Antidepressants/Bipolar (Patho) Flashcards by Madelynn Packer

what are the physiological features of depression

decreased sleep, appetite changes, fatigue, psychomotor dysfunction

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what are the psychological features of depression

dysphoria, worthlessness, excessive guild, loss of interest in all or most activities

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what are the cognitive features of depression

decreased concentration and suicide ideation

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what to rule out before diagnosing depression

drug induced depression
medical conditions
bereavement

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what drugs can induce depression

antihypertensives
sedative hypnotics
anti-inflammatory/analgesics
steroids
PD drugs or neuroleptics

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how is reserpine related to depression

depletes NE and 5HT from vesicles

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how does neuroendocrine relate to depression

overactivity of HPA axis leads to desensitization of feedback
increased CRF and symptoms of depression

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how does neurotrophic relate to depression

stress and pain decrease BDNF levels
BDNF has antidepressant activity via the sprouts that make neuro connections

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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

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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

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MOA of MAOIs

MAO-A break down NE and 5HT
MAO-B break down dopamine

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what are the 3 types of MAOIs

non-selective
MAO-B selective
MAO-A selective

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what are the non-selective MAOIs and when do you use them

phenelzine
tranylcypromine
reserved for treatment resistant depression

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what are the MAO-B selective drugs

selegiline

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what are the MAO-A selective drugs

moclobemide

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what are the issues with MAOIs

severe side effects
HTN crisis (avoid tyramine)
Interactions w/ OTCs
Irreversible (long wash out period)

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what is the major risk with tricyclics

dangerous to those with suicide ideation due to OD risk

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MOA of tertiary amines

inhibit both NE and 5HT receptors via NET and SERT

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what are tertiary amine antagonists for

antihistamines
antimuscarinics
antiadrenergics

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what are the side effects of tertiary amines

sedation, autonomic SEs, weight gain

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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