IDT Exam 2 Flashcards
8 subcategories of depression
Characterized as mild, moderate, or severe
Reactive
Agitated
Atypical
Dysthymia
PMS
Post-partum
Psychotic
SAD
Treatments for depression
Talk
Light
Antidepressants
Exercise
Electroconvulsive
What is the simple biogenic amine hypothesis
Antidepressants extend duration of biogenic amines (norepinephrine, serotonin, maybe dopamine) through blocking reuptake or metabolism (SSRIs vs. MAOIs)
Serotonin associated symptoms
Agitation
Dysphagia
Dyssomnia
Anxiety
No libido
Norepinephrine associated symptoms
Focus/alert
Memory
Energy
Problem with biogenic amine hypothesis
Biogenic amines increase in 2-3 hours
Antidepressants take weeks to months to work
Alternative antidepressant and ETC action hypothesis
Increase in biogenic amines increases neurotrophic agents (bdnf) and neuronal sprouting leading to structural changes
TCAs block
Both NE and 5-HT transporters
Examples of TCAs
Imipramine
Amitriptyline
Desipramine
Doxepin
Maprotiline
TCAs SEs
Alpha-1 antagonist → vasoconstriction
Muscarinic cholinergic antagonist
NE activation of beta adrenergic receptors
Overall: increased HR
H1 antagonist → sedation
+ alpha1 antagonist → weight gain (worst in amitriptyline and doxepin)
Death if overdosed
MAOIs block
NE and 5-HT breakdown
Examples of MAOIs
Phenylzine
Tranylcipromine
Isocarboxazid
MAOIs are used for
Treatment resistant or atypical depression
MAOI SE
Insomnia/daytime sleepiness
Dry mouth
Liver toxicity in phenylzine
Prolongs T1/2 in oxidatively deaminated drugs
What dray combos way cause serotonin syndrome
-triptans
SSRI
mepiridine
Dextromethorphan
How to treat serotonin syndrome
Oxygen
Sedation
Serotonin antagonist → Cyproheptadine
What foods can be toxic if eaten with MAOI
Tyramine rich foods
Fermented, aged, cured, and pickled foods
What is a selective MAOI
Selegiline → Parkinson’s
Why are SSRIs better than TCAs
They have no affinity for alpha adrenergic, muscarinic, histamine or dopamine receptors
Fluoxetine characteristics
Most stimulating ssri
Hyponatremia
How do SSRIs cause hyponatremia
They increase vasopressin
Mostly problematic in pts with electrolyte imbalance (bulimia)
What is discontinuation syndrome and do how you treat it
When you quit SSRI use
Nightmares
Agitation
Brain zaps
Taper dose instead of cold turkey
SNRI examples
Venlafaxine
Deafenlafaxine
Duloxetine
Levomilnacipran
Vilazodone, vortioxetine, and trazadone MOA
Serotonin receptor antagonist (5HT:1A, 3, and 7)
and block SERT
Vortioxetine is partial 5HT1A/B agonist
Trazodone is also H1 and Alpha1 antagonist
St Johns Wort characteristics
Hyperforin
Similar efficacy and SEs to SSRIs
Induces Cyp3A
Mirtazapine MOA
May potentiate NE and 5HT release by blocking autoreceptors
H1 antagonism (sleepy)
Atypical antidepressants
Mirtazapine
Bupropion
Esketamine
Dextromethorphan + bupropion
Brexanolone
Mirtazapine MOA
Presynsptic autoreceptor antagonist
Bupropion MOA
Central nicotinic receptor antagonist
Esketamine MOA
NMDA receptor antagonist
Dextromethorphan + bupropion MOA
NMDA receptor antagonist
Brexanolone MOA
Progesterone metabolite and GABAa receptor positive allosteric modulator
TCA SAR
3-4 atoms between N an ring
C3 Monohalogenation
3 amines block 5HT reuptake
2 amines block NE reuptake
3 amines can be converted to 2 amines
3 amines tend to be more
Sedating
TCAs are generally metabolized by
2D6 and 2C19
Imipramine metabolites and activity
Desipramine (desmethylimipramine)
2-hydroxydesipramine
Both active
Common TCA ring systems
Dibenzazepine
Dibenzocycloheptenes
Dibenzoxepin
Amitriptyline facts
Gets metabolized to
Highest antimuscarinic and sedative fx
Metabolized to nortryptyline which has less above SE
Tetracyclic TCA
Maprotiline
500 fold more NET inhibition than SERT
Which MAOI is prodrug
Phenelzine
Phenelzine inhibits
2B6
Non selective MAOIs
Tranylcypromine
Phenelzine
Isocarboxazid
MAOBI
Selegiline
Which MAOI are irreversible
All