Antidepressant Drugs Flashcards by Christian Wakim

5 R’s of antidepressant efficacy

Response = ≥50% reduction in sx
Remission = sx free
Recovery = 6-12 months of ongoing remission
Relapse = return of symptoms after remission but before recovery
Recurrence = return of symptoms after recovery

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average response time to antidepressants

8 weeks

if no response after this time, may switch to another antidepressant with a different MOA

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describe the withdrawal sx of antidepressants

FINISH:
flu like sx
insomnia
nausea
imbalance
sensory disturbances
hyperarousal

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SSRI MOA

selective seratonin reuptake inhibitors

via SERT

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what are the SSRIs?

citalopram
escitalopram
fluoxetine
paroxetine
sertraline ** ya girl's med 
vilazodone
vortioxetine

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which SSRI is also a partial 5HT1a agonist?

vilazodone

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which SSRI is also a partial 5HT1b agonist, full 5HT1b agonist and full 5HT1d antagonist?

vortioxetine

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why are SSRI’s preferred over TCAs?

much less impact on histamine, muscarinic and adrenergic receptors

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SSRI common side effects

sedation
sexual dysfunction
weight gain
acute withdrawal reactions

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SSRI rare side effects

QT prolongation
hyponatremia
serotonin syndrome
suicidality

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sx of serotonin syndrome

sweating
hyperreflexia
akathisia/myoclonus
shivering/tremors

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which SSRI is most likely to cause drug interactions?

fluoxetine – strong CYP450 inhibitor

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SNRI MOA

selective serotonin and norepinephrine pre-synpatic reuptake inhibitors

serotonin via SERT
norepi via NET

5HT > NE

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3˚-amide TCA MOA

inhibit both NE/5HT equally

*exception = clomipramine/amtriptyline 5HT > NE

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2˚-amide TCA MOA

inhibit NE > 5HT

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what are the SNRIs?

All TCAs
Desvenlafaxine
Duloxetine
Venlafaxine
Levomilnacipran

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what are the 3˚-amide TCAs?

"ACID"
Amitriptyline 
Clomipramine
Imipramine
Doxepin

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what are the 2˚-amide TCAs?

Amoxapine
Desipramine
Nortryptyline

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which receptors are also affected by TCAs?

histamine
muscarinic
adrenergic

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TCA activation of adrenergic receptors causes which side effects?

tachycardia
orthostatic hypotension
dysrhythmias

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TCA activation of muscarinic receptors causes which side effects?

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dry mouth
urinary retention
constipation
blurred vision

TCA activation of histamine receptors causes which side effects?

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sedation/fatigue
dizziness
seizures

3 C’s of TCA overdose

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Coma
Cardiotoxicity (Conduction abnormalities)
Convulsions

SNRI side effects

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relatively similar to SSRI’s but less risk of sexual dysfunction

Trazadone and Nefazodone MOA

SSRI + block post-synaptic a1 receptors on NE and 5HT receptors

Mirtazapine MOA

blocks pre-synaptic a2 receptors on NE and 5HT neurons + blocks post-synaptic 5HT receptors *no SERT/NET activity

side effects of SARAs

sedation orthostatic hypotension weight gain

NDRI MOA

selectively inhibits pre-synaptic reuptake of NE and DA via NET and DAT also evidence of an enhanced pre-synaptic release of NE and DA via VMAT2

what is the NDRI?

bupropion

bupropion side effects

``` agitation insomnia HTN tachy tremors weight loss seizures ```

MAOIs MOA

inhibition of monoamine oxidase which increases monoamines in neuronal vesicles and increases amounts of NE, 5HT and DA

which MAOI is the only non-selective agent

selegiline (patch)

what are the MAOI?

isocarboxazid phenelzine selegiline tranylcypromine

MAOI side effects

orthostatic hypotension sexual dysfunction weight gain insomnia/agitation

what is the primary concern of patients taking MAOIs?

hypertensive crisis *MAOIs inhibit tyramine metabolism --> causes catecholamine release

which MAOI has the lowest risk of a hypertensive crisis?

selegiline

misc antidepressants

esketamine - NMDA antagonist | brexanolone - GABAa agonist

indications for giving eskatmine

NMDA-ant: treatment-resistant depression in conjunction with ongoing antidepressant therapy *nasal administration

indications for giving brexanolone

post-partum depression - identical to endogenous allopregnanolone *60 hr IV administration

what are the mood stabilizers?

carbamazepine lamotrigine valproic acid lithium

why are anti-seizure meds used as mood stabilizers?

exact MOA unclear the just fuckin work ok?????

lithium MOA

1. alters brain structures 2. neurotransmitter modulation 3. intracellular changes

which brain structures are affected by lithium?

anterior cingulate cortex superior temporal gyrus ventral prefrontal cortex hippocampus

how does lithium modulate neurotransmitters?

inhibits DA downregulates NMDA receptor increases GABA levels

what are the intracellular effects of lithium?

inhibits IPPase and IMPase inhibits PKC, MARCKS and GSK3 activates CREB transcription factor (neuroprotective)

describe the renal effects of lithium

lithium enters principal cells of collecting duct via Na channels lithium accumulation interferes with ADH-mediated effects can lead to resistance to ADH resulting in polyuria and polydipsia

lithium renal toxicity can be confused with what other condition?

nephrogenic diabetes insipidus

what drugs interact with lithium?

diuretics ACEIs NSAIDs

lithium side effects

``` tremor mental confusion dizziness sedation thyroid goiter leukocytosis seizures serotonin syndrome ```

lithium indications

mania/bipolar 1 augmentation in unipolar depressive patients off label: reduced risk of suicide

indications for anti-seizure mood stablizers

Bipolar 1 and 2 * lamotrigine for 1 or 2 * valproic acid and carba for 1 only

Antidepressant Drugs Flashcards

(51 cards)