Ch 32: Antidepressants Flashcards

1
Q

Clinical observations in the 1960s led to formulation of the…

A

…monoamine-deficiency hypothesis of depression.

p. 339

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2
Q

What does the monoamine-deficiency hypothesis of depression assert?

A

That depression is caused by a functional deficiency of monoamine neurotransmitters (norepinephrine, serotonin, or both).

(p. 339)

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3
Q

What are the 5 classes of antidepressants?

A
SSRIs
SNRIs
TCAs
MAOIs 
atypical antidepressants

(p. 341)

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4
Q

Once an antidepressant has been selected for initial treatment, it should be used for __ to __ weeks to assess efficacy.

A

4 - 8 weeks

p. 342

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5
Q

The risk of suicidality appears _____ with all _______________.

A

equal; antidepressants

p. 343

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6
Q

Fluoxetine produces CNS…

A

…excitation rather than sedation.

p. 344

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7
Q

What are the 6 SSRI’s? (Think C-E-F-F-P-S)

A
citalopram
escitalopram
fluoxetine
fluvoxamine
paroxetine
sertraline   

(p. 346)

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8
Q

Which is the only SSRI known to cause sedation?

A

fluvoxamine

p. 346 - 347

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9
Q

What is the mechanism of action of SSRI’s?

A

blockade of 5-HT reuptake and with a resulting increase of 5-HT in the synapse

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10
Q

Venlafaxine may be cautiously combined with an SSRI or another SNRI, however, combined use with an ____ is contraindicated.

A

MAOI

p. 348

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11
Q

What are the 4 SNRI’s?

A

venlafaxine and desvenlafaxine
duloxetine
levomilnacipran

(p. 346)

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12
Q

What was the 2nd SNRI approved for major depression?

A

duloxetine (Cymbalta)

p. 348

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13
Q

Due to their similar structures, both the TCA’s and the phenothiazine antipsychotics produce the following effects:

A

sedation and anticholinergic effects, and orthostatic hypotension which is the most serious adverse effect

(p. 349)

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14
Q

How do TCA’s work?

A

They block neuronal reuptake of NE and 5-HT (although some only block reuptake of NE).

(p. 349)

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15
Q

Why are TCA’s not first-line antidepressants?

A

Because the SSRI’s and SNRI’s are generally safer and better tolerated.

(p. 351)

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16
Q

Cardiac toxicity is one of the more serious adverse effects of TCA’s. What are the 2 ways that TCA’s affect the heart?

A

1.) decreasing vagal influence on the heart secondary to muscarinic blockade
2.) acting directly on the bundle of His to slow conduction.
Both of these effects increase the risk of dysrhythmias.

(p. 351)

17
Q

What do TCA’s do to the seizure threshold?

A

lower it

p. 351

18
Q

What is the greatest concern with prescribing MAOI’s?

A

Hypertensive crisis, which can be triggered by eating foods rich in tyramine.

(p. 352)

19
Q

What is MAO, where is it, and what is its function?

A

MAO is monoamine oxidase, and it is an enzyme found in the liver, the intestinal wall, and terminals of monoamine containing-neurons.
Its function is to convert monoamine neurotransmitters (NE, 5-HT, and dopamine) into inactive products.

(p. 352)

20
Q

All of the MAOIs in current use cause ____________ inhibition.

A

irreversible

p. 352

21
Q

What is one major benefit of transdermal selegiline?

A

The risk of hypertensive crisis from dietary tyramine is much lower than with oral dosing.

(p. 355)

22
Q

Bupropion (Wellbutrin) is an atypical antidepressant similar in structure to…

A

…amphetamine. Like amphetamine, bupropion has stimulant actions and suppresses appetite.

(p. 356)

23
Q

In contrast to SSRI’s, bupropion does not cause…

A

…weight gain or sexual dysfunction. In fact, it appears to increase sexual desire and pleasure.

(p. 356)

24
Q

Bupropion is approved to treat…

A

…major depression, seasonal affective disorder, and as an aid in smoking cessation.

(p. 356)

25
Q

Antidepressant therapy should continue for how long after symptoms resolve?

A

4 to 9 months

p. 359

26
Q

What are 5 TCA drugs available which block both NE and 5-HT reuptake? (A-C-D-I-T)

The 4 which block both only NE reuptake? (D-M-N-P)

A
amitriptyline
clomipramine
doxepin
imipramine
trimipramine

desipramine
maprotiline
nortriptyline
protriptyline

(p. 350)

27
Q

What is the risk if MAOI’s are combined with an SSRI or an SNRI?

A

serotonin syndrome, symptoms of which begin 2 - 72 hours after treatment onset. Signs and symptoms include AMS, incoordination, myoclonus, hyperreflexia, excessive sweating, tremor, and fever.

(p. 345)