Case 6 DRUGS Flashcards
Reserpine
Irreversible VMAT blocker.
Causes any excess cytoplasmic monoamines in the presynaptic terminal to be broken down by MAO and CMT, and stops exocytosis of monoamines.
RESULT = LONG LASTING DEPRESSION
Iproniazid
Irreversible MAO inhibitor.
Prevents breakdown of monoamine NT’s and so increasing their availability.
Phenelzine/ Tranylcypromine
Irreversible MAO inhibitor.
Prevents breakdown of monoamine NT’s and so increasing their availability.
Moclobomide
Reversible MAO inhibitor.
Prevents breakdown of monoamine NT’s and so increasing their availability.
Amitriptyline
Tricyclic Antidepressant (TCA) Blocks re-uptake of 5-HT, NA, Dopamine.
Clomipramine
Tricyclic Antidepressant (TCA) Blocks re-uptake of 5-HT, NA, Dopamine.
Venlafaxine
Seretonin and Noradrenaline Re-uptake Inhibitors (SNRI’s).
Thus increasing their concentration in the synaptic cleft.
Sertraline
Selective Seretonin Re-uptake Inhibitor.
Increases the concentration of serotonin in the synaptic cleft.
Fluoxetine
Selective Seretonin Re-uptake Inhibitor.
Increases the concentration of serotonin in the synaptic cleft.
Paroxetine
Selective Seretonin Re-uptake Inhibitor.
Increases the concentration of serotonin in the synaptic cleft.
Citalopram
Selective Seretonin Re-uptake Inhibitor.
Increases the concentration of serotonin in the synaptic cleft.
Escitalopram
Selective Seretonin Re-uptake Inhibitor.
Increases the concentration of serotonin in the synaptic cleft.
Fluvoxamine
Selective Seretonin Re-uptake Inhibitor.
Increases the concentration of serotonin in the synaptic cleft.
Mertazapine
a2 adrenergic receptor antagonist. (a2 antagonist)
Negative feedback loop to inhibit release of noradrenaline is blocked.
Increases the release of NA and serotonin.
Antipsychotics
5-HT2A blockers. Down-regulate the 5-HT2A receptors in chronic depression.