Antidepressants Flashcards

1
Q

what is reactive depression

A

temporary reaction to real stimuli - grief

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2
Q

what is bipolar disorder

A

recurrent major depressive episodes with intervening manic, hypomanic, or mixed episodes

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3
Q

what is major depression

A

one or more major depressive episodes free of manic, mixed, or hypomanic episodes

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4
Q

what is the clinical criteria for major depression

A

at least 5 symptoms for extended period of time

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5
Q

emotional symptoms

A

cant experinces pleasure
loss of interest
pessimistic
anxiety

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6
Q

physical symptoms

A

chronic fatigue
insomnia
appetite disturbance

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7
Q

cognitive symtoms

A

poor concentration
slow thinking
poor short term memory
confusion

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8
Q

psychomotor symptoms

A

slow movements and speech

agitation

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9
Q

some non pharms for major depression

A

psychotherapy

ECT

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10
Q

what is the amine hypothesis

A

depression is related to reduced synaptic levels of NE and serotonin

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11
Q

how do antidepressants work

A

blocking normal neurotransmitter reuptake processes

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12
Q

what is the therapeutic lag

A

drugs increase NT levels right away but efficacy is delayed by weeks

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13
Q

how does phase 2 work

A

phase 1 causes agonist activity at the receptors that feedback inhibit to stop amine released causing reduced negative feedback levels and phase 2 increase

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14
Q

examples of tricyclic antidepressants

A

amitriptyline

imipramine

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15
Q

how do TCAs work

A

mixed NE and serotonin reuptake inhibitors

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16
Q

what is the cause of adverse effects of TCAs

A

blockage of cholinergic, histaminergic, alpha1 adrenergic receptors

17
Q

adverse effects of TCAs

A
orthostatic hypotension
tremour 
insomnia 
weight gain
siezure
sexual disturbance
18
Q

drug interactions of TCAs

A

cyp2D6 inhibitors
sedatives
sympathomimetics
antimuscarinics

19
Q

examples of serotonin reuptake inhibitors

A

fluoxetine
paraoxetine
sertraline

20
Q

how do ssris work

A

block serotonin reuptake more than NE

21
Q

overdose with TCAs causes

A

fatal cardiac arrthymias

22
Q

why are ssris more tolerated than tca

A

less cholinergic, histaminergic, and adrenergic blockade
higher therapeutic index
does cause platelet inhibition tho

23
Q

drug interactions with ssris

A

CYP 2D6 inhibitors
TCAs
beta blockers
antipsychotics

24
Q

advantages of ssris over tcas

A

equal efficacy with milder side effects
more favourable therapeutic index
smaller chance of addictive drug interactions

25
exampls of snris
venlafaxine
26
mechanism of snris
inhibit both serotonin and NE reuptake and weak dopamine reuptake inhibitors
27
how are snris different from tcas
no affinity for muscarinic, alppha 1 adrengergic, and histaminergic receptors
28
advantages of snris
milder side effect useful for depression with neuropathic pain fewer druginteraction lower safety margin
29
how does mirtazapine work
blocks alpha2 adrenergic receptors thus increase NE release | blocks histamine receptors
30
adverse effects of mirtazapine
sedation weight gain - major drawback less sexual side effects tho
31
drug interactions for mortazapin
none known
32
advantages of mirtazapine
anxiolytic/sedative effect | minimal drug interations
33
what is the mechanism for supropion
largely unknown | mi;d stimulant
34
how are the side effects different in bupropion
seizures major concern | no sexual dysfunction,weight gain, or sedation
35
drug interactions of bupropion
meds that lower seizure threshold | ldopa