Antidepressants Flashcards
(52 cards)
Describe the broad physiologic goal of all antidepressant medications.
Increase the concentration of neurotransmitters in the synapse
By what mechanism do anti-depressants have their effect?
There is disagreement –> some say the increased concentration of the neurotransmitters in the synapse lead to the anti-depressive effect while others argue that the effect comes from down regulation of receptors on the pre-synaptic neuron.
What evidence is there that down regulation of receptors is the reason anti-depressant medications are effective?
Because anti-depressant medications take 3-4 weeks to be effective, meaning the down regulation of receptors is likely more responsible.
List neurotransmitters (NTs) found in the synapse of CNS neurons
Epinephrine, norepinephrine, serotonin, dopamine, acetylcholine
What are two ways the body removes neurotransmitters from the synapse?
- Reuptake: recycling NTs by pumping them back into the pre-synaptic neuron
- Enzymes: acetylcholinesterase and monoamine oxidase chew up NTs in the synapse
Which class of antidepressant medications is most effective?
No one class is more effective than another –> what determines use is side effects the patient experiences
What was the original class of antidepressant medications?
Monoamine oxidase inhibitors (MAOIs)
Name two MAOIs on the market today.
Phenelzine and Tranylcypromine
What is the mechanism of action of MAOIs?
They block action of monoamine oxidase thereby increase CNS synapse levels of epi, norepi, and dopamine
What are two isoforms of MAOIs and which has the most antidepressive effect?
MAO-A and MAO-B –> MAO-A has the greatest antidepressive effect
What is the GI related AE of MAOIs and how is it mitigated?
MAO in the colon metabolizes vasoactive substances that we eat (tyramine) before they enter the bloodstream. MAOIs allow absorption of these vasoactive chemicals. Patient must adhere to a special diet or suffer risk of hypertensive emergency and urgency.
List common AEs of MAOIs other than the GI related AE.
Many drug interactions, orthostatic hypotension, palpitations, tachycardia, erectile dysfunction
Differentiate between Phenelzine and Tranylcypromine and state how it is clinically relevant.
Phenelzine: more sedating –> prescribe to people with insomnia
Tranylcypromine: more activating –> prescribe to people that sleep too much
When, after discontinuing use of MAOIs, do you no longer worry about AEs?
3 weeks after stopping medication
When should MAOIs be combined with other antidepressant medications?
Only under care of psychiatrist –> mixing more than one drug class can lead to serotonin syndrome
T/F: MAOIs are considered first line therapy for depression.
False –> patients on an MAOI have issues
What are two medications previously discussed in class that have weak MAOI properties?
Linezolid (antibiotic) and St. John’s Wort (OTC antidepressant)
Describe the use and mechanism of tricyclic antidepressants (TCAs).
- They are not commonly used –> they are dirty drugs (lots of side effects)
- They indiscriminately block NT reuptake
Why are TCAs still kept on the market?
Off label uses such as insomnia (Anti-Ach sedation), neuropathic pain, enuresis (bed wetting)
What are the three primary results of TCA toxicity?
- Tonic-clonic seizures
- Cardiac arrhythmias
- Anti-cholinergic effects (constipation, dry mouth, urinary retention, sedation, tachycardia)
How should you counsel patients when starting them on a TCA?
Anti-Ach side effects will start immediately but the antidepressant effects will not be seen for three weeks
What is the father of TCAs?
Imipramine
What is the hallmark ECG finding of TCA toxicity and what is the antidote?
Toxicity causes QRS widening on the ECG. The antidote is Bicarbonate
What are the two broad categories of TCAs?
Secondary Amines: desipramine, nortriptyline, exs
Tertiary Amines: amitriptyline, imipramine, exs
