Antidepressants Flashcards
what are the MAOI inhibitors
MAO Take Pride In Shanghai
Tranylcypromine (non hydrazine)
Phenelzine (hydrazine)
Isocarboxazid (hydrazine)
Selegiline (non hydrazine)
mechanism of MAO inhibitors (name them)
tranylcypromine, phenelzine, isocarboxazid, selegiline
- prevent the breakdown of serotonin, dopamine, norepinephrine
- PIT bind irreversibly and nonselectively to MAO-A and MAO-B
- Selegiline binds to MAO-B
use of MAOI
- depression unresponsive to other antidepressants
- Selegiline for early Parkinson’s
AE of MAOI
tranylcypromine, phenelzine, isocarboxazid, selegiline
drowsiness, insomnia, orthostatic hypotension, weight gain, muscle pain, sexual dysfunction
contraindication of MAOI (name them)
tranylcypromine, phenelzine, isocarbaxozid, selegiline
- serotonin agents: SSRI, SNRIs, or TCAs –> serotonin syndrome due to excess stimulation –> hyperthermia, muscle rigidity, myoclonus, rapid changes in mental status and vitals (so they must be stopped 2 weeks before administering MAOIs)
- tyramine containing food such as aged wine and cheese: they are broken down by MAO –> large release of catecholamines –> hypertension, tachycardia, arrhythmias, headache, stiff neck
- sympathomimetic drugs: pseudoephedrine and phenylpropanolamine (both in cold meds)
what is used to control or manage tyramine induce hypertension
Phentolamine
Prazosin
what happens if overdose on MAOI
tranylcypromine, phenelzine, isocarboxazid, selegeline
autonomic instability, hyperadrenergic symptoms, psychotic symptoms, confusion, delirium, fever
what happens with discontinuation of MAOI
discontinuation syndrome (seen with all antidepressants) –> worsening of depressive symptoms, confusion, disorientation, psychosis, anxiety
what are the TCAs
DANI and CAM
Desipramine
Amitriptyline
Nortriptyline
Imipramine
Clomipramine
Amoxapine
Maprotiline
mechanism of action of TCAs (name them)
desipramine, amitripyline, nortriptyline, imipramine, clomipramine, amoxapine, maprotiline
blocks reuptake of serotonin and NE by competitively binding their carrier protein –> increased monoamine in the cleft
block alpha adrenergic, muscarinic, histamine, and cardiac fast Na channels
AE of TCAs (name them)
desipramine, amitriptyline, nortriptyline, imipramine, clomipramine, amoxapaine, maprotiline
- block muscarinic receptors –> blurred vision, xerostomia, urinary retention, constipation, narrow angle glaucoma
- increase catecholamine receptors –> increased cardiac stimulation
- inhibit cardiac fast Na channel –> arrhythmias
- block alpha 1 receptor: orthostatic hypotension with rebound tachycardia
- H1 blocker: sedation and weight gain
- sexual effects
what metabolizes TCAs and how does it affect the population
CYP2D6 so those (esp whites) with polymorphism are associated with slow metabolism of TCAs
what occurs with overdose of TCAs
lethal arrhythmias –> v-tach and v-fib
what reverses the cardiac block caused by overdose of TCAs
sodium bicarbonate
what are the SSRIs
SEP of FFC
Sertraline Escitalopram Paroxetine Fluoxetine Fluvoxamine Citalopram
mechanism of SSRIs (name them)
Sertraline, Escitalopram, Paroxetine, Fluoxetine, Fluvoxamine, Citalopram
- inhibit the reuptake of serotonin
- unlike TCAs, they have little blocking activity at muscaranic, histamine H1, and alpha adrenergic receptors