) neurotrophins
D) cAMP response-element-binding protein (CREB)

Question 65

SSRIs possess significant anticholinergic effects resulting in dry mouth,blurred vision,and confusion for those taking the medications.

Question 66

A folate deficiency may increase the risk of depression.

Question 67

Melanie is trying a new antidepressant therapy involving low dose intravenous infusions of ketamine.She is likely to experience rapid improvement in her depression,but the effects will probably not last very long.

Question 68

No antidepressants exist that specifically and solely affect norepinephrine.

Question 69

Jacob just recently started taking an SSRI; it is likely that he will experience some insomnia while he taking his medication.

Question 70

The use of antidepressants has:

A) eliminated depression.
B) been associated with few side effects.
C) not been effective for relief of anxiety.
D) resulted in modest improvements in depression.

Question 71

The first-generation antidepressants consist of:

A) TCAs and SSRIs.
B) TCAs and MAOIs.
C) MAOIs and SSRIs.
D) MAOIs and SNRIs.

Question 72

Of the tricyclic antidepressants (TCAs),_____ is particularly effective at serotonin reuptake inhibition.

A) clomipramine (Anafranil)
B) imipramine (Tofranil)
C) desipramine (Norpramin)
D) amitriptyline (Elavil)

Question 73

Evidence suggests that _____ during antidepressant treatment provides evidence to _____ the neurogenic hypothesis of depression.

A) cAMP response-element-binding protein (CREB); discredit
B) brain-derived neurotrophic factor (BDNF); support
C) cAMP response-element-binding protein (CREB); support
D) brain-derived neurotrophic factor (BDNF); discredit

Question 74

Antidepressants have been prescribed to treat anxiety because:

A) they are less prone to induce compulsive use.
B) depression is always associated with panic disorder.
C) they are useful for treatment of psychosis.
D) mild depression often occurs with obsessive compulsive disorder (OCD).

Question 75

Tricyclic antidepressants (TCAs)affect:

A) norepinephrine and glutamate.
B) norepinephrine and serotonin.
C) dopamine and serotonin.
D) dopamine and acetylcholine.

Question 76

The dietary supplement SAMe is effective in treating severe depression.

Question 77

St.John's wort is thought to produce neurotropic effects in the hippocampus in a similar manner to BDNF.

Question 78

The dual-action antidepressant Serzone blocks both serotonin and norepinephrine reuptake as well as 5-HT₂ receptors.

Question 79

The neurogenic theory of depression involves the notion that:

A) existing neurons are unable to repair themselves in some people resulting in accumulating "depression" of the cells.
B) the brain is capable of making new neurons.
C) there is an upregulation of neurogenesis in depressed patients.
D) existing neurons are resistant to damage in depressed patients.

Question 80

In the 1960s,a patient with depression would likely have been treated with:

A) tricyclic antidepressants (TCAs).
B) selective serotonin reuptake inhibitors (SSRIs).
C) monoamine oxidase.
D) atypical second-generation antidepressants.