Ch 32: Antidepressants Flashcards
Clinical observations in the 1960s led to formulation of the…
…monoamine-deficiency hypothesis of depression.
p. 339
What does the monoamine-deficiency hypothesis of depression assert?
That depression is caused by a functional deficiency of monoamine neurotransmitters (norepinephrine, serotonin, or both).
(p. 339)
What are the 5 classes of antidepressants?
SSRIs SNRIs TCAs MAOIs atypical antidepressants
(p. 341)
Once an antidepressant has been selected for initial treatment, it should be used for __ to __ weeks to assess efficacy.
4 - 8 weeks
p. 342
The risk of suicidality appears _____ with all _______________.
equal; antidepressants
p. 343
Fluoxetine produces CNS…
…excitation rather than sedation.
p. 344
What are the 6 SSRI’s? (Think C-E-F-F-P-S)
citalopram escitalopram fluoxetine fluvoxamine paroxetine sertraline
(p. 346)
Which is the only SSRI known to cause sedation?
fluvoxamine
p. 346 - 347
What is the mechanism of action of SSRI’s?
blockade of 5-HT reuptake and with a resulting increase of 5-HT in the synapse
Venlafaxine may be cautiously combined with an SSRI or another SNRI, however, combined use with an ____ is contraindicated.
MAOI
p. 348
What are the 4 SNRI’s?
venlafaxine and desvenlafaxine
duloxetine
levomilnacipran
(p. 346)
What was the 2nd SNRI approved for major depression?
duloxetine (Cymbalta)
p. 348
Due to their similar structures, both the TCA’s and the phenothiazine antipsychotics produce the following effects:
sedation and anticholinergic effects, and orthostatic hypotension which is the most serious adverse effect
(p. 349)
How do TCA’s work?
They block neuronal reuptake of NE and 5-HT (although some only block reuptake of NE).
(p. 349)
Why are TCA’s not first-line antidepressants?
Because the SSRI’s and SNRI’s are generally safer and better tolerated.
(p. 351)