Antidepressants/Bipolar (Patho) Flashcards
what are the physiological features of depression
decreased sleep, appetite changes, fatigue, psychomotor dysfunction
what are the psychological features of depression
dysphoria, worthlessness, excessive guild, loss of interest in all or most activities
what are the cognitive features of depression
decreased concentration and suicide ideation
what to rule out before diagnosing depression
drug induced depression
medical conditions
bereavement
what drugs can induce depression
antihypertensives
sedative hypnotics
anti-inflammatory/analgesics
steroids
PD drugs or neuroleptics
how is reserpine related to depression
depletes NE and 5HT from vesicles
how does neuroendocrine relate to depression
overactivity of HPA axis leads to desensitization of feedback
increased CRF and symptoms of depression
how does neurotrophic relate to depression
stress and pain decrease BDNF levels
BDNF has antidepressant activity via the sprouts that make neuro connections
how do the hypotheses of depression relate to one another
HPA and steroids regulate BDNF
glucocorticoid receptor activated by cortisol will decrease BDNF
chronic activation of monoamine receptors will increase BDNF signaling and downregulate HPA axis
how does selectivity relate to choosing drug therapy
some drug classes will have similar selectivity which means you may have to try different classes when treating depression
MOA of MAOIs
MAO-A break down NE and 5HT
MAO-B break down dopamine
what are the 3 types of MAOIs
non-selective
MAO-B selective
MAO-A selective
what are the non-selective MAOIs and when do you use them
phenelzine
tranylcypromine
reserved for treatment resistant depression
what are the MAO-B selective drugs
selegiline
what are the MAO-A selective drugs
moclobemide
what are the issues with MAOIs
severe side effects
HTN crisis (avoid tyramine)
Interactions w/ OTCs
Irreversible (long wash out period)
what is the major risk with tricyclics
dangerous to those with suicide ideation due to OD risk
MOA of tertiary amines
inhibit both NE and 5HT receptors via NET and SERT
what are tertiary amine antagonists for
antihistamines
antimuscarinics
antiadrenergics
what are the side effects of tertiary amines
sedation, autonomic SEs, weight gain
what are the tertiary amine drugs
imipramine
amitriptyline
trimipramine
clomipramine
doxepin
MOA of secondary amines
more inhibition of NET than SERT
what are secondary amines
desipramine
protriptyline
nortriptyline
maprotiline
what are the side effects of secondary amines
same as tertiary amines but way less
MOA of SSRIs
serotonin transporter pumps are blocked and there is an increase in serotonin in synapse as a result
what are the SSRI drugs
fluoxetine
fluvoxamine
paroxetine
sertraline
citalopram
escitalopram
what are the side effects of SSRIs
N/V
headache
sexual dysfunction
anxiety
insomnia
tremor
what are the withdrawal symptoms of SSRIs
brain zaps
dizziness
sweating
nausea and vertigo
when is serotonin syndrome risk highest
SSRI given with MAOI or TCAs
serotonin syndrome symptoms
hyperthermia
muscle rigidity
restlessness
seizures
sweating
serotonin syndrome treatment
d/c med
manage symptoms
serotonin antagonist (cyproheptadine)
benzos for seizures
what are the SSRI + 5HT1a partial agonist
vilazodone
vortioxetine
what are the tetracyclic and unicyclic drugs
maprotiline
amoxapine
mirtazapine
buproprion
mirtazapine MOA
alpha 2 antagonist
5HT2 and 5HT3 antagonist
H1 antagonist
receptor antagonist not transporter
bupropion MOA
NET and SERT inhibitor
DAT inhibitor
what is the 5HT2 antagonist/SERT
trazodone
trazodone side effect
extremely sedating
what are the NMDA antagonists
ketamine
esketamine
both at low doses
MOA of SNRIs
NET and SERT inhibitors
SNRI drug examples
venlafaxine
desvenlafaxine
duloxetine
milnacipran
levomilnacipran
how to treat postpartum depression
SSRIs
venlafaxine
CBT + counseling
Brexanolone
MOA of brexanolone
GABA-A receptors resensitization
very expensive and REMS
what are the 3 treatment options for bipolar
hospitalization
psychotherapy
pharmacotherapy
what are the classes of drugs used in bipolar
mood stabilizers
atypical antipsychotics
calcium channel blockers
combo therapy
what is the main mood stabilizer used in bipolar
lithium
MOA of lithium
depletion of PIP2 and associated signaling of IP3 and PKC
modulates GSK3
what are the steps of lithium MOA
-Gq activated
-PLC activated
-IP3 made and recycled into PIP2
-Lithium blocks the recycling
-membrane has no PIP2
-PLC has no substrate so no signaling or effects
why does lithium have so many side effects
any substrate coupled to Gq will be shut down (lots of this)
what are the main problems with using lithium
small therapeutic index
lag time for effectiveness
need a loading dose
many SE
valproic and sodium valproate MOA
increase in GABAergic tone
block Na channels
Block T type Ca channels
inhibit HDAC5
Carbamazepine/Oxcarbazepine MOA
block Na channel
drug binds in inactivated state
Lamotrigine MOA
block Na and Ca channel