Antidepressants and antianxiety medication Flashcards
Most sedating SSRI
Paroxetine
Reason for paroxetine’s sedating effect
High H1 affinity
SSRI with the highest rate of discontinuation symptoms
Paroxetine
SSRIs with the highest rates of drug interactions
Fluoxetine
Fluvoxamine
Paroxetine
SSRI which causes the most short term anxiety and agitation
Fluoxetine
SSRI which causes the most short term weight loss
Fluoxetine
SSRI which has the least drug interactions
Citalopram
SSRI which is most often used with elderly patients due to its lower risk of interactions
Citalopram
SSRI which has the most evidence for safe use post-MI
Sertraline
SSRI which is most often used for children and adolescents
Fluoxetine
Most common side effect of SSRIs
GI side effects
SSRI which causes the most GI upset
Fluvoxamine
SSRIs which cause the least sexual dysfunction
Vortioxetine
Fluvoxamine
SSRI which is the most anticholinergic
Paroxetine
Medication which should be co-prescribed if a patient is taking an SSRI and NSAID
Protein pump inhibitor
Drugs where SSRIs should be avoided where possible
NSAIDs
Warfarin
Aspirin
Triptans
SSRI which does not need to be gradually reduced when stopping
Fluoxetine
SSRI discontinuation symptoms
Restlessness Insomnia, vivid dreams Unsteadiness/dizziness Sweating GI symptoms - pain, cramps, diarrhoea, vomiting Paraesthesia, shock-like symptoms Flu-like symptoms Crying spells
Half life of citalopram
33 hours
Half life of escitalopram
30 hours
Half life of fluoxetine in early use
1-3 days
Half life of fluoxetine with prolonged use
4-6 days
Half life of fluvoxamine
17-22 hours
Half life of paroxetine
22 hours
Half life of sertraline
26 hours
Mechanism of action of MAOIs
Block the monoamine oxidase enzyme, which breaks down different neurotransmitters
Where MAO A is found
Placenta, gut, liver
Where MAO B is found
Brain, liver, platelets
Neurotransmitters MAO A breaks down
Serotonin, noradrenaline, dopamine, tyramine
Neurotransmitters MAO B breaks down
Phenylethylamine, methylhistamine, tryptamine, dopamine, tyramine
Types of MAOIs
Reversible or irreversible, selective for MOA A or MOA B, or non-selective
Irreversible and selective inhibitors of MAO B
Selegiline (no longer selective at high doses)
Reversible and selective inhibitor of MAO A
Meclobemide
Most common adverse effects
Dry mouth, nausea, diarrhoea, constipation, insomnia, dizziness/light-headedness
Cause of MAOI cheese reaction
Tyramine is a monoamine found in different foods which displaces noradrenaline from neurons, causing hypertension. When MAO doesn’t break down tyramine it can build up and cause a hypertensive reaction
Foods to avoid due to risk of cheese reaction
Cheese (except cream cheese and cottage cheese) Broad beans Alcohol Banana peels Bean curd Sauerkraut Yeast extracts (e.g. marmite)
First generation TCAs (tertiary amines)
Amitriptyline Lofepramine Imipramine Dosulepin Doxepin Clomipramine
Second generation TCAs (secondary amines)
Nortriptyline
Desipramine
Amoxapine
Most dangerous TCAs in overdose
Amitriptyline
Dosulepin - possibly the most dangerous
Common side effects of TCAs
Drowsiness Dry mouth Blurred vision Constipation Urinary retention
Features of overdose of TCAs
Sedation/coma Seizures Hypertension (early) then hypotension Tachycardia Broad complex dysrhythmias Increased anticholinergic side effects
ECG features of TCA overdose
Increased QRS - >100ms in lead II
Terminal R wave >3mm in aVR
Sinus tachycardia
Specific treatments for overdose of TCAs
IV sodium bicarbonate
Hyperventilation
IV lidocaine
Avoid 1a (procainamide) and 1c (flecainide) antiarrhythmics, beta-blockers and amiodarone
Drug interactions of TCAs
Cytochrome p450 inhibitors can lead to toxicity as TCAs are highly metabolised by cytochrome p450
Cytochrome p450 inducers can lead to treatment failure
MAOIs - contraindicated with some TCAs due to serotonin syndrome like reactions
QTc prolonging drugs
Mechanism of action of TCAs
Block the serotonin transporter and the noradrenaline transporter which leads to elevated synaptic concentrations of serotonin and noradrenaline
Weak affinity for the dopamine transporter
Antagonists of multiple receptors including 5-HT2
Inhibit sodium channels leading to their cardiotoxicity in overdose
Interaction of TCAs with warfarin
TCAs increase warfarin levels - high risk of bleeding
Interaction of TCAs with clonidine
TCAs decrease clonidine levels - risk of hypertension
Interaction of TCAs with MAOIs
Increase serotonin levels via synergistic serotonergic enhancement - increased risk serotonin syndrome like reaction
Decrease tyramine entry - reduced risk cheese reaction
Interaction between TCAs and levodopa
Reduces absorption of levodopa and so lowers efficacy
Active metabolite of amitriptyline
Nortriptyline
Active metabolite of clomiprimine
Desmethyl-clomipramine
Active metabolite of dosulepin
Desmethyldosulepin
Active metabolite of doxepin
Desmethyldoxepin
Active metabolite of imipramine
Desipramine
Active metabolite of lofepramine
Desipramine
Active metabolite of fluoxetine
Norfluoxetine
Active metabolite of mirtazapine
Demethyl-mirtazapine
Active metabolite of trazadone and nefazodone
mCPP
Active metabolite of venlafaxine
O-desmethyl-venlafaxine
Start dose of citalopram for depression
10-20mg/day
Maximum citalopram dose for depression
40mg/day
Start dose of escitalopram for depression
5-10mg/day
Maximum escitalopram dose for depression
20mg/day
Start dose of sertraline for depression
50mg/day
Maximum sertraline dose for depression
200mg/day
Start dose of fluoxetine for depression
20mg/day
Maximum fluoxetine dose for depression
60mg/day
Start dose of paroxetine for depression
20mg/day
Maximum dose of paroxetine for depression
50mg/day
Start dose of vortioxetine for depression
5-10mg/day
Maximum vortioxetine dose for depression
20mg/day