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Summer 2024 > 725 Antidepressant "Book" > Flashcards

725 Antidepressant "Book" Flashcards

1
Q

What antidepressant class is very effective for depression but rarely used?

A

MAOI

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2
Q

Why are MAOI’s “last resort”?

A

HIGH potential for toxicity and lethal in ODs

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3
Q

Mechanism of action of MAOI’s/what neurotransmitters involved?

A

IRREVERSABLY destroys MAO (enzyme that breaks down neurotransmitters) in synaptic cleft which INCREASES 5-HRT, NE, & DA availability.

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4
Q

Uses of MAOIs?

A

Atypical depression

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5
Q

SEs of MAOIs?

A

Anticholinergic/antihistamine effects (xerostomia, drowsiness, dizziness, lightheadedness), nausea, diarrhea/constipation, HTN CRISES!

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6
Q

MAOI’s have ________ of drug to drug interactions and have ________ w/drawl effects.

A

a lot; severe

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7
Q

Do not take with SSRI/SNRIs due to risk of ___________ ___________ risk; wait for __ to __ wks after d/c’ing to start one.

A

serotonin syndrome; 2-5 wks

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8
Q

What MAOI is selective w/DA only and is sometimes used in Parkinson’s treatment?

A

selegiline (Emsam)

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9
Q

DO NOT consume what when taking MAOIs, why?

A

tyramine foods (aged foods like cheese & wine); combination can cause HTN crises (life threatening)

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10
Q

What group of antidepressants are typically used in primary care for things other than mental health conditions?

A

Tricyclics

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11
Q

Tricyclic antidepressants are ___________ in the treatment of depression w/high remission rates BUT have ________ of SEs and are highly ____________ in an OD.

A

effective; many; lethal

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12
Q

If rx’ing tricyclic antidepressants to someone w/SI/high risk, how long a rx should you write?

A

1 week

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13
Q

Mechanism of action of tricyclics that is COMPLEX; what does this COMPLEX mechanism cause?

A

blocks transporters site for 5-HRT & NE AND is an antagonist @ histamine, muscarinic Ach, & alpha-adrenergic receptors; which causes many SEs

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14
Q

Uses for tricyclics?

A

depression
anxiety, OCD, PTSD
pain syndromes
nocturnal enuresis

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15
Q

Most common SE of tricyclics? Other SEs?

A

orthostatic hypotension; lightheadedness*
confusion/delirium (especially w/dementia)
anticholinergic effects: sedation, xerostomia, constipation*, urine retention, blurred vision, CONFUSION
many cardiovascular effects: arrythmia
renal failure
n/v, hyperhidrosis
seizures, fine-rapid tremors, twitches of tongue/upper extremities

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16
Q

Although SEs, tricyclics are less likely to cause these compared to SSRIs/SNRIs

A

sexual dysfunction, weight gain, sleep disturbances

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17
Q

Most common reason tricyclic antidepressants are d/c’d?

A

orthostatic hypotension

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18
Q

What year was SSRIs first available in US?

A

1980

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19
Q

Compared to older antidepressants SSRIs have less potential for?

A

lethal OD

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20
Q

Mechanism of SSRIs?

A

stops re-uptake of 5-HRT into synaptic cleft which increased the amount of 5-HRT which increases the ability of post-synaptic neuron to fire -or- increases sensitivity of post synaptic receptors

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21
Q

SSRIs used for?

A

depression
GAD, OCD, PTSD
eating DOs

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22
Q

Most common SEs of SSRIs? Other SEs?

A

decreased ability to orgasm/ejaculate;
agitation, anxiety/panic
sleep disturbances, nighttime rapid muscle movements
n/v, stomach cramps, diarrhea
some QT elongation/multiple interactions

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23
Q

SEs of SSRIs are typically?

A

self-limiting

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24
Q

SSRIs take about ___ wks to take effects though SEs are seen prior; they take _____ wk for full effect

A

2; 4-6

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25
Q

Teach what when first taking an SSRI?

A

making an investment

26
Q

Most effective for what conditions:

A

anxiety r/t depression, panic, phobias, OCD, PTSD
eating DOs

27
Q

Paroxetine has a ______ 1/2 life so if misses ___ to ___ doses may feel _______; when stopping ______ slowly.

A

short; 1 to 2; w/drawl; taper

28
Q

Fluoxetine has a _____ 1/2 life so when d/c’ing it _____ tapers; if starting another antidepressant after d/c’ing you must ______ longer as it stays in system.

A

long; self; wait

29
Q

SNRIs are rx’d for same conditions of SSRIs AND?

