Antidepressants Lecture PDF Flashcards
Response to significant loss may have criteria for major depression, but…
….only after a prolonged period beyond the normal response to significant loss judged clinically
Pathophysiology of depression
Multi-factorial between genetic, social, and biochemical processes, but often focus is placed on neurotransmitter defect reflects symptoms of depression
Monoamine hypothesis of depression
Clinical observations that have provided evidence that maintains depression is caused by functional insufficiency of monoamine transmitters in the brain (serotonin, norepi) based on 2 observations -that depression was induced by reserpine (a drug that depletes monoamines from the brain) and -drugs that treat depression intensify monoamine induced neurotransmission
Electroconvulsive therapy indications (2)
-When speed is critical, when a patient has failed to respond to antidepressants
Repetitive transcranial magnetic stimulation
Production of pulsed magnetic fields that can induce electrical currents in the brain and unlike electroconvulsive therapy does not require anesthesia or induction of seizures
Light therapy
Bright light exposure that can be effective in managing SAD or nonseasonal depression
Suicide risk with antidepressants
Patients taking antidepressants should be watched closely for suicide ideation, worsening mood, and behavioral changes particularly within the first one to two months of therapy or when dosage is changed (theorized to increase energy potentiating risk of acting on suicidal thoughts) most often seen in children thru young adults creating a blackbox warning for all antidepressants
Time of response to antidepressants and maintenance treatment
Initial responses develop in 1-3 weeks, max response not seen until 12 weeks, must take at least 1 month before considered a treatment failure, low doses used initially to reduce side effects and gradually increased, if not effective, can increase dosage, switch another drug in same class, switch to drug in different class, combine 2, ad supplemental, can withdraw only via taper but long term maintenance therapy can reduce risk of recurrence for patients with recurrent depressive episodes
Only SSRI approved by FDA for treatment of major depression in children
Fluoxetine (prozac)
SSRI mech of action, ADRs (3)
- selective inhibition of serotonin reuptake
- excessive CNS excitation, sexual dysfunction, nausea
Therapeutic uses for SSRI’s (4)
- Major depressive disorder
- Generalized anxiety disorder
- OCD
- PTSD
Serotonin syndrome
Risk of often combining SSRI’s with MAOI or from overdosing or from utilizing St John’s wort, often starting 72 hours after starting drug resulting in altered mental status, agitation, confusion, hyperreflexia, tremor, and potentially death
Bruxism
Clenching or grinding of teeth usually occuring during sleep that can lead to headache, jaw pain, or dental problems, a bad side effect of SSRI’s
SSRI drug interactions
- MAOI can potentiate risk of serotonin syndrome requiring withdrawal at least 14 days before starting fluoxetine
- Warfarin can increase effect
- St. John’s wort can potentiate risk of serotonin syndrome
- small risk in pregnancy of neonatal absence syndrome (self resolving)
SNRI’s function, drug metabolism,
- Alongside SSRI considered first line option for treatment of major depression
- metabolized in the liver and excreted in the urine