Antidepressants Flashcards
A 25-year-old woman has a long history of depressive symptoms accompanied by body aches and pain secondary to a car accident 2 years ago. Physical and laboratory tests are unremarkable. Which of the following drugs might be useful in this patient? A. Amitriptyline B. Fluoxetine C. Sertraline D. Phenelzine E. Mirtazapine F. Duloxetine
A. Amitriptyline (TCAD)
F. Duloxetine** *SNRI
SSRIs are much less effective than tricyclic antidepressants in the management of: A. Bulimia B. Chronic pain of neuropathic origin C. Generalized anxiety disorder D. Obsessive-compulsive disorder E. Premenstrual dysphoric disorder
B. Chronic pain of neuropathic origin
Premenstrual depressive disorder (depressive sx during late luteal phase) responses best to
fluoxetine (Serafem)
Describe the monoamine theory of depression
Reserpine depleted brainNE and 5HT –> induced depression
BUT does not totally explain etiology of depression bc white effects on amines are immediate, mood elevating effect is delayed 2-3 weeks
What are adaptations to acute antidepressant tx and chronic antidepressant tx
acute: inhibit 5HT or NE reuptake or breakdown
Chronic: trophic actions, increased fxn and survival of cells via gene alteration
What are examples of SSRIs
- Sertraline (Zoloft)
- Citalopram (Celexa)
- Escitalopram (Lexapro)
- Fluoxetine (Prozac)
- Paroxetine (Paxil)
what are examples of SNRIs
- Venlafaxine (Effexor)
2. Duloxetine (cymbalta)
What are examples of TCAD
- amitriptyline (Elavil)
- imipramine
- despramine
What are examples of NDRI
- Bupropion (Wellbutrin)
What class of drugs are the following:
- Trazodone:
- Mirtazapine (Remeron)
- Phenelzine
- Trazodone:5HT partial agonist-SSRI
- Mirtazapine (Remeron): alpha2 antagonists
- Phenelzine: MAOI
Describe the neurodegenerative hypothesis
- Stress causes cortisol release–> detrimental gene transcription response–> neurogenesis inhibited
MOA of TCADs
NE and/or serotonin reuptake inhibitors
MOA of alpha2 antagonists
inhibition of presynaptic a2 autoreceptors that decreases NE release, such a block results in increased NE release
MOA of MAOI
(monoamine oxidase inhibitors)
*block enzyme of major degradation pathway for NE and 5HT in neuron, presumably allowing more presynaptic accumulation and subsequent release into the synapse and again leading to chronic compensatory changes at the synapse
MOA of ECT
increases the amount and activity of the rate limiting enzymes for synthesis of NE (tyrosine hydroxylase) and serotonin (tryptophan hydroxylase) resulting in increased levels of these NT
side effects of SSRIs
ACUTE
- Nausea-diarrhea
- Activation-insomnia
- Restlessness (akathisia)
- Dry mouth
DELAYED:
- Wt. gain
- Sexual dysfunction
- Cognitive blunting
- Very low likelihood of fatallties in OD
- W/D (discontinuation) symptoms–> flu-like
W/D (discontinuation) symptoms w/ SSRIs is related to
half-life (shorter=worse, paroxetine> fluoxetine)
SE of SNRIs
- HTN
- Anxiety
- Nausea
- Dizzy
- Sweating
- Sleepy
- Sexual dysfunction
- more rapid appearance of WD sx than SSRIs
SE of NDRIs
- Dizzy
- Dry mouth
- Tremor
- Insomnia
- Anxiety
- Aggravation of psychosis
- Seizure at HD
SE of Trazodone
- Drowsy- used empirically as hypnotic agent
- Dizzy
- nausea
- agitation
- OD–> minor problems only
SE of Mirtazapine
- Sleepy
- Increased appetite
- Wt. gain
- Dizzy
SE of TCAD
*poor SE profile, declining use, 2nd-3rd line agents
- Sedation (Amitriptyline > Desipramine)
- Antimuscarinic effects (no see, no pee, no spit, no shit) (Amitriptyline > Desipramine)
- Narrow angle glaucoma w/ HD
- Orthostatic hypotension
- Arrhythmias
- Sudden death in OD
- Tremor
- Seizure w/ OD
- Wt. gain (histamine blocking action)
- Sexual disturbances
SE of MOAI
- Postural hypotension via chronic increase in false NT
- Mild anticholinergic effects
- Sedation
- CNS stimulation
- liver damage
- Seizures in OD
- Shock in OD
- hyperthermia in OD