Phenomenology, psychopharmacology, counselling, hypnotics, ECT Flashcards
(166 cards)
What are antidepressants?
Antidepressants are drugs used for the treatment of moderate to severe depressive episodes
and dysthymia.
They are also used for a range of other conditions including severe anxiety and panic attacks,
obsessive–compulsive disorder (OCD), chronic pain, eating disorders and post-traumatic stress
disorder (PTSD).
All antidepressants work on the basis of the monoamine hypothesis by enhancing the activity of the monoamine neurotransmitters, noradrenaline (NA) and
serotonin (5-HT)
How do MAO Inhibitors work?
Work at presynaptic receptor to prevent breakdown of dopamine, norepinephrine and serotonin
How do TCAs work?
Work at synaptic cleft to block the reuptake of serotonin and norepinephrine
Bupropion, mirtazapine, nefazodone, trazodone, venlafaxine
How do SSRIs work?
Work at presynaptic receptor to specifically block the reuptake of serotonin
What are the neurotransmitters that are released between presynaptic and postysynaptic receptor in the cleft?
Norepinephrine
Dopamine
Serotonin
What are the classes of antidepressants
SSRI Selective Serotonin Reuptake Inhibitor
SNRI Serotonin and Noradrenaline Reuptake Inhibitor
TCA Tricyclic Antidepressant
MAOI Monoamine Oxidase Inhibitor
NARI Noradrenaline Reuptake Inhibitor
NASSA Noradrenaline-Serotonin Specific Antidepressant
SARI Serotonin Antagonist and Reuptake Inhibitor
What is considered 1st line for depression?
Evidence suggests that SSRIs are better tolerated, work more quickly and have a lower risk of
inducing mania compared with other antidepressants. Therefore, they are generally considered
first-line for depression
Examples of SSRI’s
Citalopram, escitalopram, fluoxetine, paroxetine, sertraline,
fluvoxamine
When are SSRI’s are used?
Depression (all SSRIs), panic disorder (citalopram, escitalopram,
paroxetine), social phobia (escitalopram, paroxetine), bulimia nervosa
(fluoxetine), OCD (most SSRIs), PTSD (paroxetine, sertraline), GAD
(paroxetine)
Mechanism of action of SSRI
They work by inhibiting the reuptake of serotonin from the synaptic cleft
into pre-synaptic neurones and therefore SSRIs increase the
concentration of serotonin in the synaptic cleft.
Side effects of SSRI
GI + STRESS
Gastrointestinal: nausea, dyspepsia, bloating, flatulence, diarrhoea and
constipation.
Sweating, Tremor, Rashes, Extrapyramidal side effects
(uncommon), Sexual dysfunction, Somnolence, ‘Stopping SSRI’
Nausea, headache, GI upset (5-HT3)
Agitation, akathisia, anxiety (5-HT2)
Sexual dysfunction (5-HT2)
Insomnia (5-HT2)
Hyponatraemia (SIADH)
SE of tricyclic antidepressants?
Anticholinergic effects, Alpha-1 adrenergic antagonism, Antihistaminergic (H1)
Overdose, seizures
Contraindications of SSRI
Cautions: History of mania, epilepsy, cardiac disease (sertraline is the
safest), acute angle-closure glaucoma, diabetes mellitus (monitor
glycaemic control after initiation), concomitant use with drugs that
cause bleeding, GI bleeding (or history of GI bleeding), hepatic/renal
impairment, pregnancy and breast-feeding, young adults (possible ↑
suicide risk), suicidal ideation.
Contraindications: Mania.
Dosage and Route of SSRI’s
Sertraline (50–200 mg/day), fluoxetine (20–60 mg/day), citalopram (20–
40 mg/day), escitalopram (10–20 mg/day), paroxetine (20–50 mg/day).
Oral.
Features for the monoamine of hypothesis of depression?
All antidepressant classes increase NA and 5-HT function
Amphetamines and Cocaine elevate mood
50% of depressed patients have low CSF 5-HIAA
features agains the monoamine hypothesis of depression?
Amphetamines and Cocaine less effective in depressed people
Alpha and beta blockers have no effect on BAD
Time to therapeutic effect is long
What about other treatments of depression – Ketamine (NMDA reception antagonist), ECT, TMS?
What else have we found out about depression since the monoamine hypothesis?
Stress (via the elevation of serum cortisol) is very neurotoxic, especially in the hippocampus
- It also induces Glutamate release…
- …which decreases neuronal neuroplasticity
Depressed people have decreased levels of neuroprotective chemicals such as BDNF.
Ketamine works as an NMDA receptor antagonist which decreases Glutamate release.
What is the neuroplasticity hypothesis?
Antidepressants cause slow increase in BDNF via GPCRs
Antidepressants also decrease glutamate release via other downstream mechanisms
Antidepressants may directly increase plasticity in hippocampal neurones
Do SSRIs actually work?
Do they actually work?
STAR*D (AJ Psych, 2006)
37% initial remission, 67% overall
How long do they take to work?
Potentially two weeks
Longer in the elderly and shorter in children
How long do I need to keep taking them?
6-9/12 if first episode + uncomplicated
2 years if recurrent depressive disorder, very severe episode, major relapse factors present
SNRIs examples and doses
Venlafaxine (75mg a day in divided doses)
Duloxetine (60-120mg a day)
SNRI indication
2nd or 3rd line for depression and anxiety
More rapid onset of action and are more effective than SSRIs
Mechanism of action of SNRI’s
Prevent reuptake of noradrenaline and serotonin
Dont block cholinergic receptors and do not have have as many anti-cholinergic side effects as TCAs
Side effects of SNRIs
Nausea, dry mouth, headache, dizziness, sexual dysfunction, HT
Cautions of SNRIs
Cardiac arrhythmias and HT