depression Flashcards
what is depression and theory behind it
depression - reduction in serotonin, dopamine and noradrenaline in synaptic cleft
monoamine theory - reduction in one of the monoamines - upregulation of post synaptic receptors
symptoms of depression & general management
low mood, loss of interest or pleasure in daily activities, range of cognitive behavioural and physical symptoms e.g. sleep disturbance, lack of appetite
chronic depression - depressive symptoms for at least 2 years, persistent low mood
mild - CBT
moderate-severe antidepressants
pts may feel worse in first 1-2 weeks
should be taken for 4 weeks (6 wk in elderly) before deemed ineffective
take for 6 months after remission, 1 year in elderly, 2 years in recurrent
depression treatment
1st line - SSRI
if that doesn’t work:
- increase dose
- change SSRI
- mirtazapine
- TCA or venlafaxine (severe)
- MAO-i (specialist)
if that doesn’t work - add another class, lithium or anti-psychotic
use electroconvulsive therapy in severe refractory depression
vortioxetine may be considered in patients with little to no response to at least 2 antidepressant drugs
For pts who do not respond to SSRIs or SNRIs - specialist setting/advice can consider moclobemide, irreversible MAO-i, amisulpride
fluoxetine in < 17
mirtzapine in bleeding risk
SSRI imp points + SEs
better tolerated and safer in overdose
1st line
sertraline - safest in pts with cardiac events
fluoxetine < 17
SE’s:
GI disturbances (n&v)
appetite/weight gain
sexual dysfunction
risk of bleeds
insomnia (TAKE MED IN MORNING)
QT prolongation (citalopram & escitalopram)
SSRI interactions
CYP inhibitors (avoid grapefruit juice - increases plasma conc.)
CYP inducers (reduces effectiveness e.g. St Johns Wort)
QT prolongation drugs (amiodarone, sotalol, quionolones)
drugs that increase risk of bleeds
hyponatremia (carbamazepine, diuretics)
SEROTONIN SYNDROME
serotonin syndrome
3 effects:
cognitive - headache, agitation, confusion, coma
autonomic - sweating hyperthermia
neuromuscular excitation - tremor, teeth grinding
caused by interaction with:
SSRI + TCA, MAOI
lithium
tramadol
triptans - sumatriptan
LINEZOLID
TCAs - sedating vs less sedating
sedating - better for agitated and anxious patients
- amitriptyline clomipramine dosulepin trazodone
less sedating - better for withdrawn and apathetic patients
- imipramine, lofepramine, nortriptyline
AMITRIPTYLINE + DOSULEPIN - very dangerous in OVERDOSE - avoid/not recommended in depression
TCAs in general - associated with greatest risk in overdose - although lofepramine has better safety profile
TCA - side effects
C - cardiac events
A - anti-muscarinic effects
S - seizure (lower the threshold)
H - hallucinations
DANGEROUS IN OVERDOSE (hypotension associated with OD)
TCA interactions
CYP inhibitors (avoid grapefruit juice, increases plasma conc)
CYP inducers (reduces effectiveness)
QT prolongation (amiodarone, sotalol, quionolones)
anti-muscarinics - atropine
anti-hypertensives - amlodipine
SEROTONIN SYNDROME
MAO-i imp points
specialist use only
hepatotoxicity (phenelzine + isocarboxazid)
hypertensive crisis - do not give OTC PSEUDOEHEPDRINE
avoid tyramine rich foods (meats, cheese, fermented)
interaction - tranylcypromine (MAO-I) + clomipramine (TCA) = FATAL
cheese reaction - leads to hypertensive crisis
- tyramine normally broken down by MOA
- MOA-I inhibits breakdown
- tyramine builds up - causes noradrenaline release - severe hypertension
MAO-I washout periods
MAO-I to other antidepressants - 2 weeks
MAO-I to clomipramine or imipramine - 3 weeks
others to MAO-I:
- 2 weeks after previous MAO-i stopped (0 weeks for meclobemide)
- 1/2 weeks after TCA stopped (3 wk for clomipramine or imipramine)
- 1 week after SSRI stopped ( 5 wk for fluoxetine)
