Antidepressants Flashcards
what is reactive depression
temporary reaction to real stimuli - grief
what is bipolar disorder
recurrent major depressive episodes with intervening manic, hypomanic, or mixed episodes
what is major depression
one or more major depressive episodes free of manic, mixed, or hypomanic episodes
what is the clinical criteria for major depression
at least 5 symptoms for extended period of time
emotional symptoms
cant experinces pleasure
loss of interest
pessimistic
anxiety
physical symptoms
chronic fatigue
insomnia
appetite disturbance
cognitive symtoms
poor concentration
slow thinking
poor short term memory
confusion
psychomotor symptoms
slow movements and speech
agitation
some non pharms for major depression
psychotherapy
ECT
what is the amine hypothesis
depression is related to reduced synaptic levels of NE and serotonin
how do antidepressants work
blocking normal neurotransmitter reuptake processes
what is the therapeutic lag
drugs increase NT levels right away but efficacy is delayed by weeks
how does phase 2 work
phase 1 causes agonist activity at the receptors that feedback inhibit to stop amine released causing reduced negative feedback levels and phase 2 increase
examples of tricyclic antidepressants
amitriptyline
imipramine
how do TCAs work
mixed NE and serotonin reuptake inhibitors
what is the cause of adverse effects of TCAs
blockage of cholinergic, histaminergic, alpha1 adrenergic receptors
adverse effects of TCAs
orthostatic hypotension tremour insomnia weight gain siezure sexual disturbance
drug interactions of TCAs
cyp2D6 inhibitors
sedatives
sympathomimetics
antimuscarinics
examples of serotonin reuptake inhibitors
fluoxetine
paraoxetine
sertraline
how do ssris work
block serotonin reuptake more than NE
overdose with TCAs causes
fatal cardiac arrthymias
why are ssris more tolerated than tca
less cholinergic, histaminergic, and adrenergic blockade
higher therapeutic index
does cause platelet inhibition tho
drug interactions with ssris
CYP 2D6 inhibitors
TCAs
beta blockers
antipsychotics
advantages of ssris over tcas
equal efficacy with milder side effects
more favourable therapeutic index
smaller chance of addictive drug interactions
exampls of snris
venlafaxine
mechanism of snris
inhibit both serotonin and NE reuptake and weak dopamine reuptake inhibitors
how are snris different from tcas
no affinity for muscarinic, alppha 1 adrengergic, and histaminergic receptors
advantages of snris
milder side effect
useful for depression with neuropathic pain
fewer druginteraction
lower safety margin
how does mirtazapine work
blocks alpha2 adrenergic receptors thus increase NE release
blocks histamine receptors
adverse effects of mirtazapine
sedation
weight gain - major drawback
less sexual side effects tho
drug interactions for mortazapin
none known
advantages of mirtazapine
anxiolytic/sedative effect
minimal drug interations
what is the mechanism for supropion
largely unknown
mi;d stimulant
how are the side effects different in bupropion
seizures major concern
no sexual dysfunction,weight gain, or sedation
drug interactions of bupropion
meds that lower seizure threshold
ldopa
