Anti-Depressants :) Flashcards
SHARK = concept groupings, similaries etc ~ = bold in notes and high yield * = other stuff i think is high yeild maybe
hurrah.
concept: Pathophys of depression ie NT involved
DA 5Ht NE = happy making neuotransmitters linked to a deficiency in ~signal transduction~
concept: Therefore, goal of antidepressants
increased SA, 5HT and NE to normal levels
concept: TCAs MOA
block monoamine reuptake - increases to normal levels
concept: MAO inhibitor MOA
prevent degradation of monoamines - increases to normal levels
concept: How long do a) pharmacological effects and b) clinical effects and c) beneficial effects of antidepressants take to kick in?
a) pharmaco - immediate
b) clinical - 2- 4 weeks
c) substantial benegit - 6-8 weeks
help patient through the transition
MAOi cause increase in which NT?
NE and 5HT
Name the MAOIs (SPIT + a/se dry mouth ;))
S: seregliptine P: phenylzine I: isocarboxazid T: tryanylcypromine seregliptine, phenylzine, isocarboxazid, tryanylcypromine
~*~Two reasons MAOis suck and arent really used anymore
SEROTONIN SYNDROME
the CHEESE REACTION
~*~Describe Serotonin syndrome
MAOi with anything that increases 5HT ie SSRI, SNRI, TCA, meperidine * hyperthermia * muscle rigidity * myoclonus apparently 5HT does those things
~*~Describe the Cheese reaction
Tyramine from food cant be broken down –> stimulates NE
- tachycardia
- hypertension
- arrhytmias
- seizure
- maybe stroke
List the TCAs please (NACID/naked)
N: nortryptiline A: amytriptiline C: clomipramine I: imipramine D: desipramine
List which ones are more 5HT-ergic and which ones are NE-ergic
triptylines and pramines
N: nortryptiline - more potent inhibitor of NET
A: amytriptiline - none
C: clomipramine - mroe potent inhibitor of SERT
I: imipramine - none
D: desipramine - more potentint inhibitor of NET
N-x-5-x-N @ NACID
What other receptors do TCAs affect and why do I care?
alpha adrenergic: orthostatic hypotension and reflex tachycardia
antimuscarinic: blurred vision, xerostomina, urinary retention, constipation and exacerbation of acute angle glaucoma
antihistamine: sedation and weight gain
~~~Whats your biggest concern fro someone on TCAs?
ARRHTYMIAS - largest cause of people passing away bc acts like class I antiarrhtymics by blocking FAST SODIUM CHANNELS
SHARK: how do you treat antiarrhtymias caused by TCA overdose
sodium bicarbonate
List the SSRI (SPEC-FF)
S - sertraline P - paroxetine E - es-citaloprone C - citalopram F - fluoxetine F - fluvoxamine
~*~Why are SSRIs DOC for depression
no affects at histamine, muscarinic or alpha adrenoreceptors = way less side effects than TCAs
What else can MAOis be used for
PMDD, bulimia, depression, OCD, GAD, PD, PTSD, SAD
Which SSRIs inhibit what CYPs and who cares?
high potential for drug interactions
S - sertraline = low potential
P - paroxetine = HIGH potential via - of CYP2D6
E - es-citalopram = low potential
C - citalopram = low potential
F - fluoxetien = HIGH potential via - of CYP2D6
F - fluvosamine = HIGH potential via - of CYP1A2, CYP2C19, CYP3A4
Other a/se of SSRI espeically when taking with MAOis
Serotonin Syndrome - hyperthermia, muscle rigidity, and myclonus
List the SNRIs please
Venlafexine
Duloxetine
Whats the difference between teh two SNRIs
Venlafexine - inhibits 5Ht and then Ne at higher doses + weak DA
Duloxetine - inhibits 5HT and NE at all doses
**Why would you use a SNRI instead of an SSRI?
SNRIs inhibit P450 enzymes less
(SPEC FF: HIGH - paroxetine, fluoxetine, fluvoxamine and LOW - citalopram, es-citalopraim and sertraline