A

neuralgia, fibromyalgia, & joint pain

30
Q

When you increase NE what is typically seen?

A

increased energy, focus, concentration and decreased apathy/hypersomnia

31
Q

Mechanism of SNRIs? (DUAL MECHANISM)

A

inhibits reuptake of 5-HRT and NE from synaptic cleft by DUAL MECHANISM, also impacting serotonergic and noradrenergic pain fibers from brain steam to spinal cord which increases signals which decrease or interrupt pain signals from body which decreases pain

32
Q

Conditions SNRIs are most helpful with?

A

depression, fatigue, apathy
cognitive disturbance, impaired concentration, focus/processing issues & working memory issues

33
Q

SSRI or SNRIs more effective w/depression?

A

SNRIs

34
Q

At what dose does venlfaxine effect NE?

A

150mg

35
Q

Dose-dependent risk of venlfaxine? What release can reduce risk? What should patient do?

A

HTN; ER; monitor BP

36
Q

When ETOH/drugs are used w/venlfaxine what has been reported?

A

OD

37
Q

If you stop an SNRI suddenly, what would you expect?

A

w/drawl

38
Q

Mechanism of DUAL-ACTION NDRI?

A

inhibit reuptake of NE and DA in to the presynaptic cleft

39
Q

Uses of NDRI?

A

depression BPAD-depression, ADHD, hyposexual desire DO, smoking cessation

40
Q

Because NDRI’s don’t involve serotonin, what is lessened?

A

SEs

41
Q

Don’t use NDRI w/what?

A

severe anxiety or panic DO, may acerbate

42
Q

NDRI may cause what false positive?

A

amphetamine on drug screen

43
Q

NDRI decreases the seizure threshold so don’t use with people that have a hx of?

A

seizures

44
Q

NDRI has less __________ than other antidepressants.

A

w/drawl

45
Q

Two atypical antidepressants?

A

mirtazapine (Remeron) and vilazodone (Viibryd)

46
Q

Mechanism of mirtazapine (dual-action)?

A

antagonizes A2 adrenergic, H1, and 5-HT receptors which increases 5-HRT and NE

47
Q

Mirtazapine (Remeron) causes significant ___________ and increases ___________.

A

sedation; hunger

48
Q

Uses of mirtazapine (Remeron)? What population is this often used with?

A

insomnia, depression (especially w/weight loss), agitation, co-morbid conditions where weight gain/increased hunger is needed; elderly

49
Q

What two things potentates sedation with mirtazapine (Remeron)?

A

ETOH and benzo’s

50
Q

Mirtazapine does or does not have a lot of interactions w/mother medications?

A

does not

51
Q

Mirtazapine (Remeron) is often combined w/other SSRIs OR venlafaxine to _________________ or counteract ______ ______.

A

augment; side effects

52
Q

Mechanisms (2) of vilazodone (Viibryd)?

A

SPAR - serotonin partial agonist reuptake inhibitor AND partial agonist of certain 5HRT subtype receptors … increasing serotonin

53
Q

Uses of vilazodone (Viibryd)?

A

depression, anxiety, OCD, mixed depression/anxiety DOs

54
Q

Common SEs of vilazodone (Viibryd)?

A

nausea, diarrhea, xerostomia, insomnia, dizziness, sexual dysfunction (though less than other SSRIs/SNRIs

55
Q

You have to take vilazodone (Viibryd) with _______ to ensure adequate ___________ _______________.

A

food (for absorption); drug concentrations

56
Q

Vilazodone (Viibryd) can have an ___________ onset than other antidepressants.

A

earlier

57
Q

Vilazodone (Viibryd) can be used to augment what two SEs of SSRIs/SNRIs?

A

sexual dysfunction and weight gain

58
Q

When d/c’ing vilazodone (Viibryd) what must you do?

A

taper

59
Q

Serotonin syndrome is potentially _______ because there is too much serotonin; this risk is increased when used with ______ _________ .

A

fatal; serotonergic agent

60
Q

Serotonin syndrome __________ through the symptoms of:

A

proceeds; diarrhea, restlessness/extreme agitation, hyper-reflexia, autonomic instability w/rapid changes in VS (tachycardia/HTN), myoclonus, seizures, hyperthermia, uncontrollable shivering, rigidity, delirium, coma, status epilepticus, cardiovascular collapse (DR AHAM SHS-RD-CSC)

61
Q

Tx of serotonin syndrome?

A

d/c agent(s), supportive care, meds (benzos), ventilation, paralyzing agents

Summer 2024 (12 decks)

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